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Role of Ciliary Neurotrophic Factor in Angiotensin II-Induced Hypertension.

Hypertension

January 2025

Department of Nephrology, Medical Faculty, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Germany (S.A.P., I.Q., D. Arifaj, M.K., D. Argov, L.C.R., J.S.).

Background: Ciliary neurotrophic factor (CNTF), mainly known for its neuroprotective properties, belongs to the IL-6 (interleukin-6) cytokine family. In contrast to IL-6, the effects of CNTF on the vasculature have not been explored. Here, we examined the role of CNTF in AngII (angiotensin II)-induced hypertension.

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Decapod crustaceans regulate molting through steroid molting hormones, ecdysteroids, synthesized by the molting gland (Y-organ, YO). Molt-inhibiting hormone (MIH), a neuropeptide synthesized and secreted by the eyestalk ganglia, negatively regulates YO ecdysteroidogenesis. MIH signaling is mediated by cyclic nucleotide second messengers.

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Novel approach to managing two enormous bezoars with successive snare-tip electrocautery: A case report.

World J Gastrointest Endosc

January 2025

Division of Gastroenterology and Hepatology, Department of Internal Medicine, Lukang Christian Hospital, Changhua 505002, Taiwan.

Background: Gastric bezoars are indigestible masses that can lead to gastrointestinal obstruction and ulceration. Standard treatments include endoscopic mechanical lithotripsy with a polypectomy snare and Coca-Cola dissolution therapy or a combination of both approaches. However, giant bezoars frequently require multiple treatment sessions and extended hospital stays.

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Colorectal cancer (CRC) is one of the most prevalent and deadly malignancies worldwide. Recently, ferroptosis, a novel form of regulated cell death characterized by iron dependency and lipid peroxidation, has garnered significant attention from researchers. The mechanisms underlying ferroptosis, including intracellular iron levels, lipid peroxidation, and antioxidant system regulation, offer new insights into cancer treatment strategies.

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Rationale: Acute kidney injury (AKI) is a clinical syndrome associated with a multitude of conditions. Although renal replacement therapy (RRT) remains the cornerstone of treatment for advanced AKI, its implementation can potentially pose risks and may not be readily accessible across all healthcare settings and regions. Elevated lactate levels are implicated in sepsis-induced AKI; however, it remains unclear whether increased lactate directly induces AKI or elucidates the underlying mechanisms.

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