Search

The greater omentum, a unique anatomical structure composed of adipocytes, loose connective tissue, and a dense vascular network. Plays a pivotal role beyond its traditional understanding. It houses specialized immunological units known as 'Milky spots,' making it a key player in immune response. Moreover, the omentum's capacity to enhance tissue perfusion, absorb edema fluid, boost acetylcholine synthesis, and foster neuron repair have rendered it a topic of interest in the context of various diseases, especially neurological disorders. This review provides a comprehensive overview of the intricate anatomy and histology of the greater omentum, casting light on its multifaceted functions and its associations with a spectrum of diseases. With a specific focus on neurological ailments, we delineate the intricate relationship that the omentum shares with other pathologies like stroke and we underly its contribution to serving as a therapeutic agent in neurological disorders. By deciphering the underlying mechanisms and emphasizing areas that demand further investigation. This review aims to spark renewed interest and pave the way for comprehensive studies exploring the greater omentum's potential in neurology and broader medicine overall. Given these diverse interactions that yet remain elusive, we must investigate and understand the nuanced relationship between the greater omentum and pathologies, especially its role in stroke's pathophysiology and therapeutic interventions so as to enhance patient care. [ABSTRACT FROM AUTHOR]

Our study aimed to construct a predictive model for identifying instances of futile recanalization in patients with anterior circulation occlusion acute ischemic stroke (AIS) who achieved complete reperfusion following endovascular therapy. We included 173 AIS patients who attained complete reperfusion, as indicated by a Modified Thrombolysis in Cerebral Infarction (mTICI) scale score of 3. Our approach involved a thorough analysis of clinical factors, imaging biomarkers, and potential no-reflow biomarkers through both univariate and multivariate analyses to identify predictors of futile recanalization. The comprehensive model includes clinical factors such as age, presence of diabetes, admission NIHSS score, and the number of stent retriever passes; imaging biomarkers like poor collaterals; and potential no-reflow biomarkers, notably disrupted blood-brain barrier (OR 4.321, 95% CI 1.794-10.405; p = 0.001), neutrophil-to-lymphocyte ratio (NLR; OR 1.095, 95% CI 1.009-1.188; p = 0.030), and D-dimer (OR 1.134, 95% CI 1.017-1.266; p = 0.024). The model demonstrated high predictive accuracy, with a C-index of 0.901 (95% CI 0.855-0.947) and 0.911 (95% CI 0.863-0.954) in the original and bootstrapping validation samples, respectively. Notably, the comprehensive model showed significantly improved predictive performance over models that did not include no-reflow biomarkers, evidenced by an integrated discrimination improvement of 8.86% (95% CI 4.34%-13.39%; p < 0.001) and a categorized reclassification improvement of 18.38% (95% CI 3.53%-33.23%; p = 0.015). This model, which leverages the potential of no-reflow biomarkers, could be especially beneficial in healthcare settings with limited resources. It provides a valuable tool for predicting futile recanalization, thereby informing clinical decision-making. Future research could explore further refinements to this model and its application in diverse clinical settings. [ABSTRACT FROM AUTHOR]

Acute ischemic stroke (AIS) is a serious neurological disease. Normobaric hyperoxia (NBHO) is both a non-invasive and easy method that seems to be able to improve outcomes after cerebral ischemia/reperfusion. In clinical trials, normal low-flow oxygen has been shown to be ineffective, but NBHO has been shown to have a transient brain-protective effect. Today, NBHO combined with recanalization is the best treatment available. NBHO combined with thrombolysis is considered to improve neurological scores and long-term outcomes. Large randomized controlled trials (RCTs), however, are still needed to determine the role they will have in stroke treatment. RCTs of NBHO combined with thrombectomy have both improved infarct volume at 24 hours and the long-term prognosis. These two mechanisms most likely play key roles in the neuroprotective actions of NBHO after recanalization, including the increase in penumbra oxygen supply and the integrity of the blood-brain barrier (BBB). Considering the mechanism of action of NBHO, oxygen should be given as early as possible to increase the duration of oxygen therapy before recanalization is initiated. NBHO can further prolong the existence time of penumbra, so that more patients may benefit from it. Overall, however, recanalization therapy is still essential. [ABSTRACT FROM AUTHOR]

