Cruzmchugh7435

BACKGROUND Sphenopalatine ganglion stimulation (SPG-Stim) for ischemic stroke, starting 8-24 h after onset and continuing through five days in a pooled analysis of two recent, randomized, sham-controlled trials, improved outcome of acute ischemic stroke patients with confirmed cortical involvement. As a neuromodulatory therapy, SPG-Stim differs substantially from existing pharmacologic (lytic and antiplatelets) and device (endovascular thrombectomy) acute ischemic stroke treatments. AIM Focused review of SPG anatomy, physiology, and neurovascular and neurobiologic mechanisms of action mediating benefit of SPG-Stim in acute ischemic stroke. SUMMARY OF REVIEW Located posterior to the maxillary sinus, the SPG is the main source of parasympathetic innervation to the anterior circulation. Preclinical and human studies delineate four distinct mechanisms of action by which the SPG-Stim may confer benefit in acute ischemic stroke (1) collateral vasodilation and enhanced cerebral blood flow, mediated by release of neurotransmitters with vasodilatory effects, nitric oxide, and acetylcholine, (2) stimulation frequency- and intensity-dependent stabilization of the blood-brain barrier, reducing edema (3) direct acute neuroprotection from activation of the central cholinergic system with resulting anti-inflammatory, anti-apoptotic, and anti-excitatory effects; and (4) neuroplasticity enhancement from enhanced central cholinergic and adrenergic neuromodulation of cortical networks and nitrous oxide release stimulating neurogenesis. CONCLUSION The benefit of SPG-Stim in acute ischemic stroke is likely conferred not only by potent collateral augmentation, but also blood-barrier stabilization, direct neuroprotection, and neuroplasticity enhancement. click here Further studies clarifying the relative contribution of these mechanisms and the stimulation protocols that maximize each may help optimize SPG-Stim as a therapy for acute ischemic stroke.In hypoxic-ischemic encephalopathy, the Neural Progenitors (NPs) of the developing brain fail to replenish the oligodendrocyte progenitor cells lost during hypoxic-ischemic injury (HII). Here, we aim to examine the influence of HII on the vulnerability of human NPs derived from human embryonic stem cells (hESCs) with regard to cell survival and oxidative stress, followed by assessment of cellular deregulation through measuring glutathione-levels, basal-calcium, glutamate-release and intracellular-calcium [Ca2+]i response under KCl and ATP stimulation. NPs were further evaluated for their fundamental-potential of self-renewal & proliferation, neural and glial progenitor pool and migration. Oxygen-glucose-deprivation(OGD) of 90mins was sub-lethal for NPs yet significantly increased ROS generation, oxidative-stress susceptibility and decreased glutathione-levels, along with a rise in glutamate release, basal [Ca2+]i and KCl and ATP-induced [Ca2+]i. Distinct increase in gene-expression for K+ leak channel(TASK1), purinergic-receptor P2X7 and decrease of voltage-gated Kv-channels Kv1.5, Kv4.2 & Kv4.3 were observed. OGD-insulted NPs showed reduced migration-potential and decline in glial-progenitor population. Our present study thus demonstrates for the first time that brief exposure of OGD does not reduce the neural progenitor population, its proliferation and self-renewal but can induce significant alteration in oxidative-stress susceptibility, glutamate release, [Ca2+]i response to physiological stimulus, migration and glial-progenitor pool. We thus infer that treatment strategies need to target repair of NPs of the developing brain that is affected during intra-partum asphyxia leading to varying neurologic complications such as seizure, mental retardation and/or cerebral palsy.Here, we describe a procedure to fluorescently contrast the nuclear boundary using the lipophilic carbocyanine dye DiI in cultured human cells. Our procedure is simple and is applicable to detect nuclear boundary defects, which may be relevant to studies on nuclear envelope dynamics, micronuclei formation and cancer biology.Abbreviations DiI 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate; DiO 3,3'-dioctadecyloxacarbocyanine perchlorate; NE nuclear envelope; RanBP2 Ran-binding protein 2/Nucleoporin 358.Therapeutic hypothermia (TH) is one of the few proven neuroprotective modalities in clinical practice. However, current methods to achieve TH are suboptimal. We investigated a novel esophageal device that utilizes high-flow transesophageal dry air to achieve TH via evaporating cooling. Seven Yorkshire pigs (n = 7) underwent hypothermia therapy using a novel esophageal device that compartmentalizes a segment of esophagus through which high-flow dry air freely circulates in and out of the esophagus. Efficacy (primary objective) and safety (secondary objective) were evaluated in all animals. Safety assessment was divided into two sequential phases (1) acute safety assessment (n = 5; terminal studies) to evaluate adverse events occurring during therapy, and (2) chronic safety assessment (n = 2; survival studies) to evaluate adverse events associated with therapy within 1 week of follow-up. After 1 hour of esophageal cooling (mean airflow rate = 64.2 ± 3.5 L/min), a significant reduction in rectal temperature was observed (37.3 ± 0.2°C → 36.3 ± 0.4°C, p = 0.002). The mean rectal temperature reduction was 1 ± 0.4°C. In none of the seven animals was oral or pharyngeal mucosa injury identified at postprocedural visual examination. In the two animals that survived, no reduction of food ingestion, signs of swallowing dysfunction or discomfort, or evidence of gastrointestinal bleeding was observed during the 1-week follow-up period. Open-chest visual inspection in those two animals did not show damage to the esophageal mucosa or surrounding structures. A novel esophageal device, utilizing high-flow transesophageal dry air, was able to efficiently induce hypothermia despite external heating. Therapy was well-tolerated, and no acute or chronic complications were found.The fatality rate can be dramatically reduced with the help of emergency medical services. The purpose of this study was to establish a computational algorithm to predict the injury severity, so as to improve the timeliness, appropriateness, and efficacy of medical care provided. The computer simulations of full-frontal crashes with rigid wall were carried out using LS-DYNA and MADYMO under different collision speeds, airbag deployment time, and seatbelt wearing condition, in which a total of 84 times simulation was conducted. Then an artificial neural network is adopted to construct relevance between head and chest injuries and the injury risk factors; 37 accident cases with Event Data Recorder data and information on occupant injury were collected to validate the model accuracy through receiver operating characteristic analysis. The results showed that delta-v, seatbelt wearing condition, and airbag deployment time were important factors in the occupant's head and chest injuries. When delta-v increased, the occupant had significantly higher level of severe injury on the head and chest; there is a significant difference of Head Injury Criterion and Combined Thoracic Index whether the occupant wore seatbelt.