Translation Studies Research Articles

Stroke, stemming from either hemorrhagic or ischemic cerebrovascular events, remains a leading cause of mortality and morbidity worldwide. While there is currently no effective medical therapy for hemorrhagic strokes, ischemic strokes, constituting the majority of cases, benefit from limited curative interventions, namely thrombolysis with recombinant tissue plasminogen activator and endovascular thrombectomy. However, these options are constrained by narrow post-stroke therapeutic windows. Cerebral edema, characterized by blood-brain barrier disruption and endothelial dysfunction, is a major contributor to stroke-related mortality. Endothelial progenitor cells, released by bone marrow in response to ischemic injury, have in recent years emerged as key players in vascular repair, blood- brain barrier restoration, angiogenesis and vasculogenesis. Despite accumulating evidence, the definition and characterization of endothelial progenitor cells remain inconsistent which complicates their development as so-called efficacious novel therapeutics. Concomitant targeting of markers for stemness, immaturity, and endothelial cell maturity, including CD34, CD133, and KDR, helps delineate true endothelial progenitor cells from hematopoietic cells. The synthesis, recruitment, and functionality of endothelial progenitor cells are regulated by a variety of signaling pathways, notably stromal cell-derived factor-1α/chemokine receptor 4, vascular endothelial growth factor, endothelial nitric oxide synthase/nitric oxide, and Notch1/Jagged1. These processes are influenced by several physiopathological factors such as aging, inflammation, and ischemic injury. In translational studies, endothelial progenitor cells demonstrate robust potential in attenuating infarct size, inflammation, and apoptosis while inducing angiogenesis and improving motor and cognitive functions. Although autologous and allogeneic endothelial progenitor cell-based therapies have shown safety and some efficacy in early-phase clinical trials, results remain inconclusive, and large-scale studies are required to confirm or dismiss the current findings. Issues regarding the number, route, and frequency of endothelial progenitor cell administration also need addressing. For instance, routes of endothelial progenitor cell administration present varying degrees of invasiveness, efficacy, and feasibility. Emerging research highlights the endothelial progenitor cell secretome, composed of several growth factors, cytokines, and extracellular vesicles, as a cell-free therapeutic option. Secretome-based therapeutic interventions avoid many safety and logistical challenges of cell therapies while offering comparable regenerative benefits in preclinical stroke models. Temporal dynamics in secretome composition, especially those in post-stroke pro-angiogenic and anti-angiogenic factor bioavailability, indicate the requirement for precise therapeutic timing. Clinical studies also suggest ischemic injury itself, rather than comorbid risk factors, as the principal driver of secretome alterations such as tumor necrosis factor-α upregulation. In conclusion, endothelial progenitor cells and their secretome hold significant promise as novel therapeutics for stroke. However, unresolved issues surrounding cell characterization, delivery methods, optimal time of administration, and safety must be addressed through rigorous translational and clinical studies before their use in clinical settings.

Background: While statin therapy effectively lowers plasma LDL cholesterol (LDL-C), residual cardiovascular risk remains. Emerging evidence suggests that LDL-C may exert deleterious effects beyond its role in plaque development. Even moderately elevated or borderline LDL-C levels can act as nutrient signals that chronically activate maladaptive pathways in immune cells. In particular, LDL-C can stimulate mTORC1 signaling in monocytes and macrophages — key immune cells involved in atherosclerosis — leading to autophagy suppression, unresolved inflammation, and plaque progression. Methods: In a translational study, we compared monocyte mTORC1 signaling and autophagic markers in hypercholesterolemic patients (LDL-C >160 mg/dL, n=10) and healthy controls (LDL-C <100 mg/dL, n=10). Monocyte mTORC1 activity was assessed via its downstream target, phosphorylated S6 (pS6), and mTOR–LAMP2 colocalization (lysosomal mTOR recruitment). Autophagy was measured by LC3 intensity using immunofluorescence microscopy. Follow-up samples were collected after 12 weeks of statin therapy, administered as part of routine clinical care. Mechanistic insights were supported by in vitro LDL-C stimulation in human monocyte-derived macrophages (HMDMs) and in vivo studies in ApoE-/- mice. Results: Hypercholesterolemic patients exhibited a ~3.5-fold increase in monocyte pS6/Total S6 levels and ~1.5-fold higher mTOR–LAMP2 colocalization compared to controls, consistent with elevated mTORC1 activity. LC3 intensity was reduced by approximately 50%, indicating suppressed autophagy. In vitro, LDL-C triggered mTORC1 activation, reactive oxygen species (ROS) production, and apoptosis in HMDMs. In mice, dietary cholesterol increased monocyte mTORC1 signaling, which reversed after a switch to chow. Preliminary follow-up data suggests partial normalization of mTOR activity after statin treatment. Conclusions: These findings show that elevated LDL-C is linked to increased mTORC1 activity and autophagy suppression in monocytes. Using both pS6 and lysosomal mTOR localization provided complementary evidence of pathway activation. Targeting the cholesterol nutrient-sensing mTOR–autophagy axis may offer new strategies to reduce atherosclerotic risk beyond standard lipid-lowering. This approach could support precision cardiovascular medicine by tailoring treatment to individual cellular and metabolic profiles, rather than relying solely on population-level LDL thresholds.

