Diabetes, particularly type II, is a global health concern, with current treatments like α-glucosidase inhibitors often causing gastrointestinal side effects. This study explored the antihyperglycemic potential of crude protein hydrolysate from oil palm leaves (OPL) as a plant-based α-glucosidase inhibitor. OPL protein hydrolysate was extracted under acidic, neutral, and alkaline conditions, and their α-glucosidase inhibitory activity was assessed.
View Article and Find Full Text PDFIntroduction: Aplastic anaemia (AA) is a rare disorder of bone marrow failure, characterized by bone marrow hypocellularity with pancytopenia. The annual incidence rates of AA in Asia are observed to be two to three times higher than Europe and North America. Since the introduction of immunosuppressive therapy (IST) and of allogenic stem cell transplant (SCT), the outcome of severe AA has significantly improved.
View Article and Find Full Text PDFA delicate balance between neural stem cell (NSC) quiescence and proliferation is important for adult neurogenesis and homeostasis. Small ubiquitin-related modifier (SUMO)-dependent post-translational modifications cause rapid and reversible changes in protein functions. However, the role of the SUMO pathway during NSC reactivation and brain development is not established.
View Article and Find Full Text PDFPatients with both age-related macular degeneration (AMD) and C3 glomerulonephritis (C3G) are challenged by the absence of effective therapies to reverse and eliminate their disease burden. Capitalizing on complement dysregulation as both a significant risk factor for AMD and the known pathophysiology of C3G, we investigated the potential for adeno-associated virus (AAV) delivery of complement factor H (CFH) to rescue C3G in a -/- mouse model of C3G. While past efforts to treat C3G using exogenous human CFH resulted in limited success before immune rejection led to a foreign protein response, our findings demonstrate the capacity for long-term AAV-mediated delivery of truncated CFH (tCFH) to restore inhibition of the alternative pathway of complement and ultimately reverse C3G without immune rejection.
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