Author Archives: author

I Feel (and See) My Imatinib Working – A Side Effect?

DOI: 10.31038/CST.20261114

Abstract

A previously never reported case of an unusual response to taking the chronic myeloid leukemia (CML) drug imatinib is presented. Tattoos became transiently palpable with each dose taken regardless of brand of imatinib. This did not occur with dasatinib and was not evident when the patient was off therapy. The mechanism which is still uncertain, is discussed in the context of dermatological side effects of imatinib and other CML drugs.

Introduction

I am writing to report a previously undescribed event that occurred with treatment for chronic myeloid leukemia (CML). CML is a myeloproliferative malignancy where patient outcome with the use of tyrosine kinase inhibitor (TKI) therapy, has gone from fatal without a stem cell allograft to what is now essentially a curable or chronic disease with near normal patient survival [1,2]. TKI therapy is associated with side effects/adverse events that vary with the individual drug and may help decide on the safest choice in patients with co-morbidities [3].

Case Report

A 54-year-old white male was diagnosed with asymptomatic chronic phase chronic myeloid leukemia on routine blood examination in 2006. Work up revealed classical Philadelphia chromosome and bcr: : abl1 translocation. He had no co-morbidities and his examination was unremarkable other than an abundance of tattoos of various ages and techniques. He was started on branded imatinib (Gleevec®) and achieved >MR4.5 (<0.0032%IS) by 18 months.

He had no adverse events with treatment but did have a very unusual and unique side effect. Within 30 minutes of taking the imatinib, the black components of his older tattoos became raised and palpable but not painful. This did not occur with the tattoos that were done more recently and not with any other colors. After a couple of hours, this disappeared and recurred with each dose. No changes were made. The patient declined photography but agreed to the report.

After about 6 years on therapy, he elected a treatment-free remission (TFR) attempt but failed at 4 months. As he was on a study to try a drug switch to dasatinib (Sprycel®) and see if a second TFR attempt could be successful [4]. After achieving <0.0032% log reduction for greater than a year, a second TFR attempt failed after 3 months. Interestingly, he had no recurrence of his tattoo issue while off therapy or while on dasatinib. Since he was now going to be on tyrosine kinase inhibitor (TKI) therapy indefinitely after two failed TKI discontinuation attempts, and was off study, he elected to restart imatinib as he really had no quality of life (QoL) issues while taking it. By this time imatinib was standardly available as a generic and his reimbursement would not allow brand. He went on to generic imatinib and again obtained undetectable molecular disease. Surprise, his raised tattoos were also back, confirming some kind of relationship between imatinib and the black ink of his older tattoos.

Discussion and Conclusion

The relationship here is hard to explain. A detailed PubMed® review yield not only no similar cases with imatinib, but none with other drugs. Overlooked or unreported similar cases would be interesting. Imatinib and other TKIs are known to have effects on pigmentation – vitiligo in blacks or lightening of dark skin in South Asians, hyperpigmentation of the temporal regions in Chinese, spotting in whites [5,6]. There is a definite ethnic/racial association that is cosmetically disturbing in many cases but on occasion have been noted to be beneficial in matrimonial choice in South Asians. These changes are not uncomfortable and reverse completely on stopping the imatinib [5,6]. These changes are felt to be due to alternative pathways or targets of the therapy [7,8]. Similar findings have been seen with other oncology medications [9].

What is particularly curious about this case is that the effects are reproducibly transient, time limited and related to older tattoos and oral ingestion of imatinib. They are not progressive or damaging and did not interfere with the efficacy of imatinib. Tattoo ink can cause permanent cutaneous issues [10-13] depending on the makeup. Cutaneous issues with imatinib or TKIs in general are not repeatedly transient. Although immunological issues with imatinib are known [14], they would not come and go like this. My only conclusion is that this is a very mild inflammatory response to imatinib triggering in old-time tattoo inks. A single newly reported side effect can generate thought [15,16]. This may help with better understanding of a process, inspire further thought and increase awareness leading to better safety and improvement in therapy not only of CML but other diseases. On some occasions this can lead to warnings in international guidelines [17]. Or more likely as one wag stated, “Cute but better discussed over cognac” [18].

Disclosure

No IRB was required. Patient consented and in fact wanted to be an author. There are no funding or conflicts to be noted.

References

  1. De Propris MS, Laganà A, Breccia M, De Fabritiis P (2026) Four Decades of Molecular Innovation in Chronic Myeloid Leukemia: From Antisense Targeting to Treatment-Free Remission. Cancers (Basel) [crossref]
  2. Haddad FG, Kantarjian H (2026) Chronic myeloid leukemia: incorporation of recent advances into current treatment algorithms. Blood Cancer J. [crossref]
  3. Lipton JH, Brümmendorf TH, Gambacorti-Passerini C, Garcia-Gutiérrez V, Deininger MW, Cortes JE (2022) Long-term safety review of tyrosine kinase inhibitors in chronic myeloid leukemia – What to look for when treatment-free remission is not an option. Blood Rev. [crossref]
  4. Perusini MA, Novitzky-Basso I, Atenafu EG, Forrest D, Bence-Bruckler I, Savoie L, et al. (2023) Final report of TKI discontinuation trial with dasatinib for the second attempt of treatment-free remission after failing the first attempt with imatinib: Treatment-free Remission Accomplished by Dasatinib (TRAD) study. Br J Haematol. [crossref]
  5. Dervis E, Ayer M, Akin Belli A, Barut SG (2016) Cutaneous adverse reactions of imatinib therapy in patients with chronic myeloid leukemia: A six-year follow up. Eur J Dermatol. [crossref]
  6. Di Tullio F, Mandel VD, Scotti R, Padalino C, Pellacani G (2018) Imatinib-induced diffuse hyperpigmentation of the oral mucosa, the skin, and the nails in a patient affected by chronic myeloid leukemia: report of a case and review of the literature. Int J Dermatol. [crossref]
  7. Nykaza I, Kwong B, Gordon A.J (2026) Cutaneous Toxicities of Small Molecules in Targeted Cancer Therapy Part I – Mechanisms of Toxicity. Am Acad Dermatol. [crossref]
  8. Macdonald JB, Macdonald B, Golitz LE, LoRusso P, Sekulic A.J (2015) Cutaneous adverse effects of targeted therapies: Part I: Inhibitors of the cellular membrane. Am Acad Dermatol. [crossref]
  9. Dai J, Belum VR, Wu S, Sibaud V, Lacouture ME (2017) Pigmentary changes in patients treated with targeted anticancer agents: A systematic review and meta-analysis. J Am Acad Dermatol. [crossref]
  10. Weiß KT, Schreiver I, Siewert K, Luch A, Haslböck B, Berneburg M et al. (2021) Tattoos – more than just colored skin? Searching for tattoo allergens. Dtsch Dermatol Ges. [crossref]
  11. Dodig S, Čepelak-Dodig D, Gretić D, Čepelak I (2024) Tattooing: immediate and long-term adverse reactions and complications. Arh Hig Rada Toksikol. [crossref]
  12. Giulbudagian M, Battisini B, Bäumler W, Blass Rico AM, Bocca B, Brungs C, et al. (2024) Lessons learned in a decade: Medical-toxicological view of tattooing. Eur Acad Dermatol Venereol. [crossref]
  13. Chalarca-Cañas D, Caviedes-Cleves MA, Correa-Londoño LA, Ospina-Gómez JP, Velásquez-Lopera MM (2024) Tattoos: risks and complications, clinical and histopathological approach. An Bras Dermatol. [crossref]
  14. Tiffany K. Ybarra, Ryan S. Sathianathen, Rohaum Hamidi, Nobuko Hijiya, Neil P. Shah et al. (2026) Immunological mechanisms and therapeutic advances in chronic myeloid leukemia. Leukemia. [crossref]
  15. Lipton NJ, Lipton JH (2022) Making the case for the case report – informing physicians of intracranial hypertension as an adverse event in tyrosine kinase inhibitor treated chronic myeloid leukemia patients. Leuk Lymphoma. [crossref]
  16. Alshehry NF, Kortan P, Lipton JH (2014) Imatinib-induced gastric antral vascular ectasia in a patient with chronic myeloid leukemia. Clin Case Rep. [crossref]
  17. Apperley JF, Milojkovic D, Cross NCP, Hjorth-Hansen H, Hochhaus A, Kantarjian H, Lipton JH, et al. (2025) 2025 European LeukemiaNet recommendations for the management of chronic myeloid leukemia. Leukemia. [crossref]
  18. Undisclosed Reviewer (2026) Leukemia.

Supercritical Enrichment of Boron and Cesium in Pegmatites Related to the Tin Mineralization of Ehrenfriedersdorf/Germany

DOI: 10.31038/GEMS.2026884

Abstract

The Ehrenfriedersdorf Variscan tin deposit contains pegmatite-related melt inclusions enriched in volatile and incompatible elements, including boron and cesium. This study examines the relationship among H2O, B2O3, and Cs to evaluate whether their enrichment records the influence of supercritical fluids and/or melts. We homogenized previously characterized melt inclusions and analyzed them for water, boron, cesium, and associated elements, then evaluated the results using polynomial, Lorendian, and three-dimensional compositional representations. Boron increases nonlinearly with water according to a polynomial relationship, whereas cesium displays a pronounced Lorendian distribution in the H O-Cs projection (R2=0.968), centered at approximately 26.0% H2O, with a width of 4.45% H2O, an offset of 0.48% Cs, and a height of 2.65% Cs. The projected Cs-B2O3 relationship is sigmoidal, indicating accelerated cesium enrichment at approximately 4% B2O3 and 0.5% Cs. These relationships suggest that boron and cesium became strongly concentrated during the development of volatile-rich, highly evolved residual melts and fluids associated with tin mineralization. Because binary projections may obscure the geometry of the compositional field, correction using the solvus curve is required when interpreting the complete H2O-B2O3-Cs system. The results support a model in which supercritical fluids and/or melts contributed to the transport and concentration of incompatible elements during late-stage magmatic differentiation. Boron and cesium may therefore serve as indicators of advanced pegmatitic evolution and transitions among silicate melt, aqueous fluid, and supercritical regimes, although further three-dimensional, experimental, and comparative studies are required.

Keywords

Supercritical fluids and melts, Boron enrichment, Cesium enrichment, Ehrenfriedersdorf tin deposit, Pegmatitic evolution, Melt inclusions, H2O-B2O3-Cs system, Lorentzian distribution, Volatile-rich residual melts, Solvus and critical point

Introduction

The author and coauthors [1-3] demonstrated that, in the Variscan tin deposit Ehrenfriedersdorf and similar deposits, enrichment of several elements besides Sn is directly related to supercritical fluids (SCF) and/or melts (SCM). Earlier analytical projections into the H2O-element plane were a first approximation; Thomas (2026b) [4] showed that a three-dimensional representation is more accurate. Here, the H2O-B2O3-Cs system illustrates the general behavior of such an element triple. In granitic rocks, the Clarke values of Cs and B are 5 and 15 ppm, respectively [5]. Cesium is a lithophile alkali metal found in minerals, residual solutions, and pegmatites; it also forms minerals such as pollucite and ramanite-Cs [6]. Boron occurs in the Earth’s crust as boric acid [H3BO3] and borates and is important in ore-forming processes. At relatively high concentrations, boron reduces the viscosity of silicate melts.

Sample Material and Methods

The sample material and methods for homogenization, water, boron, and element determination are given in Thomas (2000) [7], (2002) [8] and Thomas et al. (2003) [9] and 2006 [10]); the homogenization methods are presented in the predecessor publications [2,3] and the citations therein. Figure 1 shows a schematic of melt-inclusion behavior of water-rich silicate-melt systems during heating. The first observation about it dates to a presentation at the ECROFI XV meeting in 1999 [11]. A more detailed description and discussion is in Thomas et al. 2000) [12].

Figure 1: Schematic behavior of melt inclusions with different water content after homogenization at different temperatures. CP is the critical point of the resulting solvus curve (red).

Note that the inclusions shown in Figure 1 are immediately after quenching in a fully homogenized state, proved by the hydrothermal rapid-quench method or, in the same cases, the quenching in liquid nitrogen. Due to the high water content in the inclusions, they heterogenized after some hours like the schematic types shown in Figure 1.

Results

Figures 2 to 4 show the key results, which are combined into Figure 5 as a room plot, demonstrating that the triple H2O-B2O3-Cs are strongly related.

Figure 2 presents the simplified water-boron plot for the silicate melts. The following equation represents the boron curve (X=H2O; Y=B2O3):

Figure 2: Water versus boron concentration in melt inclusions on the Ehrenfriedersdorf pegmatite-related quartz. This plot represents the system’s X-Y plane.

Y=1.45255 + 0.19272 ∗ X – 0.00348 ∗ X2 – 6.38965 ∗ 10-7 ∗ X3 (1)

Figure 3 shows the concentration of Cs versus H2O and shows, in a good approximation, a Lorentzian distribution. The H2O-Cs plane projected Lorentzian data are in Table 1.

Figure 3: Lorentzian distribution of Cs versus the water content of silicate melt inclusions.

Figure 4 shows the projection of the Cs content of silicate melt inclusions in the B2O3-Cs-plane.

Figure 4: Sigmoidal Cs-B2O3 correlation in the B2O3-Cs plane.

Figure 4 shows clearly that the Lorentzian distribution of Cs begins at about 0.5% Cs, corresponding to the offset (see Table 1) and a boron concentration of about 4% B2O3. Figure 5 shows the room diagram of all three phases: H2O-B2O3-Cs, showing that all three components are well correlated, and the maximum of the Cs concentration is related to the critical point of the water-boron solvus.

Table 1: Results of the Lorentzian distribution (projection to the H2O-Cs plane (R2=0.968).

Area

Center Width Offset

Height

18.53 26.0% H2O 4.45% H2O 0.48% Cs 2.65% Cs

In the CP region, by contrast, the greatest differences occur. That could indicate that the composition there is particularly sensitive to changes in the thermodynamic conditions or phase composition.

Because the Lorentzian plot of Cs vs. H2O (Figure 3) is a projection on the H2O-Cs plane, some of the data in Table 1 must be corrected using the arc segment of the solvus curve. However, according to Figure 4, the Lorentzian curve starts, in a first approximation, at a B2O3 concentration of about 4%; we can use the uncorrected data in Table 1.

Figure 5: Room diagram H2O-B2O3-Cs. CP is the critical point.

Discussion

The results demonstrate that boron and cesium enrichment in the Ehrenfriedersdorf pegmatite-related melt inclusions is closely associated with increasing water content and, consequently, with the evolution of a volatile-rich silicate melt. The boron-water relationship follows a polynomial curve rather than a simple linear trend, indicating that boron incorporation changes as the melt becomes progressively enriched in H2O. This behavior is consistent with boron’s role as a fluxing component that can modify melt structure, reduce viscosity, and increase the capacity of residual melts to transport metals and other incompatible elements. The cesium data provide an additional indication of strong enrichment during late-stage magmatic evolution. The Lorentzian distribution of Cs versus H2O, with a coefficient of determination of R2=0.968, describes a pronounced concentration maximum near 26.0% H2O. The fitted width of 4.45% H2O, offset of 0.48% Cs, and height of 2.65% Cs indicate that cesium enrichment was not gradual throughout the entire compositional range. Instead, it became especially significant after the system reached a threshold represented by the offset. In geological terms, this threshold may mark the development of a highly evolved, water-rich fluid or melt domain in which Cs was preferentially concentrated. The projected Cs-B2O3 relationship further supports this interpretation. The sigmoidal correlation suggests that cesium enrichment accelerated once the boron concentration reached approximately 4% B2O3, corresponding to the beginning of the Lorentzian increase at about 0.5% Cs. Boron and cesium therefore appear to be linked through the progressive development of a volatile-rich residual melt rather than behaving as independent components. Their association is significant because both elements can indicate advanced fractionation and conditions favorable for concentrating and transporting tin in granite-pegmatitic systems.

The three-dimensional H2O-B2O3-Cs representation is important because two-dimensional projections can conceal the geometry of the underlying compositional field. In particular, the Lorentzian parameters obtained from the H2O-Cs projection cannot necessarily be applied directly to the complete three-component system. Correction using the arc segment of the solvus curve is therefore required. This observation emphasizes that apparent correlations in projected plots may partly reflect the projection of a curved three-dimensional surface, and it provides a methodological reason for treating binary diagrams as approximations rather than complete descriptions of melt evolution. These findings broaden the interpretation of the Ehrenfriedersdorf deposit by showing that Cs and B enrichment is not merely a chemical peculiarity of individual inclusions. Instead, it records interactions among volatile enrichment, melt structure, and phase relations during the late stages of magmatic differentiation. The results are compatible with a model in which supercritical fluids and/or melts contribute to the redistribution and concentration of incompatible elements, including components relevant to tin mineralization. They also suggest that B and Cs concentrations may be useful geochemical indicators for recognizing highly evolved pegmatitic environments and for tracing transitions between silicate melt, aqueous fluid, and supercritical regimes. Several limitations should nevertheless be considered. The boron relationship is based on a simplified projection, and interpreting the cesium distribution depends on the quality and representativeness of the melt-inclusion data. A high R2 value shows that the Lorentzian function fits the available projected data well, but it does not, by itself, establish a unique genetic mechanism. The effects of pressure, temperature, inclusion re-equilibration, post-entrapment modification, analytical uncertainty, and possible loss or redistribution of volatile components must also be evaluated. In addition, the cited Clarke values provide a useful crustal reference but do not represent the composition of the specific parental magma or the full range of processes affecting the deposit. We already know that the Lorentzian element distribution curves can vary from place to place in the Sauberg deposit. At some places, the Cs concentration in the critical region can reach 8.88% (indicated by the appearance of Ramanite-(Cs) in melt inclusions trapped near the critical point of the evolved H2O-silicate system; see Thomas and Rericha, 2023 [13].

For this case, we present the data in Table 2. Further work using calibrated three-dimensional phase relations, independent fluid-inclusion constraints, and broader sampling would help test whether the observed thresholds and correlations are characteristic of Ehrenfriedersdorf alone or apply to comparable Variscan tin-pegmatite systems. First results on the Variscan Zinnwald tin deposits point to this possibility. However, boron is in the E-Erzgebirge only weak enriched. Here, fluorine has greater meaning. Boron increases westward and reaches its maximum around Ehrenfriedersdorf.

Table 2: Results of the Lorentzian distribution (projection to the H2O-Cs plane (R2=0.994) for extreme Cs- and H2O-rich silicate melts.

Area

Center Width Offset

Height

13.309 30.0% H2O 0.9% H2O 5.36% Cs 8.88% Cs

Figure 6 shows a boron-rich silicate melt drop in granite quartz from Ehrenfriedersdorf. Thomas and Rericha (2023) [13] provide more information on boron in melt inclusions in granite quartz.

Figure 6: BSE image of a B-rich melt inclusion in granite quartz from Ehrenfriedersdorf. The silicate melt contains 10.6% B2O3.

Conclusions

In this contribution, together with the precede work [1-4,14], we see clearly that a row of elements like Li, Be, B, P, Cl, Zn, As, Sn, Sb, Cs, Ta, W are highly enriched and show a general Lorentzian distribution which cannot be explained with a conventional enrichment process. The Lorentzian distribution clearly indicates a strong or moderate input of water and some critical elements via supercritical fluids (SCF) and/or supercritical melts (SCM) from mantle regions. Indicators are the sporadic appearance of diamond, lonsdaleite, moissanite, coesite, cristobalite X-I, α- and γ-AlB12, as well as the orthorhombic cassiterites of the CaCl2– and cotunnite-types (e.g., Thomas, 2024) [15]. According to Schröcke’s Figures C-D (1954) [16,17], the Sauberg mine (e.g., Prinzler-West) contains many pegmatites and pegmatite-like bodies that cannot be explained by water from the surrounding granites. These figures also show that the mineral-forming media are not homogeneous; the source is non-uniform and varies strongly in composition and consistency. Swarms of SCF and SCM of different thickness and power come from different depths. At the transition between the supercritical, critical, and subcritical stages, processes occur which cannot be reduced to well-known pieces.

Acknowledgment

The contribution is dedicated to Dr. Adolf Rericha from Falkensee/ Germany, who, despite his health problems, was always open to discussions.

References

  1. Thomas R (2026a) Attempt to interpret the exceptional element enrichment and distribution in pegmatite related to the Variscan tin deposit at the example of Ehrenfriedersdorf, Geol Earth Mar Sci 8: 1-8.
  2. Thomas R, Davidson P, Appel K (2019) The enhanced element enrichment in the supercritical states of granite-pegmatite systems. Acta Geochim 38: 335-349.
  3. Thomas R, Davidson P, Rericha A, Voznyak DK (2022) Water-rich melt inclusions as “frozen” samples of the supercritical state in granites and pegmatites reveal extreme element enrichment resulting under non-equilibrium Mineral J (Ukraine) 44: 3-15.
  4. Thomas R (2026b) Lorentzian distribution of Sn in the Ehrenfriedersdorf Geol Earth Mar Sci 8: 1-4.
  5. Rösler HJ, Lange H (1975) Geochemische VEB Deutscher Verlag für Grundstoffindustrie Leipzig. Pg: 675.
  6. Thomas R, Davidson P, Hahn A (2008) Ramanite-(Cs) and ramanite-(Pb): new cesium and rubidium pentaborate tetrahydrate minerals identified with Raman American Mineralogist 93: 1034-1042.
  7. Thomas R, Webster JD, Heinrich W (2000) Melt inclusions in pegmatite quartz: complete miscibility between silicate melts and hydrous fluids at low Contrib Mineral Petrol 139: 394-401.
  8. Thomas R (2002) Determination of the H3BO3 concentration in fluid and melt inclusions in granite pegmatites by laser Raman microprobe American Mineralogist 87: 56-68.
  9. Thomas R, Förster H-J, Heinrich W (2003) The behavior of boron in a peralumonous granote-pegmatite system and associated hydrothermal solutions: a melt and fluid-inclusion study. Contrib Mineral Petrol 144: 457-472.
  10. Thomas R, Kamenetsky VS, Davidson P (2006) Laser Raman spectroscopic measurements of water in unexposed glass inclusions. Am Mineralogist 91: 467-470.
  11. Thomas R, Webster JD, Heinrich W (1999) Melt inclusions in pegmatite quartz: Complete miscibility between silicate melts and hydrous Terra Nostra 99: 305-307.
  12. Thomas R (2000) Determination of water contents of granite melt inclusions by confocal laser Raman microprobe American Mineralogist 85: 868-872.
  13. Thomas R, Rericha A (2023) Extreme enrichment of Cs during the crystallization of the Ehrenfriedersdorf pegmatite melt related ti the Variscan tin mineralization. Geol Earth Mar Sci 5: 1-4.
  14. Thomas R (2025) Interpretation of the Lorentzian distribution of tin in the Variscan Ehrenfriedersdorf deposit, Geol Earth Mar Sci 7: 1-5.
  15. Thomas R (2024) The CaCl2-to rutile phase transition in SnO2 from high to low pressure in Geol Earth Mar Sci 6: 1-4.
  16. Schröcke H (1954) Zur Paragenese erzgebirgischer Zinnlagerstätten. Neues Mineral. Abh 87: 33-109.
  17. Thomas R (2023a) Unusual cassiterite mineralization related to the Variscan tin mineralization of the Ehrenfriedersdorf deposit, Aspects Min Miner Sci 11: 1233-1236.

