Potential role of myo-inositol to improve ischemic stroke outcome in diabetic mouse.

Brain edema is one of the critical factors causing hightened disability and mortality in stroke patients, which is exaggerated further in diabetic patients. Organic osmolytes could play a critical role in the maintenance of cytotoxic edema. The present study was aimed to assess the role of myo-inositol, an organic osmolyte, on stroke outcome in diabetic and non-diabetic animals.

Superperc: A new technique in minimally-invasive percutaneous nephrolithotomy.

Introduction: Percutaneous nephrolithotomy (PCNL) has undergone significant changes in recent years in the quest for improving efficacy and reducing morbidity. Newer minimally-invasive modalities of PCNL such as mini-PCNL, ultra-mini PCNL, and micro-PCNL have evolved with advancement in optics and technology. However, with these newer advancements, migration of small fragments produced with laser lithotripsy remains a concern, which may result in incomplete stone clearance.

Passage Variation of PC12 Cells Results in Inconsistent Susceptibility to Externally Induced Apoptosis.

The PC12 cell line is a widely used in vitro model for screening the neuroprotective activity of small molecule libraries. External insult due to serum deprivation or addition of etoposide induces cell death by apoptosis. While this screening method is commonly used in early stage drug discovery no protocol accounting for cell passage number effect on neuroprotective activity has been disclosed.

Nicotine pre-exposure reduces stroke-induced glucose transporter-1 activity at the blood-brain barrier in mice.

Background: With growing electronic cigarette usage in both the smoking and nonsmoking population, rigorous studies are needed to investigate the effects of nicotine on biological systems to determine long-term health consequences. We have previously shown that nicotine exerts specific neurovascular effects that influence blood brain barrier (BBB) function in response to stroke. In this study, we investigated the effects of nicotine on carrier-mediated glucose transport into ischemic brain.

Functional up-regulation of endopeptidase neurolysin during post-acute and early recovery phases of experimental stroke in mouse brain.

In this study, we provide evidence for the first time that membrane-bound endopeptidase neurolysin is up-regulated in different parts of mouse brain affected by focal ischemia-reperfusion in a middle cerebral artery occlusion model of stroke. Radioligand binding, enzymatic and immunoblotting experiments in membrane preparations of frontoparietal cortex, striatum, and hippocampus isolated from the ischemic hemisphere of mouse brain 24 h after reperfusion revealed statistically significant increase (≥ twofold) in quantity and activity of neurolysin compared with sham-operated controls. Cerebellar membranes isolated from the ischemic hemisphere served as negative control supporting the observations that up-regulation of neurolysin occurs in post-ischemic brain regions.

The role of blood-brain barrier transporters in pathophysiology and pharmacotherapy of stroke.

Cerebral ischemia is one of the major causes of disability worldwide. In cerebral ischemic stroke, occlusion of a major cerebral artery by an embolus or local thrombosis can result in transient or permanent reduction of cerebral blood flow to a portion of the brain, resulting in deprivation of glucose and oxygen. Since the brain relies on a continuous supply of nutrients and ions via mostly carrier mediated processes across the blood-brain barrier (BBB), any irregularity in these transport mechanisms dramatically affects neuronal function and outcome after acute and chronic stroke.

The role of glucose transporters in brain disease: diabetes and Alzheimer’s Disease.

The occurrence of altered brain glucose metabolism has long been suggested in both diabetes and Alzheimer’s diseases. However, the preceding mechanism to altered glucose metabolism has not been well understood. Glucose enters the brain via glucose transporters primarily present at the blood-brain barrier.

An in vitro model of ischemic stroke.

Brain stroke is a devastating cerebrovascular disease and ranks as the third most common cause of death and disability in the US. Altered blood-brain barrier (BBB) signaling and permeability characteristics during stroke can increase the risk for life-threatening hemorrhagic transformation or damaging brain edema. The BBB plays a crucial role in maintaining the permeability and CNS homeostasis under physiological/pathological conditions by protecting the brain from the fluctuations in plasma constituents.

In vitro models of the blood-brain barrier.

The chapter provides an introduction and brief overview of currently available in vitro blood-brain barrier models, pointing out the major advantages and disadvantages of the respective models and potential applications. Bovine brain microvessel endothelial cell isolation, culture, and transendothelial permeability measurement procedures are discussed in detail as a model system for a laboratory to begin brain vascular investigations.

Characterization of neuroprotective effects of biphalin, an opioid receptor agonist, in a model of focal brain ischemia.

Approximately 795,000 people experience a new or recurrent stroke in the United States annually. The purpose of this study was to assess the protective effect of a nonselective opioid receptor agonist, biphalin, in brain edema and infarct damage by using both in vitro and in vivo models of stroke. In an in vivo model of ischemia, biphalin significantly decreased edema (66.

Opioid receptor agonists reduce brain edema in stroke.

Cerebral edema is a leading cause of mortality in stroke patients. The purpose of this study was to assess a non-selective opioid receptor agonist, biphalin, in decreasing reducing brain edema formation using both in vitro and in vivo models of stroke. For the in situ model of ischemia, hippocampal slices were exposed to oxygen glucose deprivation (OGD) conditions and we observed that hippocampal water content was increased, compared to normoxia.

Neuroprotective effects of NU1025, a PARP inhibitor in cerebral ischemia are mediated through reduction in NAD depletion and DNA fragmentation.

Oxidative stress induced cell injury is reported to contribute to the pathogenesis of cerebral ischemia. Reactive oxygen species such as hydrogen peroxide (H2O2) and superoxide radical along with nitric oxide and peroxynitrite generated during ischemia-reperfusion injury, causes the overactivation of poly (ADP-ribose) polymerase (PARP) leading to neuronal cell death. In the present study we have evaluated the effects of PARP inhibitor, 8-hydroxy-2 methyl-quinazolin-4-[3H]one (NU1025) in H2O2 and 3-morphilinosyndonimine (SIN-1) induced cytotoxicity in PC12 cells as well as in middle cerebral artery occlusion (MCAO) induced focal cerebral ischemia in rats.