Ischemic stroke is an extremely common pathology with strikingly high morbidity and mortality rates. The endoplasmic reticulum (ER) is the primary organelle responsible for conducting protein synthesis and trafficking as well as preserving intracellular Ca2+ homeostasis. Mounting evidence shows that ER stress contributes to stroke pathophysiology. Moreover, insufficient circulation to the brain after stroke causes suppression of ATP production. Glucose metabolism disorder is an important pathological process after stroke. Here, we discuss the relationship between ER stress and stroke and treatment and intervention of ER stress after stroke. We also discuss the role of glucose metabolism, particularly glycolysis and gluconeogenesis, poststroke. Based on recent studies, we speculate about the potential relationship and crosstalk between glucose metabolism and ER stress. In conclusion, we describe ER stress, glycolysis, and gluconeogenesis in the context of stroke and explore how the interplay between ER stress and glucose metabolism contributes to the pathophysiology of stroke. [ABSTRACT FROM AUTHOR]

Understanding the regional propensity differences of atherosclerosis (AS) development is hindered by the lack of animal models suitable for the study of the disease process. In this paper, we used 3SASCVD dogs, an ideal large animal human-like models for AS, to interrogate the heterogeneity of AS-prone and AS-resistant arteries; and at the single-cell level, identify the dominant cells involved in AS development. Here we present data from 3S-ASCVD dogs which reliably mimic human AS pathophysiology, predilection for lesion sites, and endpoint events. Our analysis combined bulk RNA-seq with single-cell RNA-seq to depict the transcriptomic profiles and cellular atlas of AS-prone and AS-resistant arteries in 3S-ASCVD dogs. Our results revealed the integral role of smooth muscle cells (SMCs) in regional propensity for AS. Notably, TNC+ SMCs were major contributors to AS development in 3S-ASCVD dogs, indicating enhanced extracellular matrix remodeling and transition to myofibroblasts during the AS process. Moreover, TNC+ SMCs were also present in human AS-prone carotid plaques, suggesting a potential origin of myofibroblasts and supporting the relevance of our findings. Our study provides a promising large animal model for pre-clinical studies of ASCVD and add novel insights surrounding the regional propensity of AS development in humans, which may lead to interventions that delay or prevent lesion progression and adverse clinical events. [ABSTRACT FROM AUTHOR]

Stroke is one of the most prevalent causes of death around the world. When a stroke occurs, many cellular signaling cascades and regulators are activated, which results in severe cellular dysfunction and debilitating long-term disability. One crucial regulator of cell fate and function is mammalian Forkhead box protein O1 (FoxO1). Many studies have found FoxO1 to be implicated in many cellular processes, including regulating gluconeogenesis and glycogenolysis. During a stroke, modifications of FoxO1 have been linked to a variety of functions, such as inducing cell death and inflammation, inhibiting oxidative injury, affecting the blood brain barrier (BBB), and regulating hepatic gluconeogenesis. For these functions of FoxO1, different measures and treatments were applied to FoxO1 after ischemia. However, the subtle mechanisms of posttranscriptional modification and the role of FoxO1 are still elusive and even contradictory in the development of stroke. The determination of these mechanisms will lead to further enlightenment for FoxO1 signal transduction and the identification of targeted drugs. The regulation and function of FoxO1 may provide an important way for the prevention and treatment of diseases. Overall, the functions of FoxO1 are multifactorial, and this paper will summarize all of the significant pathways in which FoxO1 plays an important role during stroke damage and recovery. [ABSTRACT FROM AUTHOR]