Diamond-like Carbon (DLC) in Herderite from Namibia

DOI: 10.31038/GEMS.2026883

Abstract

Raman spectroscopy offers a nondestructive approach to differentiate and characterize sp2– and sp3-bonded carbon. In sp2-rich materials, the defect-activated D band generally appears near 1350 cm-1, whereas the graphite G band occurs near 1580 cm-1. Enhanced graphitic ordering may additionally generate a second-order 2D band near 2700 cm-1. Diamond exhibits a characteristic first-order Raman line at approximately 1332 cm-1, corresponding to the zone-center optical phonons of its sp3-bonded lattice. Band position, linewidth, and relative intensity provide valuable information on bonding configuration, crystallinity, defects, and structural disorder. Mechanical stress shifts Raman bands by altering lattice strain; compressive and tensile stresses generally induce opposite frequency changes, although the precise response depends on crystallographic orientation and bonding structure. Temperature modifies the spectra through phonon anharmonicity and thermal expansion, commonly producing redshift and linewidth broadening as temperature increases. Accordingly, analysis of peak positions, linewidths, and intensity ratios supports assessment of carbon-phase composition, structural quality, stress state, and thermal behavior. Prerequisites are strong reducing conditions.

Keywords

Raman spectroscopy, DLC in herderite, sp2– bonded carbon, sp3– bonded carbon, D band, G band, Reducing conditions, Supercritical fluids

Introduction

During Raman studies of herderite and hydroxylherderite samples, we found that many herderite samples from Namibia contain numerous small black flats (some micrometer thick) over wide areas. Raman studies show that these black, mostly irregularly shaped areas correspond to diamond-like carbon (DLC), but not in the sense of Irmer and Dorner-Reisel (2005) [1]. In industrial applications, DLC is a class of amorphous carbon materials that contain significant amounts of sp³-hybridized carbon atoms, giving it diamond-like hardness, while also incorporating sp² carbon for flexibility and lubricity. The purest form, tetrahedral amorphous carbon (ta-C), consists almost entirely of sp³ bonds, whereas other forms may include hydrogen, different metals, or graphitic carbon depending on the production process. In this context, DLC refers to a carbon-based coating with diamond-like properties, such as high hardness, low friction, and good wear and chemical resistance. A typical Raman spectrum of diamond-like carbon (DLC) shows two broad bands: the D band around 1350 cm⁻¹ associated with disorder and defects in sp²-bonded carbon. The G band is around 1580 cm⁻¹ associated with the stretching of sp² carbon bonds. Diamond-rich material may additionally show a sharp diamond peak near 1332 cm⁻¹, which can overlap with the DLC D band. Because crystallization in nature is fast and more chaotic, the black areas are not expected to occupy very large, undisturbed areas, as in the technique. However, the underlying processes are probably the same. In topaz from the Klein Spitzkoppe, Namibia, similar black areas are also present. They are generally rarer. However, a large part consists of moissanite [SiC], and a smaller part consists of DLC.

Sample and Methods

Herderite [CaBe(PO4]F from Namibia, Erongo Mountains, farm Davib-Ost

Cairncross and Bahmann (2006) [2,3] described the mineral as hydroxylherderite. Thomas (2026) [4] identified the material as herderite using Raman spectroscopy. However, there are water-clear, small areas with a tendency toward hydroxylherderite, particularly at the crystal rims. The herderite sample (about 2 x 1.5 x 0.5 cm) comes from miarolitic cavities in the Erongo Mountains. According to Cairncross and Bahmann (2006) [2,3], herderite is associated with small (less than 2 cm) schorl crystals, muscovite, and orthoclase. A single pocket opened in July 2003 yielded a small amount of the herderite material. Most specimens are thumbnail- to small-cabinet-size clusters composed of individual crystals measuring less than 1 cm. The largest crystal found thus far measures 6.2 cm and is studded by small schorl crystals.

Two different colors of hydroxyl-herderite were described from Erongo: pale green and off-white. X-ray diffraction analysis of crystals of both colors at the University of Johannesburg revealed that they are the same species; the cause of the color difference is not known. While working on herderite samples from the Erongo, the author was surprised to find that many crystals (the white type) contain relatively large DLC aggregates. Figures 1 to 4 show such aggregates as examples. Single diamonds with the same characteristic as the large DLC areas are also present.

Microscopy and Raman Spectroscopy

All microscopic and Raman spectroscopic investigations were conducted using a petrographic polarization microscope (BX 43) equipped with a rotating stage and coupled to an EnSpectr Raman spectrometer R532 (Enhanced Spectrometry, Inc., Mountain View, CA, USA). Measurements were performed in both reflection and transmission modes. All measurements were carried out with the EnSpectr R532. Measurements covered the spectral range from 0 to 4000 cm⁻¹ and were conducted with a single-mode 532 nm laser operating at a maximum output of 50 mW. Analytical settings included a 20 µm entrance aperture, a holographic grating of 1800 g mm⁻¹, and a spectral resolution of approximately 4 cm⁻¹ across the measured range. For most analyses, we used a long-working-distance Olympus LMPlanFL 100× objective, which allows a measuring field about 1 µm in diameter on the sample. Laser power at the sample surface was continuously adjustable down to 0.02 mW. Higher powers, up to 50 mW, were used only for overview measurements. For measurements over the range 0–4000 cm-1, we generally set the laser power to 30 mW at the sample. For minerals located deep under the polished surface, we generally also used 30 mW laser power; however, we used a significantly longer measurement time. We calibrated Raman-band positions before and after each measurement series using the Si band of a semiconductor-grade single-crystal silicon chip. Based on 20 repeated measurements, run-to-run reproducibility was ± 0.2 cm⁻¹ for silicon (520.2 ± 0.2 cm⁻¹) in the range from 0 to 2000 cm⁻¹. As a second reference, we used a water-clear diamond crystal from Brazil. We measured the first-order diamond line at 1333.4 ± 0.6 cm⁻¹, with a FWHM of 5.1 ± 0.1 cm⁻¹ (see also Solin and Ramdas, 1970) [5]. FWHM is the full width at half maximum. However, scrutiny of the Brazil diamond shows small heterogeneities (different ¹³C content).

Results

During the determination of the fluorine content of hydroxylherderite/herderite [4], we observed many irregular black areas (for example, Figures 1 to 4). Examination with Raman spectroscopy indicated diamond-like carbon (DLC). Figure 5 shows such a Raman spectrum from DLC. Crystalline diamond and graphite show very low FWHM values (~5 cm-1), opposite to DLC.

Figure 1: Herderite (white) fragment from a miarolitic cavity from Namibia. The black parts are DLC-like material. Light brown parts are hydroxylherderite.

Figure 2: Herderite (Hrd) with DLC and small hydroxylherderite (h-Hrd) from Namibia.

Figure 3: Diamond-like carbon (DLC) aggregate in herderite (Hrd) from Namibia.

Figure 4: DLC in herderite (Hrd) from Namibia.

Figure 5a: Raman spectrum of diamond-like carbon (DLC) in herderite from Namibia. Hrd – herderite from the matrix.

This spectrum (Figure 5b) shows a broad diamond line at 1328.2 cm-1; broad carbon D-lines at 1357.1 and 1379.7 cm-1 with FWHM = 28.3 and 46.3 cm-1; and a broad G-band at about 1585 cm-1. Figure 5b is an example of the decomposition of the first-order region of the Raman spectrum of DLC. The diamond band at 1328.2 cm-1 has a FWHM of 46.9 cm-1, and the G-band has two components at 1567.3 and 1594.1 cm-1 with FWHMs of 65.2 and 53.2 cm-1, respectively.

Figure 5b: Decomposition of a DLC Raman spectrum. D1 at about 1350 cm-1 is typical for poorly ordered carbons. The same applies to the D2 and D3 bands. The G-band, or graphite band, occurs at 1580 cm-1. Laser heating causes a partial shift downward to 1567 cm-1 [6]. According to Zaitsev (2001) [7], the band around 1567 cm-1 is typical for low-quality CVD diamond films.

To confirm whether the black material is real DCL, we recorded Raman spectra in the first-order range using different laser powers (5 to 50 mW). We found a “plateau-like” range (15-35 mW) with a more or less identical position of the diamond line at ≤ 1324 cm-1 (see Figure 6). Across the entire laser-energy range, the diamond-line position forms a sigmoid curve, probably produced by the interaction of sp2 and sp3 species in different carbon phases diamond, carbon, amorphous carbon).

Figure 6: Shift of the diamond line of first order with the laser power on the DLC in the herderite sample from Namibia.

The sigmoid trend shows that the position of the first-order diamond line depends nonlinearly on the applied laser power. The line position changes most strongly within an intermediate power range and tends toward a limiting value at higher power, indicating a saturation-like response. The power-dependent shift of the first-order diamond Raman line is attributed primarily to laser-induced heating. sp²- rich regions may enhance laser absorption and facilitate heat transfer to the diamond phase. The sigmoid response suggests a nonlinear, saturating thermal process, possibly caused by changes in absorption and heat dissipation as the local temperature increases. Further temperature calibration or comparison with samples having different sp² contents would be required to confirm this mechanism. Natural diamond crystals (e.g., the reference diamond from Brazil) show a nearby linear course from 4.3 to 50 mW: 1333.4 ± 0.6 cm-1, differ strongly from DLC in herderite from Namibia. The lonsdaleite-like carbon from fluorite from Zinnwald [8] shows a clear linear decline of the 1312 cm-1 line from 4.3 to 1296.8 at 50 mW laser power on the sample. Figure 7 shows the Raman shift of the first-order diamond line as a function of the used laser energy [9,10].

Figure 7: Raman shift (cm-1) versus laser (532 nm) energy (mW) obtained using the Brazil reference diamond. The sigmoid (Boltzmann) fit starts at 1302.5 cm-1, 0.8 mW and ends at 1333.6 cm-1 and 50 mW. The correlation coefficient is R2 = 0.99914.

Discussion

Raman spectroscopy responds differently to sp2– and sp3-bonded carbon: sp2 carbon produces strong, broad Raman features. The G band appears near 1580 cm-1 and is associated with in-plane stretching of sp2 bonds. The D band appears near 1350 cm-1 and indicates disorder, defects, or finite-sized sp2 clusters. The sp3 carbon in crystalline diamond. produces a sharp first-order Raman line near 1332 cm-1. In amorphous or DLC materials, sp3 bonding usually does not produce a distinct peak; instead, it affects the position, width, and intensity of the broad D and G bands. For DLC, the Raman spectrum is therefore mainly used to analyze the sp2 network. The ID/IG intensity ratio, along with the G-band position and width, can indicate changes in disorder and sp2/sp3 bonding. However, Raman alone does not provide a fully reliable quantitative sp3 concentration; techniques such as XPS, EELS, or NEXAFS are often used to confirm it [9,10].

Conclusion

In conclusion, Raman spectroscopy effectively distinguishes sp2-and sp3-bonded carbon by identifying their characteristic vibration features. In diamond, the dominant signature is a sharp line near 1332 cm-1, corresponding to the ordered sp3-bonded crystal lattice. DLC, by contrast, generally exhibits broader D and G bands: the D band is associated with disordered or defect-rich carbon structures, while the G band reflects graphitic sp2 binding. Temperature can broaden, shift, or reduce the intensity of these features by increasing phonon interactions and promoting structural rearrangement, whereas Raman spectroscopy provides a sensitive means of distinguishing sp2-and sp3-bonded carbon and evaluating their structural environments. In sp2-rich carbon, the characteristic G band, typically near 1580 cm-1, arises from in-plane bond-stretching vibrations of graphitic carbon, whereas the defect-activated D-band, commonly near 1350 cm-1, reflects disorder, finite crystallite size, and defects. In sp3-bonded diamond, the Raman spectrum is dominated by the first-order line near 1332 cm-1, corresponding to the zone-center optical phonon. This line is highly responsive to external conditions: increasing temperature generally causes phonon softening, producing a shift toward lower wavenumber and often linewidth broadening, while compressive stress shifts the line upward and tensile stress shifts it downward. The magnitude and direction of the shift therefore provide information about the thermal and mechanical state of the diamond lattice. Together, the relative intensities and positions of the sp2 G and D bands and the diamond Raman line enable assessment of bonding configuration, structural disorder, temperature, and stress in carbon-based materials. Mechanical stress commonly shifts the Raman peaks and may alter their widths. Thus, the position, intensity, and shape of the D, G, and diamond-related bands provide a practical means of evaluating bonding configuration, disorder, crystallinity, and environmental effects in carbon-based materials. The presence of DLC in pegmatitic herderite suggests that strong reducing conditions are a prerequisite for its formation. The input of supercritical fluids is therefore probable.

References

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  2. Cairncross B, Bahmann U (2006) Famous mineral localities: the Erongo Mountains The Mineralogical Record 37: 361-470.
  3. Cairncross B (2005) Klein Spitzkoppe The Mineralogical Record 36: 317-335.
  4. Thomas R (2026) Remarks on herderite [CaBe(PO4)F] and hydroxylherderite [CaBe(PO4)(OH)]. Geology, Earth and Marine Sciences 8: 1-4.
  5. Solin SA, Ramdas AK (1970) Raman spectrum of Physical Review B 1: 1687-1698.
  6. Beyssac O, Goffe C, Chopin C, Rouzaud JN (2002) Raman spectra of carbonaceous material in metasediments: a new geothermometer. Metamorphic Geol 20: 859-871.
  7. Zaitsev AM (2001) Optical Properties of Diamond – A Data Berlin, Heidelberg, New York. Springer. Pg: 502.
  8. Thomas R, Trinkler M (2024) Monocrystalline lonsdaleite in REE-rich fluorite from Sadisdorf and Zinnwald/E-Erzgebirge, GEMS 6: 1-5.
  9. Lafuente B, Downs RT, Yang H, Stone N (2015) The power of databases: the RRUFF In: Armbruster T, Danisi RM (eds). Highlights in Mineralogical Crystallography. Berlin, Germany, Walter de Gruyter: 1-30.
  10. Thomas R (1982) Ergebnisse der thermobarogeochemischen Untersuchungen an Flüssigkeitseinschlüssen in Mineralen der postmagmatischen Zinn-Wolfram. Mineralisation der Freiberger Forschungshefte FFH C 370. Pg: 85.

Simplifying Neuroanatomical Diagnosis in Dogs and Cats Based Twelve Functional Regions and Associated Clinical Signs

DOI: 10.31038/IJVB.20261015

Abstract

Neuroanatomical diagnosis is a crucial clinical assessment in animals with neurological disease. Given the complexity of the nervous system, however, it can be challenging for the primary care practitioner to recall and clinically integrate the plethora of neuroanatomical structures and their functions to form this important assessment. While it is sometimes necessary to have advanced knowledge of how discrete neuroanatomical elements of the nervous system as isolated entities, it is pragmatically important for the practicing clinician to have a “functional” understanding of how discrete neuroanatomical structures are integrated, interrelated, and coordinated into a functional unit. These functional units can then be used for neuroanatomical localization. In this review the important functional regions of the nervous system that are responsible for animals performing various normal functions will be discussed in the context of making a neuroanatomical diagnosis. Concurrently, classic clinical abnormalities associated with dysfunction of these functional units will be provided. Using this functional system, the clinician can make practical decisions about disease location with the nervous system. With accurate neuroanatomical diagnosis, the clinician can subsequently formulate an accurate differential diagnosis list followed by an appropriate diagnostic plan to ultimately identify the primary neurologic disease process.

Keywords

Clinical neurology, Clinical evaluation, Neuroanatomical diagnosis, Clinical signs

Introduction

During performance of the neurological examination in animals, abnormalities of nervous system function are identified and categorized. Each clinical abnormality provides a “clue” to the location of the dysfunction within nervous system. Fundamentally, an understanding of the neuroanatomic structures that are responsible for a particular neurologic examination finding are necessary when attempting to determine the location of the lesion resulting in the neurologic dysfunction. Most importantly, however, the practicing clinician needs to understand how these neuroanatomical structures coordinate as functional units to create clinically detectable outputs. Abnormalities found during the neurologic examination help to determine 1) that an abnormality exists in the nervous system and 2) the location of this abnormality within the nervous system. While the neuroanatomical structures are foundational, it is most important that the functional outputs from these anatomical structures which are evaluated clinically are identified and collated.

The determination of where the nervous system is abnormal is referred to as the neuroanatomic diagnosis. This assessment is the fundamental process that underpins clinical neurologic assessment in animals [1-13]. Determining the location of any abnormality in the nervous system is arguably the most important aspect of appropriate clinical evaluation of animals with neurologic disease. Only after determining the location of any abnormality can an appropriate differential diagnosis of disease processes affecting that region of the nervous system be logically generated. Once a list of possible disease processes is formulated, appropriate diagnostic tests to establish the specific disease processes can logically be decided upon, performed, and interpreted in this context.

Recalling specific locations of discrete neuroanatomical structures in the day-to-day clinical evaluations of affected patients, however, can be challenging. This difficulty in making neuroanatomical connections may be a component of a known neurophobia among medical professionals [14-17]. While the nervous system is exceedingly complex, the practicing clinician ultimately identifies the functional outputs of the nervous system through clinically detectable signs such as postures and movements. The astute clinician, then, needs to have a “functional” understanding of how the nervous system is organized and integrated to subsequently understand how disease manifests in clinical dysfunction. While it is sometimes necessary to possess knowledge of how discrete neuroanatomical elements of the nervous system function as isolated entities, it is most important for the practicing clinician to have an operational understanding of how these separate neuroanatomical entities are integrated, interrelated, and interacted as a functional unit. These functional units are interconnected forming functional relationships which are responsible for clinically detectable body functions. An understanding of neurologic functionality promotes an understanding of how information is transmitted or “flows” back and forth between structures within the nervous system and expressed as clinically observable activities. When abnormalities exist within the nervous system, these functional relationships are disrupted or disconnected resulting in clinical signs as evidence of this dysfunction.

Diseases involving individual functional units within the nervous system tend to result in a “classic” set of corresponding clinical signs [1-13]. One, some, or all these classic clinical signs may be present in any individual animal. For this discussion, disease may also be referred to as a lesion (a pathologic or traumatic discontinuity of tissue or loss of function of a part) or an abnormality (any deviation from or interruption of the normal structure or function of a body part). These terms are not to be taken to designate any specific disease process or etiology. Based on regions with similar functionality and the associated clinical signs, nervous system abnormalities can be pragmatically localized into one of twelve main anatomical/functional regions (Figure 1).

Figure 1: Image depicting the 12 Functional Regions (Zones) that can be used for neuroanatomical localization in dogs and cats.

For simplicity, these anatomical/functional regions will be referred to as “Zones” for this review. While attempting to be as specific as possible with a neuroanatomical diagnosis, a practical initial goal for most clinicians is to determine if disease within the nervous system is present in either the intracranial region (and associated cranial nerves), spinal cord segments, or the peripheral/neuromuscular junction/muscle complex. Answering a series of prompted questions is helpful in determining the neuroanatomical diagnosis during a clinical evaluation (Table 1).

Table 1: Clinical Questions associated with neuroanatomical localization.

Important clinical questions relative to neuroanatomical diagnosis
1 Is the abnormality rostral to, or caudal to, the foramen magnum?
2 If the abnormality is rostral to the foramen magnum, is the disease affecting the rostrotentorial (“forebrain”) structures, the brain stem, the cerebellum, or individual cranial nerves?
3 If the abnormality is caudal to the foramen magnum, does this disease involve the spinal cord, the peripheral nerve, neuromuscular junction, or muscle?
4 If the disease involves the spinal cord, which segment (s) (C1-C5, C6-T2, T3-L3, L4-S3, Caudal segments)
5 If the abnormality involves the peripheral nervous system, which nerve (s)?
6 Does the abnormality primarily/exclusively involve the neuromuscular junction?
7 Does the abnormality primarily/exclusively involve the muscle?
8 Do all the clinical signs localize to multiple regions within the nervous system?

Question 1. Is the Abnormality Rostral to or Caudal to the Foramen Magnum?

Anatomical structures rostral to the foramen magnum include the intracranial nervous system (rostrotentorial, caudotentorial (brain stem, cerebellum)) and the specific cranial nerves [18]. Structures caudal to the foramen magnum include the spinal cord segments, specific peripheral nerves, neuromuscular junction, or muscular systems.

Clinical Signs Reflecting Intracranial Dysfunction

Clinical signs suggestive of intracranial disease include, but are not limited to, alterations in mental acuity, behavior abnormalities, cranial nerve abnormalities, seizures, various head posture abnormalities, propulsive circling movements, and conscious proprioceptive deficits in the limbs. Once it has been determined that an intracranial abnormality exists, further delineation of the location of the lesion may be possible based on the specific clinical signs present.

Question 2. Is the Abnormality Affecting the Rostrotentorial Structures, Brain Stem Structures, Cerebellum, or Individual Cranial Nerves?

