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Introduction: Early Brain Injury (EBI) significantly contributes to poor neurological outcomes and death following subarachnoid hemorrhage (SAH). The mechanisms underlying EBI post-SAH remain unclear. This study explores the relationship between serial cerebral blood flow (CBF) changes and neurological symptoms, as well as the mechanisms driving CBF changes in the ultra-early stages after experimental SAH in mice.

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Purpose: Studying the effect of interleukin-17 (IL-17) on the mechanism of CD4+ T-cell immune regulation and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway may offer new ideas and methods for the therapy of dilated cardiomyopathy.

Methods: Naive CD4+ T cells were isolated from mice using a magnetic bead sorting reagent and manipulated by overexpression or knockdown of IL-17. Protein levels of Janus kinase 2 (JAK2), phosphorylated JAK2 (p-JAK2), signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), matrix metalloproteinase-2 (MMP-2), and matrix metalloproteinase-9 (MMP-9) were determined by Western blotting.

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Neutrophils in MASLD and MASH.

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Department of Physiology, School of Medicine, Kyungpook National University, Daegu 41944, Korea; Cell & Matrix Research Institute, Kyungpook National University, Daegu 41944, Korea.

Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) and its progressive form, Metabolic Dysfunction Associated Steatohepatitis (MASH), represent significant health concerns associated with the metabolic syndrome. These conditions are characterized by excessive hepatic fat accumulation, inflammation, and potential progression to cirrhosis and hepatocellular carcinoma. Neutrophils are innate immune cells that play a pivotal role in the development of MASLD and MASH.

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Biomaterials

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Department of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, PR China; State Key Laboratory of Organ Failure Research, Southern Medical University, Guangzhou, 510515, PR China. Electronic address:

Chronic diabetic wounds are a prevalent and severe complication of diabetes, contributing to higher rates of limb amputations and mortality. N6-methyladenosine (mA) is a common RNA modification that has been shown to regulate tissue repair and regeneration. However, whether targeting mA could effectively improve chronic diabetic wound healing remains largely unknown.

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Background: Overexpression of tear matrix metalloproteinases-9 (MMP-9) on the ocular surface tissues has been reported to result in ocular surface damage. MMP-9 levels in tears have been listed as one of many tools for confirming dry eye disease (DED).

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