It is well known that atherosclerotic vascular disease (ASVD) in the elderly is a global disease with high morbidity, mortality and disability, and plasma LDL-C correction is the most important strategy for ASVD control. However, a large proportion of patients failed to achieve their ideal LDL-C goals after statins use. Ezetimibe, a newly non-statin lipid-lowering agent, is an inhibitor of exogenous cholesterol absorption. Whereby, ezetimibe plus statins may reduce LDL-C more strongly than statins alone. Differed from any other papers published previously, which only involved ezetimibe plus statins for coronary heart disease, the highlight of this paper is to summarize the efficacy and safety of ezetimibe plus statins in all kinds of ASVD subtypes and their related diseases, mainly included aortic atherosclerosis, coronary artery disease, cerebrovascular and peripheral artery diseases. Obviously, this paper is inimitable, which will provide the readers an important reference, especially in treating the elderly with multi-organs atherosclerosis. [ABSTRACT FROM AUTHOR]

White matter lesion (WML), also known as white matter hyperintensities or leukoaraiosis, was first termed in 1986 to describe the hyperintense signals on T2-weighted imaging (T2WI) and fluid-attenuated inversion recovery (FLAIR) maps. Over the past decades, a growing body of pathophysiological findings regarding WMLs have been discovered and discussed. Currently, the generally accepted WML pathogeneses mainly include hypoxia-ischemia, endothelial dysfunction, blood-brain barrier disruption, and infiltration of inflammatory mediators or cytokines. However, none of them can explain the whole dynamics of WML formation. Herein, we primarily focus on the pathogeneses and neuroimaging features of vascular WMLs. To achieve this goal, we searched papers with any type published in PubMed from 1950 to 2020 and cross-referenced the keywords including "leukoencephalopathy", "leukoaraiosis", "white matter hyperintensity", "white matter lesion", "pathogenesis", "pathology", "pathophysiology", and "neuroimaging". Moreover, references of the selected articles were browsed and searched for additional pertinent articles. We believe this work will supply the robust references for clinicians to further understand the different WML patterns of varying vascular etiologies and thus make customized treatment. [ABSTRACT FROM AUTHOR]

Physical exercise is an effective therapy for neurorehabilitation. Exercise has been shown to induce remodeling and proliferation of astrocyte. Astrocytes potentially affect the recruitment and function of neurons; they could intensify responses of neurons and bring more neurons for the process of neuroplasticity. Interactions between astrocytes, microglia and neurons modulate neuroplasticity and, subsequently, neural circuit function. These cellular interactions promote the number and function of synapses, neurogenesis, and cerebrovascular remodeling. However, the roles and crosstalk of astrocytes with neurons and microglia and any subsequent neuroplastic effects have not been studied extensively in exercise-induced settings. This article discusses the impact of physical exercise on astrocyte proliferation and highlights the interplay between astrocytes, microglia and neurons. The crosstalk between these cells may enhance neuroplasticity, leading to the neuroplastic effects of exercise. [ABSTRACT FROM AUTHOR]

Cognitive impairment is closely associated with the slowing of glucose metabolism in the brain. Glucose transport, a rate-limiting step of glucose metabolism, plays a key role in this phenomenon. Previous studies have reported that limb remote ischemic conditioning (LRIC) improves cognitive performance in rats with chronic cerebral hypoperfusion (CCH). Here, we determined whether LRIC could ameliorate cognitive impairment in rats with CCH by regulating glucose transport. A total of 170 male Sprague-Dawley rats were used. Animals subjected to permanent double carotid artery occlusion (2VO) were assigned to the control or LRIC treatment group. LRIC was applied beginning 3 days after the 2VO surgery. We found that LRIC can improve learning and memory; decrease the ratio of ADP/ATP; increase glucose content; upregulate the expression of pAMPKa, GLUT1 and GLUT3; and increase the number of GLUT1 and GLUT3 transporters in cerebral cortical neurons. The expression of GLUT1 and GLUT3 in the cortex displayed a strong correlation with learning and memory. Pearson correlation analysis showed that the levels of GLUT1 and GLUT3 are correlated with neurological function scores. All of these beneficial effects of LRIC were ablated by application of the AMPK inhibitor, dorsomorphin. In summary, LRIC ameliorated cognitive impairment in rats with CCH by regulating glucose transport via the AMPK/GLUT signaling pathway. We conclude that AMPK-mediated glucose transport plays a key role in LRIC. These data also suggest that supplemental activation of glucose transport after CCH may provide a clinically applicable intervention for improving cognitive impairment. [ABSTRACT FROM AUTHOR]

