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Total 108 results found since Jan 2013.

GPR39 Knockout Worsens Microcirculatory Response to Experimental Stroke in a Sex-Dependent Manner
AbstractNo current treatments target microvascular reperfusion after stroke, which can contribute to poor outcomes even after successful clot retrieval. The G protein –coupled receptor GPR39 is expressed in brain peri-capillary pericytes, and has been implicated in microvascular regulation, but its role in stroke is unknown. We tested the hypothesis that GPR39 plays a protective role after stroke, in part due to preservation of microvascular perfusion. We gener ated GPR39 knockout (KO) mice and tested whether GPR39 gene deletion worsens capillary blood flow and exacerbates brain injury and functional deficit after focal ...
Source: Translational Stroke Research - October 1, 2022 Category: Neurology Source Type: research

Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury
In this study, we used multimodal imaging to assess edema formation and quantify the amount of metabolically functional brain salvaged after a rat model of stroke reperfusion. TRPM4 upregulation in endothelium emerges as early as 2  h post-stroke induction. Expression of TRPM4 channel was suppressed directly in vivo by treatment with siRNA; scrambled siRNA was used as a control. T2-weighted MRI suggests that TRPM4 inhibition successfully reduces edema by 30% and concomitantly salvages functionally active brain, measured by18F-FDG-PET. These in vivo imaging results correlate well with post-mortem 2,3,5-triphenyltetrazolium...
Source: Translational Stroke Research - March 22, 2018 Category: Neurology Source Type: research

Effects of the New Thrombolytic Compound LT3001 on Acute Brain Tissue Damage After Focal Embolic Stroke in Rats
In this study, we tested the effects of LT3001 as a potential alternative thrombolytic in focal embolic ischemic stroke rat model. Stroked rats received intravenous injection of 10  mg/kg LT3001 or tPA at 1.5, 3, or 4.5 h after stroke, respectively, and the outcomes were measured at different time points after stroke by performing multi-parametric MRI, 2,3,5-triphenyltetrazolium chloride (TTC) staining, and modified neurological severity score. Lastly, we assessed the effect of LT3001 on the tPA activity in vitro, the international normalized ratio (INR), and the serum levels of active tPA and plasminogen activator inhib...
Source: Translational Stroke Research - November 29, 2022 Category: Neurology Source Type: research

Recombinant Human Perlecan DV and Its LG3 Subdomain Are Neuroprotective and Acutely Functionally Restorative in Severe Experimental Ischemic Stroke
AbstractDespite recent therapeutic advancements, ischemic stroke remains a major cause of death and disability. It has been previously demonstrated that  ~ 85-kDa recombinant human perlecan domain V (rhPDV) binds to upregulated integrin receptors (α2β1 and α5β1) associated with neuroprotective and functional improvements in various animal models of acute ischemic stroke. Recombinant human perlecan laminin-like globular domain 3 (rhPDVLG3), a 21-kDa C-terminal subdomain of rhPDV, has been demonstrated to more avidly bind to the α2β1 integrin receptor than its parent molecule and consequently was postulated to evok...
Source: Translational Stroke Research - December 12, 2022 Category: Neurology Source Type: research

PAI-1 but Not PAI-2 Gene Deficiency Attenuates Ischemic Brain Injury After Experimental Stroke
The objectives of the present were twofold: first, to characterize the time-dependent cerebral mRNA expression of the plasminogen activator system (PAS) after brain ischemia and second, to investigate the impact of PAI-1 and PAI-2 on brain infarct volume using gene-deficient mice. AdultC57Bl/6J mice were subjected to unilateral transient middle cerebral artery occlusion (MCAO) followed by reperfusion for 3, 24, 72, or 120  h. Quantitative PCR revealed that brain mRNA expression levels of the PAS components, and particularly of PAI-1 (237-fold) and PAI-2 (19-fold), peaked at 24 h after stroke. Accordingly, PAI-1 plasma ac...
Source: Translational Stroke Research - July 5, 2018 Category: Neurology Source Type: research

Effect of TTC Treatment on Immunohistochemical Quantification of Collagen IV in Rat Brains after Stroke
AbstractAlthough used extensively in stroke research, there is limited knowledge of how 2, 3, 5-triphenyltetrazolium chloride (TTC)-treated rat brain sections are altered and if they can be used for immunohistochemical quantification after staining with TTC. In the present study, we hypothesized that TTC treatment (TTC+) would not interfere with collagen IV immunohistochemical staining compared with non-TTC-treated (TTC −) brain slices. We further hypothesized that there would be no difference in autofluorescence or nonspecific secondary antibody fluorescence between TTC+ and TTC− brain slices. Coronal brain sections o...
Source: Translational Stroke Research - January 8, 2018 Category: Neurology Source Type: research

Stroke Dysbiosis Index (SDI) in Gut Microbiome Are Associated With Brain Injury and Prognosis of Stroke
Conclusions: We developed an index to measure gut microbiota dysbiosis in stroke patients; this index was significantly correlated with patients' outcome and was causally related to outcome in a mouse model of stroke. Our model facilitates the potential clinical application of gut microbiota data in stroke and adds quantitative evidence linking the gut microbiota to stroke. Introduction Ischemic stroke imposes a heavy burden on society, with 24.9 million cases worldwide (1). Although intravenous thrombolysis and endovascular treatment greatly improve some patients' prognosis, the prognosis for most pa...
Source: Frontiers in Neurology - April 23, 2019 Category: Neurology Source Type: research

Protective effect of low-intensity transcranial ultrasound stimulation after differing delay following an acute ischemic stroke.
CONCLUSION: In the event of an acute ischemic stroke, LITUS can inhibit the decrease of ADC and the effect is closely related to the delay in treatment. The earlier the ultrasound intervention, the better the protective effect. PMID: 30552999 [PubMed - as supplied by publisher]
Source: Brain Research Bulletin - December 12, 2018 Category: Neurology Authors: Liu L, Du J, Zheng T, Hu S, Dong Y, Du D, Wu S, Wang X, Shi Q Tags: Brain Res Bull Source Type: research

Bumetanide: A review of its neuroplasticity and behavioral effects after stroke.
Authors: Tao D, Liu F, Sun X, Qu H, Zhao S, Zhou Z, Xiao T, Zhao C, Zhao M Abstract Stroke often leads to neuronal injury and neurological functional deficits. Whilst spontaneous neurogenesis and axon regeneration are induced by ischemic stroke, effective pharmacological treatments are also essential for the improvement of neuroplasticity and functional recovery after stroke. However, no pharmacological therapy has been demonstrated to be able to effectively improve the functional recovery after stroke. Bumetanide is a specific Na +-K +-Cl- co-transporter inhibitor which can maintain chloride homeostasis in neuro...
Source: Restorative Neurology and Neuroscience - July 16, 2019 Category: Neurology Tags: Restor Neurol Neurosci Source Type: research

Evaluation of anti-inflammatory diphenyldihaloketone EF24 in transient ischemic stroke model
CONCLUSIONS: EF24 controls infarct growth and suppresses tissue inflammation in ischemic stroke, which can be monitored by 18F-FGA uptake.PMID:35254869 | DOI:10.1080/02699052.2022.2034959
Source: Brain Injury - March 7, 2022 Category: Neurology Authors: Alexander Mdzinarishvili Hailey Houson Andria Hedrick Vibhudutta Awasthi Source Type: research