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gelatinase/edema
Врската е зачувана во таблата со исечоци
Страница 1 од 55 резултати
The sensitivity of versican from rabbit lung to gelatinase A (MMP-2) and B (MMP-9) and its involvement in the development of hydraulic lung edema.
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Large chondroitinsulphate-containing proteoglycan (versican) isolated from rabbit lung was cleaved by purified gelatinase A (MMP-2) and gelatinase B (MMP-9), as well as by crude enzyme extract from rabbit lung with hydraulic edema. Gelatine zymography, performed after purification of gelatinases by
Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke.
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BACKGROUND
While gelatinase (MMP-2 and -9) activity is increased after focal ischemia/reperfusion injury in the brain, the relative contribution of neutrophils to the MMP activity and to the development of hemorrhagic transformation remains unknown.
RESULTS
Anti-PMN treatment caused successful
Prognostic role of maternal neutrophil gelatinase-associated lipocalin in women with severe early-onset preeclampsia.
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BACKGROUND
The association between maternal plasma levels of neutrophil gelatinase-associated lipocalin (NGAL) and maternal complications in women admitted with severe early-onset preeclampsia was evaluated.
METHODS
Plasma levels of NGAL were measured at admission in patients with severe early-onset
Cotreatment with Furosemide and Hypertonic Saline Decreases Serum Neutrophil Gelatinase-associated Lipocalin (NGAL) and Serum Creatinine Concentrations in Traumatic Brain Injury: A Randomized, Single-Blind Clinical Trial.
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Acute kidney injury (AKI) occurs both after traumatic brain injury (TBI) and after hypertonic saline administration; furosemide may be useful in preventing AKI indirectly. Serum neutrophil gelatinase-associated lipocalin (sNGAL) is superior to serum creatinine (sCr) in diagnosing early AKI. We
Injury-induced 92-kilodalton gelatinase and urokinase expression in rat brain.
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BACKGROUND
Proteolytic disruption of the extracellular matrix is important in pathologic processes. We have shown that activated 72-kilodalton (kd) type IV collagenase injected intracerebrally attacks brain extracellular matrix and opens the blood-brain barrier. Therefore, we tested the hypothesis
EPH-gestosis (pre-eclampsia)-induced decrease of gelatinase activity may promote an accumulation of collagen in the umbilical cord artery.
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It was found in our previous paper that edema, proteinuria, hypertension (EPH)-gestosis-associated accumulation of collagen in the umbilical cord artery (UCA) is a result of increased biosynthesis and decreased degradation of this protein. It is known that the activity of collagenolytic enzymes is a
Moderate and severe traumatic brain injury induce early overexpression of systemic and brain gelatinases.
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OBJECTIVE
Recent experimental evidence suggests that matrix metalloproteinases (MMPs) are implicated in the pathophysiology of traumatic brain injury (TBI) by increasing blood-brain barrier permeability and exacerbating posttraumatic edema. We examined the acute profile of MMP-2 and MMP-9 in the
Neutrophil gelatinase-associated lipocalin predicts myocardial dysfunction and mortality in severe sepsis and septic shock.
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BACKGROUND
This study examines the clinical utility of plasma neutrophil gelatinase-associated lipocalin (NGAL) as an indicator of myocardial dysfunction and mortality in severe sepsis and septic shock.
METHODS
We designed a prospective cohort study in an intensive care unit, and 53 patients with
Serum neutrophil gelatinase associated lipocalin and plasma nitric oxide levels in healthy and preeclamptic pregnants.
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OBJECTIVE
The authors aimed to evaluate serum neutrophil gelatinase associated lipocalin (NGAL) and plasma nitric oxide (NO) levels in preeclamptic and healthy pregnant women above 24 gestation weeks.
METHODS
Forty-nine healthy and 21 preeclamptic (total 70) pregnant women participated voluntarily
Estimation of gelatinase content in rat brain: effect of focal ischemia.
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Matrix metalloproteinases degrade the extracellular matrix and are involved in a variety of diseases, including inflammatory diseases of the central nervous system. Here we estimated the content of gelatinase in rat brain under control conditions and 4 h after transient focal ischemia using
Cerebral mast cells mediate blood-brain barrier disruption in acute experimental ischemic stroke through perivascular gelatinase activation.
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OBJECTIVE
Perivascularly positioned cerebral mast cells (MC) have been shown to participate in acute blood-brain barrier disruption and expansive brain edema following experimental transient cerebral ischemia. However, the underlying molecular mechanisms remain unknown. Because proteolytic
Radiation-induced blood-brain barrier damage in astrocytoma: relation to elevated gelatinase B and urokinase.
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Successful management of brain tumors prolongs life, raising the risk of delayed injury secondary to the treatment. Radiation therapy, a mainstay of brain tumor treatment, can damage the cerebral blood vessels. Acutely a breakdown of the blood-brain barrier (BBB) may be seen, but fibrosis
Vasogenic edema due to tight junction disruption by matrix metalloproteinases in cerebral ischemia.
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Cerebral ischemia causes cell swelling and breakdown of the blood-brain barrier (BBB). Cytotoxic edema results from energy failure, and vasogenic edema occurs when the blood vessels are damaged. Proteases and free radicals are the end result of a molecular injury cascade. Matrix metalloproteinases
SIRT1 inhibition by sirtinol aggravates brain edema after experimental subarachnoid hemorrhage.
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Secondary brain injury following subarachnoid hemorrhage (SAH) is poorly understood. We utilized a rat model of SAH to investigate whether SIRT1 has a protective role against brain edema via the tumor suppressor protein p53 pathway. Experimental SAH was induced in adult male Sprague-Dawley rats by
Expression of matrix metalloproteinase-9 in thrombin-induced brain edema formation in rats.
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Recent evidence has demonstrated that thrombin plays an important role in the development of brain edema by the blood-brain barrier disruption in intracerebral hemorrhage. Matrix metalloproteinases (MMPs), a family of proteolytic enzymes that degrade the extracellular matrix, are implicated in
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