In the early eighteenth century, Dominique Parennin, a French Jesuit missionary in China, wrote at the behest of the Emperor Kangxi a manuscript in the Manchu language which combined some of the theories of traditional Chinese medicine with Western medical concepts. One of the surviving manuscripts of this "Manchu Anatomy," sent by Parennin to the French Royal Academy of Sciences in 1723, is now kept in the Muséum d'Histoire Naturelle in Paris. This work, "Ge ti ciowan lu bithe," has recently been translated into modern Mongolian, affording an opportunity to research Parennin, his life and work, and the significance of the "Manchu Anatomy."

Introduction: Following infarction, heart often undergoes pathological remodeling and dysregulation of sodium and calcium homeostasis, predisposing patients to heart failure and arrhythmias. While current pharmacological therapies can slow disease progression, they are not aimed to directly address deficits in both cardiac contraction and action potential conduction. Previously, we have demonstrated that AAV-mediated gene therapy with the prokaryotic voltage-gated sodium channel (BacNav) can restore cardiac electrical and mechanical function in a setting of pressure-overload heart failure. Hypothesis: We hypothesized that AAV-BacNav gene therapy could rescue contractile and electrical dysfunction in a clinically relevant setting of chronic post-myocardial infarction. Method: 8-to-10-week-old male rats underwent a 45-min left anterior descending artery ligation followed by reperfusion. Two weeks after the ischemia/reperfusion surgery, we delivered a total of 1E12 viral genomes of either myo2A-cTnT-BacNav-HA-mScarlet (BacNav group) or myo2A-cTnT-mScarlet (mock group) via direct injection around the scar area in the left ventricle (a total of 200uL, split into 6-8 sites) (n=3 for BacNav group, n=5 for mock group). Cardiac contractile and electrical function was non-invasively monitored over the following four weeks using echocardiography and electrocardiography, respectively, followed by ex vivo epicardial voltage mapping in Langendorff-perfused hearts. Results: At 2 weeks post-surgery, all rats exhibited left ventricular ejection fraction (LVEF) reduction (BacNav: 46.45+/-3.81%; mock: 50.92+/-2.50%). The LVEF continued to deteriorate in the mock group during the following 4 weeks, while in the BacNav group it significantly improved (BacNav: 54.71+/-3.26%; mock: 42.66+/-3.34%). While both groups exhibited rare incidences of spontaneous arrhythmias in ECG, the BacNav group had reduced cardiac axis deviation (BacNav: 37.53-69.18°; mock: -152.14-135.54°). Ex vivo epicardial voltage mapping to test for arrhythmia vulnerability revealed spontaneous reentry in 100% of mock group hearts, compared to only 33.3% in the BacNav group. Conclusion: AAV-BacNav therapy significantly improved both contractile and electrical function in a rat model of ischemia-reperfusion heart failure, providing foundation for the future translational studies.