The rostrotentorial (often referred to as the “forebrain”) structures (Zone 1) include the cerebral hemispheres, basal nuclei, diencephalon, rostral portion of the mesencephalon, and associated structures such as the meninges, blood vessels, and ventricles (lateral, third, and mesencephalic aqueduct). These structures are located rostral to an imaginary transverse plane extending from the tentorium cerebelli ventrally separating the intracranial nervous system into two components. The rostrotentorial nervous system structures are responsible for many functions requiring consciousness, awareness, and associated responses. Classic clinical signs of an abnormality of rostrotentorial structures are found in Table 2. The most common clinical signs of a rostrotentorial abnormality include alterations in their mental acuity or behavior, a menace response abnormality from poor or absent vision, facial sensation recognition abnormalities, true seizure activity, proprioceptive abnormalities in the limbs, a tendency to walk propulsively in a circular direction, “hemi-inattention” or “hemi-neglect”, head pressing, and or head turning. Unilateral lesions involving the rostrotentorial region predominantly result in clinical signs on the side of the body opposite (contralateral) to the abnormality.

Table 2: Classic Clinical Signs of Rostrotentorial Abnormalities.

Classic Clinical Signs of Rostrotentorial (“Forebrain”) Abnormalities
Alterations in mental acuity and behavior (listless, lethargy, somnolence, stupor, coma)
“Head Pressing”
Hemi-inattention or Hem-neglect
Contralateral Menace Response Deficit with concurrent normal Facial Nerve Function and Pupillary Light Reflex (PLR) (unilateral abnormality)
Contralateral Facial Sensation Deficit (unilateral abnormality)
Contralateral Hemiparesis/Hemiplegia (unilateral abnormality)
Tetraparesis/Tetraplegia (bilateral abnormality)
Seizures
Head turning (usually in the direction of a unilateral abnormality)
Circling (usually in the direction of a unilateral abnormality)

Importantly, while there is a constellation of clinical signs that may be present in any individual animal with a rostrotentorial disease, all these clinical signs may not be present in every affected animal. In some instances, for example, only a single clinical sign may be present to indicate an abnormality in these neuroanatomical structures. Additionally, because of the somatotopic organization of the nervous system, very discrete abnormalities may result in focal or localized clinical signs (for example, dysfunction of a single limb). The type and extent of any disease process ultimately will determine the specific associated clinical signs.

Clinical Signs of Caudotentorial (Brain Stem) Disease

The caudotentorial structures include the commonly defined brain stem (Zone 2), the cerebellum (Zone 3), and associated structures such as the meninges, blood vessels, and ventricles (mesencephalic aqueduct and fourth) [18]. The predominate clinical signs of a brain stem abnormality are found in Table 3. These include abnormal mental acuity and awareness, proprioceptive abnormalities in the limbs, abnormalities of Cranial Nerves III through XII, decerebrate posturing (midbrain abnormalities), and, in severe instances, respiratory irregularities or failure of respiratory function.

Table 3: Classic Clinical Signs of Caudotentorial Abnormalities (Brain Stem).

Classic Clinical Signs of Brain Stem Abnormalities
Alterations in mental acuity and behavior (listless, lethargy, somnolence, stupor, coma)
Cranial nerve abnormalities (Cranial nerves III through XII)
Vestibular signs – head tilting, ataxia, wide-based posturing, nystagmus, positional strabismus
Ipsilateral Hemiparesis/Hemiplegia (unilateral abnormality)
Tetraparesis/Tetraplegia (bilateral abnormality)
Abnormalities of respiration

Clinical Signs of Caudotentorial Disease Involving the Cerebellum

The cerebellum (Zone 3) is a unique structure of the central nervous system anatomically and functionally. Because of the important proprioceptive functions of the cerebellum, clinical signs of cerebellar disease are often characteristic as described as “uncoordinated” because of dysfunction of unconscious proprioception [1-13]. Unilateral lesions of the cerebellum result in ipsilateral clinical signs. Common clinical signs of cerebellar disease are found in Table 4. These include ataxia, dysmetria, Intention tremors, lack of balance, head tilting, nystagmus, broad or wide-based stance postures, a menace response deficit (ipsilateral to a unilateral cerebellar lesion) with normal vision, and, in severe instances, decerebellate posturing.

Table 4: Classic Clinical Signs of Caudotentorial Abnormalities (Cerebellum).

Classic Clinical Signs of Cerebellar Abnormalities
Uncoordinated movements
Ataxia
Hypermetria
Falling
Intention tremor
Absent menace response with normal vision, normal palpebral reflex, and pupillary light reflex (ipsilateral to a unilateral abnormality)
Pupillary abnormalities (rare)

Clinical Signs of Individual Cranial Nerves

Common clinical signs of individual cranial nerve abnormalities (Zone 4) are found in Table 5. The challenge with cranial nerve abnormalities is determining if the abnormality involves the central (primarily the cranial nerve nuclei) or peripheral components (ganglion and peripheral nerve axons) of the cranial nerve. If the central nervous system elements of the cranial nerves are abnormal, these are a component of the rostrotentorial (CN I and II) and brain stem (CN III – XII) localization schemata.

Table 5: Classic Clinical Signs of Cranial Nerve Abnormalities.

Classic Clinical Signs of Cranial nerve Abnormalities
CN I Anosmia or dysosmia
CN II Visual abnormalities; menace response abnormalities
CN III Strabismus; ocular movement abnormalities (medial direction); pupillary dilation
CN IV Strabismus; ocular movement abnormalities (rotational)
CN V Facial sensation abnormalities; ocular sensation abnormalities; temporalis and masseter muscle abnormalities
CN VI Strabismus; ocular movement abnormalities (lateral direction)
CN VII Abnormalities of the muscles of facial expression; keratoconjunctivitis sicca
CN VIII Head tilting; falling; nystagmus; positional strabismus
CN IX Swallowing abnormalities; stridor
CN X Swallowing abnormalities; stridor; abnormalities of gastrointestinal functionality
CN XI Neck positional abnormalities (lateral direction)
CN XII Tongue movement abnormalities; tongue atrophy

Question 3. If the Abnormality is Caudal to the Foramen Magnum, is this Abnormality Affecting the Spinal Cord, Peripheral Nerve, Neuromuscular Junction, and or Muscle?

Neuroanatomical structures caudal to the foramen magnum include the spinal cord and the peripheral nerves as well as the associated neuromuscular junction and muscles [18]. Based on clinical signs such as proprioceptive abnormalities of limbs, spinal reflex function, and painful areas, the clinician can differentiate the abnormality into one of these two general functional systems.

Question 4. If the Abnormality Involves the Spinal Cord, Which Segments?

If the clinical signs suggest an abnormality within the spine or spinal cord, the next step is to determine the location relative to the various spinal segments of that abnormality. Based on the associated clinical signs, the clinician should be able to localize the abnormality to one or more of five functional regions within the spinal cord. Importantly, spinal cord localization schemata are based on spinal cord segments, not vertebral segments as these two separate anatomical entities do not align in all regions of the spine.

Clinical Signs and Localization of Spinal Cord Disease

Clinical signs of spinal cord disease vary with the location of the disease within the spinal cord. As pathways to and from the intracranial nervous system structures travel cranially and caudally through the spinal cord to influence limb function, abnormalities of limb conscious or general proprioception are often found with spinal cord disease. Once the affected limb (s) are identified, spinal reflex assessments are performed to determine if the abnormality involves the central or peripheral nervous system structures (historically referred to as upper motor neuron (UMN) or lower motor neuron (LMN) systems) [1-13]. After collecting this information, the examiner should be able to localize the lesion into one of five spinal cord areas.

The spinal cord is divided into functional areas based primarily on the presence of either central (historically “UMN”) or peripheral (historically “LMN”) clinical signs to the limbs. The presence or absence of these characteristic signs is based upon the concept of a local spinal reflex (that is, a function that does not require conscious control) and the normal control of these reflex functions from intracranial and central spinal cord nervous system. A central (“UMN”) is a neuron or group of neurons that does not exit the central nervous system, and influences, either positively or negatively, peripheral nerve (“LMN”) functionality. Clinical signs of central nervous system disease include proprioceptive abnormalities, increased or normal spinal reflexes, increased or normal limb muscle tone, and, if present, disuse atrophy (Tables 6 through 10).

Table 6: Classic Clinical Signs of Cervical Segment 1 to Cervical Segment 5 Abnormalities.

Classic Clinical Signs of a Cervical Segment 1 to Cervical Segment 5 Abnormality
Limb movement abnormalities
Proprioceptive abnormalities when moving (ataxia, hypermetria, limb dragging)
Ipsilateral Hemiparesis/Hemiplegia (unilateral abnormality)
Tetraparesis/Tetraplegia (bilateral abnormalities)
Painful reactions (cervical region)
With severe abnormalities, impairment of respiration

The peripheral nervous system and the effector organs (muscles) are components of what is commonly referred to as “the final common pathway.” This functional unit, however, also includes the cell bodies of the peripheral nervous system in the grey matter of the spinal cord. Clinical signs of peripheral nerve (“LMN”) disease include proprioceptive abnormalities, decreased or absent spinal reflexes, decreased or absent limb muscle tone, and neurogenic atrophy and may result from a spinal cord abnormality that involves the gray matter or reflex interneurons within the local spinal cord segments. As both central and peripheral nervous system abnormalities can result in proprioceptive deficits, evaluation of spinal reflex function becomes important in separating abnormalities of these two functional systems.

Lesions of the Cervical (C)1-C5 spinal segments (Zone 5) classically result in limb dysfunction such as ataxia, hypermetria, and tetraparesis or, if severe, tetraplegia (Table 6). Caudally projecting pathways from the respiratory nuclei of the brain stem to the peripheral nerves for respiration (phrenic nerve to the diaphragm and the intercostal nerves to the intercostal muscles) are located in the cervical spinal cord. Therefore, disease that interrupts these pathways may compromise respiratory functions. Respiratory function is usually only severely compromised in animals that lose voluntary movement (i.e., are tetraplegic). Often, animals will have a concurrent “whispery” bark due to inadequate tidal volumes and decreased projection of that air mass through the larynx and pharynx.

If the disease occurs unilaterally within the cervical spinal cord, hemiparesis may be found on the side ipsilateral to the abnormality as the spinal cord is functionally located caudal to the functional crossover within the intracranial nervous system. Cervical hyperesthesia is often present with many cervical spinal cord diseases but not, for example, in diseases associated with primary nervous system degeneration. One caveat: some animals with intracranial diseases may also have cervical hyperesthesia and this feature of intracranial disease should be considered when localizing an abnormality exclusively to the cervical spinal cord. Components of Horner’s syndrome (sympathetic dysregulation) may be present due to involvement of the caudally projecting sympathetic fibers in the lateral tectotegmental spinal tract from the intracranial central nervous system structures. With unilateral lesions, components of Horner’s syndrome can be found in the eye ipsilateral to the abnormality. Spinal reflex function should be normal or potentially exaggerated, as the peripheral nerves in the cervical and lumbar intumescence are not affected with an exclusive C1-C5 spinal cord segment abnormality.

Lesions of the C6- Thoracic (T)2 spinal segments (cervical intumescence – Zone 6) may also result in abnormalities of limb movements including ataxia, tetraparesis or tetraplegia similarly as with lesions of the C1-C5 spinal segments (Table 7). Spinal reflexes in the pelvic limb will be normal or exaggerated, while those in the thoracic limbs should be decreased to absent due to involvement of the motor neuron cell bodies and axons that make up the nerves to the thoracic limb. This decrease in thoracic limb reflex function is an important clinical feature for localization in these spinal segments.

Table 7: Classic Clinical Signs of Cervical Segment 6 to Thoracic Segment 2 Abnormalities.

Classic Clinical Signs of a Cervical Segment 6 to Thoracic Segment 2 Abnormality
Limb movement abnormalities
Proprioceptive abnormalities when moving (ataxia, hypermetria, limb dragging)
Ipsilateral Hemiparesis/Hemiplegia (unilateral abnormality)
Tetraparesis/Tetraplegia (bilateral abnormalities)
Painful reactions (cervical; cranial thoracic regions)
Decreased to absent thoracic limb spinal reflexes
Decreased to absent thoracic limb muscle tone
Neurogenic Muscle atrophy of thoracic limb muscles
With severe abnormalities, impairment of respiration
Horner’s syndrome (miosis, ptosis, enophthalmos, elevated nictitating membrane) ipsilateral to a unilateral abnormality
Abnormalities of the cutaneous trunci reflex (due to a lateral thoracic nerve abnormality)

If the abnormality is unilateral, hemiparesis is seen with similar reflex changes (decreased to absent thoracic limb spinal reflexes and normal to increased pelvic limb reflexes). Horner’s syndrome (sympathetic denervation) or only a component such as a miotic pupil may be present as the caudal cervical intumescence (T1 to T3 spinal segments) is the location of the preganglionic cell bodies lie and concurrently where the corresponding nerves exit the spinal cord and vertebral canal. With unilateral lesions, Horner’s syndrome will be found in the eye ipsilateral to the abnormality.

If the abnormality involves the C8-T1 spinal segments or nerves, the cutaneous trunci reflex may be abnormal. If the abnormality is unilateral, the ipsilateral cutaneous trunci muscle will not contract with stimulation on either side of the body. The nonaffected side, however, should still contract with stimulation on either side confirming the integrity of the T3-Lumbar (L)3 spinal region.

Abnormalities of the T3-L3 spinal segments (Zone 7) may result in abnormalities of limb movements including ataxia paraparesis or, if severe, paraplegia (Table 8). With unilateral abnormalities, a central nervous system monoparesis of the pelvic limb may be found. While the pelvic limbs are dysfunctional, spinal reflex function in the pelvic limbs will be normal or in some instances exaggerated. The thoracic limbs, however, should function normally.

Table 8: Classic Clinical Signs of Thoracic Segment 3 to Lumbar Segment 3 Abnormalities.

Classic Clinical Signs of a Thoracic Segment 3 to Lumbar Segment 3 Abnormality
Limb movement abnormalities
Proprioceptive abnormalities when moving (ataxia, hypermetria, limb dragging)
Ipsilateral monoparesis/monoplegia (unilateral abnormality)
Paraparesis/Paraplegia (bilateral abnormalities)
Painful reactions (thoracolumbar region)
Abnormalities of the cutaneous trunci reflex
Urination (larger bladder; “firm” feeling; difficult to express; incontinence) and defection abnormalities (incontinence; normal anal tone)

The cutaneous trunci reflex may be absent caudal to the location of the abnormality, especially with more severe spinal lesions. The level where the cutaneous trunci reflex cannot be elicited is usually within one to three spinal segments of the spinal cord abnormality. With severe spinal cord abnormalities in this location, Schiff-Sherrington posture (that is, hyper-extended thoracic limbs) may be seen. Hyperesthesia may be present on palpation or manipulation of the vertebral segments in this region. Focal hyperesthesia is a helpful neuroanatomical localizing sign in all regions of the spinal cord.

Urinary function may be abnormal with T3 to L3 spinal segment lesions. This is more common with abnormalities that impair voluntary movement. In these instances, the animal similarly cannot urinate voluntarily. The bladder is often large, has appropriate muscle tone on palpation, and can be difficult to manually express due to excessive tone in the urinary sphincters.

Abnormalities of the L4-Sacral (S) S3 spinal segments (lumbar intumescence – Zone 8) may also result in paraparesis/plegia (Table 9). Pelvic limb reflexes, however, will be decreased or absent which is the most important clinical distinction compared to spinal cord abnormalities occurring cranial to these segments. Depending upon which area of the intumescence is involved, specific reflexes may be abnormal. With an abnormality of the L4-L6 spinal segments (femoral nerve), the patella reflex is reduced or absent. Quadriceps muscle atrophy may be present from neurogenic atrophy or a combination of neurogenic and disuse atrophy if the animal has not been using the pelvic limbs for an extended period. Sensation on the distal medial side of the pelvic limb may be reduced or absent due to involvement of the sensory functions of the femoral nerve.

Table 9: Classic Clinical Signs of Lumbar Segment 4 to Sacral Segment 3 Abnormalities.

Classic Clinical Signs of a Lumbar Segment 4 to Sacral Segment 3 Abnormality
Limb movement abnormalities
Ipsilateral monoparesis/monoplegia (unilateral abnormality)
Paraparesis/Paraplegia (bilateral abnormalities)
Proprioceptive abnormalities when moving pelvic limbs (ataxia, hypermetria, limb dragging)
Painful reactions (lumbosacral region)
Decreased to absent pelvic limb spinal reflexes
Decreased to absent pelvic limb muscle tone
Neurogenic Muscle atrophy of pelvic limb muscles
Urination (larger bladder; “flaccid” feeling; easy to express; incontinence) and defection abnormalities (dilated anal sphincter; incontinence)

With abnormalities of the L6-S1,2,3 spinal segments (sciatic nerve), the withdrawal reflex is reduced or absent. The patellar reflex may appear exaggerated due to the loss of antagonist muscles to this reflex because of the sciatic involvement (referred to as “pseudohyperreflexia”). Atrophy of the muscles innervated by the sciatic nerve may be present. Atrophy can occur in any muscle innervated by the sciatic nerve but is often most obvious in the cranial tibial muscle.

Correlation between the vertebral and the spinal segments is important as well. In the lumbar area, the spinal cord segments are more cranially located compared to the corresponding vertebral segments. The spinal cord usually terminates in the cranial half of the L7 vertebrae in dogs [18]. In larger breeds of dogs, the spinal cord may terminate more cranially, and in smaller breeds, more caudally [18]. In cats, the spinal cord ends at the L7 or the sacral vertebrae [18]. In dogs, the sacral spinal cord segments tend to lie over L5 vertebra with some variability among individual breeds and individual animals [18]. In cats, the sacral spinal cord segments are found more distally (S2-S3 lie over L6 vertebrae) [18]. Generally, the L1 and L2 spinal cord segments are located within the L1 and L2 vertebrae, respectively. Spinal cord segments L3-L7 are located between L3 and L5 vertebrae.

With abnormalities of the S1-S3 spinal cord segments, bladder and colonic dysfunction may be present. The external anal sphincter may be dilated and have poor muscle tone for contraction. The bladder may be large, flaccid feeling on palpation, and easily expressed. Many animals with peripheral nerve innervation abnormalities or damage primarily to the detrusor muscle (detrusor muscle atrophy) will expel urine with minimal abdominal pressure.

With abnormalities of the caudal spinal cord segments (Zone 9), tail movement dysfunction and reduced or absent tail sensation are commonly present (Table 10). The tail often cannot be extended dorsally or is located in an abnormal position, ventrally or laterally. Hyperesthesia may be present on palpation or manipulation of the sacral or caudal vertebral segments.

Table 10: Classic Clinical Signs of Caudal Segment Abnormalities.

Classic Clinical Signs of Caudal Segment Abnormalities
Tail movement abnormalities
Abnormal tail position
Painful reactions

Clinical Signs and Localization of Peripheral Nerve, Neuromuscular Junction, and Muscle Disease

Question 5. If the abnormality involves the peripheral nerves (Zone 10), which nerves?

The peripheral nervous system includes any nerve myelinated by a Schwann cell [18]. Schwann cells begin myelinating peripheral nerves to the limbs at the intervertebral foramen. Using this strict definition, other components of the peripheral nervous system, such as the cell body of the motor neuron in the ventral grey of the spinal cord, would not be included in this strict definition of the peripheral nervous system. Functionally, however, an abnormality of the peripheral nerve or cell body, the neuromuscular junction (NMJ), an or the muscle can result in a similar constellation of clinical signs.

In animals, peripheral nerve (Zone 10), neuromuscular junction (Zone 11), and or muscle (Zone 12) disease primarily results in “weakness” of muscle function (Table 11 through 13). “Weakness” in this is used to indicate a muscle strength problem, however, often is equally used to describe movement dysfunction. If the animal can generate stepping movements, the limb movements are usually associated with shorter step distances, often referred to colloquially as “choppy”. Animals are sometimes described as “stiff” due to inability to advance an appropriate step distance and concurrently with a more extended limb posture. In other instances, the limbs may appear flaccid, have tremoring movements, and buckle primarily with weight bearing. Animals may stand with the limbs placed more centrally under the body. In some instances, this may result in a kyphotic spine or even cow-hocked posture. Animals with both peripheral nerve and muscle disease may also have abnormalities of limb posture. The limb joint angulation during the stance or swing phase of the gait cycle is abnormal, usually with an over-flexion during standing and lack of flexion during forward swing movements.

Table 11: Classic Clinical Signs of Peripheral Nerve Abnormalities.

Classic Clinical Signs of a Peripheral Nerve Abnormality
Limb movement abnormalities
Proprioceptive abnormalities when moving pelvic limbs (limb dragging)
Ipsilateral monoparesis/monoplegia (unilateral abnormality)
Paraparesis/Paraplegia (bilateral abnormalities pelvic limbs only)
Tetraparesis/Tetraplegia (bilateral abnormalities all limbs)
Short inter-step distances/Shorten strides
Abnormal flexed or extended postures of the limbs
Exercise intolerance
Kyphotic posturing when exercising
Facial muscle weakness; decreased palpebral reflexes; excessive salivation
Decreased to absent limb spinal reflexes
Decreased to absent limb muscle tone
Neurogenic Muscle atrophy of limb muscles
Lateral recumbency (when severe)
Abnormal vocalization (indicative of poor air movement by the respiratory muscles)

Abnormal muscle functionality may be seen in visceral structures such as the esophagus resulting in megaesophagus in animals with peripheral nerve disease. This may result in regurgitation, decreased swallowing, excessive salivation, gagging, or aspiration pneumonia. Peripheral nerve, neuromuscular junction, and or muscle involvement of the cranial nerves, such as the glossopharyngeal and vagus, may result in dysphagia, dysphonia, gagging, swallowing abnormalities, and coughing. Inspiratory stridor may be present with laryngeal paralysis seen in association with some peripheral nerve diseases. If the diaphragm and intercostal muscles are involved, decreases in effective respiration may result. Animals with respiratory muscle weakness tend to become tachypneic to compensate for decreased inspiratory volume. As the condition worsens, abdominal breathing, wherein the abdomen moves out during inspiration may be present.

Table 12: Classic Clinical Signs of Neuromuscular Junction Abnormalities.

