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ribonucleic acid/وذمة

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الصفحة 1 من عند 45 النتائج

Apolipoprotein E affects the central nervous system response to injury and the development of cerebral edema.

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Apolipoprotein E has been implicated in modifying neurological outcome after traumatic brain injury, although the mechanisms by which this occurs remain poorly defined. To investigate the role of endogenous apolipoprotein E following acute brain injury, noninvasive magnetic resonance imaging was

Tenascin in meningioma: expression is correlated with anaplasia, vascular endothelial growth factor expression, and peritumoral edema but not with tumor border shape.

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OBJECTIVE Tenascin is an extracellular matrix glycoprotein that is expressed during embryogenesis, inflammation, angiogenesis, and carcinogenesis. The aim of this study was to investigate how tenascin expression relates to histological grade, angiogenesis, and radiological findings in

Brain edema in meningiomas is associated with increased vascular endothelial growth factor expression.

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OBJECTIVE Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF), an endothelial cell-specific cytokine, induces proliferation of endothelial cells and increases vascular permeability dramatically. All gliomas secrete significant amounts of VEGF, whereas meningiomas are variable

Case of a healthy infant born following antenatal enterovirus myocarditis and hydrops.

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Fetal hydrops and myocarditis were diagnosed in a woman at 32 weeks of gestation (WG). Transplacental enterovirus infection was suspected because all other causes of myocarditis and hydrops were excluded, it was during an endemic period, and there was a setting of maternal infection (fever a few

Forebrain ischemia-reperfusion simulating cardiac arrest in mice induces edema and DNA fragmentation in the brain.

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Brain injury affects one-third of persons who survive after heart attack, even with restoration of spontaneous circulation by cardiopulmonary resuscitation. We studied brain injury resulting from transient bilateral carotid artery occlusion (BCAO) and reperfusion by simulating heart attack and

[Micro-ribonucleic acids participate in electroacupuncture intervention-induced improvement of ischemic stroke].

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Ischemic stroke is a major cause of permanent disability and death in adults, and electroacupuncture (EA) intervention has a positive role in improving neurological function in patients with ischemic stroke through a series of complex processes. In the present paper, we make a review about the

Meningiomas: role of vascular endothelial growth factor/vascular permeability factor in angiogenesis and peritumoral edema.

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OBJECTIVE Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF) is a potent angiogenic growth factor implicated in the tumor angiogenesis/metastasis of a number of human cancers. Activation of receptors for VEGF/VPF is specifically mitogenic to endothelial cells and increases

RNase therapy assessed by magnetic resonance imaging reduces cerebral edema and infarction size in acute stroke.

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Ischemic stroke causes cell necrosis with the exposure of extracellular ribonucleic acid (RNA) and other intracellular material. As shown recently, extracellular RNA impaired the blood-brain-barrier and contributed to vasogenic edema-formation. Application of ribonuclease 1 (RNase 1) diminished

Poldip2 mediates blood-brain barrier disruption and cerebral edema by inducing AQP4 polarity loss in mouse bacterial meningitis model

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Background: Specific highly polarized aquaporin-4 (AQP4) expression is reported to play a crucial role in blood-brain barrier (BBB) integrity and brain water transport balance. The upregulation of polymerase δ-interacting protein 2

Cellular expression and hormonal regulation of neuropilin-1 and -2 messenger ribonucleic Acid in the human and rhesus macaque endometrium.

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Although much is known about the biology of vascular endothelial growth factor (VEGF) and its cognate receptors (VEGFRs), VEGFR1 and VEGFR2, little is known about the roles of the VEGFRs neuropilin (NP)-1 and NP-2 in the primate endometrium. In this study, we investigated the cellular localization

Long noncoding ribonucleic acid NKILA induces the endoplasmic reticulum stress/autophagy pathway and inhibits the nuclear factor-k-gene binding pathway in rats after intracerebral hemorrhage.

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Long noncoding RNAs (lncRNAs) have emerged as an important class of molecules that have been associated with brain function and neurological disease, but the expression profiles of lncRNAs after intracerebral hemorrhage (ICH) remain to be elucidated. In this study, we determined the expression

Mitoquinone attenuates blood-brain barrier disruption through Nrf2/PHB2/OPA1 pathway after subarachnoid hemorrhage in rats.

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Mitochondrial dysfunction is involved in the mechanism of early brain injury (EBI) following subarachnoid hemorrhage (SAH). Blood-brain barrier disruption is a devastating outcome in the early stage of SAH. In this study, we aimed to investigate the role of a mitochondria-related drug

Relationship between NogoA/NgR1/RhoA signaling pathway and the apoptosis of cerebral neurons after cerebral infarction in rats.

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The aim of this study was to investigate the effect and the mechanism of the NogoA/NgR1/RhoA signaling pathway on the apoptosis of neurons in cerebral infarction (CI) rats. Our findings might provide references for clinical prevention and treatment of CI.A

Effects of lncRNA MALAT1-mediated β-catenin signaling pathway on myocardial cell apoptosis in rats with myocardial ischemia/reperfusion injury.

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To investigate the effects of long non-coding ribonucleic acid (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on myocardial ischemia/reperfusion (I/R) injury in rats and its mechanism, and to provide a certain reference for the clinical prevention and

Aquaporin-11 (AQP11) Expression in the Mouse Brain.

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Aquaporin-11 (AQP11) is an intracellular aquaporin expressed in various tissues, including brain tissues in mammals. While AQP11-deficient mice have developed fatal polycystic kidneys at one month old, the role of AQP11 in the brain was not well appreciated. In this study, we examined the AQP11
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