Background: High-density lipoprotein (HDL) is classically recognized for its atheroprotective functions, including facilitating reverse cholesterol transport and reducing vascular inflammation and oxidative stress. However, growing evidence reveals that HDL is functionally heterogeneous. Human plasma HDL can be fractionated chromatographically into five subfractions (H1-H5), with increasing electronegativity and progressively impaired protective functions. H5, the most electronegative subfraction, is associated with increased inflammation, impaired cholesterol efflux capacity, and other features suggestive of a potential atherogenic role. Purpose: To evaluate the clinical and mechanistic relevance of H5 in atherosclerotic cardiovascular disease (ASCVD), we performed a translational study integrating human data with in vivo mouse experiments. Given the elevated ASCVD risk among individuals with metabolic syndrome (MetS), we investigated correlations between H5 levels, the number of MetS criteria met, and key ASCVD-related risk indicators. We hypothesized that H5 enrichment contributes directly to vascular pathology. Methods: Asymptomatic individuals ( n =83) who met diagnostic criteria for MetS and exhibited at least one ASCVD risk factor were enrolled. Carotid artery ultrasonography was used to measure stenosis as a surrogate of subclinical ASCVD. To explore causality, purified human H5 was intravenously administered to C57BL/6J mice. H1, the least electronegative HDL subfraction, and saline served as controls. Aortic lipid deposition and fibrosis were assessed via Oil Red O and Picro-Sirius Red staining, respectively. Results: Plasma H5% positively correlated with systolic blood pressure, ankle-brachial index (ABI), and carotid artery stenosis ( Table 1 ). A representative case of a 63-year-old male with T2DM and a MetS history—yet otherwise favorable lipid profile—revealed 38.46% carotid stenosis associated with elevated H5 (4.4%), despite no history of statin use ( Figure 1 ). In vivo, H5-treated mice exhibited marked lipid-rich aortic plaques and increased collagen deposition, while H1 and saline controls showed minimal pathology ( Figure 2 ). Conclusion: This study provides both clinical and experimental evidence that electronegative HDL, specifically H5, contributes to vascular dysfunction and ASCVD progression. H5 may serve as a novel biomarker and therapeutic target, enabling more refined cardiovascular risk stratification and personalized preventive strategies.

Background: Inhaled cannabis has been associated with increased risk of acute coronary events, yet the mechanisms remain unknown. Hypothesis: Using a novel ex vivo mechanistic atherogenesis assay, the purpose of this translational study was to test the hypothesis that combusted cannabis use increases two early steps in atherogenesis, monocyte transendothelial migration (MTEM) and monocyte-derived foam cell formation (MDFCF), in people who use combusted cannabis, and that these changes are further increased in people who co-use combusted cannabis with nicotine electronic cigarettes (nECIGs), the tobacco product of choice in young people. Methods: In a cross-sectional study, using PBMCs and plasma from healthy adults (21-30 y) who chronically 1) use inhaled combusted cannabis, 2) co-use combusted cannabis and nECIGs, and 3) non-using controls, proatherogenic monocyte factors were measured using our ex vivo atherogenesis assay (Fig 1A) and compared amongst the 3 groups. Outcomes were 1) MTEM (% of blood monocytes that undergo transendothelial migration through a collagen gel), and 2) MDFCF as determined by flow cytometry and 3) the median fluorescence intensity (MDFCF-MFI) of the lipid staining fluorochrome BODIPY in monocytes. Results: A total of 134 participants were enrolled (combusted cannabis use=59, combusted cannabis/nECIG co-use=26, control=49). The demographics of the groups did not differ. The MTEM was significantly greater in people who use cannabis (27.8 + 4.4%, p<0.00001, mean±SD) or co-use cannabis/nECIG (33.2 + 7.8%, p<0.0001) vs controls (24.8 + 2.8%) and tended to be greater in people who co-use cannabis/nECIG vs cannabis alone (p=0.056, Fig 1B). Similarly, MDFCF and MDFCF-MFI were greater in people who use cannabis (35.8 + 6.5%,1155.0 + 159.6 u, respectively) or co-use cannabis/nECIG (44.7 + 10.0%, 1464.2 + 253.1 u) vs controls (25.8 + 8.6%, 967.2 + 170.2 u; p<0.00001 for all) and were significantly greater in people who co-use cannabis/nECIG vs cannabis alone (p=0.03; Figs 1C &1D). Conclusions: Chronic use of combusted cannabis is associated with higher monocyte transendothelial migration and monocyte-derived foam cell formation, two early instigators of atherogenesis, in a novel ex vivo atherogenesis assay. The changes are further increased in people who co-use combusted cannabis with nicotine electronic cigarettes. These findings provide mechanistic insights into the observation that cannabis use is associated with increased risk of myocardial infarction.

