Osteopontin infusion into normal adult rat brain fails to increase cell proliferation in dentate gyrus and subventricular zone.

In the first week after focal ischemia in adult brain, the basal level of neurogenesis increases dramatically in two distinct areas: The dentate gyrus (DG) of the hippocampus and the subventricular zone (SVZ) of the lateral ventricles. It is possible that this remotely induced neurogenesis is the result of a proliferation inducing factor, or factors, diffusing from the infarction to the neurogenic regions. The secreted protein osteopontin (OPN) is a possible factor.

Inhibition of intercellular adhesion molecule-1 protein expression by antisense oligonucleotides is neuroprotective after transient middle cerebral artery occlusion in rat.

Background And Purpose: The present study was performed to determine whether antisense inhibition of intercellular adhesion molecule-1 (ICAM-1) protein expression decreases focal ischemic brain damage.

Methods: Male spontaneously hypertensive rats underwent 1-hour middle cerebral artery occlusion (MCAO) and 24-hour reperfusion. Rats were infused with ICAM-1 antisense or control oligodeoxynucleotides (ODNs) (48 nmol/d ICV) or vehicle, starting 24 hours before MCAO and continuing until the time of death.

Ornithine decarboxylase activity in in vivo and in vitro models of cerebral ischemia.

Ornithine decarboxylase (ODC) is considered the rate-limiting enzyme in polyamine biosynthesis, and an increase in putrescine after central nervous system (CNS) injury appears to be involved in neuronal death. Cerebral ischemia and reperfusion trigger an active series of metabolic events, which eventually lead to neuronal death. In the present study, ODC activity was evaluated following transient focal cerebral ischemia and reperfusion in rat.

Phospholipase A2, hydroxyl radicals, and lipid peroxidation in transient cerebral ischemia.

Phospholipid degradation is an important promoter of neuronal death after transient cerebral ischemia. Phospholipid hydrolysis by phospholipase A2 (PLA2) after transient cerebral ischemia releases arachidonic acid. Arachidonic acid metabolism results in formation of reactive oxygen species, lipid peroxides, and toxic aldehydes (malondialdehyde, 4-hydroxynonenal, and acrolein).

Stroke-induced progenitor cell proliferation in adult spontaneously hypertensive rat brain: effect of exogenous IGF-1 and GDNF.

Progenitor cells in the dentate gyrus of hippocampus (DG) and the subventricular zone of lateral ventricles (SVZ) generate new neurons throughout the life of mammals. Cerebral ischemia increases this basal progenitor cell proliferation. The present study evaluated the time frame of proliferation, length of survival and the phenotypes of the new cells formed after transient middle cerebral artery occlusion (MCAO) in adult spontaneously hypertensive rats.

L-arginine in focal cerebral ischemia.

Nitric oxide and its precursor, L-arginine, have a great importance in cerebrovascular studies. In this study, we elucidate the dose dependent L-arginine effects on cerebral ischemia. The study involved 96 New Zealand albino rabbits, which were randomly allocated into four groups.

Cytidinediphosphocholine treatment to decrease traumatic brain injury-induced hippocampal neuronal death, cortical contusion volume, and neurological dysfunction in rats.

Object: In previous studies at their laboratory the authors showed that cytidinediphosphocholine (CDP-choline), an intermediate of phosphatidylcholine synthesis, decreases edema formation and blood-brain barrier disruption following traumatic brain injury (TBI). In the present study the authors investigate whether CDP-choline protects hippocampal neurons after controlled cortical impact (CCI)-induced TBI in adult rats.

Methods: After adult male Sprague-Dawley rats had been anesthetized with halothane, a moderate-grade TBI was induced with the aid of a CCI device set at a velocity of 3 m/second, creating a 2-mm deformation.

Is there an association between athletic amenorrhea and endothelial cell dysfunction?

Purpose: To test the hypothesis that young females with athletic amenorrhea and oligomenorrhea show signs of early cardiovascular disease manifested by decreased endothelium-dependent dilation of the brachial artery.

Methods: Ten women with athletic amenorrhea (mean +/- SE, age 21.9 +/- 1.

