gliosis/وذمة

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Antisense oligodeoxynucleotides targeting connexin43 reduce cerebral astrocytosis and edema in a rat model of traumatic brain injury.

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OBJECTIVE Brain injury induces an acute increase in the expression of gap junction protein connexin43 (Cx43). It also leads to cerebral edema, probably due to the swelling and proliferation of astrocytes reactive to the injury. Antisense oligodeoxynucleotides (AS-ODN) targeting Cx43 were tested for

Chemical preconditioning-induced reactive astrocytosis contributes to the reduction of post-ischemic edema through aquaporin-4 downregulation.

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Aquaporins are a family of membrane proteins that promote the transmembrane diffusion of water. Aquaporin-4 (AQP4) is a predominant water channel protein in the brain and is concentrated in the end-feet of astrocytes. A critical question is what role astrocytic AQP4 plays in pathological conditions.

Purinergic 2Y1 receptor stimulation decreases cerebral edema and reactive gliosis in a traumatic brain injury model.

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Traumatic brain injury (TBI) is the leading cause of death and disability in children and young adults. Neuroprotective agents that may promote repair or counteract damage after injury do not currently exist. We recently reported that stimulation of the purinergic receptor subtype P2Y(1)R using

The effects of glucosteroids upon cold-induced brain edema. 3. Prevention of gliosis following brain edema.

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Assessment of demyelination, edema, and gliosis by in vivo determination of T1 and T2 in the brain of patients with acute attack of multiple sclerosis.

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This study intended to investigate the possibility of magnetic resonance (MR) to characterize the acute plaque due to multiple sclerosis (MS). To obtain information, in vivo measurements of relaxation processes were performed in 10 patients with known acute MS plaques, using a whole-body

Response of Postoperative and Chronic Uveitic Cystoid Macular Edema to a Dexamethasone-Based Intravitreal Implant (Ozurdex).

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To survey the clinical responses to treatment of chronic postoperative and uveitic cystoid macular edema (CME) with a dexamethasone-based intravitreal implant (Ozurdex(®)). This retrospective, interventional case series reports on patients with chronic CME after uncomplicated vitrectomy for

Cerebrospinal fluid edema and its sequelae in hydrocephalus.

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CSF edema is observed in the periventricular white matter in acute hydrocephalus especially when the intraventricular pressure is elevated; there is usually no detectable disturbance of the blood-brain barrier. Histological and ventricular perfusion studies suggest that CSF flows through the intact

Time course of tissue elasticity and fluidity in vasogenic brain edema.

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We examined chronological changes in regional tissue elasticity (stiffness) and fluidity (1/viscosity) of the white matter during the development and resolution of vasogenic brain edema. Cryogenic injury was created in the cortex of cat brain, and the brain was prepared for measurement of regional

Intrauterine anoxic brain damage in nonimmune hydrops fetalis.

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A case is presented of a live-born infant with nonimmune hydrops fetalis who survived for 9 h. Neuropathological examination revealed extensive neuronal loss and gliosis in the subcortical gray nuclei suggestive of anoxic brain damage some weeks before birth. In addition the cerebellum was found to

The efficacy of shunting the hydrocephalic edema.

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The efficacy of shunting the hydrocephalic edema was evaluated by means of transmission electromicroscopical observation (TEM) comparing ultrastructural alterations seen in either valid or invalid shunted feline hydrocephalus. Owning to shunt placement, deteriorated clinical symptoms recovered and

Delayed radiation necrosis with extensive brain edema after gamma knife radiosurgery for multiple cerebral cavernous malformations--case report.

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A 39-year-old man presented with multiple intracranial cavernous malformations manifesting as intractable seizures persisting for more than 20 years. He underwent gamma knife radiosurgery (GKRS) for right frontal and left temporal cavernous malformations. He began to suffer from progressive left

Effects of antiperoxidants on FeCl2-induced lipid peroxidation and focal edema in rat brain.

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Head trauma with contusion or cortical laceration and hemorrhage causes focal edema with encephalomalacia and gliosis. Because cerebral hemorrhage ultimately results in deposition of heme compounds and iron into the neuropil, we injected an aqueous solution of iron salts to simulate the

Apparent diffusion coefficient in vasogenic edema and reactive astrogliosis.

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BACKGROUND Distinguishing between vasogenic edema and reactive astrogliosis may be difficult in some instances. This study was performed to test the hypothesis that diffusion-weighted (DW) imaging with apparent diffusion coefficient (ADC) maps can be used to differentiate these two types of

Respiratory failure without pulmonary edema following injection of a glutamate agonist into the ventral medullary raphe of the rat.

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Injection of ibotenic acid (IA), a glutamate agonist, into the ventral medullary raphe (VMR; especially the nucleus raphe magnus) of the rat produced respiratory failure and death following a predictable course of events. The response to the IA injection was characterized initially by increased

Sequential changes in ischemic edema following transient focal cerebral ischemia in rats: magnetic resonance imaging study.

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Sequential and regional changes in ischemic edema following various durations of focal cerebral ischemia were studied by magnetic resonance (MR) imaging in a rat unilateral intraluminal middle cerebral artery occlusion model. Occlusion was performed from 5 minutes to 5 hours. T2-weighted images were

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