Background: Understanding mechanisms activating the cardiomyocyte (CM) cell-cycle in large mammals is essential to designing molecular therapies for treating injured hearts. Pig CMs are known to exist cell-cycle shortly after birth; however, we have shown that pig CMs actively proliferate when apical resection surgery is performed on postnatal day 1 (AR P1 ), and active CM proliferation starts on postnatal day (P)8 following injury. CM single-nucleus RNA-sequencing (snRNAseq) data were collected and processed from uninjured (CTL) pigs and AR P1 pig hearts on P1, P4, P8, and P28 at the border zone. Before P8, expressions of two heat-shock proteins, HSPA5 and HSP90B1, significantly decreased on P4 and remained low at later timepoints in naïve hearts. Hypothesis: Stress-responsive heat-shock proteins are upregulated in pig AR P1 cardiomyocytes before AR P1 P8 and promote CM proliferation. Approach: Heat-shock protein expressions were evaluated via immunohistological analysis in blindly-selected areas in naïve fetal, CTL-P7, and AR P1 P8 pig hearts. The capability of heatshock proteins in inducing CM cell-cycle was demonstrated in human AC16 CM cell line via lentivirus-mediated overexpression and knockdown of HSPA5 and HSP90B1. Cell-cycle marker PH3 and cell-cycle regulators FOXM1, P53, and antioxidant molecule PRX-V were quantified in AC16 cells via Western blotting. Results: Following AR P1 , both snRNAseq and immunohistological analysis showed that the expression of heat-shock proteins remained high in AR P1 P8 CMs. In AC16 cells, overexpression (or knockdown) of HSPA5 and HSP90B1 increased (or decreased) the cell cycle. Overexpressing (or knocking down) HSPA5 resulted in an increase (or decrease) of PH3, FOXM1, and PRX-V; while P53 expression decreased (or increased). Overexpressing (or knocking down) HSP90B1 increased (or decreased) PH3 and HSPA5. Conclusion: HSPA5 and HSP90B1 were upregulated in pig AR P1 CMs before the active CM proliferation timepoints, and promoted cardiomyocyte cell-cycle activity; the mechanism involved the downstream effectors, including FOXM1, PRX-V, and P53. Designing molecular therapies targeting these genes may promote CM proliferation and protection in translational studies of heart diseases.

An RNS mouse model was established using a “24-hour sleep deprivation and 48-hour recovery cycle” repeated for 5 cycles. RNS mice exhibited elevated peripheral inflammation and myocardial injury. Single-cell RNA sequencing (scRNA-seq) combined with flow cytometry revealed increased infiltration of macrophages in cardiac tissues of RNS mice, primarily originating from the bone marrow. Reactome enrichment analysis identified significant activation of the Dectin-1 signaling pathway in cardiac-infiltrating monocytes and macrophages, and genetic knockout of Dectin-1 (Dectin-1-/-) markedly attenuated RNS-induced macrophage infiltration and myocardial injury. Epigenetic profiling (ATAC-seq and CUT–Tag) demonstrated that even after a 4-week recovery period, RNS-exposed hematopoietic stem and progenitor cells (HSPCs) maintained increased chromatin accessibility at genes related to leukocyte migration and myeloid cell differentiation, accompanied by persistent enrichment of H3K4me3 modifications at these loci, suggesting the establishment of trained immunity. Furthermore, RNS-induced trained immunity could be transferred to recipient mice via bone marrow transplantation, leading to exaggerated inflammatory responses upon secondary challenges such as RNS or ischemia-reperfusion injury. Mechanistic studies showed that sympathetic activation elevated norepinephrine levels in bone marrow, which primarily via β1-adrenergic receptor (β1-AR) upregulated EGR1 expression in HSPCs. ChIP-qPCR and dual-luciferase reporter assays confirmed that EGR1 directly binds to and transactivates the promoters of histone methyltransferases SETD1B and KMT2B. EGR1 knockout significantly suppressed norepinephrine-induced pro-inflammatory reprogramming and trained immunity in bone marrow. In vitro siRNA knockdown experiments further revealed that SETD1B depletion more potently inhibited H3K4me3 establishment compared to KMT2B, implicating the β1-AR/EGR1/SETD1B axis as dominant in sympathetic-driven trained immunity. Clinical translational studies detected consistent H3K4me3 enrichment and upregulated Dectin-1 signaling pathway genes in peripheral blood monocytes of night-shift workers. In animal models, EGR1-/- mice exhibited suppressed Dectin-1 signaling pathway and reduced myocardial injury, while AAV-mediated Dectin-1 overexpression reversed this protection, confirming that RNS-activated trained immunity exacerbates myocardial injury via the Dectin-1 pathway.