Although revascularization rates after endovascular thrombectomy for large vessel acute ischemic stroke (AIS) are high (71%), only 46% of patients achieve functional independence at 90 days. The present study was designed to explore a new method for predicting the functional prognosis of AIS patients after endovascular recanalization. A total of 200 anterior circulation stroke patients who received endovascular therapy were enrolled. Logistic regression analysis of clinical characteristics on functional independence were performed. The predictive power of sub-items in National Institute of Health stroke scale (NIHSS) and the combination of NIHSS consciousness and Alberta Stroke Program Early CT Score (ASPECTS) on functional independence were assessed by Receiver Operating Characteristic (ROC) curves and the latter was compared with 3 previously published prediction models by AUC (the area under ROC curve). The AUC for the NIHSS consciousness score to predict functional independence was higher than whole NIHSS and other sub-items (0.716 v 0.705, 0.586, 0.573, 0.552 and 0.559). Low NIHSS consciousness score, high ASPECTS score, short time from onset to recanalization, and high rate of successful recanalization were demonstrated to be significantly associated with the functional independence (OR 0.697, 2.226, 0.994 and 28.643). The prediction power of the combination was significantly better than NIHSS and ASPECTS alone (AUC 0.793 v 0.705 and 0.752). Compared with 3 other prediction models, the combination was found to be the strongest predictor for functional independence (AUC 0.793 v 0.791, 0.671 and 0.564). NIHSS which has been shown to be a strong predictor of functional outcomes after endovascular recanalization is largely dependent on the consciousness component. NIHSS consciousness score combined with ASPECTS appears to be a favorable predictor of functional independence. These findings may have broad reaching effects for isolated centers around the world without advanced imaging for triage and prognostication. [ABSTRACT FROM AUTHOR]

Acute ischemic stroke due to basilar artery occlusion (BAO) carries a very poor prognosis. Functional outcomes in BAO patients undergoing endovascular therapy (EVT) may differ according to the specific pathological mechanisms. We aimed to explore the impact of the underlying pathological mechanisms on prognosis at 90-days and long-term follow-up in BAO patients treated with EVT. We analyzed consecutive BAO patients undergoing EVT from December 2012 to December 2018 at a single center (Xuanwu Hospital). Patients were classified into either an intracranial atherosclerotic disease (ICAD) group or an embolic group according to the corresponding angiographic findings. The baseline characteristics and functional outcomes were compared between the two groups. Multivariable logistic regression analysis was performed. Among the 167 patients enrolled, 78 patients (46.7%) were in the ICAD group and 89 patients (53.3%) were assigned to the embolic group. Overall, 149 patients (89.2%) achieved successful reperfusion post-EVT. There were no significant differences in functional outcomes at 90-days and long-term follow-up between the two groups. Similarly, a Kaplan-Meier survival analysis showed similar long-term survival probabilities (P = 0.438). The pathological mechanism was not associated with functional independence (OR, 1.818; 95% CI, 0.694-4.761; P = 0.224), favorable outcome (OR, 1.476; 95% CI, 0.592-3.681; P = 0.403), or mortality (OR, 1.249; 95% CI, 0.483-3.226; P = 0.646). However, based on subgroup analysis, embolic BAO versus ICAD was significantly associated with better functional independence in those aged 60 years and younger (OR, 4.513; 95% CI, 1.138-17.902). In this study, no differences in either 90-days or long-term functional outcomes between ICAD-related BAO and embolic BAO patients undergoing EVT were observed. However, in BAO patients aged = 60 years, the pathological mechanism of embolism was associated with better functional independence. [ABSTRACT FROM AUTHOR]

