2022

Metabolomic Evidence for Peroxisomal Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

2026-02-18T06:14:57Z

Metabolomic Evidence for Peroxisomal Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Roy, Ayan Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic and debil- itating disease characterized by unexplained physical fatigue, cognitive and sensory dysfunction, sleeping disturbances, orthostatic intolerance, and gastrointestinal problems. People with ME/CFS often report a prodrome consistent with infections. Using regression, Bayesian and enrichment analyses, we conducted targeted and untargeted metabolomic analysis of plasma from 106 ME/CFS cases and 91 frequency-matched healthy controls. Subjects in the ME/CFS group had significantly de- creased levels of plasmalogens and phospholipid ethers (p < 0.001), phosphatidylcholines (p < 0.001) and sphingomyelins (p < 0.001), and elevated levels of dicarboxylic acids (p = 0.013). Using machine learning algorithms, we were able to differentiate ME/CFS or subgroups of ME/CFS from controls with area under the receiver operating characteristic curve (AUC) values up to 0.873. Our findings provide the first metabolomic evidence of peroxisomal dysfunction, and are consistent with dys- regulation of lipid remodeling and the tricarboxylic acid cycle. These findings, if validated in other cohorts, could provide new insights into the pathogenesis of ME/CFS and highlight the potential use of the plasma metabolome as a source of biomarkers for the disease.

Emergence of SARS-like coronavirus in China: An update

2026-02-18T06:15:01Z

Emergence of SARS-like coronavirus in China: An update Roy, Ayon

Strategies to trace back the origin of COVID-19

2026-02-18T06:15:25Z

Strategies to trace back the origin of COVID-19 Roy, Ayon

b-sitosterol conjugated silver nanoparticle-mediated amelioration of CCl4-induced liver injury in Swiss albino mice

2026-02-18T06:15:03Z

b-sitosterol conjugated silver nanoparticle-mediated amelioration of CCl4-induced liver injury in Swiss albino mice Roy, Ayan Objective: Drug induced hepatocyte death is a major contributor to acute liver failure. We aimed to deter- mine whether b-sitosterol conjugated silver nanoparticles (BSAgNPs) could ameliorate carbon tetrachlo- ride (CCl4)-induced liver injury in Swiss albino mice. Methods: Biogenic silver nanoparticles were synthesized from b-sitosterol to produce b-sitosterol (BS) conjugated silver nanoparticles. Serum liver function assays in mice model with CCl4-induced liver injury revealed that alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), bilirubin and cholesterol levels decreased markedly after treatment with b-sitosterol and BSAgNPs. In vivo liver enzymatic assays, including superoxide dismutase (SOD), catalase and reduced glu- tathione (GSH) were conducted to assess the antioxidant activity of the treatments. Results: Liver tissue from BSAgNP treated mice displayed significantly elevated SOD activity (73.57 ± 1. 48%) when compared to positive control group with silymarin treatment. Catalase activity decreased drastically in CCl4 treated mice (47.14 ± 1.08%), but increased with the administration of BSAgNPs (72. 24 ± 2.25%). An increase in transforming growth factor b (TGF-b1) in liver tissue homogenate accompa- nied a reduction in nuclear factor erythroid-2-related factor 2 (Nrf2) in CCl4 treated mice. b-sitosterol and BSAgNPs mediated the reduction of TGF-b1. In the BSAgNPs treated mice, Nrf2 level was significantly ele- vated; however, no change was detected following b-sitosterol treatment. Conclusion: Our findings reveal that b-sitosterol conjugated silver nanoparticles (BSAgNPs) may cause activation of the Nrf2 gene, through potential inhibition of TGF b1/Smad signaling. Antifibrotic effect of BSAgNPs may promote the lowering of chronic inflammation, oxidative stress and collagen deposition. Nanoparticle-mediated drug delivery of b-sitosterol may therefore have therapeutic promise against hep- atic complications.