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Novel gap junction protein beta-1 gene mutation associated with a stroke-like syndrome and central nervous system involvement in patients with X-linked Charcot-Marie-Tooth Type 1: A case report and literature review.
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Gap junction protein beta-1 (GJB1) gene mutations lead to X-linked Charcot-Marie-Tooth Type 1 (CMTX1). We studied a Chinese family with CMTX1 and identified a novel GJB1 point mutation. Our patient had a transient stroke-like clinical manifestations and magnetic resonance imaging (MRI) changes. An
Therapeutic effects of JLX-001 on ischemic stroke by inducing autophagy via AMPK-ULK1 signaling pathway in rats.
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(3β,5α,16α,20S)-4,4,14-trimethyl-3,20-bis(methylamino)-9,19-cyclopregnan-16-ol-dihydrochloride (JLX-001), a structural analogue of cyclovirobuxine D (CVB-D), is a novel compound from synthesis. This study aims to confirm the therapeutic effects of JLX001 on ischemic stroke (IS) and research its
Roles of electro-acupuncture in glucose metabolism as assessed by 18F-FDG/PET imaging and AMPKα phosphorylation in rats with ischemic stroke.
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Targeted energy metabolism balance contributes to neural survival during ischemic stroke. Herein, we tested the hypothesis that electro‑acupuncture (EA) can enhance cerebral glucose metabolism assessed by 18F‑fluorodeoxyglucose/positron emission tomography (18F‑FDG/PET) imaging to prevent
Effects of amino acids on alcohol intake in stroke-prone spontaneously hypertensive rats.
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Examination was made of the effects of amino acids on alcohol intake in stroke-prone spontaneously hypertensive rats (SHRSP). The animals were divided into two groups according to dietary protein level, normal (15%) and low (5%). The two groups were further divided into two groups according to
TRPM7 (Transient Receptor Potential Melastatin-Like 7 Channel) Kinase Controls Calcium Responses in Arterial Thrombosis and Stroke in Mice.
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OBJECTIVE
TRPM7 (transient receptor potential cation channel, subfamily M, member 7) is a ubiquitously expressed bifunctional protein comprising a transient receptor potential channel segment linked to a cytosolic α-type serine/threonine protein kinase domain. TRPM7 forms a constitutively active
Premature Stroke Secondary to Severe Hypertension Results from Liddle Syndrome Caused by a Novel SCNN1B Mutation
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ACE-Triggered Hypertension Incites Stroke: Genetic, Molecular, and Therapeutic Aspects.
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Stroke is the second largest cause of death worldwide. Angiotensin converting enzyme (ACE) gene has emerged as an important player in the pathogenesis of hypertension and consequently stroke. It encodes ACE enzyme that converts the inactive decapeptide angiotensin I to active octapeptide,
Prophylactic trials for stroke in stroke-prone SHR. (3) Amino acid analysis of various diets and their prophylactic effect.
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This study confirmed again that high protein diet feeding decreased the incidence of stroke, and high fish protein diet did attenuate severe hypertension but high soybean protein diet did not affect the hypertension. Dietary amino acid analyses indicated that increases in total amino acids,
miR‑126a‑5p‑Dbp and miR‑31a‑Crot/Mrpl4 interaction pairs crucial for the development of hypertension and stroke.
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The present study aimed to integrate the mRNA and microRNA (miRNA) expression profiles of spontaneously hypertensive rats (SHR rats) and stroke‑prone spontaneously hypertensive rats (SHRSP rats) to screen for potential therapeutic targets for hypertension and stroke. The datasets GSE41452, GSE31457,
Cyclin-dependent kinase-5 targeting for ischaemic stroke.
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Recovery from ischaemic stroke is dependent on survival of neurones, particularly in peri-infarcted regions. Angiogenesis is critical for the development of new microvessels resulting in the re-formation of collateral circulation associated with enhanced neuronal survival and reduced morbidity and
Effect of long-term 'corn peptide' ingestion on alcohol metabolism in stroke-prone spontaneously hypertensive rats with alcohol loading.
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The effect of long-term 'corn peptide (CP)' ingestion on alcohol metabolism was investigated in stroke-prone spontaneously hypertensive rats (SHR-SP) with alcohol loading. Long-term CP ingestion in the EtOH/CP group did not significantly increase plasma GOT and GPT activities but markedly increased
Bone marrow stromal cells increase astrocyte survival via upregulation of phosphoinositide 3-kinase/threonine protein kinase and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase pathways and stimulate astrocyte trophic factor gene expression after anaerobic insult.
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Transplantation of bone marrow stromal cells improves animal neurological functional recovery after stroke. Astrocytes are known to provide structural, trophic and metabolic support for neurons. Thus astrocytes are critical for neural survival during post-ischemia. However, information on the
Discovering Biomarkers and Pathways Shared by Alzheimer's Disease and Ischemic Stroke to Identify Novel Therapeutic Targets.
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Background and objectives: Alzheimer's disease (AD) is a progressive neurodegenerative disease that results in severe dementia. Having ischemic strokes (IS) is one of the risk factors of the AD, but the molecular mechanisms that underlie IS and AD are not well understood. We thus aimed to
Nicotinamide phosphoribosyltransferase protects against ischemic stroke through SIRT1-dependent adenosine monophosphate-activated kinase pathway.
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OBJECTIVE
Stroke is a leading cause of mortality and disability. Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)(+) biosynthesis and contributes to cell fate decisions. However, the role of Nampt in brain and stroke
Necroptosis is one of the modalities of cell death accompanying ischemic brain stroke: from pathogenesis to therapeutic possibilities.
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Due to very limited therapeutic options, ischemic brain injury is one of the leading causes of death and lifelong disability worldwide, which imposes enormous public health burden. One of the main events occurring with ischemic brain stroke is cell death. Necroptosis is a type of cell death
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