Inhibition of Na(+)-K(+)-Cl(-) cotransporter during focal cerebral ischemia decreases edema and neuronal damage.

Our previous study demonstrated that pharmacological inhibition of the Na(+)-K(+)-Cl(-) cotransporter isoform 1 (NKCC1) during ischemia and reperfusion attenuated neuronal damage and edema. In this study, we further investigated whether NKCC1 activity contributes to ischemic damage during either ischemia or reperfusion. Immunoblotting revealed that expression of NKCC1 protein was increased following 2-h focal ischemia in cerebral cortex.

Traumatic brain injury-induced acute gene expression changes in rat cerebral cortex identified by GeneChip analysis.

Proper CNS function depends on concerted expression of thousands of genes in a controlled and timely manner. Traumatic brain injury (TBI) in mammals results in neuronal death and neurological dysfunction, which might be mediated by altered expression of several genes. By employing a CNS-specific GeneChip and real-time polymerase chain reaction (PCR), the present study analyzed the gene expression changes in adult rat cerebral cortex in the first 24 hr after a controlled cortical impact injury.

Does oral creatine supplementation improve strength? A meta-analysis.

Objectives: Oral creatine is the most widely used nutritional supplement among athletes. Our purpose was to investigate whether creatine supplementation increases maximal strength and power in healthy adults.

Study Design: Meta-analysis of existing literature.

Gene expression analysis of spontaneously hypertensive rat cerebral cortex following transient focal cerebral ischemia.

Identification of novel modulators of ischemic neuronal death helps in developing new strategies to prevent the stroke-induced neurological dysfunction. Hence, the present study evaluated the gene expression changes in rat cerebral cortex at 6 and 24 h of reperfusion following transient middle cerebral artery occlusion (MCAO) by GeneChip analysis. Transient MCAO resulted in selective increased mRNA levels of genes involved in stress, inflammation, transcription and plasticity, and decreased mRNA levels of genes which control neurotransmitter function and ionic balance.

Gender differences in the retention of Swahili names for unfamiliar odors.

Several studies, using different techniques, have established that women typically outperform men in naming odors. The mechanism for this effect was explored here in two experiments. In experiment 1, men and women learned randomly assigned Swahili names for a set of seven unfamiliar odors.

GeneChip analysis shows altered mRNA expression of transcripts of neurotransmitter and signal transduction pathways in the cerebral cortex of portacaval shunted rats.

Identifying the gene expression changes induced by hepatic encephalopathy (HE) leads to a better understanding of the molecular mechanisms of HE-induced neurological dysfunction. Using GeneChip and real-time PCR, the present study evaluated the gene expression profile of rat cerebral cortex at 4 weeks after portacaval shunting. Among 1,263 transcripts represented on the chip, mRNA levels of 31 transcripts were altered (greater than twofold; 16 increased and 15 decreased) in the portacaval shunted (PCS) rat compared to sham control.

Polyamines and central nervous system injury: spermine and spermidine decrease following transient focal cerebral ischemia in spontaneously hypertensive rats.

Polyamines (putrescine, spermidine and spermine) are ubiquitous cellular components, but their specific role in central nervous system (CNS) injury has yet to be characterized. CNS injury results in increased activities of ornithine decarboxylase and spermidine/spermine-N(1)-acetyltransferase, and accumulation of putrescine. The present study determined the polyamine profile in three models of CNS injury, in two different species (gerbil and rat) and two strains of rats (Sprague-Dawley and spontaneously hypertensive): (1) transient focal cerebral ischemia in spontaneously hypertensive rats (SHR); (2) traumatic brain injury in Sprague-Dawley rats; and (3) transient forebrain ischemia in gerbils.

Diffusion tensor MR imaging in diffuse axonal injury.

Background And Purpose: Disruption of the cytoskeletal network and axonal membranes characterizes diffuse axonal injury (DAI) in the first few hours after traumatic brain injury. Histologic abnormalities seen in DAI hypothetically decrease the diffusion along axons and increase the diffusion in directions perpendicular to them. DAI therefore is hypothetically associated in the short term with decreased diffusion anisotropy.