Doxorubicin (DOX), a widely used chemotherapeutic agent, is effective against various malignancies, but its clinical application is limited by cumulative dose-dependent cardiotoxicity. The objective of this review is to systematically explore the molecular mechanisms involved in DOX-induced cardiotoxicity (DIC) and evaluate the cardioprotective potential of plant-derived bioactive compounds. A comprehensive literature search was conducted using databases, such as PubMed, Scopus, and Web of Science, focusing on studies published in the last two decades. Emphasis was placed on experimental and preclinical models that investigated molecular pathways of DIC and the therapeutic role of phytochemicals. DOX-induced cardiotoxicity is mediated through a cascade of molecular events, including excessive oxidative and nitrosative stress, mitochondrial damage, apoptosis, impaired autophagy, and altered activity of signaling pathways, such as AMPK, Nrf2, TGF-β1/Smad2, and HIF-1α. Epigenetic dysregulation also contributes to myocardial injury. Phytochemicals, such as flavonoids, polyphenols, and alkaloids, have shown significant cardioprotective effects. These compounds exert their actions by modulating redox homeostasis, preserving mitochondrial function, regulating apoptotic markers, and restoring signaling imbalances. The pleiotropic nature of phytocompounds enables them to target multiple pathological mechanisms associated with DIC. Despite promising in vitro and in vivo evidence, limitations, such as poor bioavailability, lack of standardized dosing, and inadequate clinical data, hinder their translational potential. Novel delivery systems and well-controlled clinical trials are necessary to overcome these challenges. Plant-derived bioactive compounds show potential in mitigating doxorubicin-induced cardiotoxicity, as supported by preclinical evidence. However, further translational studies are warranted to validate these findings, optimize pharmacokinetics, and evaluate their feasibility in clinical oncology settings.

This seminar presents a comparative linguistic study of French and Yoruba adverbs, emphasizing their forms, classifications, functions, and pedagogical implications. The paper examines how adverbs in both languages act as essential modifiers that enrich the meanings of verbs, adjectives, and other adverbs. Drawing on the works of Grevisse (1988), Dubois and Lagane (2006), and Bamgbose (1966), the study identifies the main categories of adverbs — those of manner, time, place, quantity, affirmation, and negation — and analyzes their syntactic behavior. In French, adverbs are primarily formed through morphological derivation (especially with the suffix -ment), while in Yoruba, they are mostly produced through reduplication, a process that reflects the rhythmic and tonal character of the language. The research shows that although French adverbs tend to occupy fixed positions in sentences, Yoruba adverbs exhibit syntactic flexibility and are strongly influenced by context and cultural expression. Despite these differences, both languages share the communicative goal of enhancing clarity, precision, and emphasis in discourse. The study concludes that a deeper understanding of adverbial structures in both languages contributes significantly to effective bilingual pedagogy, translation studies, and linguistic competence.

Abstract Ku Hung-Ming 辜鴻銘 (pinyin: Gu Hongming, 1857–1928) was the first Chinese translator who translated Confucian classics into English, breaking the long-time monopoly of translation of Confucian classics by Western missionaries. He also translated Western poems into Chinese and elaborated on his thought on translation in his writings. However, Ku is peripheralized in contemporary Chinese historiography of translation. This article investigates this striking phenomenon, arguing that Ku’s peripheralization is due to Chinese translation historiographers’ subscription to the dual meta-narratives of individual enlightenment and national salvation, their colonial mentality, and the impact of the century-long trivialization of Ku in China. This article throws into relief the intricate relationship between translation historiography and its socio-political context, calling for attention to this under researched area of translation studies. It also sheds important light on contemporary Chinese intellectual landscape, calling for a decolonized understanding of Chinese culture.

This study aims to analyze the translation techniques used in the English version of Selera Nusantara, a mobile video game developed by Gambir Game Studio that highlights Indonesia’s culinary and cultural richness. The research focuses on Season 1, Episode 1 of the game, which introduces the main narrative and characters. Using Anthony Pym’s (2018) typology of translation solutions as the analytical framework, this study identifies and categorizes the translation strategies applied in rendering the game’s dialogue and cultural references from Indonesian to English. The research employed a descriptive qualitative method, with data collected through documentation and content analysis of the game’s bilingual scripts. The findings revealed a total of 1,196 translation solutions, with Perspective Change being the most dominant (373 instances), followed by Cultural Correspondence (327) and Density Change (259). The subcategory Relocation of Culture-Specific Referents emerged as the most frequently used strategy within Cultural Correspondence. These results suggested that translators prioritized cultural adaptability and narrative clarity to make the game accessible to a global audience while preserving its Indonesian identity. The study contributed to translation studies by demonstrating the applicability of Pym’s typology to interactive digital content and highlighting the importance of translation in promoting local culture through global media like video games.