Classic Clinical Signs of a Neuromuscular Junction Abnormality
Limb movement abnormalities
Ipsilateral monoparesis/monoplegia (unilateral abnormality)
Paraparesis/Paraplegia (bilateral abnormalities pelvic limbs only)
Tetraparesis/Tetraplegia (bilateral abnormalities all limbs)
Short inter-step distances/Shorten strides
Exercise intolerance
Kyphotic posturing when exercising
Facial muscle weakness; decreased palpebral reflexes; excessive salivation

Animals with peripheral nerve disease often have abnormalities of general or conscious proprioceptive testing (Table 11). When evaluating general or conscious proprioception in animals with suspected peripheral nerve, neuromuscular junction, and or muscle disease, it is important to evaluate the animal when full weight-bearing and again when the animal’s weight is supported by the examiner, as some diseases affect only the motor functionality of the nerve. With exclusive motor function abnormalities, when the animal’s weight is supported by the examiner, these animals can generate normal conscious proprioception or paw placement due to normal sensory function. With many peripheral nerve and central nervous system lesions, however, animals often have both motor and sensory weakness occurring concurrently. Conscious proprioceptive deficits will be present in these animals regardless of weight-bearing status in these animals.

Table 13: Classic Clinical Signs of Primary Muscle Abnormalities.

Classic Clinical Signs of Primary Muscle Abnormalities
Limb movement abnormalities
Short inter-step distances/Shorten strides
Exercise intolerance
“Crabbing”
Kyphotic posturing when exercising
Facial muscle weakness; decreased palpebral reflexes; excessive salivation
Primary Myopathic Muscle atrophy of limb muscles

Spinal reflexes are reduced or absent in animals with peripheral nerve disease. This is an important clue to the location of the abnormality in the peripheral nerve. Resting muscle tone and muscle resistance to passive range of motion in the limbs will be poor or absent.

With peripheral nerve disease involving motor nerve innervation, neurogenic atrophy of muscles occurs. This atrophy evolves relatively rapidly after a peripheral nerve injury (within 5 to 10 days) and results in significant amounts of muscle atrophy. Often the underlying bony structures become prominent due to the significant degree of atrophy. With single nerve disease, muscle atrophy may be in focal muscles or muscle groups corresponding to the distribution of the affected peripheral nerve innervation.

Individual peripheral nerves may be selectively involved with various pathological processes that involve the motor or sensory functional components. Primary sensory nerve disease often results in exaggerated uncoordinated movements resulting from the associated proprioceptive deficits. Animals with primary afferent or sensory neuropathies may have an awkward gait wherein they tend to “flap” the limbs and strike the ground on the more dorsal palmar and plantar regions of the paw and lower limb. Evaluation of the sensory distribution loss may be helpful in localization with sensory components of the peripheral nerve are abnormal. The sensory deficiencies can be present in the dermatomes and autonomous zones innervated by these nerves. In general, however, clinical assessment of skin innervation is inconsistent.

Question 6. Does the Abnormality Involve the Neuromuscular Junction (Zone 11)?

Animals with disease primarily involving the neuromuscular junction classically have overlapping clinical signs with peripheral nerve and primary muscle abnormalities. Short stepping is one of the more classical signs. With some neuromuscular diseases, muscle weakness is exacerbated with exercise (e.g., myasthenia gravis, hypoglycemia). Dogs and cats with neuromuscular junction, and muscle disease may lie down frequently. Cats particularly may rest their head on their thoracic limbs when lying down. Cats tend to have ventral neck flexion, or inability to lift their heads, presumably due to cervical muscle weakness. Animals with disease of the neuromuscular junction or muscle abnormalities may have proprioceptive deficits during weight bearing, but not when their weight is supported by the examiner as discussed previously. In diseases of the neuromuscular junction (e.g., myasthenia gravis) and muscle, spinal reflexes are classically normal as relatively minimal muscle strength is necessary to perform simple reflex functions.

Question 7. Does the Abnormality Primarily or Exclusively Involve the Muscle (Zone 12)?

Animals with disease primarily involving the muscle also have clinical signs overlapping with peripheral nerve and neuromuscular junction abnormalities. Weakness of muscle function is the most consistent clinical abnormality. Short stepping and muscle atrophy are clinical clues. Animals with primary muscle disease, however, should have normal conscious proprioceptive testing when the examiner supports the animal’s body weight.

Primary muscle abnormalities may result in dysfunction of visceral structures such as the esophagus resulting in megaesophagus similar to peripheral nerve disease [1-13]. This muscle weakness may result in regurgitation, swallowing abnormalities, excessive salivation, gagging, or aspiration pneumonia. Muscle involvement of muscles innervated by cranial nerves, such as the glossopharyngeal and vagus, may equally result in dysphagia, dysphonia, swallowing abnormalities, gagging, and coughing. If the diaphragm and intercostal muscles are involved, decreases in effective respiration may result.

With most primary diseases of muscle, muscle mass is classically decreased. In contrast, animals with myotonia or some other muscle disorders may have hypertrophy of their muscles. Their muscle groups may be well defined (prominent) anatomically. They similarly have short step distances when gaiting and often with extended limb postures. Equally, animals with muscle cramping or myotonia may have episodic bouts of extended limb postures. As with some neuromuscular diseases, muscle weakness may be exacerbated with exercise.

Multifocal or Diffuse Lesions of the Nervous System

Question 8. Do all the Clinical Signs Localize to a Focal Region in the Nervous System?

Some diseases can affect multiple regions of the nervous system simultaneously. Additionally, two or more different diseases can concurrently affect the nervous system in differing areas. If the clinical signs cannot be adequately explained by a single focal abnormality, then consideration should be given to a single disease with multifocal pathology or that there are multiple disease processes present affecting multiple functional units. Diffuse diseases such as inflammatory conditions would be an example.

Conclusion

The ability to make an accurate neuroanatomical diagnosis is the essential step in determining possible disease processes that affect that location within the animal’s nervous system. Correctly determining the location of any abnormality in the nervous system of animals is foundational to completing a logical differential diagnosis list and subsequently diagnostic plan. While seemingly complex, there are essentially twelve functional regions of the nervous system for neuroanatomical diagnosis. Based on the classic clinical signs associated with these twelve functional regions, an accurate neuroanatomical location of any neurologic abnormalities is possible. Once an accurate neuroanatomical diagnosis is identified, further clinical assessment can logically be performed to ultimately make a definitive diagnosis.

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Bispectral Analysis of NIRS Muscle Oxygenation in Type 2 Diabetes During Treadmill Walking

DOI: 10.31038/EDMJ.20261032

Abstract

Background: Type 2 Diabetes Mellitus (T2D) impairs peripheral microvascular reactivity and skeletal muscle oxygen consumption during locomotion causing impaired exercise tolerance in a poorly understood manner. While linear spectral measures of NIRS capture total oxygen signal power, they fail to capture the complex and chaotic dynamics of muscle oxygen control.

Aim: Using bispectral analysis to quantify non-linear harmonic interactions and quadratic phase coupling (QPC) of muscle oxygenation in T2DM participants with and without DM complications.

Methods: Participants were stratified into two distinct cohorts ( n =12 each) based on T2DM severity: Group 1 (T2D with complications: elevated HbA1c, extended disease duration, clinical neuropathy/vasculopathy) and Group 2 (Well-controlled/no complications). Time-series continuous tissue oxygenation (StO2) data (N = 1,826 frames per series at fs = 10 HZ ) were collected from participants performing a standardized treadmill walking task at self-selected usual walking pace. Higher-order spectral analysis—specifically bispectrum magnitude |B (f1 , f2)|  and normalized bicoherence b (f1 , f2) —was computed across the principal non-linear domain ( f2 ≤ f1 ,  f1+ f2 ≤ 5.0).

Results: Group 1 exhibited an 84.1-fold increase in mean total bispectral energy ( 1.28 x 1011 vs. 1.52 x 109 arbitrary units p < 0.001 ) and an 8.7-fold higher peak bispectral magnitude ( 2.42 x 105 vs. 2.79 x 104 p < 0.001 ) compared to Group 2. Quadratic phase coupling concentrated along the fundamental diagonal (f1= f2), with Group 1 peaking at 0.94 Hz ( f3= 1.88 Hz second harmonic) and Group 2 peaking at  ( second harmonic). Peak normalized bicoherence reached 0.886 in Group 1 versus 0.785 in Group 2. Group1 generated severe non-linear distortion and exaggerated low-frequency harmonic coupling in active muscle oxygenation during locomotion.

Conclusions: More advanced diabetes, or complications of T2DM, not only have direct impact on exercise capacity but also disrupt the poorly understood complex, dynamic local control of muscle oxygenation. Bispectral analysis of NIRS signals serves as a sensitive, non-invasive biomarker for evaluating the deterioration in oxygen dynamics, seen in more advanced diabetes, which is not detectable by conventional NIRS techniques and shows promise for early detection of clinical deterioration.

Introduction

Type 2 Diabetes Mellitus (T2D) is characterized by exercise intolerance (as characterised by a lower muscle oxygen consumption at VO2max compared with non-diabetes [1] although the precise mechanisms are not fully understood due to the complex interactions of local mechanisms controlling the balance of oxygen consumption and supply in local muscle tissue. During physical activity, skeletal muscle requires precise, real-time matching of local microvascular oxygen delivery to dynamic metabolic demand. In healthy individuals, local vasomotion, autonomic sympathetic tone, and endothelial nitric oxide release regulate local perfusion in a balanced, quasi-linear oscillatory manner, and each with distinct frequencies. Significant skeletal muscle deoxygenation is known to occur during exercise in type 2 diabetes [2]. Local recruitment of microvascular blood volume/hematocrit, blood flow, and VO2peak are normally all mutually correlated but uncouple in T2DM [3]. In advanced T2D—marked by prolonged disease duration, poor glycaemic control (HbA1c > 8.0%) and microvascular structural remodeling, vasodilatory responsiveness becomes severely compromised [4].

When analysing oxygen levels in muscle (often measured via Near-Infrared Spectroscopy (NIRS) as Oxygenated Haemoglobin (HbO) or tissue oxygenation index (TSI), traditional linear signal processing techniques (e.g., Fourier Transform, Power Spectral Density) quantify energy distribution across isolated frequency bands. But this only indicates which frequencies are present, not the interactions and coupling effects between (e.g., myogenic, neurogenic, endothelial rhythms). As a result, overall NIRS oxygen dynamics in exercise often appear normal in T2DM [5,6]. These linear spectrums inherently assume phase independence between frequency components and mask higher-order non-linear dynamics. In contrast, the mean bispectrum magnitude reveals how these frequencies interact with each other and therefore serves as a powerful tool to detect nonlinear physiological control mechanisms and microvascular regulation [7]. The bispectrum |B (f1 , f2)| evaluates higher-order statistics by identifying quadratic phase coupling (QPC)—a mechanism where non-linear interactions between two frequencies f1 and f2 and  generate a coupled harmonic component at f3= f1 + f2 . It extends the traditional power spectrum (which uses two-point correlations) to a three-point frequency correlation or third order statistic. It evaluates how three frequency components—f₁, f₂, and their sum f₁ + f₂—relate to one another in terms of both amplitude and phase. Because it is derived from a triple product of Fourier transforms, the bispectrum is a complex number possessing both a phase (biphase) and a magnitude. The 3 practical benefits of Bispectral compared to traditional power spectra are; Phase information to determine whether frequency components are interdependent. Quadratic phase coupling to reveal when two frequencies combine to create a third frequency. Gaussian noise suppression, making non-Gaussian or hidden signals easier to analyse.

Because the raw bispectrum magnitude is dependent on the amplitude of the underlying signal, a large peak can simply mean the oxygen level fluctuations have increased in volume, not necessarily that their coordination increased. To separate pure coordinate coupling from raw amplitude changes during muscle contraction or rest, the analysis is paired with bicoherence b (f1 , f2),. Bicoherence normalizes the mean bispectrum magnitude to a scale of 0 to 1, indicating the true strength of the phase coupling.

This study therefore applies bispectrum analysis to 24 recordings of skeletal muscle oxygenation (StO2) recorded during treadmill walking in participants with T2DM. We tested the hypothesis that advanced diabetic complications (neuropathy, vasculopathy, extended duration, high HbA1c) reduce oxygenation dynamical complexity and instead induce structural non-linear distortions manifesting as significantly higher bispectral energy and altered quadratic phase coupling compared to spectra of no complications diabetes as the control.

Materials and Methods

Study Design and Dataset

Study sample size was based on previous studies [8] where DM affected oxygenation HbO by 11%. To detect a difference between complications and no complications T2DM groups with 80% power and 5% significance requires 24 individuals (12 in each group). To allow for missing data of 10%, sample size was set at 24.

Ethical Considerations

The study was conducted in accordance with ethical guidelines for observational research within a larger research program: IRAS Project ID: 67269. An amendment for further recruitment and data collection was approved on 5 March 2024. (10002.NSA6.5.03.2024) (Appendix 1) Patient confidentiality was maintained throughout the study, and all data were fully anonymised for analysis. Only data relevant to the statistical analysis was extracted from records. (Appendix 1)

Inclusion and Exclusion Criteria

Inclusion criteria included confirmed diagnosis of type 2 diabetes mellitus and age 18 years or older. The diabetes with complications group included T2DM adults with coded diagnoses of confirmed CVD, PAD, DPN in medical records or T2DM >12years, while the comparison group comprised T2DM adults with no such codes in the records.

Exclusion criteria were applied to ensure participant safety and data quality. Patients with mobility problems that would prevent gait assessment on a treadmill were excluded, as were individuals lacking mental capacity to provide informed consent or follow testing instructions.

Group Assignment

  • Group 1 (Advanced T2D/Complications):  n = 12 participants corresponding clinically to elevated HbA1c levels, longer diabetic duration, and high prevalence of diabetic peripheral neuropathy and peripheral artery disease.
  • Group 2 (Controlled T2D/no complications): n = 12 participants corresponding clinically to well-managed glycemia and minimal vascular/neuropathic complications.

Treadmill Testing

Participants were priorly provided with a participant information sheet and if in agreement signed consent forms. Participants familiarised themselves with treadmill walking starting at a slow pace and self-adjusting the speed control up to self-perceived natural walking pace. NIRS measurements of walking at steady pace for 2minutes were recorded.

Muscle Oxygenation Testing

Throughout the exercise, continuous non-invasive measurements of muscle oxygenation/deoxygenation status were measured with near-infrared spectroscopy (NIRS) (PortaMon; Artinis Medical Systems, Gelderland, the Netherlands) at 10 Hz. The portaMon was placed on the lateral head of gastrocnemius muscle of the dominant limb, secured using a Velcro strap, and covered with a cloth bandage to exclude ambient light. The NIRS monitor emits two wavelengths (780 and 850 nm) which interact with oxyhaemoglobin and deoxyhaemoglobin. Using the Beer–Lambert law to account for scattering we determined changes of relative concentrations of oxy (HbO) and deoxygenated (HHb)

Datasets

Continuous tissue oxygenation time-series signals were acquired from N = 24 adult participants diagnosed with T2D during a standardized treadmill walking protocol (TMv3). Each participant dataset comprised 1,826 sequential temporal data points recorded at a uniform sampling frequency fs = 10.0 Hz (Δt=0.1 s), yielding a total continuous measurement window of  182.6 seconds.

Analysis

Analysis was performed using a dedicated script coded in python (Appendix 1).

Higher-Order Spectral Analysis Formulation

For a discrete zero-mean time series x(t), segment-averaged Fourier transforms X(f) were calculated using Welch’s modified periodogram approach with Hann windowing ( Nperseg = 128 points,  50% overlap). The discrete bispectrum B ( f1 , f2) measures the complex third-order correlation between three spectral components satisfying the resonant condition f1 + f2= f3 :

where IE[·] denotes the expectation operator across time segments and X*(·) represents the complex conjugate. To eliminate magnitude dependence and quantify true non-linear phase coupling independent of signal amplitude, the normalized bicoherence index b ( f1 , f2)  was calculated:

Total Bispectral Energy (EB) was evaluated over the alternating region ( f1 , f2 ≥ 0.15 Hz):

Results

Individual Participant Bispectral Profiles

Rank-ordering the 24 diabetic participants by total bispectral energy revealed a strong, multi-order-of-magnitude separation between the advanced disease cohort (Group 1) and the controlled cohort (Group 2) (Table 1) (Appendix 2).

Table 1: Demographics of the patients and of the healthy controls.

Characteristic

Group 1 T2DM+ Complications (N=12)

 Group 2-no comps (N=12)

Age (years)

63.7 ± 5.7

61.0 ± 6.2

Males

7

5

HbA1c (%)

9.1 ± 1.0

7.4 ± 0.9

HbA1c (mmol/mol)

62 ± 14

57 ± 14

BMI (kg/m2)

27.2 ± 2.2

25.5 ± 1.9

Duration diabetes (years)

19.0 ± 9.9

3.2 ± 2.1

DM peripheral neuropathy (DPN)

10

1

Group Comparative Analysis

Non-Linear Energy Disparity: Group 1 exhibits over 84 times greater total bispectral energy ( 1.28 x 1011 vs. 1.52 x 109 ) than Group 2. Harmonic Phase Coupling: Both groups display focused quadratic phase coupling along the diagonal ( f1= f2), generating strong second-harmonic interactions ( f3=f1 + f2 ≈ 2f1). (Table 2). Crucially, while the normalized bicoherence magnitude is comparable between groups ( bmax ≈ 0.52), the absolute bispectral magnitude |B| is 8.7 times higher in Group 1. The Bispectrum magnitude reflects the degree of quadratic phase coupling or nonlinear interactions between triads of frequencies of controllers of oxygenation in response to exercise. This demonstrates that while both groups display intrinsic non-linear phase coupling, the magnitude of non-linear wave interaction and dynamic amplitude distortion is vastly magnified in the group with more advanced diabetes disease.

Table 2: Comparative Group Statistics (Mean  SD).

The mean bispectrum magnitude (6.6x higher in Group 1), taken over multiple epochs, ensures that random, incoherent noise and phase fluctuations cancel out toward zero, isolating stable, phase-coupled harmonic components. The higher value indicates that fluctuations are more driven by deterministic, nonlinear physiological systems rather than random variations (Figures 1 and 2).

Figure 1: Log-Bispectrum and bicoherence contour plots averaged for Groups 1 and 2. Log scaling reveals underlying harmonically coupled structures across 0.5 Hz ≤ f1 ≤ 2.5 Hz. Group 1 shows a higher baseline magnitude ( log10 ≈ 4.5 to 7.5). Group 2 shows similar coupling but lower overall magnitude intensity ( log10 ≈ 0.75 to 6.15) indicating higher diversity/complexity in oxygenation signals.

Figure 2: 3D contour maps of the bispectrum magnitude (vertical axis) and the geometric distribution of quadratic phase coupling for a) participant in Group 1 T2DM with diabetic complications and b) participant in group 2 without complications. Note the reduction and clustering of spectral energy and peaks in (a) reflecting muscle oxygen changing in a highly predictable, inflexible and restricted pattern, compared to (b). (b) shows a wider energy dispersal, and a more complex peak signature reflecting the complex, fluid, and non-linear variations seen in healthy tissues.

Discussion

The primary finding of this study is the high increase in total bispectral energy in participants with advanced/complicated T2D (Group 1) relative to those with T2D without complications (Group 2). High bispectral energy reflects muscle oxygen levels changing to a highly predictable, rigid and strictly coupled harmonic pattern, rather than showing the complex, fluid, and chaotic variations seen in healthy tissues. This shift in frequencies is quantified by the mean bispectrum magnitude. Chaotic systems have the advantage of being rapidly adaptable to changes in local conditions without the need for central control. Therefore, while a more inflexible pattern of oxygenation appears more organised (hence higher spectral energy/lower entropy) it loses the dynamic ability to adapt to changes in local oxygen demand. As a result, oxygenation not meeting the demands of muscle, over time, leads to muscle degenerative changes and sarcopenia [9]. The results accord with those only other bispectral NIRs muscle study by Molinari, where spectral energy reduced in muscle after 1 year of exercise training in diabetes [8]. The physiological and metabolic reasons behind why more advanced T2DM exhibits high bispectral energy (and thus lower signal entropy) in muscle oxygenation patterns results from three main factors:

Microvascular Stiffness

In healthy microvasculature, vasomotion is mediated by smooth muscle cell electromechanical coupling, endothelial nitric oxide release, and sympathetic innervation operating within a flexible, linear regulation envelope. The microvasculature supplying the muscle is incredibly dynamic. It constantly adjusts to minor local changes via endothelial nitric oxide release, neural inputs, and metabolic demands. This creates a highly complex, chaotic, and “organic” oxygenation signal (low bispectral energy, high entropy). Capillary basement membrane and advanced glycation end-product (AGE) cross-linking reduce arterial compliance. When subjected to the mechanical pumping of treadmill locomotion, stiffened microvessels generate non-linear pressure-flow wave interactions The capillaries lose their ability to dynamically fluctuate. The oxygenation signal becomes strictly bound to macro-hemodynamic forces—like the mechanical, repetitive pumping of the heart or rigid breathing rates. This strong phase-locking to external cyclic rhythms drives up bispectral quadratic phase coupling (QPC), creating high bispectral energy. Loss of sympathetic nerve fibre density impairs smooth vasomotor control, transforming smooth sinusoidal vasomotion into abrupt, asymmetric flux variations that generate strong higher-order harmonics [10].

Mitochondrial Dysregulation

Healthy muscle tissue rapidly and flexibly switches between metabolic substrates (carbohydrates and fatty acids) and continuously adjusts oxygen extraction based on immediate cellular needs [11]. Diabetic myocytes become metabolically inflexible and unable to dynamically “demand” and extract oxygen in a rapid and responsive manner. [12,13]. The oxygen extraction rate becomes severely impaired and fixed. The oxygenation signal loses its internal biological complexity and flattens into a simple, repetitive cycle dictated purely by systemic delivery.

De-conditioning and Structural Muscle Changes (Sarcopenia)

T2DM causes structural changes in the muscle, including muscle wasting (sarcopenia), fatty infiltration, and a shift in muscle fibre types (often a loss of capillaries wrapping around the fibres) [14]. When muscle is structurally simplified, alongside reduced capillary density, the diffusion path for oxygen into the tissue becomes uniform and restricted [15]. Localized oxygen pools that create complex signals are replaced by homogenous tissue saturations which translate mathematically into cleaner, highly coupled harmonic waves and high bispectral energy.