Citicoline: neuroprotective mechanisms in cerebral ischemia.

Cytidine-5'-diphosphocholine (citicoline or CDP-choline), an intermediate in the biosynthesis of phosphatidylcholine (PtdCho), has shown beneficial effects in a number of CNS injury models and pathological conditions of the brain. Citicoline improved the outcome in several phase-III clinical trials of stroke, but provided inconclusive results in recent clinical trials. The therapeutic action of citicoline is thought to be caused by stimulation of PtdCho synthesis in the injured brain, although the experimental evidence for this is limited.

GeneChip analysis after acute spinal cord injury in rat.

Spinal cord injury (SCI) leads to induction and/or suppression of several genes, the interplay of which governs the neuronal death and subsequent loss of motor function. Using GeneChip, the present study analyzed changes in the mRNA abundance at 3 and 24 h after SCI in adult rats. SCI was induced at T9 level by the New York University impactor by dropping a 10-g weight from a height of 25 mm.

Protective effects of glial cell line-derived neurotrophic factor on hippocampal neurons after traumatic brain injury in rats.

Object: The purpose of this study was to evaluate whether glial cell line-derived neurotrophic factor (GDNF) can protect against hippocampal neuronal death after traumatic brain injury (TBI).

Methods: Male Sprague-Dawley rats were subjected to moderate TBI with a controlled cortical impact device while in a state of halothane-induced anesthesia. Then, GDNF or artificial cerebrospinal fluid ([aCSF]; vehicle) was infused into the frontal horn of the left lateral ventricle.

Effects of citicoline on phospholipid and glutathione levels in transient cerebral ischemia.

Background And Purpose: Cytidine-5'-diphosphocholine (citicoline or CDP-choline) is an essential intermediate in the biosynthesis of phosphatidylcholine, an important component of the neural cell membrane. Citicoline provided significant neuroprotection after transient forebrain ischemia in gerbils. This study was undertaken to examine changes and effects of citicoline on phospholipids and glutathione synthesis after transient cerebral ischemia and reperfusion.

Attitudes and approaches to acute ischemic stroke in Wisconsin hospitals.

Although acute stroke is a common presentation to an emergency room, the presentation of a patient with acute ischemic stroke, within a limited time window as an appropriate candidate for cerebral thrombolysis, is not common. In many of these patients, their candidacy can be improved through community education toward emergent transfer to an emergency room if they manifest symptoms of stroke. This would improve the "symptom-to-door" time.

Transient focal cerebral ischemia down-regulates glutamate transporters GLT-1 and EAAC1 expression in rat brain.

Transient focal cerebral ischemia leads to extensive excitotoxic neuronal damage in rat cerebral cortex. Efficient reuptake of the released glutamate is essential for preventing glutamate receptor over-stimulation and neuronal death. Present study evaluated the expression of the glial (GLT-1 and GLAST) and neuronal (EAAC1) subtypes of glutamate transporters after transient middle cerebral artery occlusion (MCAO) induced focal cerebral ischemia in rats.

Neuroprotection by memantine, a non-competitive NMDA receptor antagonist after traumatic brain injury in rats.

This study investigated whether memantine, a non-competitive NMDA receptor antagonist is neuroprotective after traumatic brain injury (TBI) induced in adult rats with a controlled cortical impact device. TBI led to significant neuronal death in the hippocampal CA2 and CA3 regions (by 50 and 59%, respectively), by 7 days after the injury. Treatment of rats with memantine (10 and 20 mg/Kg, i.

Expression of Na(+)-K(+)-Cl(-) cotransporter in rat brain during development and its localization in mature astrocytes.

Na(+)-K(+)-Cl(-) cotransporter has been proposed to play an important role in the regulation of intracellular Cl(-) concentration in neurons during development. In this study, the expression pattern of the cotransporter in different regions of rat brain was examined at birth (P0), postnatal days 7 (P7), P14, P21, and adult by Western blotting analysis. In cortex, thalamus, cerebellum and striatum, the cotransporter expression level was low at P0 and significantly increased at P14 (P<0.