In keeping with its status as one of the major causes of disability and mortality worldwide, brain damage induced by cerebral arterial disease has been the subject of several decades of scientific investigation, which has resulted in a vastly improved understanding of its pathogenesis. Brain injury mediated by venous etiologies, however, such as cerebral, jugular, and vertebral venous outflow disturbance, have been largely ignored by clinicians. Unfortunately, this inattention is not proportional to the severity of cerebral venous diseases, as the impact they exact on the quality of life of affected patients may be no less than that of arterial diseases. This is evident in disease sequelae such as cerebral venous thrombosis (CVT)-mediated visual impairment, epilepsy, and intracranial hypertension; and the long-term unbearable head noise, tinnitus, headache, dizziness, sleeping disorder, and even severe intracranial hypertension induced by non-thrombotic cerebral venous sinus (CVS) stenosis and/or internal jugular venous (IJV) stenosis. In addition, the vertebral venous system (VVS), a large volume, valveless vascular network that stretches from the brain to the pelvis, provides a conduit for diffuse transmission of tumors, infections, or emboli, with potentially devastating clinical consequences. Moreover, the lack of specific features and focal neurologic signs seen with arterial etiologies render cerebral venous disease prone to both to misdiagnoses and missed diagnoses. It is therefore imperative that awareness be raised, and that as comprehensive an understanding as possible of these issues be cultivated. In this review, we attempt to facilitate these goals by systematically summarizing recent advances in the diagnosis and treatment of these entities, including CVT, CVS stenosis, and IJV stenosis, with the aim of providing a valid, practical reference for clinicians. [ABSTRACT FROM AUTHOR]

Among cerebral venous thrombosis (CVT) patients, those with venous infarction have more severe clinical presentations and worse outcomes. Identifying biomarkers associated with venous infarction in CVT may help understand the pathogenesis and provide potentially useful therapeutic markers. Fifty-two CVT patients were prospectively recruited and divided into three groups: acute/subacute CVT with venous infarction (ASVI, n=30), without venous infarction (ASOVI, n=13), and chronic CVT (n=9). Blood brain barrier (BBB) permeability- related proteins, including claudin-5, occludin, matrix metalloproteinase-9, glial fibrillary acidic protein, and S100B, and inflammation-related factor high-sensitivity C-reactive protein (hs-CRP), were tested in serum and/or cerebrospinal fluid upon admission. We compared these biomarkers between the three groups and investigated their associations with venous infarction and clinical symptom severity in acute/subacute CVT patients on admission using the NIH Stroke Scale (NIHSS). Serum hs-CRP was significantly higher in acute/subacute CVT patients than chronic CVT patients. For acute/subacute CVT patients, levels were significantly higher in the ASVI group than the ASOVI group for serum claudin-5 (medians 2.80 vs. 2.50 mg/I, respectively, P = 0.039) and hs-CRP (medians 17.25 vs. 2.27 mg/l, respectively, P = 0.003). Both these biomarkers, analyzed as categorical or continuous variables, were also significantly associated with venous infarction in acute/subacute CVT patients after logistic regression analysis. Additionally, hs-CRP was positively correlated with the NIHSS (r = 0.710, P < 0.001) on admission in acute/subacute CVT patients. In CVT patients, venous infarction was associated with BBB disruption and potentially inflammation. Hs-CRP might serve as a biomarker reflecting the clinical severity of CVT in the acute/subacute stages. [ABSTRACT FROM AUTHOR]

Acute ischemic stroke (AIS) is a perpetual threat to life and functionality due to its high morbidity and mortality. In the past several decades, therapeutic hypothermia has garnered interest as an effective neuroprotective method in the setting of AIS. However, traditional hypothermic methods have been criticized for their low cooling efficiency and side effects. Intra-arterial cold saline infusion (IA-CSI), as a novel hypothermic method, not only minimizes these side effects, but is also perfectly integrated with widely accepted recanalization modalities in AIS, thereby serving as a promising prospect for clinical translation. In this article, we review the historical development of IA-CSI, summarize major studies of IA-CSI in rodents, large animals, and humans to date, and suggest insight into future development prospects in the field of AIS. We hope that this article will provide inspiration for the future application of hypothermia in AIS patients. [ABSTRACT FROM AUTHOR]