Clinical Implications as a Diagnostic Biomarker

Bispectral energy analysis, combining both phase alignment and third-order amplitude variance, acts as a highly sensitive non-linear biomarker that can detect loss of microvasculature complex dynamics, not visible by standard spectral analysis of NIRS signals and likely before clinical signs of deterioration. The separation observed between Group 1 and Group 2 suggests that bispectral profiling during walking tests could provide a non-invasive diagnostic tool to screen for:

  • Subclinical diabetic peripheral neuropathy before sensory loss manifest.
  • Microvascular diabetic vasculopathy and peripheral artery risk.
  • Objective tracking of therapeutic interventions aimed at restoring vascular flexibility.
  • Early diabetic myopathy prior to diabetic sarcopenia.

NIRS already has advantages over other methods of assessing muscle oxygen content (portable, low cost, non-invasive) and research also shows that NIRS provides reliable measures of exercise-induced oxygen responses regardless of the protocol used [16].

Conclusions

Bispectral analysis of skeletal muscle tissue oxygenation during locomotion provides novel insights into muscle oxygenation dysfunction in Type 2 Diabetes. Advanced diabetic complications—including neuropathy, vasculopathy, prolonged disease duration, and poor glycemic control—are characterized by an 84-fold surge in total non-linear bispectral energy and significant phase coupling, overall indicating a loss of physiological adaptability. Higher-order spectral analysis represents a promising, non-invasive approach for identifying muscle oxygenation dysfunction in T2DM and the potential for earlier detection of disease progression.

Funding

No funding was provided for this study.

Conflict of Interest

RB, SH and LC declare no conflicts of interest.

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  9. Yang L, Wu H, Chen J, Wang W, Zhang Z, Feng J, Qiu W, Dong F, Lin N, Yuan F (2025) Muscle oxygen saturation stratification by photoacoustic imaging in diabetic sarcopenia: Association with disease status. Photoacoustics. [crossref]
  10. Dipla K, Triantafyllou A, Koletsos N, Papadopoulos S, Sachpekidis V, Vrabas IS, Gkaliagkousi E, Zafeiridis A, Douma S (2017) Impaired Muscle Oxygenation and Elevated Exercise Blood Pressure in Hypertensive Patients: Links With Vascular Stiffness. Hypertension. [crossref]
  11. Palmer BF, Clegg DJ (2022) Metabolic Flexibility and Its Impact on Health Outcomes. Mayo Clin Proc. [crossref]
  12. van de Weijer T, Sparks LM, Phielix E, Meex RC, van Herpen NA, Hesselink MK, Schrauwen P, Schrauwen-Hinderling VB (2013) Relationships between mitochondrial function and metabolic flexibility in type 2 diabetes mellitus. PLoS One. [crossref]
  13. Scheuermann-Freestone M, Madsen PL, Manners D, Blamire AM, Buckingham RE, Styles P, Radda GK, Neubauer S, Clarke K (2003) Abnormal cardiac and skeletal muscle energy metabolism in patients with type 2 diabetes. Circulation. [crossref]
  14. Ghosh M, Heo Y, Kushwaha GS, Cho C, Son YO (2026) Interplay between sarcopenia and type 2 diabetes: mechanisms, implications, and therapeutic prospects. Nutr Diabetes. [crossref]
  15. Larsson L, Degens H, Li M, Salviati L, Lee YI, Thompson W, Kirkland JL, Sandri M (2019) Sarcopenia: Aging-Related Loss of Muscle Mass and Function. Physiol Rev. [crossref]
  16. Tandirerung FJ, Jamieson A, Hendrick E, Hughes AD, Jones S (2024) Near-infrared spectroscopy (NIRS) in vivo assessment of skeletal muscle oxidative capacity: a comparison of results from short versus long exercise protocols and reproducibility in non-athletic adults. Front Physiol. [crossref]

Targeting the Tumor Microenvironment with Plant-Derived Immunomodulators: An Emerging Therapeutic Strategy

DOI: 10.31038/CST.20261113

 

The publication “Plant-derived immunomodulators in cancer: Balancing immune activation and suppression within the tumor microenvironment” (Beier V, Wink W, Samstag Y (2026). Adv Biol Regul. 99: 101132) serves as a valuable entry point for a wider and increasingly significant discussion in oncology and immunology. It addresses a highly relevant challenge in modern tumor immunology: the targeted modulation of the immune system within the tumor microenvironment using plant-derived compounds. Instead of merely listing phytochemicals, the article emphasizes a key conceptual issue: natural substances are not intrinsically “immune enhancing” or inherently “safe”; rather, they are pharmacologically active compounds that may either promote or hinder antitumor immune responses, depending on the specific context and dosage. This perspective is particularly important for the field, as it encourages researchers and clinicians to move beyond overly simplistic distinctions between “natural” and “synthetic,” and to approach plant-derived compounds as potent immunological tools whose mechanisms of action require rigorous investigation.

An especially important insight is that the tumor microenvironment should not be understood as a passive setting, but rather as a dynamic immunological niche.

Cancer cells actively exploit inflammatory and regulatory pathways to establish conditions in which immune activation is tightly restricted and often transient, while immunosuppressive processes are strengthened and maintained.

Plant-derived immunomodulators such as piperlongumine, berberine, and epigallocatechin gallate (EGCG) do not act as universally immune-stimulating agents but instead exert complex and sometimes opposing effects on T cells and regulatory immune networks. A compound that appears advantageous in a simplified in vitro system may, within the complex environment of a tumor, unintentionally promote regulatory T cells, myeloid derived suppressor cells, or other immunosuppressive populations. Conversely, a molecule that dampens inflammation in one context may, in another, relieve inhibitory constraints on effector immune responses. This apparent duality should not be interpreted as a limitation of the field, but rather as an indication that any agent targeting the immune system – whether natural or synthetic – must be, in addition, assessed within a biological system that inherently integrates both activation and suppression.

From clinical-research perspective, the subject of plant-derived immunomodulators also underscores a broader tension between traditional practices and evidence-based medicine. Compounds such as berberine, EGCG, curcumin, and resveratrol have longstanding roles in various traditional medical systems, and their application is frequently supported by anecdotal reports or historical use. These natural products can be regarded as multi-target drugs as they can interfere with several molecular targets, mostly proteins, in the body. However, contemporary oncology increasingly requires precision, including clearly defined molecular targets, measurable pharmacokinetic properties, reproducible immunological outcomes, and well-established clinical endpoints. The central issue is therefore not only whether and in what way plant-derived compounds shift the balance between immune activation and immune suppression in patients, but whether their effects are sufficiently predictable, controllable, and compatible with current immuno-oncology treatment strategies.

Pharmacokinetic limitations – low bioavailability, complex metabolism, and uncertain tissue distribution – are often underappreciated in phytochemical research, all of which makes it difficult to translate promising preclinical findings into consistent clinical benefit. In addition, patients are increasingly using phytochemicals as dietary supplements on their own initiative while undergoing chemotherapy, targeted therapies, or treatment with immune checkpoint inhibitors, often without clear recommendations regarding appropriate dosing, timing, or possible interactions. This leads to a situation in which “natural” compounds are effectively incorporated into an unregulated, real world polypharmacy context. Consequently, the subject addressed in the publication intersects with broader pharmacological challenges, including the need for standardized formulations, comprehensive pharmacokinetic and pharmacodynamic characterization, and vigilant monitoring of immune related adverse effects.

Finally, this topic points toward an emerging opportunity: Plant-derived immunomodulators may prove most valuable not as standalone treatments, but as context dependent adjuvants that fine tune immune responses. In certain scenarios, they may help to overcome PD L1-mediated resistance mechanisms, modulate excessive cytokine release, or reduce chronic inflammation that contributes to tumor progression. In other situations, however, they could compromise immune surveillance or intensify immune related toxicities. The key challenge moving forward lies in establishing a framework in which such agents are selected on the basis of their mechanisms of action, the patient’s immune profile, and concurrent therapies, rather than on tradition or marketing claims alone. In this regard, the review functions as a conceptual anchor for a more rigorous and integrative approach to the use of natural products in cancer immunology, in which plant-derived immunomodulators are regarded not as harmless adjuncts, but as pharmacologically significant factors within the broader landscape of immuno-oncology.

References

  1. Beier V, Wink W, Samstag Y (2026) Plant-derived immunomodulators in cancer: Balancing immune activation and suppression within the tumor microenvironment. Adv Biol Regul 99: 101132. [crossref]

HPLC Determination of Pharmaceutical Strength of Expired Oral Hypoglycemics Containing Metformin, Pioglitazone and Alogliptin

DOI: 10.31038/JPPR.2026912

Abstract

Objective: To evaluate the strength of expired medications commonly used in free clinics, with the goal of determining whether their shelf lives can be safely extended. Given the limited literature in this area, the study intends to generate evidence that could inform cost-saving strategies and reduce pharmaceutical waste without compromising patient safety.

Methods: Samples from expired metformin, pioglitazone, and alogliptin products were analyzed using a validated high performance liquid chromatography [HPLC] method to determine the levels of their active ingredients. Quantitative analysis was performed using a HyPurity® column [C18, 150 4.6 mm, 3 μ, Thermo Scientific] column with gradient elution at a flow rate of 1mL/min. Detection wavelength for metformin, pioglitazone, and alogliptin was 250, 270, and 276 nm, respectively.

Results: Expiry dates of analyzed batches ranged from April 2007 to April 2017 for metformin, December 2005 to November 2015 for pioglitazone, and October 2015 to April 2017 for alogliptin. Despite the wide range in expiry dates for the selected oral hypoglycemic agents, all analyzed samples maintained an average strength within 10% of their listed concentrations [metformin: 96.5%, alogliptin: 98.1%, and pioglitazone 100.3%].

Conclusion: Our results provide support for utilizing near-expiry metformin, pioglitazone, and alogliptin in the free clinic setting with patient and physician consent. With an extended post-expiry shelf life, the use of these oral hypoglycemic agents can contribute to reducing the financial burden of expired medication disposal and increased storage life, as well as being available for the management of type 2 diabetes mellitus in free clinic patients.

Keywords

Oral hypoglycemics, Metformin, Pioglitazone, Alogliptin, HPLC analysis, Drug expiration

Introduction

Type 2 diabetes mellitus [T2DM] is an endocrine disorder affecting approximately 38.4 million individuals in the United States, [11.6% of the population] and in which the body loses sensitivity to insulin [1]. Different classes of oral and injectable hypoglycemic agents are effective in managing T2DM. Selection of hypoglycemic agents may differ depending on the patient’s A1c goal, comorbidities, concomitant medications, and cost. Metformin is a biguanide hypoglycemic agent approved by the Food and Drug Administration [FDA] in 1994 and is one of the most common oral hypoglycemic agents used in T2DM treatment due to its effectiveness, cost, and relative tolerability [2]. According to the American Diabetic Association [ADA], metformin is the preferred first-line medication used to treat T2DM [3] and is currently used world-wide by more than 200 million patients daily [4], making it one of the most commonly used daily medications. Metformin acts through multiple mechanisms affecting liver metabolism, e.g. suppression of gluconeogenesis, and host-gut microbiota [enhanced anerobic glucose utilization] [4,5], resulting in lower blood glucose levels and increased insulin sensitivity in appropriately treated patients [4]. When used alone, metformin is capable of reducing A1c by approximately 1.12%, making it one of the most effective oral hypoglycemic agents, while also avoiding undesirable adverse effects such as weight gain and hypoglycemia [6]. Metformin has also found its way onto the WHO’s list of essential medicines [7]. Pioglitazone is a thiazolidinedione [TZD] agent that functions as an agonist to PPAR-alpha and PPAR-gamma nuclear receptors, increasing sensitivity to insulin naturally produced by the body [8]. Pioglitazone was FDA approved in July of 1999 for the treatment of T2DM in adults as an adjunct to healthy diet and exercise [8]. According to the 2025 ADA Standards of Care in Diabetes, pioglitazone is typically not a first line agent for treatment of T2DM but can be used in combination with or as an alternative to metformin therapy if it is not tolerated [3]. Pioglitazone is considered to be a highly effective agent in lowering blood glucose to achieve a goal A1c. Alogliptin is a dipeptidyl peptidase-4 [DPP-4] inhibitor that works by preventing the deactivation of the incretin hormones glucose-dependent insulinotropic polypeptide [GIP] and glucagon-like peptide-1 [GLP-1] [9]. By prolonging the action of these peptides, insulin secretion and sensitivity are increased while glucagon secretion is decreased. The FDA approved alogliptin in January 2013 to improve glycemic control in adults with T2DM. This included alogliptin alone, as well as two combination formulations: one with metformin and the other with pioglitazone. Alogliptin and other DPP-4 inhibitors are not typically first line agents for glycemic control in T2DM but are often used as adjunctive agents to help reach a goal A1c [10].

Of the three medications, the cost of metformin is relatively low with a median 30-day average wholesale price [AWP] as low as $3 compared to alogliptin and pioglitazone at $234 and $345, respectively. Also, there is still a statistically significant gap between insured and uninsured patients when it comes to medication adherence and affordability. Per the 2017-2018 National Health Interview Survey, 35.7% of uninsured patients with diabetes did not take their medication as prescribed and 42.6% asked their doctor for a lower-cost medication [10]. While there are approaches to lower prescription drug costs, such as discount programs and manufacturer coupons, this is a time where free clinics play a vital role in lowering the financial burden and providing healthcare to underserved populations. Free clinics are a nationwide healthcare model that exists in every State, including Wisconsin. They were introduced to assist populations that struggle to access healthcare, including individuals who are without health insurance, by bridging this gap to help uninsured Americans. The 1000+ free clinics and pharmacies in the United States are members of the National Association of Free & Charitable Clinics [NAFC, https: // nafcclinics.org/]. These clinics operations are based on voluntary work by various healthcare providers and diverse public and private gifts/ donations. However, one major challenge to free clinics is increasing demand with decreased funding [11]. One way to address decreased funding is to use donated medications that may be close to expiry in the treatment of patients at free clinics.

Providing close-to-expiry or even expired medications to those who cannot afford them may appear as disregarding this group’s health, and the debate continues between opposers and supporters [12,13]. Despite the controversy, meaningful care would still be provided if the medications are still effective, especially when low-income individuals experience T2DM at a higher rate than others. It is reported that patients with very low income have 55% higher incidence rate of T2DM than those who have never experienced low or very low income [14]. This presents an opportunity to provide effective hypoglycemic drugs to this population. If such drugs are proven to retain their potency beyond expiry date, these donated medications even if they are close to expiration date can greatly improve management of a disease state that disproportionally affects patients with a high social deprivation index. The expiration date assigned to a medication is the date until which the manufacturer can guarantee its established strength and purity at its designated storage conditions, i.e. this is the date that manufacturers disclose for a product based on the limited time within which stability studies are conducted [15]. However, does this mean that drugs would lose potency once they are beyond the listed expiration date? Not necessarily so. Relatively few literature reports address this question but there are plausible indications that many medications retain active ingredient stability beyond manufacturer-provided expiration dates. For example, through the Shelf-Life Extension Program [SLEP], the FDA collaborated with the US Department of Defense to analyze, verify drug levels, and extend expiration dates of more than 100 strategic medications in army stockpiles to reduce waste and cost of replacing these technically expired medications. In 2009, the program was able to provide expiration date extensions of up to 5 years through analytical verification methods [16]. In alignment with the SLEP study, the British Antarctic Survey Medical Unit examined the stability of five expired drugs [atropine, nifedipine, flucloxacillin, naproxen, and bendroflumethiazide analyzed 15-51 months past expiry dates] that experience extreme temperature variations while in transport and storage [17]. After analysis, it was found that all drugs had retained stability, and only one of the five drugs had vials of freeze-dried solid medication that exhibited some potential degradation products in one-third of vials. Additionally, two studies investigated EpiPen injectors up to 50 months after expiry. One study reported a retained potency in 61% of injectors [18], while the other study found that 35 EpiPens retained 84-96% potency up to 36 months after expiration [19]. These studies and others, including a comprehensive review by Zilker et al., [20], show that many pharmaceutical products may display extended stability, especially if they are in solid dosage forms, e.g. tablets and capsules.

As a result of widespread availability of expired medication batches at free clinics affiliated with the Wisconsin Association of Free and Charitable Clinics, including various anti-diabetic agents, we extended our earlier investigation of expired respiratory tract medications [21] to include the oral hypoglycemic products reported in this study. The study evaluated the levels of three active constituents in expired oral hypoglycemics [metformin, alogliptin, and pioglitazone] utilizing a validated HPLC analytical method. Our results provide further evidence to support the post-expiry stability of pharmaceutical products and offer reassurance that select oral hypoglycemic medications within a few months or even days of expiry can still be utilized when other alternatives are not available.

Methods and Materials

Chemicals and Reagents

Analytical standard metformin, alogliptin, and pioglitazone were purchased from Sigma Aldrich [St. Louis, MO], AChemBlock [Hayward, CA], and Alfa Aesar [Ward Hill, MA], respectively. Analytical solvents were purchased from Fisher Scientific. All analyzed batches were provided by the Greater Milwaukee Free Clinic [GMFC] in Milwaukee, WI, which ceased operations in May 2019. While at the clinic, samples were stored at standard room conditions, except for occasional power outages that may have impacted heating and cooling systems. All samples remained sealed and unopened unless stated otherwise in this report.

Instruments

Analytical procedures were conducted using an HPLC system [Prominence LC-2030, Shimadzu, Japan] equipped with a quaternary pump, autosampler, and photodiode array [PDA] detector.

Standard Solutions

For each analytical standard, two aliquots each weighing 100.0 mg, were separately placed into 100-mL volumetric flasks designated as MS-A/MS-B, PS-A/PS-B, and AS-A/AS-B for metformin, pioglitazone, and alogliptin, respectively. Methanol was added to the mark in each flask, which was sealed and stored at 2°C. The XS-A solutions were utilized for constructing calibration curves, whereas XS-B solutions were used for validating accuracy and precision.

Analytical Method Development

Gradient elution was performed with a flow rate of 1 mL/min which started at 5% acetonitrile [solvent A] in 0.1% aqueous formic acid [solvent B] for 1 minute, followed by a linear increase from 5% to 100% [A] over 6 minutes, maintaining 100% [A] for 1 minute, returning to 5% [A] and running for 2 minutes. Column temperature was maintained at 25 °C and injection volume set to 10 μL. All hypoglycemics were separated using a HyPurity® column [C18, 150 4.6 mm, 3μ, Thermo Scientific] with detection at 250, 270, and 276 nm for metformin, pioglitazone, and alogliptin, respectively.

Method Validation

The developed method was validated for selectivity, calibration curve linearity, accuracy, and precision, following FDA/ICH guidelines for pharmaceuticals and biologics [22]. Multipoint calibration curves were constructed for the three drugs using standard solutions at different concentrations. Accuracy and precision were validated at 3 different standard solution concentrations for each drug. All samples were injected in triplicate for analysis. A detailed description of method validation is included in Supplement A.

Sample Preparation and Analysis

All samples were in the form of film-coated tablets. For each batch, a subset of tablets totaling 30% of the entire lot (3-10 tablets depending on batch size) was selected for analysis. The selected tablets were ground into a fine powder, and the equivalent of one tablet was transferred to a 10-mL volumetric flask. Any remaining powder was stored at 4°C. The transferred aliquots were suspended in 10 mL of methanol and ultrasonicated for 20 minutes. Approximately 2 mL of the resulting solution was filtered through a 0.45μ filter into an HPLC vial, with the initial 1 mL discarded, before being injected onto the column in triplicate. Samples were diluted as necessary for concentrations to fall within the calibration curve range.

Results

Based on validation results included in Appendix A, the developed method was selective [specific for detecting the exact ingredients], accurate and reproducible. Thus, it could be reliably utilized to determine concentrations of all three drugs in their respective dosage forms. The examined samples included single and combination products of the three hypoglycemics in tablet form. The out-of-date samples (23 total) comprised four batches of metformin, two batches of metformin/alogliptin, six batches of metformin/pioglitazone, nine of pioglitazone, and two of alogliptin/pioglitazone. Additionally, one in-date sample was analyzed for metformin and for pioglitazone. No significant degradation product peaks were identified in any of the analyzed samples. Representative chromatograms for three analyzed products are depicted in Figure 1.

Figure 1: Representative chromatograms of out-of-date samples of combinations of each oral hypoglycemic.

The manufacturer expiration dates ranged from April 2007 to April 2017 for metformin, December 2005 to November 2015 for pioglitazone, and October 2015 to April 2017 for alogliptin. As illustrated in Table 1 and Figure 2, all samples exhibited drug levels between 90-110% of target concentration [metformin: 95.7+3.1%], [pioglitazone: 100.4+4.5%], and [alogliptin: 98.1+8.3%].

Table 1: Concentrations of hypoglycemic drugs in expired samples and in-date samples relative to label concentrations.

    Determined concentration relative to label (%)
Brand Expiry Date LOT# Metformin Pioglitazone

Alogliptin

Actoplus June 2007

A11314

98.4 105.4

–

Actoplus April 2007

A11443

92.5 104

–

Actoplus May 2007

A11133

100.2 102.5

–

Actoplus May 2007

A11191

92.3 90.6

–

Actoplus July 2007

A11332

97.8 105.4

–

Actoplus July 2007

A11330

96.8 97.4

–

Actavis August 2019

1259918M

94.5 –

–

Ascend May 2018

3116062

92.6 –

–

Teva February 2019

100001905

92.8 –

–

Fortamet April 2008

575G0464A

92.6 –

–

Actos December 2005

C10376

– 106.4

–

Actos April 2007

C11109

– 103.4

–

Actos November 2007

C11616

– 102.2

–

Actos April 2007

A11157

– 97.7

–

Actos February 2006

C10363

– 101.9

–

Actos July 2007

C11708

– 101.2

–

Actos August 2007

A11608

– 100.2

–

Actos March 2006

C10385

– 100.9

–

Actos April 2007

C11152

– 98.9

–

Kazano April 2017

C20121

98.8 –

90.4

Kazano February 2017

C20106

99.2 –

98.6

Oseni October 2015

A18640

– 96.9

93.9

Oseni November 2015

A18646

– 91.2

109.5

Metformin (Generic) April 2024

1010262

103.3 –

–

Pioglitazone (Generic) November 2023

M2017437

– 103.3

–

Figure 2: Concentration Distribution of hypoglycemic ingredients in expired samples and one in-date sample (2024) as percentage of label concentrations.

