NLRP3-mediated autophagy dysfunction links gut microbiota dysbiosis to tau pathology in chronic sleep deprivation.

Emerging evidence indicates that sleep deprivation (SD) can lead to Alzheimer's disease (AD)-related pathological changes and cognitive decline. However, the underlying mechanisms remain obscure. In the present study, we identified the existence of a microbiota-gut-brain axis in cognitive deficits resulting from chronic SD and revealed a potential pathway by which gut microbiota affects cognitive functioning in chronic SD.

Intestinal dysbiosis mediates cognitive impairment via the intestine and brain NLRP3 inflammasome activation in chronic sleep deprivation.

Growing evidence suggests the involvement of the microbiota-gut-brain axis in cognitive impairment induced by sleep deprivation (SD), however how the microbiota-gut-brain axis work remains elusive. Here, we discovered that chronic SD induced intestinal dysbiosis, activated NLRP3 inflammasome in the colon and brain, destructed intestinal/blood-brain barrier, and impaired cognitive function in mice. Transplantation of "SD microbiota" could almost mimic the pathological and behavioral changes caused by chronic SD.

Construction of circRNA-Mediated Immune-Related ceRNA Network and Identification of Circulating circRNAs as Diagnostic Biomarkers in Acute Ischemic Stroke.

Background And Purpose: Accumulating evidence suggests that circular RNAs (circRNAs) are involved in immune and inflammatory processes after acute ischemic stroke (AIS). However, the roles of circRNA-mediated competing endogenous RNA (ceRNA) in modulating immune inflammation of AIS have not yet been determined. This study aimed to construct a circRNA-mediated immune-related ceRNA network and identify novel circRNAs in AIS.

Endovascular Treatment With and Without Intravenous Thrombolysis in Large Vessel Occlusions Stroke: A Systematic Review and Meta-Analysis.

Previous studies have shown conflicting results about the benefits of pretreatment with intravenous thrombolysis before endovascular treatment (EVT) in patients with acute ischemic stroke (AIS) with large vessel occlusions (LVOs). This study aimed to investigate the clinical efficacy and safety of EVT alone vs. bridging therapy (BT) in patients with AIS with LVOs.

Unhealthy Lifestyle Is an Important Risk Factor of Idiopathic BPPV.

Benign paroxysmal positional vertigo (BPPV) is a self-limiting and recurrent disease but the cost is considerable. The number of patients with BPPV increased significantly under the quarantine policy in Hangzhou. The unhealthy lifestyle risk factors of BPPV have not yet been investigated.

Accuracy of Transcranial Doppler Ultrasound Compared with Magnetic Resonance Angiography in the Diagnosis of Intracranial Artery Stenosis.

 One of the most common causes of acute cerebral infarction (ACI) is intracranial artery stenosis (ICAS). The goal of our study was to evaluate the accuracy of transcranial Doppler (TCD) compared with magnetic resonance angiography (MRA) for diagnosing ICAS in patients with ACI.  Consecutive patients presenting with ACI to the neurology department underwent both MRA and TCD examination within 6 hours of difference.

The Short-term Prognostic Value of the Triglyceride-to-high-density Lipoprotein Cholesterol Ratio in Acute Ischemic Stroke.

The triglyceride (TG)-to-high-density lipoprotein cholesterol (HDL-C) ratio (TG/HDL-C) is a simple approach to predicting unfavorable outcomes in cardiovascular disease. The influence of TG/HDL-C on acute ischemic stroke remains elusive. The purpose of this study was to investigate the precise effect of TG/HDL-C on 3-month mortality after acute ischemic stroke (AIS).

β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke.

Background: Stroke-induced immunodeficiency syndrome (SIDS) is regarded as a protective mechanism for secondary inflammatory injury as well as a contributor to infection complications. Although stroke-induced hyperactivation of the sympathetic system is proved to facilitate SIDS, the involved endogenous factors and pathways are largely elusive. In this study, we aim to investigate the function of beta-arrestin-2 (ARRB2) in the sympathetic-mediated SIDS.

