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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
D-myo-inositol-1,2,6-trisphosphate (IP3) is an isomer of the naturally occurring second messenger D-myo-inositol-1,4,5-trisphosphate, and exerts anti-inflammatory and antiedematous effects in the lung. Myo-inositol (Inos) is a component of IP3, and is thought to play an important role in the
Oxidants released from inflammatory cells contribute to the pathogenesis of acute inflammatory edema in many models. Chemically produced oxidants can reversibly alter the barrier properties of cultured endothelial and epithelial monolayers. This report examines the effects of nonlytic doses of H2O2
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
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
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
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.,
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
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
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
The biological and immune-protective properties of surfactant-derived phospholipids and phospholipid subfractions in the context of neonatal inflammatory lung disease are widely unknown. Using a porcine neonatal triple-hit acute respiratory distress syndrome (ARDS) model (repeated airway lavage,
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
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
Treatments to improve the neurological outcome of edema and cerebral ischemic stroke are severely limited. Here, we present the first in vivo single cell images of cortical mouse astrocytes documenting the impact of single vessel photothrombosis on cytotoxic edema and cerebral infarcts. The volume