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myo inositol/edema
L'enllaç es desa al porta-retalls
Pàgina 1 des de 64 resultats
Glutamine, myo-inositol, and organic brain osmolytes after portocaval anastomosis in the rat: implications for ammonia-induced brain edema.
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Brain myo-inositol, an organic osmolyte, is decreased in cirrhotic patients with hepatic encephalopathy but appears unchanged in fulminant hepatic failure. An osmoregulatory response to the increase in brain glutamine may explain the decrease in brain myo-inositol; if this is the case, organic
Glutamine, myo-inositol, and brain edema in acute liver failure.
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Is myo-inositol a measure of glial swelling after stroke? A magnetic resonance study.
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OBJECTIVE
To determine whether the hypothesis that the phenomenon of persistent cytotoxic edema in the subacute stage of ischemic stroke is in fact associated with the glial population. This is done by assessing the evolution of both the apparent diffusion coefficient (ADC) and the glial-specific
Reduced albumin extravasation in experimental rat skin and muscle burn injury by D-myo-inositol-1,2,6-trisphosphate treatment.
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This study investigated the effects of the anti-inflammatory agent D-myo-inositol-1,2,6-trisphosphate (IP3) on burn edema. Two sets of experiments were performed. In the first set, a full-thickness burn injury was induced in the abdominal skin of anesthetized rats. Postburn intravenous treatment was
Lowering of interstitial fluid pressure will enhance edema in trachea of albumin-sensitized rats.
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Interstitial fluid pressure (Pif) has recently been found to play an important role in edema formation in acute airway inflammation. Because airway inflammation is important in the pathogenesis of asthma, Pif was measured in rat trachea after albumin challenge to rats previously sensitized to
Alpha-Trinositol inhibits edema generation and albumin extravasation in thermally injured skin.
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Pharmacologic attempts to reduce edema generation and albumin extravasation into thermally injured skin have until recently been disappointing unless the drugs (usually antiphlogistic or anti-inflammatory drugs) were given before injury. We have studied the effect of alpha-trinositol (PP56, i.e.,
Effect of alpha-trinositol on interstitial fluid pressure, edema generation, and albumin extravasation after ischemia-reperfusion injury in rat hind limb.
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Reperfusion of ischemic tissue often leads to an acute inflammatory response, which acts directly to aggravate the injury in the reperfused zone, characterized by adhesion and subsequent infiltration of inflammatory cells that injure the tissue through the generation of oxygen-derived free radicals
Effects of D-myo-Inositol-1,2,6-triphosphate on eicosanoid formation in burned skin.
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D-myo-Inositol-1,2,6-triphosphate (IP3) has been shown to reduce edema and progressive ischemia following experimental skin burns. The mechanism(s) are not identified but could be related to antiinflammatory effects of the agent. In the present ex vivo study we compared the effects of IP3 with those
Myo-inositol-derived glycolipids with anti-inflammatory activity from Solanum lanceolatum.
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Lanceolitols A1-A7 (1-7) and B1-B7 (9-15), two series of new myo-inositol-derived glycolipid analogues, in which a sugar moiety is replaced by a fatty acid esterified myo-inositol moiety, were isolated from the leaves of Solanum lanceolatum. Their structures were elucidated on the basis of
Brain edema dynamics in patients with overt hepatic encephalopathy A magnetic resonance imaging study.
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The aim of our study was to investigate the dynamics of brain water content assessed by magnetic resonance imaging (MRI) applications in patients with cirrhosis and overt episodic hepatic encephalopathy (HE).
METHODS
Twenty-four patients with cirrhosis and overt HE, 9 healthy controls and 9 controls
Alpha-trinositol reduces edema formation at the site of scald injury.
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BACKGROUND
The effects of alpha-trinositol (1D-myo-inositol-1,2,6-triphosphate, IP3) on burn-induced edema formation were investigated.
METHODS
Lymph flow (QL; microliter/min) and lymph-to-plasma protein ratio (CL/CP) were monitored in groups of five to six dogs before and 4 hours after (1) a
alpha-Trinositol decreases lung edema formation after smoke inhalation in an ovine model.
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Inhalation injury is a dominant cause of mortality in thermally injured individuals. After acute lung injury induced by smoke inhalation, lung lymph flow (QL) increased and pulmonary microvascular reflection coefficient to protein (sigma) decreased. alpha-Trinositol (PP56, 1D-myo-inositol
Osmoregulatory changes in myo-inositol content and Na+/myo-inositol cotransport in rat cortical astrocytes.
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Exposure of cortical astrocytes to 325, 350, or 390 mosM culture media for 48 h caused a 1.4-, 2.1-, and 3.5-fold increase, respectively, in cellular content of the compatible osmolyte myo-inositol. Elevated myo-inositol levels accounted for approximately 56-100% of the solute needed by the cells
Potential role of myo-inositol to improve ischemic stroke outcome in diabetic mouse.
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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
Induction of Na+/myo-inositol co-transporter mRNA after rat cryogenic injury.
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Myo-inositol is one of the major organic osmolytes in the brain. It is stored in the cells by the Na+/myo-inositol co-transporter (SMIT) which is regulated by extracellular osmolality. First, in order to confirm that local change of the osmolality induces alteration of the SMIT mRNA in brain, we
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