Discussion

The pharmaceutical industry adheres to FDA rules and regulations to determine drug stability and indicate expiration dates on product labels. These expiration dates assure and guarantee consumers that the drug will maintain its potency if stored properly and used before a specific date. However, exceeding an expiration date doesn’t necessarily mean the product loses effectiveness. In fact, it is not uncommon that expired medications are disposed of in a manner that could harm the environment, kept for personal use, or donated to free clinics rather than being properly disposed of. Healthcare practitioners at free clinics frequently encounter the ethical challenge of deciding whether to dispense expired medications, especially when they represent the sole treatment option for their patients. Under these circumstances, it would be beneficial to provide physicians with accurate data to inform their choices regarding the utilization or avoidance of expired medications for specific medical conditions. Based on the interactive health compass Milwaukee database, there are many uninsured people in the Milwaukee area. In the 53206 zip code, for example, the uninsured rate has most recently been documented at 19.24% [23]. This population is generally unable to afford medical care and utilize free clinics in the area. Data suggests that chronic diseases, including diabetes, have high rates [24]. Diabetes alone increases the risk of cardiovascular problems significantly, without comorbid conditions [25]. Free clinics, often underfunded and resource-limited, frequently struggle to provide patients with first-line medication therapies due to constraints in cost and availability. For many patients, even metformin which is considered ‘inexpensive’, a small copay may not be affordable. Providing free clinics with information about long-term stability of specific agents allows for providers within these settings to better ethically manage uninsured patients and provide more first-line therapy, which ultimately increases the health of the communities involved. Due to Medicaid policy changes within the next few years, almost 10 million people may lose access to insurance [26]. As we have found with the new agents coming to market for diabetes, drugs are becoming more expensive [27]. This work is imperative to continue for the improvement of health outcomes for uninsured patients now, and may even become more important as Medicaid policy changes occur.

The findings from this study demonstrate that all tested metformin samples maintained a potency exceeding 90% of their specified strength for up to 16 years post their designated expiration dates. It can be noted that, excluding lots 100001905, 1259918M, and 3116062, all other metformin samples were sealed and unopened. The pre-opening of these specific lots may have introduced potential sources of degradation within the samples, such as air and moisture. Additionally, sample lot 575G0464A exhibited a thicker film-coating, a characteristic that may have affected the observed metformin concentration in that sample due to potential inclusion of the film coating in the prepared samples. For reference, an in-date sample of metformin was analyzed and had a concentration within 90-110% of its expected potency. Similarly, all alogliptin and pioglitazone products exhibited a retention of more than 90% of their specified strength for periods exceeding 8 and 18 years, respectively. Sample lots A18640 and A18646 which were combination tablets of alogliptin and pioglitazone, had a hard-to-remove film-coating, which may have contributed to an increased variability in the observed drug concentrations. The lack of significant degradation product peaks further supports active ingredient stability in analyzed samples. One in-date sample of pioglitazone was analyzed and produced a similar result to that of the in-date metformin sample. However, we were unable to acquire any in-date alogliptin samples despite reaching out to different manufacturers. Expiry dates varying from 2007 to 2017 between the three hypoglycemics and results that all samples tested were above the 90% concentration threshold, suggest that such drugs could maintain potency in excess of 10 years post-expiry. Based on the above results and as noted in our earlier study [21], the potential impact of the data is far-reaching, and can influence various facets and modalities, ranging from clinical and home use to the global availability of medications. With 38.4 million individuals in the U.S alone struggling with T2DM, our study supports the notion of increased availability to many who may not be able to afford monthly prescriptions. Valid global implications may be considered especially for regions where economical deprivation may contribute to higher incidence of T2DM.

The use of expired drugs that have retained active ingredient concentrations can be a viable option for free clinic patients. With that said, the potential risks and benefits of an expired medication may still be evaluated on a drug-to-drug basis. In the future, other drugs will need to be studied to determine if they show extended potency past the manufacturing expiry date. This study helps in addressing the broader question of risk and benefit. With all the samples proving to be within ±10% of the intended concentration, there is not a clear and obvious risk due to loss of potency or development of potentially toxic degradation products. While there could be further risks that are unknown, it appears that the use of expired oral hypoglycemics similar to those tested in this study can provide minimal risk and great benefit to patients who cannot afford otherwise. This is in line with a 2019 commentary which recommended that long-term stability testing should be conducted to support use of medications beyond their initially disclosed expiration dates [28].

Conclusion

Our findings demonstrate the sustained strength of metformin, pioglitazone, and alogliptin, and provides evidence for their utilization at home and in free clinics. Our results were generated by a selective, accurate, and reproducible HPLC method developed in-house for measuring the concentrations of these drugs in expired batches of film-coated tablets. Our findings show that all three hypoglycemics maintained their expected concentration levels for extended periods up to 18 years beyond their labeled expiration dates. These results offer valuable insights for pharmacists, physicians, and patients considering the use of expired medications in various contexts, including at home use and within free clinics. Any ethical issues related to this concept should be further investigated.

Acknowledgements

The authors thank Dr. Rachel Kavanaugh and Jacob Dyer in providing in-date samples of metformin and pioglitazone, respectively, for comparative analysis.

Author Contributions

M. Hawi, A. Little, C. White: analytical lab work, data management, manuscript creation and review. J. Dyer: data review, manuscript creation and review

E. Abourashed: principal investigator, project planning and lab oversight, data review, final manuscript editing, formatting and submission.

Declaration of Generative AI and AI-Assisted Technologies In The Writing Process

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  28. Gikonyo D, Gikonyo A, Luvayo D, Ponoth P (2019) Drug expiry debate: the myth and the Afr Health Sci. 19: 2737-2739. [crossref]

Brief Report: Facilitators to Mental Health Service Access among Refugees: A Systematic Review and Thematic Synthesis

DOI: 10.31038/PSYJ.2026821

Abstract

Refugees permanently resettled in high-income countries experience increased rates of psychological distress, yet consistently underutilise statutory mental health services. While existing literature focuses predominantly on structural and cultural barriers, this systematic review synthesises evidence on factors that facilitate service access and ongoing engagement from the direct perspectives of refugees. A search across four electronic databases yielded 12 qualitative studies encompassing 195 refugees and asylum seekers across diverse host nations. Thematic synthesis identified three primary themes: (1) Utilising Local Resources, (2) Trust and Transparency, and (3) Adaptive Approaches. Findings demonstrate that service engagement is maximised when care is embedded within trusted community structures, supported by transparent therapeutic alliances, and tailored through flexible, culturally integrated practices.

Introduction

Over 82 million individuals globally are forcibly displaced, with approximately one million resettled in high-income nations. The compounding impact of pre-migration trauma and post-migration stressors elevates psychological distress among refugees beyond the level of other migrant populations [1,2]. Despite high clinical need, refugees encounter significant system-level and cultural obstacles that impede service utilisation [3,4]. Prior systematic reviews have largely integrated provider perspectives or focused narrowly on structural barriers, inadvertently omitting initial access points and contributing to a deficit-oriented understanding. To address this gap, this review systematically synthesises empirical qualitative literature to identify service-level and social facilitators of mental health access and engagement, centring exclusively on the lived experiences of refugee service users.

Methods

Literature Review and Selection

Conducted in accordance with PRISMA guidelines [5], four electronic databases (CINAHL, PsycInfo, Medline, and Web of Science) were searched for peer-reviewed studies published between 2011 and 2022. Search strings combined terms for refugee populations, access/engagement phenomena, and mental health service contexts.

Eligibility Criteria

Quality Appraisal and Data Synthesis

Methodological quality was evaluated using the Critical Appraisal Skills Programme (CASP) qualitative tool [6]. Studies were retained regardless of score due to the limited scope of available literature. Data were extracted and synthesized inductively using Thomas and Harden’s [7] three-stage thematic synthesis approach (line-by-line coding, descriptive theme generation, and analytical synthesis).

Results

Study Characteristics

The 12 included studies represented 195 refugees (103 males, 107 females across single/overlapping cohorts) aged 16–65 from diverse origin regions (Africa, Middle East, South Asia, South America, Eastern Europe). Eight studies were rated high quality and four medium quality via CASP criteria.

Utilising Local Resources

  • Physical Environment: Proximity and structural accessibility significantly promoted initial Integrating mental health services within familiar non-clinical hubs (e.g., schools, walk-in community centres) reduced geographical barriers and mitigated fears of institutional stigma associated with major hospital facilities.
  • Social Environment: Trusted social networks served as primary mediators. Encouragement, shared positive experiences, and direct navigation assistance from family, community leaders, teachers, and sponsors helped demystify complex Western referral pathways.

Trust and Transparency

  • Therapeutic Alliance: Sustained engagement depended on relational authenticity, empathy, active listening, and explicit cultural curiosity from Continuity of care with a single practitioner fostered security comparable to supportive personal networks.
  • Professional Practice: Perceived clinical competence and strict adherence to confidentiality were Concerns regarding interpreter discretion within small ethnic communities often hindered disclosure, highlighting the need for transparent boundary enforcement across all care personnel.

Adaptive Approaches

  • Holistic Care: Services that concurrently addressed post-migration material stressors (e.g., asylum claim navigation, housing assistance, social welfare support) demonstrated higher retension.
  • Culturally Integrated Care: Frameworks accommodating diverse explanatory models of illness—including collaboration with traditional or religious healers—validated client worldviews and enhanced intervention acceptability.
  • Patient Autonomy: Flexible session scheduling, adaptable session lengths, and non-prescriptive, collaborative choices regarding trauma disclosure empowered service users and reinforced self-agency.

Discussion

This systematic review confirms that refugee mental health service engagement in high-income resettlement nations is optimized when care models move beyond traditional, clinic-bound paradigms. Facilitators operate ecologically across structural, interpersonal, and methodological domains. Embedding care in local, accessible sites overcomes transportation and bureaucratic barriers, while social networks function as critical bridge-builders [8,9]. Within clinical encounters, relational trust and holistic responsiveness take precedence over specific Western therapeutic modalities. Furthermore, the importance of addressing housing, legal processes, employment, and social integration alongside psychological care supports ecological models of refugee mental health which emphasise the interaction between trauma and post migration stressors Flexibility regarding trauma disclosure aligns with emerging evidence that non-directive, collaborative treatment models best prevent re-traumatisation and support long-term recovery.

Recommendations for Clinical Practice

  1. Service Architecture: Transition toward community-based, co-located delivery models (e.g., school or community centre based clinics) with walk-in capabilities and direct transport assistance.
  2. Multi-Agency Integration: Establish cross-sector partnerships with social housing, legal assistance, and third-sector organizations to provide comprehensive, non-siloed support.
  3. Workforce Training: Implement mandatory cultural humility and cross-cultural mental health training for clinicians and professional medical interpreters.
  4. Community Engagement: Develop “cultural broker” systems and psychoeducational outreach programs to foster health literacy and destigmatize formal care within refugee networks.

References

  1. Miller KE, Rasmussen A (2010) War exposure, daily stressors, and mental health in conflict and post-conflict settings: Bridging the divide between trauma-focused and psychosocial Social Science & Medicine 70: 7-16. [crossref]
  2. Silove D, Ventevogel P, Rees S (2017) The contemporary refugee crisis: An overview of mental health World Psychiatry 16: 130-139. [crossref]
  3. Kirmayer LJ, Narasiah L, Munoz M, Rashid M, Ryder AG, et al. (2011) Common mental health problems in immigrants and refugees: General approach in primary Canadian Medical Association Journal 183: E959-E967. [crossref]
  4. Satinsky E, Fuhr DC, Woodward A, Sondorp E, Roberts B (2019) Mental health care utilisation and access among refugees and asylum seekers in Europe: A systematic Health Policy 123: 851-863. [crossref]
  5. Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, et al. (2021) The PRISMA 2020 statement: An updated guideline for reporting systematic BMJ 372: n71. [crossref]
  6. Critical Appraisal Skills Programme (2024) CASP checklist: 10 questions to help you make sense of qualitative research.
  7. Thomas J, Harden A (2008) Methods for the thematic synthesis of qualitative research in systematic BMC Medical Research Methodology 8: 45. [crossref]
  8. Colucci E, Minas H, Szwarc J, Guerra C, Paxton G (2015) In or out? Barriers and facilitators to refugee-background young people accessing mental health services. Transcultural Psychiatry 52: 766-790. [crossref]
  9. Posselt M, McDonald K, Procter N, de Crespigny C, Galletly C (2017) Improving the provision of services to young people from refugee backgrounds with comorbid mental health and substance use problems: Addressing the barriers. BMC Public Health 17: 280.

Engineering Microalgae for Enhanced Immunotoxin Therapy: From Production to Delivery

DOI: 10.31038/JPPR.2026911

Abstract

Immunotoxins (ITs), promising agents for targeted cancer therapy by fusing targeting moieties with potent toxins, face significant clinical translation hurdles including poor stability, systemic toxicity, inefficient tumor delivery, and a lack of scalable production platforms. This review highlights engineered microalgae as an innovative integrated “production-delivery” platform to address these limitations. Capitalizing on their high biocompatibility, genetic tractability, and costeffective cultivation, microalgae can be engineered via surface functionalization and chloroplast/nuclear genetic manipulation to directly produce and deliver ITs, thereby bypassing complex chemical conjugation and enhancing therapeutic integrity. Beyond serving as efficient carriers, these engineered systems demonstrate unique synergistic capabilities: their motility or externally guided (e.g., light/magnetic) navigation improves deep tumor penetration; photosynthetic activity alleviates tumor hypoxia and modulates the immunosuppressive microenvironment; and inherent immunomodulatory components (e.g., polysaccharides) activate innate immune cells, creating a favorable context for IT efficacy. Despite remaining challenges in expression optimization and precise in vivo targeting, the convergence of synthetic biology and smart material design positions engineered microalgae as a transformative platform poised to advance the next generation of safe, effective, and affordable IT based cancer therapeutics.

Keywords

Immunotoxin, Engineered microalgae, Drug delivery, Biocompatibility cancer therapy

Introduction

Cancer ranks as the second leading cause of death globally, with incidence rates showing a persistent upward trend year on year [1]. National cancer statistics reveal that approximately 10 million people die from cancer annually, with global cancer cases projected to rise to 28.4 million by 2040 [2]. Cancer cells pose a major threat to the life and health of patients due to their uncontrolled proliferation and easy metastasis to other organs or tissues. However, traditional therapies such as chemotherapy and radiotherapy often have limited clinical efficacy due to poor specificity, strong systemic toxicity, and tumor drug resistance [3-5]. In recent years, new anticancer therapies have been emerging. Among them, biological targeted therapy can achieve the dual goals of accurately killing cancer cells and protecting normal tissues, and its side effects are significantly lower than those of synthetic drugs, which has attracted wide attention. ITs are a typical representative of this strategy [6-9]. Composed of a targeting moiety (usually a monoclonal antibody or antibody fragment) and a cytotoxic payload (such as gelonin toxin or Pseudomonas aeruginosa exotoxin A) via chemical conjugation or recombinant fusion, they can selectively induce cell death by recognizing specific antigens on the surface of cancer cells (Figure 1) [10,11], providing a highly efficient targeted approach for cancer therapy [12]. Although preclinical studies of ITs have shown good prospects, its clinical application is still restricted by multiple factors [13]: (1) Systemic toxicity caused by nonspecific binding to normal cells; (2) It is easily degraded by protease in the blood; (3) The toxin induces neutralizing antibodies and induces immunogenicity; (4) low penetration efficiency for solid tumors; (5) It is difficult to maintain its biological activity during large-scale production. Among these, two issues are particularly prominent: the high immunogenicity induced by exogenous toxins and the lack of a suitable large-scale production platform. The former readily triggers an anti-ITs anti-body response in the body, accelerating drug clearance and increasing the risk of adverse reactions such as allergies and cytokine release syndrome; The latter limitation arises from traditional platforms failing to meet the production requirements for soluble expression and low toxin residue levels of ITs, thereby hindering industrialization progress [14,15].

Figure 1: Schematic diagram of IT structure and tumor targeting mechanism. A. Structure of IT B. Tumor Targeting Mechanism: 1. The target molecule of IT binds specifically to the antigen (or receptor) on the surface of tumor cells. 2. ITs are internalized into tumor cells by receptor-mediated endocytosis. 3. Upon entry into the cell, the IT is transported to the lysosome where it undergoes degradation to release the free cytotoxic payload. 4. The cytotoxic payload acts in the cytoplasm: it either disrupts the DNA strand or inhibits protein synthesis. 5. Apoptosis of tumor cells was induced to complete targeted killing.

To address these challenges, there is an urgent need to develop highly efficient integrated drug “production-delivery” systems that enhance the stability, targeting, and bioavailability of ITs while overcoming bottlenecks in large-scale production. As a kind of diverse photosynthetic microorganisms, microalgae have become a research hotspot of new biological carriers due to their inherent advantages [16,17]. More importantly, as an expression platform with both eukaryotic modification ability and low-cost culture characteristics, eukaryotic microalgae can not only directly produce the core functional modules of ITs (such as targeting fragments, toxic molecules, and immune activation elements), but also provide an important reference for the optimization of ITs by developing special expression systems and delivery technologies. In recent years, relevant research results have preliminarily verified its feasibility (Table 1). In addition, microalgae can regulate the tumor microenvironment (TME) and tumor-associated microbiome (TAM) through engineering, creating favorable conditions for ITs to play a therapeutic role [18-20].

Table 1: IT functional components and other functional proteins produced by eukaryotic microalgae.

Recombinant protein

Function Expression host Genome engineered

Core Highlights

References

IT components          
CD22-targeting ITs (αCD22PE40, αCD22CH23PE40) Treatment of B-cell lymphoma Chlamydomonas reinhardtii Chloroplast Chloroplast Expresses both monomeric and dimeric forms, which are soluble and enzymatically active; specifically binds CD22-positive B cells for efficient killing; significantly prolongs survival of tumor-bearing mice; avoids in vitro chemical conjugation, reducing off-target toxicity (Tran et al., 2013) [21]
Human IgG antibody against Hepatitis B Virus surface protein (CL4mAb) Prevention of Hepatitis B virus infection Phaeodactylum tricornutum Nuclear genome Efficiently secretes fully assembled functional antibodies, with a maximum concentration of 2550 ng/mL in culture medium; high purity of secreted antibodies eliminates complex purification steps, enabling low-cost production (Hempel and Maier, 2012) [22]
Attenuated E7 protein of Human Papillomavirus 16 (E7GGG) Prevention of HPV-related lesions and cancer C. reinhardtii Chloroplast Chloroplast High solubility and strong immunogenicity; induces specific antibody production and T-cell proliferation; provides effective protection against HPV-related tumors; can be produced under sterile and controlled conditions complying with Good Manufacturing Practice(GMP) standards (Demurtas et al., 2013) [23]
Fusion protein of multiple antihypertensive peptides (RPLKPW, LKPNM, AINPSK) Treatment of hypertension C. reinhardtii Chloroplast Chloroplast Fusion expression of multiple angiotensin-converting enzyme inhibitory peptides; in vivo experiments confirm antihypertensive effect, with the most significant blood pressure reduction 6 hours after oral administration; suitable for direct development of functional foods without complex purification (Carrizalez-López et al., 2018) [24]
Major birch pollen allergen (Bet v 1.0101) Allergen immunotherapy (AIT) for allergic diseases C. reinhardtii Chloroplast Chloroplast Similar secondary structure and immunological activity to Escherichia coli-expressed counterparts; effectively binds human IgE and mouse-specific IgG; serves as a safe and efficient production platform for oral desensitization vaccines (Hirschl et al., 2017) [25]
Other Functional Proteins          
Plasmodium falciparum PfCelTOS-IL2 antigen-adjuvant fusion protein Malaria prevention (pre-erythrocytic and transmission-blocking vaccine) C. reinhardtii Chloroplast Chloroplast Mixotrophic culture (low light) promotes protein accumulation; the fusion protein is soluble, correctly folded, and immunologically active; IL-2 adjuvant enhances antigen immunogenicity (Shamriz and Ofoghi, 2018, 2019) [26-27]
White Spot Syndrome Virus (WSSV) VP28 protein Prevention and control of WSSV infection in shrimp C. reinhardtii Chloroplast Chloroplast Codon optimization enables efficient expression; the algal strain tolerates the weakly acidic environment (pH 4.0) and 0.3% bile salts in shrimp digestive tracts; oral administration results in a shrimp survival rate of 87%, serving as a carrier for aquatic animal oral vaccines (Kiataramgul et al., 2020) [28]
Hyperthermophilic endoglucanase (CelB)-PTXD chimeric protein Lignocellulosic degradation, biofuel production C. reinhardtii Chloroplast Chloroplast Cultivable in non-sterile, phosphite-containing medium to avoid contamination; enzyme activity reaches 7.37–8.57 U/g dry weight; PTXD endows the algal strain with phosphorus source selectivity, ensuring culture stability (Cutolo et al., 2021) [29]

The engineering strategy further expands the potential of microalgae as IT delivery vectors, and surface modification technology can enhance the specific binding to tumors by coupling targeting ligands [30]. Genome engineering can achieve stable expression of ITs in the chloroplast or nucleus [31,32]. Microalgae-based micro-robots have the ability of autonomous movement and responsiveness to environmental stimuli, and can actively navigate to tumor sites [33,34]. These engineered microalgal systems not only protect ITs from degradation but also reduce off-target toxicity, increase tumor accumulation, and synergistically regulate anti-tumor immune responses [35,36]. In this review, we systematically review the latest progress of engineered microalgae in IT-mediated tumor therapy, including the inherent characteristics of vectors, targeted engineering strategies, synergistic mechanisms, challenges, and prospects, in order to provide a prospective reference for technological innovation and clinical translation in this field.

The Core Potential of Eukaryotic Microalgae as an Integrated “Production-Delivery” Platform for ITs

Recent advances in biopharma have laid the foundation for the research and development of complex protein drugs. However, due to the structural characteristics of macromolecules, industrial production of these drugs is still facing challenges. Cell-free protein synthesis cannot achieve large-scale manufacturing at present, and the production of protein drugs (such as ITs) mainly relies on living cell-based expression systems. Different expression systems have their own advantages and disadvantages (Table 2) [37-41]. Eukaryotic microalgae have unique advantages, such as prokaryotic operation convenience and eukaryotic modification ability, which are extremely promising alternative platforms. Their core advantages are reflected in the synergistic adaptation of “production” and “delivery” dimensions.