To investigate the safety and efficacy of intravenous administration of a standard dose of glycoprotein-IIb/IIIa inhibitor tirofiban after vessel recanalization by mechanical thrombectomy in acute ischemic stroke. A consecutive series of patients (n=112) undergoing endovascular ischemic stroke intervention therapy were enrolled. 81 patients were eligible for intravenous (IV) tirofiban treatment for 24 hours after mechanical thrombectomy. The incidence of symptomatic intracranial hemorrhage (sICH), death, National Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS) were assessed. In the 81 patients receiving tirofiban, 52 patients (64.2%) were treated with IV rt-PA before mechanical thrombectomy. sICH was found in 2 (2.5%) patients with no fatal ICH. Four patients died during 3 months after stroke onset. Successful recanalization with thrombolysis in cerebral infarction (TICI) score =2b was achieved in 75 of 81 patients (92.6%) after mechanical thrombectomy. The average number of passes with Solitaire stent retriever was 1.3. At 3 months, 55 of 81 patients (67.9%) had favorable outcomes (mRS<=2). The intravenous application of a standard dose of tirofiban post-Solitaire stent retriever thrombectomy and intravenous thrombolysis appears to be safe and relatively effective in acute ischemic stroke. [ABSTRACT FROM AUTHOR]

To evaluate the incidence of post-interventional contrast staining (PICS) in acute ischemic stroke (AIS) Chinese patients who were treated with endovascular thrombectomy (ET) and investigate potential association of PICS with functional outcome and intracerebral hemorrhage (ICH). This observational study was based on a single-center prospective registry study. AIS patients who underwent ET from January 2013 to February 2017 were recruited into this study. All patients had dual-energy CT (DECT) scan of the head at 12 to 24 hours post-ET. The primary outcome was the incidence of PICS. Secondary outcomes were total ICH, symptomatic ICH (sICH), 3-month functional outcome, and long-term functional outcome. One hundred and eighty patients were enrolled in this study. PICS was detected in 50 patients (28%) based on the post-interventional CT scan. We first used basic statistical analyses, showing that the incidence of both total ICH (60% vs. 25%, p<0.001) and sICH (18% vs. 8%, p=0.044) were higher in patients with PICS than those without, and fewer patients achieved no disability (mRS≤1) in the PICS group compared to the control group at both 3-month and long-term follow-up (p<0.01 each). However, multivariate regression analysis further revealed that PICS only increased total (adjusted odds ratio, 7.38; 95% confidence interval 1.66 to 32.9; p=0.009) but not sICH risk. Furthermore, the logistic regression analyses did not show statistical difference in good clinical outcomes or mortality between the two groups. PICS is a common phenomenon in Chinese AIS patients. It is associated with total ICH after ET, but it seems to have no effect on functional outcome and sICH. Further large-scale studies are warranted to validate these results. [ABSTRACT FROM AUTHOR]

Hypothermia is considered as a promising neuroprotective treatment for ischemic stroke but with many limitations. To expand its clinical relevance, this study evaluated the combination of physical (ice pad) and pharmacological [transient receptor potential vanilloid channel 1 (TRPV1) receptor agonist, dihydrocapsaicin (DHC)] approaches for faster cooling and stronger neuroprotection. A total of 144 male Sprague Dawley rats were randomized to 7 groups: sham (n=16), stroke only (n=24), stroke with physical hypothermia at 31°C for 3 h after the onset of reperfusion (n=24), high-dose DHC (HHC)(1.5 mg/kg, n=24), low-dose DHC (L-DHC)(0.5 mg/kg, n=32) with (n=8) or without (n=24) external body temperature control at ~38 °C (L-DHC, 38 °C), and combination therapy (L-DHC+ ice pad, n=24). Rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h. Infarct volume, neurological deficits and apoptotic cell death were determined at 24 h after reperfusion. Expression of pro- and anti-apoptotic proteins was evaluated by Western blot. ATP and reactive oxygen species (ROS) were detected by biochemical assays at 6 and 24 h after reperfusion. Combination therapy of L-DHC and ice pad significantly improved every measured outcome compared to monotherapies. Combination therapy achieved hypothermia faster by 28.6% than ice pad, 350% than L-DHC and 200% than H-DHC alone. Combination therapy reduced (p<0.05) neurological deficits by 63% vs. 26% with L-DHC. No effect was observed when using ice pad or H-DHC alone. L-DHC and ice pad combination improved brain oxidative metabolism by reducing (p<0.05) ROS at 6 and 24 h after reperfusion and increasing ATP levels by 42.9% compared to 25% elevation with L-DHC alone. Finally, combination therapy decreased apoptotic cell death by 48.5% vs. 24.9% with L-DHC, associated with increased anti-apoptotic protein and reduced pro-apoptotic protein levels (p<0.001). Our study has demonstrated that combining physical and pharmacological hypothermia is a promising therapeutic approach in ischemic stroke, and warrants further translational investigations. [ABSTRACT FROM AUTHOR]