Ultrasound-induced blood-brain barrier opening and selenium-nanoparticle injection lower seizure activity: A mouse model of temporal lobe epilepsy.

Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage breakdown and chronic inflammation. Current therapies mainly relieve symptoms but do not halt disease progression. We developed collagen hydrogels incorporating propolis-loaded zeolitic imidazolate framework-8 (ZIF-8) nanoparticles (PROZIF) and menstrual blood-derived stem cells (MenSCs). Invitro assays evaluated microstructure, cell viability, anti-inflammatory activity, drug release, and cytoprotection. An osteoarthritis model was induced in rats by monosodium iodoacetate (MIA). Animals received intra-articular injections of hydrogels, and outcomes were assessed by histology, enzyme-linked immunosorbent assay (ELISA), knee swelling, and locomotor function. Collagen-PROZIF-MenSCs hydrogels with 2% nanoparticle content (COL-PROZIF-MenSCs-2) preserved MenSC viability, showed strong anti-inflammatory effects, and provided sustained propolis release. Invivo, this group significantly reduced cartilage degeneration, decreased tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), and increased transforming growth factor-beta (TGF-β) and fibroblast growth factor (FGF) levels compared to controls. Knee swelling was reduced, and locomotor scores improved. Combining ZIF-8 nanoparticles with MenSCs in collagen hydrogels synergistically mitigated OA progression in rats by reducing inflammation and supporting cartilage repair. This approach demonstrates promise as a localized, cell- and drug-based therapy for OA, warranting further long-term and translational studies.

Genomic profiling of high tumor mutational load in microsatellite-stable colorectal cancer uncovers MAPK signaling pathway alterations following anti-EGFR therapy.

ABSTRACT Drawing from Lawrence Venuti's concept of ‘invisibility’ (1995/2018), this study examines Jhumpa Lahiri's efforts to enhance her visibility in the paratexts of her translations and self-translations. Taking advantage of her status as a Pulitzer Prize-winning author, Lahiri experiences linguistic transmigrations between English and Italian. This analysis explores her transition to a translingual author, beginning with her first book written in Italian, her interlinguistic translation of Domenico Starnone's novels, and, finally, her self-translation strategies. All these literary shifts serve as a means to redefine her literary identity and assert her presence as a (self-)translator. By exploring the paratexts accompanying her (self-)translations, this paper highlights how Lahiri challenges traditional perceptions of translator invisibility, contributing to contemporary discussions in translation studies.

Rewiring amino acids in cancer.

Multiple system atrophy (MSA) is a rare and progressive neurodegenerative disorder characterized by Parkinsonism, cerebellar dysfunction, and autonomic failure. Emerging evidence suggests that gut microbiota may contribute to neurodegeneration, but whether these associations are causal remains unclear. We conducted a two-sample Mendelian randomization (MR) analysis using genome-wide association study (GWAS) summary statistics of gut microbiota (n = 18,340) from the MiBioGen consortium and MSA (888 cases, 7,128 controls) from a recent European study. Single nucleotide polymorphisms associated with 196 bacterial taxa were selected as instrumental variables. The primary MR method was inverse-variance weighting, complemented by weighted median, MR-Egger, and MR-PRESSO. Sensitivity analyses assessed pleiotropy, heterogeneity, and robustness. Six taxa showed nominal associations with MSA risk. Lentisphaeria (OR = 1.57, p = 0.035), Oscillospira (OR = 1.76, p = 0.034), Victivallales (OR = 1.57, p = 0.035), and Peptococcus (OR = 1.46, p = 0.025) were positively associated with increased risk, whereas Veillonella (OR = 0.40, p = 0.004) and Erysipelotrichaceae UCG-003 (OR = 0.60, p = 0.041) were associated with reduced risk. No evidence of pleiotropy or heterogeneity was found. None survived multiple-testing correction. This MR study provides hypothesis-generating evidence suggesting potential causal relationships between gut microbiota and MSA. These taxa nominate candidate microbial targets for future mechanistic and translational studies.

Mass spectrometry-based proteomics in glioblastoma - current understanding and future impact.

Development of succinate dehydrogenase subunit B-deficient tumor models for preclinical immunotherapy testing.