Table 2: Comparison of different recombinant protein expression systems.

Evaluation Indicator

Eukaryotic Microalgae (e.g. C. reinhardtii) Bacteria (e.g. Escherichia coli) Yeast (e.g. Saccharomyces cerevisiae) Transgenic Plants (e.g. Tobacco) Plant Viruses (e.g. Tobacco Mosaic Virus) Mammalian Cells (e.g. CHO Cells)

Transgenic Animals (e.g. Cattle and Sheep)

Glycosylation Ability Eukaryotic: mammalian – like; Prokaryotic: None None Incorrect (high – mannose type) Correct (mammalian – like) Correct (mammalian – like) Correct (mammalian – like) Correct (mammalian – like)
Target Protein Folding Quality Good Poor Medium Good Good Excellent Excellent
Genetic Manipulation Convenience Highly Convenient Highly Convenient Relatively Convenient Highly Convenient Relatively Convenient Moderately Convenient Highly Convenient
Scale up production feasibility Easily Achievable Easily Achievable Easily Achievable Easily Achievable Easily Achievable Moderate Difficulty Good Feasibility
Proliferation Rate Rapid Extremely Fast Relatively Fast Slow Relatively Fast Slow Slow
Product Output Level Medium Extremely High Relatively High Relatively High Extremely High Relatively Low Relatively Low
Cost of cultivation Extremely Low Extremely Low Relatively Low Relatively Low Relatively Low High High
Biosafety Level High Safety Low Safety Safety Unknown High Safety High Safety Moderate Safety High Safety
Potential Contamination Type Low Contamination Risk Endotoxin Contamination Low Contamination Risk May contain pesticides, herbicides and toxic plant metabolites Unknown Contamination Status May carry viruses, prions and oncogenic DNA May carry viruses, prions and oncogenic DNA

These photosynthetic microorganisms belong to the kingdom Protista, encompassing two major groups: prokaryotic cyanobacteria (blue-green algae) and eukaryotic microalgae. They are widely distributed across marine, terrestrial, and extreme ecosystems, and their rich species diversity enables adaptation to diverse applications [42]. Most clinically relevant species (e.g., C. reinhardtii, Dunaliella salina, Chlorella vulgaris, Haematococcus pluvialis) are FDA-approved Generally Recognized as Safe (GRAS) level, with no human pathogen host risk and outstanding biosafety [43]. Its chloroplasts can stably express foreign proteins, and the correct folding rate of over 90% can be achieved by the eukaryotic folding system, and the products are not contaminated by endotoxin. It has the ability of post-translational modification, such as disulfide bond formation, and there is no transgene silencing mechanism. It has successfully expressed SCFV, full-length human IgG1, and a variety of recombinant proteins [44,45]. The nuclear genome also supports efficient transformation. Although the amount of protein accumulation is slightly lower than that of the chloroplast, the resources of alternative markers, promoters, and reporters are abundant, and the expression efficiency can be improved through strategies such as codon optimization [46,47]. Genetic modification techniques for microalgae have become increasingly sophisticated, with transformation methods including DNA-coated nanoparticle uptake, CRISPR-Cas9-mediated transformation, electroporation, gene gun delivery, and Agrobacterium-mediated transformation [48,49]. In addition, the nuclear genome, chloroplast genome, and mitochondrial genome can all realize foreign gene integration, which goes far beyond some expression platforms that can only undergo nuclear transformation [50]. C. reinhardtii, as a model organism, possesses comprehensive molecular genetic tools and genomic databases. It exhibits rapid growth rates (doubling every 8 hours) and can be cultured under phototrophic, mixed-trophic, or heterotrophic conditions. Non-toxic and capable of low-cost protein secretion, its chloroplasts have successfully synthesized complex therapeutics such as foot-and-mouth disease virus VP1-toxin fusion proteins [51]. Diatoms (e.g., P. tricornutum) have attracted attention due to their silicified cell walls and unique ecological functions. Both the nuclear genome and plastidial genome have been stably transformed, and functional monoclonal antibodies can be efficiently secreted and expressed [52,53], providing more species options for IT production. Prokaryotic cyanobacteria have also been genetically engineered to achieve the synthesis of biofuels, bioplastics, and secondary metabolites [54]. Their genetic manipulation technologies (such as plasmid expression systems and homologous recombination) have laid the foundation for the subsequent expression of Its [55].

Biocompatibility and Low Immunogenicity Biocompatibility and Low Immunogenicity

Most clinically relevant microalgae are of the FDA-approved GRAS grade and have a long history of use in the field of food supplements. Their core advantage lies in the dual biocompatibility encompassing production host tolerance and in vivo therapeutic safety. At the production level, microalgae can tolerate the expression of complex ITs by means of the chloroplast sequestration mechanism [21]. At the level of in vivo application, its cell wall polysaccharide (predominantly β-1,3-glucan), photosynthetic proteins (sharing 30%-40% similarity with human homologous proteins), and phospholipid composition similar to that of human cell membranes can minimize immune rejection to the greatest extent [56]. They can also be enzymatically cleaved into non-toxic metabolites, combining host tolerance with in vivo therapeutic safety. Unlike traditional hosts, they do not rely on protease-deficient mutations or balanced lethal systems to circumvent toxin toxicity [57]. In the C57BL/6 mouse model, the drug delivery system constructed with microalgae showed no obvious inflammatory response within 72 hours after intravenous injection (the serum IL-6 level increased by ≤15% compared with the control group), and no inflammatory infiltration was observed in liver tissue sections [58]. By comparison, traditional expression systems have significant limitations: ITs expressed by Escherichia coli are prone to residual endotoxins, which can trigger inflammatory reactions such as fever and vascular leak syndrome [59]. The high-mannose glycan modification of Pichia pastoris tends to induce anti-carrier antibodies, with the antibody positive rate increasing with the frequency of administration [60]. Mammalian cells (e.g., CHO cells) are liable to retain animal-derived components, which increases the risk of allergies [61]. Microalgal microrobots can also be engineered to enhance safety: erythrocyte membrane, macrophage membrane, or PEG molecules can be coated on the surface to achieve immune escape, reduce macrophage phagocytosis rate, and prolong the circulation half-life [62]. Biodegradable materials such as GRAS strain and Fe₃O₄@SiO₂ are selected to ensure that the carrier is enzymatically metabolized without long-term accumulation, which makes it suitable for intravenous, oral, local injection, and other routes of delivery [63]. For example, oral administration of microalga-adriamycin complex can avoid intestinal mucosal injury and penetrate the intestinal barrier, providing new possibilities for the treatment of gastrointestinal tumors [64-66].

Surface Modification of Microalgae: A Key Support for Targeted Delivery of ITs

The surface of microalgae cells is naturally rich in active functional groups. Through a variety of flexible ways, such as covalent coupling, electrostatic interaction, membrane coating, and bioorthogonal reaction, microalgae can modify antibodies, peptides, aptamers, and other targeting elements to significantly improve the specific binding and enrichment ability of ITs to tumor tissues. In traditional modification strategies, microalgae such as C. reinhardtii and Arthrospira platensis are naturally negatively charged on their surfaces, enabling them to efficiently adsorb positively charged ITs (e.g., PE38 toxin domain, saponin) or targeting ligands through electrostatic interaction [67]. For instance, the spirulina-based drug delivery system (SP@Dox) developed by Zhou Min’s team from Zhejiang University achieved targeted tumor accumulation in a breast cancer lung metastasis model. Compared with the unmodified group, the tumor selectivity was increased by 2-3 fold, and the drug accumulation in normal lung tissues was reduced by more than 40% [68]. The chlorella-based biomimetic carrier coated with macrophage cell membrane can precisely deliver ITs by virtue of its inflammation-homing property. This not only increases the drug concentration in inflammation-associated tumor tissues by 3.2-4.5 fold but also reduces the non-specific distribution in normal organs such as the liver and kidneys [69]. In addition, microalgae can be adapted to different tumor targets to form a “one carrier and multiple targets” mode, which can be conjugated with trastuzumab, hyaluronic acid, and cetuximabfor HER2-positive breast cancer, CD44 high expression pancreatic cancer, and EGFR positive lung cancer, respectively, and the preparation cost is more than 40% lower than that of synthetic vectors such as liposomes [70-72].

Different from traditional systems that can only produce ITs, microalgae can achieve the integration of “production-modification”. For example, C. reinhardtii chloroplast can stably express ITs, and the carboxyl group on ITs surface can be directly covalently coupled with RGD peptide without additional purification steps [73], and the specific binding rate is over 85%; The modification of ITs expressed in Escherichia coli requires at least five steps of inclusion body dissolution, renaturation and multiple chromatography, which easily leads to the loss of toxin activity [74]. The targeted modification of ITs expressed in mammalian cells is easily interfered with by serum components [75]. The emerging bioorthogonal reaction (click chemistry) further amplifies the advantages of microalgae modification: Cu (I) -catalyzed azido-alkyne cycloaddition (CuAAC) can form a stable covalent bond between the targeted molecules and microalgae, and the tumor cell binding rate is 5-7 times higher than that of the unmodified group [76]; Strain-enhanced azido – alkyne cycloaddition (SPAAC) can achieve specific coupling under physiological conditions without metal catalyst [77], and retain ITs activity and carrier biocompatibility to the greatest extent. The surface modification of microalgae not only achieves efficient targeted delivery of ITs but also simplifies operation and reduces cost through an integrated process, which provides key technical support for the clinical transformation of ITs.

Structural Stability and High Loading Capacity of Microalgae: The Key to Efficient Delivery of ITs

The unique multi-level cellular structure of microalgae (rigid cell wall, phospholipid bilayer cell membrane, chloroplast and other intracellular compartments) can not only provide a physical barrier for ITs to resist acid-base environment and enzymatic degradation, but also achieve high-capacity loading by means of porous structure and intracellular storage, simultaneously solving the core defects of ITs which are easy to degrade and conformational instability. At the same time, it reduces the process complexity of in vitro loading and provides a double guarantee for efficient delivery.

(1) The multilayered structure confers strong stability and prolongs the active period of ITs

The rigid cell wall (containing cellulose, peptidoglycan, silica, and other components) acts as a “first line of defense” to physically isolate proteases, nucleases, and acidic environments in the blood [78], such as the siliceous shell of diatoms and the model toxin encapsulated by the cellulose-pectin complex cell wall of Chlorella. After incubation in the simulated fluid containing 1mg/mL trypsin for 72 hours, the activity retention rate was more than 70%, which was much higher than 15%-20% of the free toxin [79]; Spirulina-peptidoglycan cell wall could reduce the contact between protease and intracellular toxin, and the toxin activity could maintain more than 65% after 48 hours of incubation in pH 5.0 acidic environment [80]; The phospholipid bilayer can isolate pH-sensitive toxins (e.g., Pseudomonas aeruginosa exotoxin A) from the acidic environment of endosomes and lysosomes through hydrophobic interaction, resulting in a 3.3-fold longer half-life in vivo than the free form [81,82]; The thylakoid membrane of chloroplast can also provide a “secondary protection”, which can achieve a continuous and slow release of ITs in the cytoplasm even if the microalgal cell membrane is destroyed by lysosomes, avoiding toxic burst or rapid degradation [83]. In contrast, ITs expressed by Escherichia coli (e.g., PE38, DT388) require additional modification with BSA or PEG to resist degradation, with a half-life of only 2-4 hours [84]. ITs expressed by Pichia pastoris lose more than 60% of their activity within 24 hours in a simulated intestinal environments [85]. For ITs expressed by mammalian cells (e.g., CHO cells), low-temperature storage and stabilizers are necessary. Moreover, their stability decreases significantly in the presence of an acidic environment and proteases, making them unable to tolerate the complex tumor microenvironment [86,87]. In contrast, microalgae can achieve the stable existence of ITs without additional modification by virtue of their natural structure.

(2) Multiple load mechanism to achieve high-capacity delivery and adapt to different types of ITs

Microalgae support three loading modes, including physical encapsulation, chemical conjugation, and intracellular expression and storage, which can be flexibly adapted according to the hydrophilicity, hydrophobicity, and molecular size of ITs. The loading capacity of microalgae is significantly higher than that of synthetic vectors and traditional expression system-derived vectors. In terms of physical encapsulation, the porous silica shell of diatoms and the intracellular cavity of Chlorella can encapsulate small-molecule toxins or bioactive conjugates in batch, and the loading capacity of some microalgae-based carriers is better than that of traditional liposomes [88]. In the chemical coupling mode, the active groups, such as the hydroxyl group and the carboxyl group, on the cell wall surface could form covalent bonds with ITs to achieve stable loading. Microalgae such as Spirulina had high coupling efficiency and could well retain the loading molecular activity [89]. Under the mode of intracellular expression and storage, the chloroplast genome of microalgae can directly express ITs and store them [90]. The chloroplast of C. reinhardtii has been proven to be an efficient expression platform for recombinant therapeutic proteins. The products exhibit excellent solubility and comparable activity to those from traditional systems. Meanwhile, the thylakoid membranes of the chloroplast can provide protection for the expressed products, endowing them with greater advantages in activity retention compared to prokaryotic expression systems. Additionally, mild ultrasonic treatment can form nanoscale micropores in the chlorella cell wall to enhance encapsulation efficiency. Regulating the nitrogen source concentration in the culture medium can induce microalgae to accumulate lipid droplets, significantly increasing their loading capacity for hydrophobic molecules [91].

(3) Synergy of Stability and Loading Capacity, Adapting to Diversified Therapeutic Scenarios

In local long-acting tumor therapy, embedding the microalgae-bioactive molecule complex in sodium alginate bio-degradable hydrogel and implanting it locally at the tumor site can not only protect the loaded molecules from degradation by hydrolytic enzymes but also achieve sustained release through the porous structure, thereby extending the local effective treatment cycle [92]; In the scenario of systemic delivery, bioactive molecules encapsulated by spirulina can resist degradation by metabolic enzymes in the body after intravenous injection, enhance the enrichment efficiency at tumor sites, and alleviate off-target toxicity to organs such as the kidneys [93,94]. Traditional expression systems have long faced the core bottleneck of stability and load imbalance. Microalgae, through the synergistic advantages of structural protection and high capacity loading, simultaneously solve the key problems of insufficient stability and low delivery efficiency of ITs, providing a more suitable integrated solution for diverse clinical scenarios.

Complementary Applications of Microalgae and Conventional Platforms

Different expression platforms exhibit distinct adaptabilities, and there is no absolute superiority or inferiority among them: the microalgae platform is suitable for ITs that do not require complex glycosylation and demand low-cost, large-scale production (e.g., CD22-targeted ITs). Its culture cost is only 1/5 to 1/3 of that of Escherichia coli and more than 80% lower than that of CHO cells [95]; Mammalian cells are still the preferred choice for highly active ITs requiring precise glycosylation, which can achieve complex post-translational modifications and ensure ITs in vivo stability and targeted binding activity [96]. E. coli can be used for rapid expression of short peptide toxin fragments with a short turnaround time (only 24-48 hours), which is suitable for preliminary functional verification in the laboratory stage [97]. For practical applications, a strategy of “segmented production + in vitro assembly” can be used, such as microalgae expressing the target ligand and toxin backbone, followed by mild chemical coupling (e.g., SPAAC click chemistry) to achieve functional assembly, which takes both production cost and product activity into consideration.

Limitations of Existing Loading Strategies and Breakthroughs in Microalgal Recombinant Expression Systems

The production and delivery of traditional targeted drugs (including “magic bullet” drugs such as ITs) have long faced core technical bottlenecks, which seriously restrict their clinical translation efficiency. Currently reported microalgae-based microrobots (Figure 2), while integrating the natural motility of microalgae with engineered modification properties, achieve autonomous movement driven by flagella and can be precisely regulated via external stimuli such as light and magnetic fields [98,99]. These robots offer a promising solution for the active navigation and targeted delivery of ITs. However, such systems primarily achieve targeted drug delivery through chemical modification strategies like covalent binding and electrostatic adsorption, or physical loading methods such as biomembrane encapsulation [100,101], and thus still possess significant inherent limitations.

Figure 2: schematic depicts the natural properties, actuation methods, functionalization strategies, and biomedical applications of microalgae-based robots.

The first is the “single-use” limitation. The microalgae and the drug are not integrated in the design, and the micro-algae carrier has no regenerative loading capacity after the loaded part works, which is eventually removed by immune cells and cannot be reused. For example, the C. reinhardtii -red blood cell membrane-coated nanoparticle robot developed by the University of California, San Diego, can specifically deliver doxorubicin to lung metastatic tumor sites, significantly reduce tumor volume, and extend the median survival time of model mice from 27 days to 37 days [102]. However, it still fails to overcome this limitation. Second, large-scale production is limited, chemical modification requires secondary treatment, and biofilm encapsulation is limited by capacity, proliferation, and transmission, which leads to a cumbersome process and about 40% reduction in efficiency [103]. Thirdly, there is insufficient loading stability and adaptability. Chemically modified drugs are prone to detachment, leading to off-target toxicity. Biomembrane encapsulation has a narrow adaptability range for drugs with different molecular weights and hydrophilic-hydrophobic properties. For instance, ITs with a molecular weight greater than 100 kDa are difficult to load efficiently, while the loading rate of chemically modified small-molecule toxins may drop to less than 50% of the initial value after 24 hours of in vivo circulation [104]. For example, in the spirulina delivery system modified with Fe₃O₄ nanoparticles, the detachment rate of the loaded doxorubicin reaches 58% after 24 hours of in vivo circulation, resulting in toxic reactions induced by drug accumulation in some normal tissues [105].

The recombinant expression system in eukaryotic microalgae provides an innovative way to break through these limitations and is expected to solve the key challenge of the lack of efficient adaptation production platforms for ITs. The core breakthroughs focus on three aspects: first, the integrated production of carrier and drug. Microalgae are genetically engineered to directly express ITs or functional antibodies, and then stably stored or directed released by means of chloroplast isolation, signal peptide-mediated secretion, and other mechanisms, without in vitro modification or encapsulation steps, to avoid the loss of drug activity and the risk of contamination. For example, Synechocystis sp. PCC 6803 ex-pression system constructed by Zhang et al. successfully expressed phycocyanin (C-PC) and prepared polyclonal anti-bodies with a titer as high as 1: 1,025,000. Western blot analysis confirmed its high specificity, and due to the absence of in vitro chemical modification throughout the process, the antibody activity retention rate exceeded 95% [106]. Another study confirmed that when using chloroplast engineering technology to express fish virus subunit vaccines, the isolation and protection effect of the thylakoid membrane could make the antigen activity retention rate up to 94%, and the production efficiency was 38% higher than that of the traditional process [107]. Second, it possesses the capability of sustainable proliferation and stable expression. The engineered microalgae, after modification, can reproduce repeatedly under simple conditions, and their progeny can still stably carry and express ITs, achieving “one-time modification and continuous production.” This eliminates the need for repeated synthesis and significantly simplifies the production process. For example, the glass bead transformation method established by Kindle et al. successfully achieved nuclear transformation of Chlamydiae reinhardtii, which provided a reliable technical basis for the introduction of exogenous genes [108,109] further optimized the exogenous gene expression system of C. rhinophylla by inserting endogenous regulatory elements into the transgenic sequence, which significantly improved the expression stability. After successive passages, the expression of exogenous genes in the recombinant algal strain did not decrease significantly, and the growth rate was consistent with that of the wild-type algal strain [109]. Third, it enhances delivery safety and efficiency. ITs are expressed and stored by microalgae themselves, avoiding the reduction in biocompatibility caused by chemical modification. Meanwhile, by integrating the natural motility of microalgae with engineered navigation modules such as light and magnetic responsiveness, it enables full-chain controllable delivery encompassing “autonomous movement – targeted enrichment – endogenous release.” For example, the functionalized diatom delivery system constructed by De la Soie et al., which is modified with vitamin B₁₂-targeting molecules and a light-responsive module on its surface, achieves a 2-fold increase in targeted enrichment and photoactivated toxicity against colorectal cancer cells [110].

Although there is no direct study on the delivery of ITs mediated by microalgae, microalgae, as a natural delivery carrier with excellent biocompatibility, have accumulated a large number of successful cases in the delivery of “magic bullet” drugs (targeted chemotherapy drugs, immunomodulators, etc.), which provides an important reference for the application of ITs (Table 3). The nuclear and chloroplast genomes of the model microalgae have been transformed efficiently, and the CRISPR-Cas9 precision editing technology is mature. The chloroplast expression system has no transgene silencing and can complete key post-translational modifications. The commercial application of large-scale culture technology lays a solid foundation for the mass production of ITs. This integrated mode of “production-delivery” not only breaks through the limitations of existing microalgal robotics but also builds a low-cost, sustainable, and high-safety system, which is expected to become an ideal platform for the production and delivery of ITs. Subsequent optimization of microalgal surface targeting modifications (such as coupling with specific ligands, such as anti-CD22 and anti-HER2) and IT expression systems (such as chloroplast promoter optimization and signal peptide screening) can achieve synergistic optimization of efficient production and precise delivery, providing a new path for the clinical transformation of “magic bullet” drugs.

Table 3: Targeted delivery and clinical application of microalgae-based robots.