Hibernation is a unique physiological state that evolved to survive periods of food shortages. It is characterized by profound decreases in metabolic rate, body temperature and physiological functions. Studies have shown that animals in hibernation can resist neurological damage. Here, we aimed to study whether hypoxia can induce a hibernation-like state in a traditionally non-hibernating animal and whether it is neuroprotective. All procedures were conducted according to international guidelines on laboratory animal safety. Mice C57BL/6 (19-21g) were placed into a 125 mL jar with fresh air and the jar was sealed with a rubber plug. For each run, the tolerance limit was judged by the animals' appearance for ''air hunger". The animal was removed from the jar as soon as its first gasping breath appeared and was moved to another fresh-air-containing jar of similar volume. This procedure was performed in four runs. The hypoxia exposure significantly decreased oxygen (O2) consumption, carbon dioxide (CO2) production, respiratory rate and heart rate. Meanwhile, rectal temperature reached a minimum of 12.7±2.56°C, which is lower than a wide range of ambient temperatures. The mimicked hibernation decreased the infarct size in a focal cerebral ischemia mouse model. Our findings suggest the possibility of inducing suspended animation-like hibernation states for medical applications post injury. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a major cause of death and disability globally, and its incidence is increasing. The only treatment approved by the US Food and Drug Administration for acute ischemic stroke is thrombolytic treatment with recombinant tissue plasminogen activator. As an alternative, therapeutic hypothermia has shown excellent potential in preclinical and small clinical studies, but it has largely failed in large clinical studies. This has led clinicians to explore the combination of therapeutic hypothermia with other neuroprotective strategies. This review examines preclinical and clinical progress towards developing highly effective combination therapy involving hypothermia for stroke patients. [ABSTRACT FROM AUTHOR]

Motor imagery (MI), defined as the mental implementation of an action in the absence of movement or muscle activation, is a rehabilitation technique that offers a means to replace or restore lost motor function in stroke patients when used in conjunction with conventional physiotherapy procedures. This article briefly reviews the concepts and neural correlates of MI in order to promote improved understanding, as well as to enhance the clinical utility of MI-based rehabilitation regimens. We specifically highlight the role of the cerebellum and basal ganglia, premotor, supplementary motor, and prefrontal areas, primary motor cortex, and parietal cortex. Additionally, we examine the recent literature related to MI and its potential as a therapeutic technique in both upper and lower limb stroke rehabilitation. [ABSTRACT FROM AUTHOR]

