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Página 1 desde 32 resultados
Posttreatment with uridine and melatonin following traumatic brain injury reduces edema in various brain regions in rats.
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Traumatic brain injury (TBI) is a major health problem and a significant cause of death, disability, and neurobehavioral deficits. We investigated the effect of posttreatment with uridine and melatonin, separate and in combination, on edema in various brain regions following TBI via lateral fluid
Effect of uridine 5'-diphosphate on cryogenic brain edema in rabbits.
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This study was undertaken to examine the effect of uridine 5'-diphosphate, administered intravenously or intraperitoneally, on cold injury-induced brain edema in rabbits. Bolus injection or continuous intravenous infusion of uridine 5'-diphosphate 26 hours after a lesion was established had adverse
Effects of uridine, isomatitol and 4-thiouridine on in vitro cell adhesion and in vivo effects of 4-thiouridine in a lung inflammation model.
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Since leukocyte adhesion to endothelial cells is crucial for extravasation of leukocytes to sites of inflammation, inhibition of cell-cell adhesion has been suggested as a means to achieve selective modulation of the immune system. We have, using a static in vitro adhesion assay involving adhesion
[Pharmacology of uridine and cytidine].
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It was established that with intraperitoneal introduction of uridine and cytidine their DL50 for mice equals 5100 and 2700 mg/kg, respectively. In doses of 1/27 and 1/50 of DL50 cytidine reduces by 50 per cent the edema of the rat's paw in a dextran-and formaldehyde-induced inflammation, brings down
Targeted deletion of both thymidine phosphorylase and uridine phosphorylase and consequent disorders in mice.
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Thymidine phosphorylase (TP) regulates intracellular and plasma thymidine levels. TP deficiency is hypothesized to (i) increase levels of thymidine in plasma, (ii) lead to mitochondrial DNA alterations, and (iii) cause mitochondrial neurogastrointestinal encephalomyopathy (MNGIE). In order to
Cellular accumulation of extravasated serum protein and DNA fragmentation following vasogenic edema.
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Accumulation of serum protein has been demonstrated in injured brain cells following vasogenic brain edema. The present study was conducted to test whether this phenomenon is also observed in apoptotic cells as well as in necrotic cells. Apoptotic cell death has been implicated in a variety of brain
Occurrence of apoptosis following cold injury-induced brain edema in mice.
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Apoptosis has been known to contribute to neuronal death following a variety of brain insults. However, the role of vasogenic brain edema in neuronal apoptosis is unknown. We studied the temporal pattern of brain edema and neuronal apoptosis following cold injury. Cold injury-induced brain edema,
Bacillus anthracis edema factor substrate specificity: evidence for new modes of action.
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Since the isolation of Bacillus anthracis exotoxins in the 1960s, the detrimental activity of edema factor (EF) was considered as adenylyl cyclase activity only. Yet the catalytic site of EF was recently shown to accomplish cyclization of cytidine 5'-triphosphate, uridine 5'-triphosphate and inosine
Cold injury in mice: a model to study mechanisms of brain edema and neuronal apoptosis.
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Small rodents, mice in particular, have been widely used for genetic manipulation because of the extensive knowledge in development, embryology and other molecular aspects of this species. However, the use of mice for neurobiology research in the area of brain edema and neuronal injury has not been
Cytidylyl and uridylyl cyclase activity of bacillus anthracis edema factor and Bordetella pertussis CyaA.
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Cyclic adenosine 3',5'-monophosphate (cAMP) and cyclic guanosine 3',5'-monophosphate (cGMP) are second messengers for numerous mammalian cell functions. The natural occurrence and synthesis of a third cyclic nucleotide (cNMP), cyclic cytidine 3',5'-monophosphate (cCMP), is a matter of controversy,
Hydrogen-rich saline alleviates early brain injury via reducing oxidative stress and brain edema following experimental subarachnoid hemorrhage in rabbits.
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BACKGROUND
Increasing experimental and clinical data indicate that early brain injury (EBI) after subarachnoid hemorrhage (SAH) largely contributes to unfavorable outcomes, and it has been proved that EBI following SAH is closely associated with oxidative stress and brain edema. The present study
A comparative biochemical, pharmacological and immunological study of Clostridium novyi alpha-toxin, C. difficile toxin B and C. sordellii lethal toxin.
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The three clostridial cytotoxins, i.e. alpha-toxin of C. novyi (Tox alpha-nov), toxin B of C. difficile (ToxB-dif) and lethal toxin of C. sordellii (LT-sor) consist of single peptide chains of about 200,000 (Tox alpha-nov), 250,000 (LT-sor) and 275,000 (ToxB-dif) mol. wts. ToxB-dif and LT-sor but
Pharmacological and biochemical studies of cytotoxicity of Clostridium novyi type A alpha-toxin.
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The actions of apparently homogeneous alpha-toxin from Clostridium novyi type A were studied in order to develop an in vitro system which closely mimics its in vivo effects and to search for the mode of poisoning. Time to death (by intravenous injection of mice) was inversely related to dose, with a
Lung injury induced by butylated hydroxytoluene: cytodynamic and biochemical studies in mice.
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Butylated hydroxytoluene, a common food additive, is known to produce proliferative pulmonary changes characterized by increased DNA, RNA, and lung weight. In the present study, reactive hyperplasia and fibrosis were produced within 9 days after a single intraperitoneal injection of 400 mg. per kg.
Cannabinoid receptor type 2 agonist attenuates apoptosis by activation of phosphorylated CREB-Bcl-2 pathway after subarachnoid hemorrhage in rats.
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Early brain injury (EBI) which comprises of vasogenic edema and apoptotic cell death is an important component of subarachnoid hemorrhage (SAH) pathophysiology. This study evaluated whether cannabinoid receptor type 2 (CB2R) agonist, JWH133, attenuates EBI after SAH and whether CB2R stimulation
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