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Department of Anaesthesia, Rabin Medical Centre, Beilinson Hospital, Petach Tikva, Israel; Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel. Electronic address:
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Department of Biotechnology, College of Biomedical & Health Science, Konkuk University, Chungju, Republic of Korea; Research Institute for Biomedical & Health Science (RIBHS), Konkuk University, Chungju, Republic of Korea. Electronic address:
Many patients with liver diseases are exposed to the risk of hepatic encephalopathy (HE). The incidence of HE in liver patients is high, showing various symptoms ranging from mild symptoms to coma. Liver transplantation is one of the ways to overcome HE.
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National Council of Research (CNR), Institute of Biochemistry and Cell Biology, 00015 Monterotondo (RM), Italy.
Botulinum neurotoxin type A (BoNT/A) has expanded its therapeutic uses beyond neuromuscular disorders to include treatments for various pain syndromes and neurological conditions. Originally recognized for blocking acetylcholine release at neuromuscular junctions, BoNT/A's effects extend to both peripheral and central nervous systems. Its ability to undergo retrograde transport allows BoNT/A to modulate synaptic transmission and reduce pain centrally, influencing neurotransmitter systems beyond muscle control.
View Article and Find Full Text PDFSpleen tyrosine kinase aggravates intestinal inflammation through regulating inflammatory responses of macrophage in ulcerative colitis.
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Cheeloo College of Medicine, Shandong University, Jinan 250012, China; Department of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining 272000, China. Electronic address:
Background: Ulcerative colitis (UC) is a persistent chronic, non-specific inflammatory disease, and macrophages play a crucial role in its pathogenesis. Spleen tyrosine kinase (Syk) is strongly associated with the pathogenesis of several inflammatory diseases. However, the role of Syk in the pathogenesis of UC is still obscure.
View Article and Find Full Text PDFEngineered extracellular vesicles for TGF-β encapsulation as a therapeutic strategy against LPS-induced systemic inflammation.
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National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, Key Laboratory of Medicinal Resources and Natural Pharmaceutical Chemistry (Shaanxi Normal University), The Ministry of Education, College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi 710119, China. Electronic address:
Inflammation underlies a wide variety of physiological and pathological processes, the Lipopolysaccharide (LPS)-induced inflammation model is widely recognized as a classical inflammatory paradigm, while Transforming growth factor-β (TGF-β) serves as a potent immunosuppressant capable of inhibiting immune responses and mitigating inflammation. However, its in vivo instability and the high cost associated with purification have imposed limitations on its clinical application. Therefore, we propose a therapeutic strategy for genetically modifying extracellular vesicles (HEVs) derived from HEK-293 T cells to incorporate TGF-β which holds potential for mitigating LPS-induced inflammation.
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