Dural venous sinus thrombosis (DVST) is a rare cause of stroke, which typically affects young women. The importance of identifying pre-disposing factors that lead to venous stasis lies in the foundation of understanding the etiology, pathophysiology and clinical presentation. The precise therapeutic role of interventional therapies is not fully understood though the current data do suggest potential applications. The aim of the study was to perform a systematic review and meta-analysis to evaluate the utility of and short-term 30-day survival after endovascular therapy for patients with DVST. Standard PRISMA guidelines were followed. Data sources included PubMed keywords and phrases, which were also incorporated into a MeSH search to yield articles indexed in Medline over a 5-year period. All RCTs, observational cohort studies, and administrative registries comparing or reporting DVST were included. Sixty-six studies met inclusion criteria. 35 articles investigating treatment in a summation of 10,285 patients were eligible for data extraction and included in the review of treatment modalities. A total of 312 patients were included for statistical analysis. All patients included received endovascular intervention with direct thrombolysis, mechanical thrombectomy or both. 133 (42.6%) patients were documented to have a neurologic decline, which prompted endovascular intervention. All patients who had endovascular interventions were those who were started on and failed systemic anticoagulation. 44 patients were reported to have intracranial hemorrhages after intervention. Regardless of systemic anticoagulation, patients were still reported to have complications of VTE and PE. Primary outcome at 3-6 month follow up revealed mRS⩽1 in 224 patients. DVST presents with many diagnostic and therapeutic challenges. The utility of invasive interventions such as local thrombolysis and mechanical thrombectomy is not fully understood. It is exceedingly difficult to conduct large randomized trials for this low incidence disease process with large pathophysiological heterogeneity. [ABSTRACT FROM AUTHOR]

Remote ischemic perconditioning (PerC) has been proved to have neuroprotective effects on cerebral ischemia, however, the effect of PerC on the BBB disruption and underlying mechanisms remains largely unknown. To address these issues, total 90 adult male Sprague Dawley (SD) rats were used. The rats underwent 90-min middle cerebral artery occlusion (MCAO), and the limb remote ischemic PerC was immediately applied after the onset of MCAO. We found that limb remote PerC protected BBB breakdown and brain edema, in parallel with reduced infarct volume and improved neurological deficits, after MCAO. Immunofluorescence studies revealed that MCAO resulted in disrupted continuity of claudin-5 staining in the cerebral endothelial cells with significant gap formation, which was significantly improved after PerC. Western blot analysis demonstrated that expression of tight junction (TJ) protein occludin was significantly increased, but other elements of TJ proteins, claudin-5 and ZO-1, in the BBB endothelial cells were not altered at 48 h after PerC, compared to MCAO group. The expression of matrix metalloproteinase (MMP-9), which was involved in TJ protein degradation, was decreased after PerC. Interestingly, phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2), an upstream of MMP-9 signaling, was significantly reduced in the PerC group. Our data suggest that PerC inhibits MMP-9-mediated occludin degradation, which could lead to decreased BBB disruption and brain edema after ischemic stroke. [ABSTRACT FROM AUTHOR]

Along with thrombolytic therapy, which has a number of limitations, stroke outcome may be improved with neuroprotective therapies that disrupt ischemic cell death. Recent research has shown a neuroprotective role of ethanol administration during ischemic stroke, such as its ability to reduce infarct volume and neurologic deficit. In order to investigate this further, we assessed the hypothesis that ethanol's neuroprotective effect is through reduction of apoptosis and the modulation of the important apoptotic PKCδ and Akt signaling pathway. Ethanol (1.5 g/kg) was given by intraperitoneal injections to 54 Sprague-Dawley rats after 2 hours of middle cerebral artery (MCA) occlusion, followed by 3 or 24 hours of reperfusion. We measured apoptotic cell death, PKC-δ, and Akt mRNA and protein expressions in each of ischemic groups with or without ethanol treatment using ELISA, real-time PCR and Western blot analysis. Our results showed that cell death was significantly increased in rats following 2 hour MCA occlusion and 24 hour reperfusion. Subsequently, cell death was significantly reduced by an administration of ethanol. We further found that ethanol administration, prior to either 3 or 24 hours of reperfusion, significantly decreased the expression of PKC-δ while simultaneously increasing the expression Akt at both mRNA and protein levels at the two points. In conclusion, our study suggests that ethanol administration following ischemic stroke modulates the gene and protein profile in such a way that it increased expression of anti-apoptotic Akt and decreased the pro-apoptotic PKC-δ. This ultimately results in a decrease in neuronal apoptosis, thus conferring neuroprotection. [ABSTRACT FROM AUTHOR]