Microalgae Category

Modification Techniques

Carrier Substances

Targeting Methods

Clinical Application

References 

C. reinhardtii Electrostatic interaction load Doxorubicin Light signal-regulated guidance Bioactive substance delivery (Akolpoglu et al., 2020b) [111]
  Click on chemical coupling Ciprofloxacin Passive enrichment in lung capillaries Acute bacterial pneumonia intervention (Zhang et al., 2022b) [112]
  Click chemical modification Vancomycin + Ciprofloxacin Light-controlled targeted delivery Bacterial infectious disease prevention and treatment (Shchelik et al., 2021) [113]
  Cell-penetrating modification Functional drugs Magnetic field-driven navigation Bioactive substance delivery, fluorescence tracing (Santomauro et al., 2018) [114]
C. pyrenoidosa Electrostatic adsorption loading Doxorubicin In situ direct injection Osteosarcoma targeted therapy (Liang et al., 2024b) [115]
  Electrodeposition modification Doxorubicin Magnetic field-regulated navigation Targeted drug delivery efficacy enhancement (Gong et al., 2022) [116]
  Calcium phosphate coating modification / Active dispersion targeting Improvement of radiotherapy resistance in hypoxic tumors (Zhong et al., 2021b) [117]
  Cell membrane coating process Chloroquine + Hematoporphyrin dihydrochloride Immune-mediated targeting Antitumor immunotherapy efficacy enhancement (Gao et al., 2023) [118]
  Hydrogel composite modification Doxorubicin In situ injection administration Hypoxic breast cancer treatment (Lee et al., 2019) [119]
Spirulina Electrostatic adsorption loading Doxorubicin Passive targeting to lung capillaries Breast cancer lung metastasis treatment (Zhong et al., 2020) [120]
  Electrostatic interaction-based loading Doxorubicin In situ injection administration Osteosarcoma clinical treatment (An et al., 2024) [121]
  Electrostatic adsorption technology Astaxanthin Passive entrapment by intestinal villi Radiotherapy-related injury protection (Zhang et al., 2023) [122]
  Cell encapsulation technology Curcumin Passive retention by intestinal villi Oral drug delivery for intestinal diseases (Zhong et al., 2021d) [123]
  Cell encapsulation process Amifostine Passive entrapment by intestinal villi Intestinal radiotherapy injury protection (Zhang et al., 2022a) [124]
  Cell encapsulation technology Metformin In situ injection administration Targeted intervention for osteoarthritis (Liang et al., 2024d) [125]
  Electrodeposition modification process Doxorubicin Magnetic field-driven navigation Chemo-photothermal synergistic therapy (Wang et al., 2019) [126]
  Hydrogel composite modification Resveratrol Floating retention in gastric juice Alcohol-related disease treatment (Hua et al., 2024) [127]

Mechanisms of Enhanced Efficacy in Engineering Microalgae-Mediated IT Therapy

Engineered microalgae can significantly improve the therapeutic effect of ITs through multidimensional mechanisms such as enhancing tumor penetration, regulating tumor microenvironment and tumor-associated microbiome, and cooperative immune regulation. It can effectively solve the key bottleneck of clinical application of traditional ITs and provide core technical support for their clinical transformation.

Enhancement of Tumor Penetration

Microalgae-based microrobots, leveraging the advantages of natural flagella-driven autonomous motility and small size (1-10 μm), exhibit superior penetration capability into solid tumors compared to passive delivery systems such as liposomes and nanoparticles. McCord et al. confirmed via optical tweezers technology that the flagellar propulsive force of wild-type C. reinhardtii is significantly higher than that of flagellar structure-deficient mutants, providing a dynamic basis for its penetration through dense biological matrices [128]; Related studies have shown that C. reinhardtii can effectively cross the physical barrier composed of collagen fibers and glycosaminoglycans in the tumor extracellular matrix (ECM) by means of the voluntary movement driven by two flagella, and its tissue penetration ability is significantly better than that of static nanoparticles [129]. The advantages of self-driven microrobots in solid tumor penetration have been demonstrated in many studies. For example, the Fe₃O₄-mediated self-driven nanobots constructed by Banerjee et al. can penetrate into the core of the tumor in the HCT116 colorectal cancer tumor sphere in vitro, and the drug distribution is significantly better than that of free drug delivery and passive delivery vehicles. The disintegration of tumor spheres can be induced within 72 hours, which effectively solves the problem of uneven distribution of therapeutic agents and insufficient killing of deep cells, and significantly improves the killing efficiency of tumor cells [130].

Regulation of Tumor Microenvironment and Tumor-associated Microbiome

Polysaccharides, proteins, and antioxidant substances in microalgae can reduce inflammatory response, alleviate tumor hypoxia, and enhance anti-tumor immunity. In terms of microenvironment regulation, studies have shown that spirulina can significantly reduce the levels of TNF-α and other pro-inflammatory cytokines in tissues by inhibiting the NF-κB signaling pathway, and play an anti-inflammatory role [131]; Seaweed polysaccharides can inhibit macrophage activation by blocking the nuclear translocation of NF-κB, thereby reducing the release of IL-6 and TNF-α [132]; In addition, spirulina polysaccharides can effectively inhibit the polarization of tumor-associated macrophages (TAM) towards the tumor-promoting M2 phenotype (an anti-inflammatory macrophage subtype that promotes tumor angiogenesis, invasion, and metastasis), thereby collectively improving the tumor inflammatory microenvironment [133]. More importantly, the photosynthesis of microalgae can produce oxygen continuously in the tumor site, which not only enhances the killing activity of ITs against hypoxic cancer cells but also enhances the activity of immune cells. In terms of microbiome regulation, Ge et al. [134] confirmed that oral administration of spirulina can selectively regulate the structure of intestinal flora and increase the abundance of beneficial bacteria through its rich β-glucan and other prebiotics, thereby improving the body’s immune function [134]. Relevant studies have further confirmed that the increase in the abundance of beneficial intestinal bacteria can promote the maturation of dendritic cells and indirectly enhance the anti-tumor immune response of immunotherapy, which provides a mechanism to support the synergistic effect of engineered spirulina [135].

Synergistic Immunoregulatory Effects

The engineered characteristics of microalgae not only enhance their ability as IT delivery vectors, but also achieve synergistic effects with ITs through a variety of ways to improve the effect of anti-tumor immunity. Bioactive components released by microalgae can directly affect the function of immune cells. Polysaccharides (such as β-glucan) can bind to innate immune cell receptors, activate macrophages and dendritic cells, and induce the secretion of key cytokines, including IL-12 and TNF-α, which lay the foundation for the initiation of the acquired immune response. Enhance the body’s recognition and attack of tumor cells [136]; At the same time, its specific compounds can regulate the production of cytokines, reduce the level of immunosuppressive factors in the tumor microenvironment, inhibit the activity of MDSC (tumor-associated myeloid suppressor cells), and create favorable conditions for T cells and NK cells to exert anti-tumor effects [137,138]. Engineered microalgae also have the potential to activate long-term memory immune cells, such as memory T cells, which provides the possibility of improving the long-term efficacy of treatment and enhancing the immune system’s long-term monitoring and elimination ability against cancer cells. This direction is worthy of further exploration [139-141]. Additionally, microalgae can combine with immune-activating particles, such as CpG oligonucleotides, to further stimulate the anti-tumor activity of immune cells. Through the coordination of delivery systems and immune activation mechanisms, microalgae can significantly enhance cell-specific immune responses [142]. In the combination therapy scenario, microalgae can achieve an amplification of efficacy when combined with other cancer therapies, such as checkpoint inhibitors and CAR-T cell therapy. This combi-nation can not only provide sustained release of immunomodulatory factors but also efficiently deliver ITs to form synergistic effects through multiple mechanisms [143,144]. Through continuous improvement of the coordination strategy of microalgae and ITs, the killing ability of tumor cells can be greatly improved, and exploring the differences in the roles of different microalgae species in activating different immune pathways also opens up a new direction for follow-up research in this field.

Challenges and Future Prospects

Although engineered microalgae have shown significant potential in IT production, they still face several technical bottlenecks. Firstly, the expression efficiency is low. At present, the expression level of microalgal recombinant proteins is generally low, which is difficult to meet the needs of large-scale clinical application; Secondly, the purification process is complex, the microalgae cell wall structure is dense, which increases the difficulty of protein extraction, and the traditional fragmentation method may also lead to the degradation of the target protein; In addition, the immunogenicity problem should not be ignored. The glycosylation pattern of the microalgae expression system is different from that of mammalian cells, which may cause the expressed ITs to trigger non-specific immune responses in the host. In terms of targeted delivery, the tumor enrichment efficiency of microalgal vectors still needs to be improved. During oral administration, gastric acid and digestive enzymes in the gastrointestinal tract will cause significant damage to microalgal cells, resulting in low bioavailability. When injected intravenously, unmodified microalgae are easily cleared by the reticuloendothelial system and shorten the half-life of blood circulation. Synthetic biology technology has provided a clear optimization path to solve the above bottlenecks. By introducing heterologous signal peptide genes into model microalgae such as C. reinhardtii and reconstructing the ER-Golgi secretion pathway, the secretion efficiency and extracellular recovery rate of recombinant proteins can be significantly improved [145]; At the same time, the central carbon metabolism network and amino acid synthesis pathway were optimized to increase the supply of key amino acids and provide raw material support for the efficient synthesis of special structure Its [146].

The development of intelligent delivery systems is also the core of future research. The integration of blue-light-inducible promoters can realize the precise activation and release of ITs by light [147], and the pH-sensitive modification technology can make the microalgal vectors respond to the acidic tumor microenvironment to achieve targeted release and increase the local therapeutic concentration [148]. Advancing clinical translation requires multidisciplinary collaboration, with breakthroughs focused on three key areas. First, establish GMP-compliant large-scale microalgae cultivation and purification processes. Optimize parameters in closed photobioreactors—including light intensity (120–150 μE·m⁻²·s⁻¹), temperature (25±1°C), and pH (7.0–7.5)—to ensure batch consistency of products (purity ≥95%, coefficient of variation in activity ≤10%) [149]; second, enhancing immunogenicity-related research by conducting systematic safety evaluations (including acute toxicity, chronic toxicity, and immunogenicity assessments) and developing standardized clinical assessment methods (e.g., measuring anti-microalgal carrier IgG and IgE antibody titers in patient serum) [150]; Third, optimize the administration method by using enteric coating or targeted nano-suspensions to increase oral bioavailability from 10%–15% to over 30%, thereby reducing the required dosage and the risk of adverse reactions [151,152].

At present, preliminary progress has been made in the preclinical study of microalgae-mediated ITs. For example, anti-CD22 ITs expressed by C. reinhardtii were intraperitoneally injected consecutively at a dose of 10 mg/kg for 4 weeks in a mouse model of B-cell lymphoma; the tumor inhibition rate reached 58%-72%, with no significant weight loss or liver and kidney function damage observed. In the future, combination therapy and personalized treatment will become the core development direction. Micro-algal IT combined with CAR-T cell therapy can alleviate tumor hypoxia through microalgal oxygen generation, inhibit M2 macrophage polarization, and increase the infiltration rate of CAR-T cells by 2-3 times [153]; Based on patient-derived tumor organoids, suitable combinations of microalgae-expressing ITs (such as anti-HER2 ITs + immune activation module for HER2-positive breast cancer) can be rapidly screened to achieve “tailored” precision treatment and reduce the incidence of adverse reactions [154].

Conclusion

Engineered microalgae, as an emerging platform for IT production and delivery, offer innovative solutions for cancer treatment through their exceptional biosynthetic capabilities, outstanding cost-effectiveness, and favorable biocompatibility. From fundamental research to clinical translation, this platform has achieved significant progress in IT design, efficient production, and elucidation of the mechanism of action, demonstrating remarkable potential, particularly in targeted therapies for hematological malignancies and solid tumors. In the future, with the continuous development of synthetic biology, gene editing and nanobiotics, engineered microalgal systems will be iteratively upgraded to the direction of intelligence and precision. By optimizing expression efficiency, innovating delivery systems and developing combined treatment strategies, microalgal IT expression is expected to become one of the core technologies of the next generation of cancer immunotherapy. It provides a new way to solve the key problems such as drug resistance and side effects in current cancer treatment.

Author Contributions

Yuxin Xie: Conceptualization, Visualization, Data curation, Writing – original draft. Xiaoyu Deng: Formal analysis, Writing – review & editing. Quan Wang: Supervision, Writing – review & editing. Jishi Lv: Project administration, Supervision, Funding acquisition.

Funding

This research was funded Hubei University of Science and Technology Cultivate Scientific Research Project (2025-26X11).

Conflicts of Interest

The authors declare that the research was conducted in the absence of any.

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Decolonising Medical Education in Low- and Middle-Income Countries: From Institutional Autonomy to Institutional Responsibility

DOI: 10.31038/JCRM.2026914

Introduction

In our first commentary, we argued that commercialisation and neo-colonial influences have progressively shifted medical education in low- and middle-income countries (LMICs) away from its public purpose, replacing societal needs with market-driven measures of institutional success. We proposed reclaiming social accountability as a guiding principle through which medical schools could realign education with the health priorities of the populations they serve [1]. In our second commentary, we argued that this aspiration cannot be realised unless medical schools possess sufficient institutional autonomy to define educational priorities according to local health needs rather than predominantly responding to externally rewarded indicators of excellence [2]. Together, these arguments explain why reform is necessary and who should determine educational priorities. They leave, however, one important question unanswered: once medical schools possess that autonomy, how should it be exercised?

This commentary argues that the next stage in this progression is institutional responsibility. Institutional autonomy determines who has the authority to define educational priorities; institutional responsibility determines how that authority should be exercised. If medical schools seek greater freedom to determine their educational missions, they must also accept a broader role in strengthening the health systems and societies they serve.

By institutional responsibility, we do not suggest that medical schools replace governments or become solely responsible for healthcare delivery. Governments remain responsible for financing, regulating, and delivering healthcare. Medical schools, however, are not passive educational organisations operating outside health systems. Through their admissions policies, curricula, teaching hospitals, faculty practice, research agendas, partnerships with health services, and graduate outcomes, they exert substantial influence over the capacity, priorities, and future direction of national health systems. The question is therefore not whether medical schools influence healthcare, but whether they consciously accept responsibility for the influence they already possess.

We therefore propose institutional responsibility as the logical progression of the arguments advanced in our previous commentaries. Social accountability establishes the public purpose of medical education, while recent scholarship has increasingly recognised that educational institutions must contribute directly to health system strengthening rather than functioning solely as centres of professional training [3-6].

From Institutional Autonomy to Institutional Responsibility

Institutional autonomy is frequently interpreted as independence from external influence or freedom from regulatory constraints. We use the term differently. Institutional autonomy refers to the capacity of medical schools to determine educational priorities that reflect the health needs of their own societies while continuing to meet internationally recognised standards of educational quality. It is therefore neither isolation from international collaboration nor rejection of accreditation or external evaluation. Rather, it is the ability to exercise independent educational judgement within a globally connected academic community.

Autonomy, however, is not a sufficient objective in itself. Institutions that seek greater authority to determine educational priorities must also demonstrate that this authority is exercised in ways that advance the public good rather than institutional prestige alone. Autonomy without responsibility risks replacing one form of external dependence with another form of institutional self-interest. The important question is therefore no longer who determines educational priorities, but how educational authority should be exercised once it has been reclaimed.

This question is particularly important in LMICs. Over recent decades many countries have expanded medical education considerably while continuing to experience shortages of healthcare workers, inequitable distribution of services, weak primary healthcare systems, and substantial migration of health professionals. Increasing the number of medical schools or graduates has not consistently translated into stronger health systems. These challenges arise from complex political, economic, and social factors and cannot reasonably be attributed solely to medical schools. Nevertheless, educational institutions are influential participants within these systems. Decisions concerning student selection, clinical training, research priorities, postgraduate education, and partnerships with health services directly shape the future health workforce and influence the capacity of health systems to respond to national needs.

Institutional responsibility therefore broadens the traditional understanding of educational success. Medical schools have historically been evaluated through measures such as graduate competence, accreditation status, research productivity, international rankings, and academic reputation. These indicators remain important and should not be abandoned. However, they capture only part of an institution’s contribution. Equally important is the extent to which medical schools strengthen health systems, contribute to workforce sustainability, generate knowledge relevant to national priorities, and improve health equity. Educational excellence and societal contribution should therefore be understood as complementary rather than competing dimensions of institutional success.

Viewing medical schools as civic institutions rather than simply educational providers represents an important conceptual shift. Universities have long been recognised as institutions that contribute to economic development, public policy, and social progress beyond their teaching functions. Medical schools should similarly be understood as anchor institutions within healthcare systems. Their responsibility extends beyond producing competent graduates to fostering partnerships with communities, supporting healthcare delivery, informing public policy, generating locally relevant evidence, and strengthening the resilience of the health systems within which they operate. This conception is consistent with calls for medical schools to function as socially accountable institutions that actively contribute to strengthening health systems [3-6].

This perspective does not diminish the legitimate aspirations of students or faculty. Medicine remains an important profession that offers opportunities for career development, international collaboration, and social mobility. Nor does institutional responsibility imply that graduates should be prevented from pursuing opportunities abroad. Rather, it asks institutions to consider whether their collective strategies—including admissions policies, educational programmes, research priorities, and relationships with health services—are contributing meaningfully to the long-term health needs of the societies that support them.

Recognising this broader institutional role requires moving beyond general principles towards practical action. Institutional responsibility should not remain an abstract aspiration. Instead, it should provide an operational framework through which medical schools can evaluate their decisions, priorities, and societal contributions. This requires institutions to evaluate success not only through educational outcomes but also through their contribution to health system improvement [3,4].

Institutional Responsibility Framework (IRF)

To translate these principles into practice, we propose a Institutional Responsibility Framework (IRF) comprising five interconnected domains through which medical schools can operationalise their broader societal role. The IRF is not intended to replace accreditation standards or regulatory requirements. Rather, it provides a conceptual framework through which medical schools can align educational excellence with meaningful contributions to health systems and society.

Educational Responsibility

Educational responsibility requires medical schools to align admissions policies, curricula, assessment, and postgraduate training with nationally identified health priorities. This extends beyond ensuring that graduates meet internationally accepted standards of competence. Educational programmes should prepare future physicians to respond effectively to the epidemiological, demographic, social, and health system challenges most relevant to the communities they will serve. Success should therefore be evaluated not only by examination performance or postgraduate placement, but also by graduate preparedness to address local healthcare needs. This aligns with international calls for health professions education that is responsive to societal needs and national health priorities [3-6].

Service Responsibility

Medical schools should recognise their contribution to healthcare delivery as an integral component of their institutional mission.

Teaching hospitals, university clinics, community outreach programmes, and rural training platforms should function not only as educational settings but also as mechanisms through which institutions contribute directly to improving access to healthcare and strengthening local health services. This reflects the growing recognition that academic institutions function as anchor organisations capable of contributing directly to health system performance [3,4]. Long-term partnerships with communities should replace episodic outreach activities, allowing educational institutions to participate meaningfully in improving population health while simultaneously enriching student learning.

Workforce Responsibility

Medical schools substantially influence the quality, distribution, and sustainability of the future health workforce. They should therefore work collaboratively with governments, professional regulators, healthcare providers, and employers to support workforce planning and development. The Commission on the Education of Health Professionals argued that medical schools should actively participate in workforce transformation rather than limiting their role to producing graduates [3]. Institutional responsibility includes promoting career pathways that encourage service in underserved areas, strengthening primary healthcare, supporting postgraduate training in priority specialties, and contributing to strategies that improve workforce retention. Graduate migration is influenced by numerous economic and political factors beyond the control of educational institutions; however, medical schools can help create educational environments and professional opportunities that strengthen national workforce sustainability.

Knowledge Responsibility

Research agendas should increasingly emerge from locally identified health priorities rather than being driven solely by international funding priorities or publication incentives. Similar arguments have been advanced within contemporary scholarship on decolonising medical education, which calls for greater recognition of locally generated knowledge and contextually relevant research agendas [7]. Academic excellence should encompass implementation research, health systems improvement, policy engagement, quality improvement, and community impact alongside conventional bibliometric indicators. Medical schools should aspire not only to consume internationally generated evidence but also to produce knowledge that informs national policy, strengthens healthcare systems, and addresses contextually relevant health challenges.

Governance Responsibility

Institutional responsibility also requires more inclusive models of governance. Communities should move beyond being recipients of educational activities to becoming meaningful partners in institutional decision-making. Patients, community representatives, healthcare professionals, policymakers, and civil society organisations should contribute to strategic planning, curriculum development, institutional evaluation, and priority setting. Inclusive governance also reflects the principles of socially accountable institutions advocated in international guidance [4-6]. Such participation strengthens institutional legitimacy, ensures that educational priorities remain responsive to societal needs, and reinforces trust between medical schools and the communities they ultimately serve.

These five domains are mutually reinforcing. Educational reform cannot succeed without workforce planning; research cannot achieve societal impact without engagement with healthcare systems; and institutional autonomy cannot generate public trust without responsible governance. Together, they reposition medical schools as civic institutions whose responsibilities extend beyond educating future physicians to strengthening the health systems within which those physicians will practise.

Conclusion

Our first commentary argued that medical education in LMICs must reclaim its public purpose by resisting the growing influence of commercialisation and externally driven measures of success [1]. Our second commentary proposed that this objective cannot be achieved unless medical schools possess sufficient institutional autonomy to determine educational priorities according to the needs of the societies they serve [2]. This commentary completes that progression by arguing that autonomy alone is insufficient unless it is accompanied by institutional responsibility.

Institutional responsibility does not ask medical schools to replace governments or assume sole responsibility for healthcare delivery. Rather, it recognises that medical schools are influential institutions whose decisions shape future health workforces, research agendas, clinical services, and relationships with communities. Their educational mission cannot therefore be separated from their broader contribution to the health systems within which they operate.

Taken together, these three commentaries propose a progressive framework for reforming medical education in LMICs. Social accountability establishes the public purpose of medical education. Institutional autonomy enables medical schools to determine locally relevant educational priorities. Institutional responsibility provides the practical framework through which those priorities can be translated into meaningful institutional action. This perspective complements contemporary efforts to strengthen socially accountable and health-system-oriented medical education while extending them through a stronger emphasis on institutional responsibility [3-7].

Ultimately, the success of a medical school should not be judged solely by the physicians it graduates, the research it publishes, or the rankings it achieves. Equally important is the extent to which it contributes to stronger health systems, healthier communities, and more equitable societies. Ultimately, medical schools should be judged not only by the physicians they graduate, but also by the societies those physicians help to build. Institutional responsibility therefore represents not an additional obligation, but the fullest expression of the public purpose of medical education.

Declarations

Competing Interests

The author declares that there are no competing interests.

Funding Information

No external funding was received for this work.

Author Contribution

AFK conceptualised the commentary, conducted the literature review, drafted the manuscript, and approved the final version for submission.

Acknowledgements

The author would like to acknowledge the contributions of researchers whose work informed the development of this commentary.

Keywords

Institutional responsibility, Medical education, Institutional autonomy, Social accountability, Health systems strengthening, Decolonisation, Low- and middle-income countries (LMICs)

References

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