Potential specific immunological indicators for stroke associated infection are partly modulated by sympathetic pathway activation.

Background: Evidence has led to the consideration of immunodepression after stroke as an important contributor to stroke associated infection (SAI). However, so far no specific immunological indicator has been identified for SAI, and the underlying mechanism remains poorly understood.

Results: SAI patients had significantly higher IL-6 and IL-10 levels and lower HLA-DR levels than no-infection patients within 48h after stroke onset.

Blocking Sympathetic Nervous System Reverses Partially Stroke-Induced Immunosuppression but does not Aggravate Functional Outcome After Experimental Stroke in Rats.

Stoke results in activation of the sympathetic nervous system (SNS), inducing systemic immunosuppression. However, the potential mechanisms underlying stroke-induced immunosuppression remain unclear. Here, we determined the SNS effects on functional outcome and explored the interactions among SNS, β-arrestin2 and nuclear factor-κB (NF-κB) after experimental stroke in rats.

Splenectomy following MCAO inhibits the TLR4-NF-κB signaling pathway and protects the brain from neurodegeneration in rats.

Background And Purpose: The Toll-like receptor 4(TLR4)/nuclear factor kappa B NF-κB inflammatory pathway contributes to secondary inflammation in many diseases including stroke. Moreover, the neuroprotective effect of splenectomy in stroke is supported by a vast body of experimental evidence. Nevertheless, the underlying mechanism(s) by which splenectomy enhance neuroprotection in stroke is still poorly understood.

Role of the sympathetic nervous system and spleen in experimental stroke-induced immunodepression.

Background: The mechanism of stroke-induced immunodepression syndrome (SIDS) remains uncertain. Some studies suggest that hyperactivation of the sympathetic nervous system (SNS) may be the key factor underlying SIDS. Catecholamines impair early lymphocyte response, which can increase the risk of stroke-associated infection (SAI).

[Male sexual dysfunction and Parkinson's disease: a preliminary investigation].

Objective: To investigate the prevalence of male sexual dysfunction in males with Parkinson's disease and the pathogenesis and related factors of the problem.

Methods: We evaluated the sexual function of 140 men with Parkinson's disease using Mini-mental State Examination (MMSE), Unified Parkinson's Disease Rating Scale (Part III) (UPDRS III), Hoenhn-Yahr Staging (HYS), Hamilton Depression Scale (HAMD) and Sexual Dysfunction Standard of ICD-10. We calculated the Levodopa equivalent doses (LED) for all the patients.

Cytotoxic role of advanced glycation end-products in PC12 cells treated with β‑amyloid peptide.

Alzheimer's disease (AD) is the most common type of dementia afflicting the elderly. Recent studies have increasingly suggested that a high concentration of advanced glycation end products (AGEs) may be important in AD pathogenesis. However, the mechanisms and pathways involved remain unknown.

Effects of ginkgo biloba extract EGb761 on expression of RAGE and LRP-1 in cerebral microvascular endothelial cells under chronic hypoxia and hypoglycemia.

Alzheimer's disease (AD), characterized by accumulation of amyloid-beta protein (Abeta) in brain parenchyma, is closely associated with brain ischemia. Decreased clearance of Abeta from brain is the main cause of Abeta accumulation in sporadic AD. However, the mechanisms underlying ischemia-mediated AD pathogenesis remain unclear.

[mRNA expression and activity of ADAM17 in hippocampus after chronic cerebral hypoperfusion: experiment with aged rats].

Objective: To explore the effect of alpha-secretase on the pathogenesis of cognitive impairment following cerebral ischemia.

Methods: Forty-eight 12~16-months-old Wistar rats were randomly divided into 2 equal groups: hypoperfusion group, undergoing permanent occlusion of bilateral common carotid arteries to mimic cerebral hypoperfusion, and sham-operation group. Each group was further divided into 1, 2, 4, and 16 week subgroups.