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3 beta galactosidase/hemorragia
O link é salvo na área de transferência
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Reversible activation of a cryptic cleavage site within E. coli beta-galactosidase in beta-galactosidase fusion proteins.
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The VP60 capsid protein of rabbit haemorrhagic disease virus (60 kDa) has been fused to the C-terminus of beta-galactosidase and produced in E. coli from two related expression vectors. One of these vectors, carries a 429 bp DNA segment encoding the N-terminus peptide of VP60, and directs the
Association between the organoleptic scores, oral condition and salivary β-galactosidases in children affected by halitosis.
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OBJECTIVE
The goal of this work is to evaluate the association between organoleptic scores, oral condition and salivary β-galactosidases, to facilitate the differential diagnosis of halitosis in children.
METHODS
Fifty systemically healthy children with a primary complaint of oral malodour were
Molecular cloning, sequencing and expression in Escherichia coli of the capsid protein gene from rabbit haemorrhagic disease virus (Spanish isolate AST/89).
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We describe the cloning, nucleotide sequencing and expression in Escherichia coli of the major capsid component (VP60) from the Spanish field isolate AST/89 of rabbit haemorrhagic disease virus (RHDV). The sequence of the 3'-terminal 2483 nucleotides of the genome was found to be 95.4% identical to
In utero transplantation of wild-type fetal liver cells rescues factor X-deficient mice from fatal neonatal bleeding diatheses.
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Factor X (FX)-deficient embryos suffer partial embryonic lethality with approximately 30% of the embryos arresting at midgestation. The remaining animals survive to term but die perinatally mainly from abdominal or intracranial hemorrhage. We have rescued FX-deficient mice by transplanting fetal
Gene transfer to cerebral blood vessels after subarachnoid hemorrhage.
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OBJECTIVE
Vasospasm remains a major cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage. One step toward gene therapy to prevent spasm of cerebral vessels is to determine whether subarachnoid blood prevents transgene expression.
METHODS
Vasospasm was induced in mongrel dogs
Role of endothelial NO synthase phosphorylation in cerebrovascular protective effect of recombinant erythropoietin during subarachnoid hemorrhage-induced cerebral vasospasm.
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OBJECTIVE
In the present study, the effect of subarachnoid hemorrhage (SAH) on the phosphorylation of endothelial NO synthase (eNOS) and the ability of recombinant erythropoietin (Epo) to augment this vasodilator mechanism in the spastic arteries were studied.
METHODS
Recombinant adenoviral vectors
Expression and function of recombinant endothelial nitric oxide synthase gene in canine basilar artery after experimental subarachnoid hemorrhage.
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OBJECTIVE
Gene transfer with recombinant viral vectors encoding vasodilator proteins may be useful in therapy of cerebral vasospasm after subarachnoid hemorrhage (SAH). Relaxations mediated by nitric oxide are impaired in cerebral arteries affected by SAH. The present study was designed to determine
Macular cherry-red spots and beta-galactosidase deficiency in an adult. An autopsy case with progressive cerebellar ataxia, myoclonus, thrombocytopathy, and accumulation of polysaccharide in liver.
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An adult patient with macular cherry-red spots, a gargoyle-like physical appearance, cerebellar ataxia, myoclonus, convulsive seizures, and pyramidal tract signs showed a profound deficiency of beta-galactosidase in liver and brain. Thrombocytopathy of undetermined etiology was evident since
Retinoic acid receptor status in mouse spleen during a primary immune response against beta-galactosidase.
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OBJECTIVE
Evaluation of the dynamics of all-trans retinoic acid receptor binding properties in mouse spleen nuclear extracts during a primary immune response against beta-galactosidase.
METHODS
Female BALB/c mice, aged between 5 and 6 weeks were immunized intradermally into the shaved back (4 spots
Effect of glucocorticoids on release of lysosomal enzymes in liver ischemia and hemorrhagic shock in pigs.
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The effect of glucocorticoids on the release of lysosomal enzymes was studied in liver ischemia created by dearterialization and in hemorrhagic shock in pigs. In shock the treatment with glucocoticoids suppressed the release of beta-glucosidase and beta-galactosidase into the circulation. The
Effect of adenovirus-mediated nitric oxide synthase gene transfer on vasospasm after experimental subarachnoid hemorrhage.
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OBJECTIVE
Evidence indicates that vasospasm after subarachnoid hemorrhage (SAH) is caused in part by a decrease in the vasodilator nitric oxide (NO), which is produced mainly in endothelial cells. This study tested whether intracisternal injection of adenovirus-expressing endothelial NO synthase
Acute hemorrhagic pancreatic necrosis in mice: the activity of lysosomal enzymes in the pancreas and the liver.
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The activity of lysosomal enzymes of the pancreas and the liver has been studied during induction and onset of acute hemorrhagic pancreatic necrosis with fat necrosis (AHPN) in mice. We induced AHPN by feeding the animals a choline-deficient (CD) diet containing 0.5% DL-ethionine (CDE). Control
Heme oxygenase 1 protects against hepatic hypoxia and injury from hemorrhage via regulation of cellular respiration.
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Heme oxygenase 1 (HO-1) is an important regulator of the cellular response to stress and inflammation. These investigations test the hypothesis that HO-1 overexpression protects against hemorrhage-induced hypoxia by regulating cellular respiration and oxygen availability. Male C57BL/6 mice or
Brain transplantation of immortalized human neural stem cells promotes functional recovery in mouse intracerebral hemorrhage stroke model.
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We have generated stable, immortalized cell lines of human NSCs from primary human fetal telencephalon cultures via a retroviral vector encoding v-myc. HB1.F3, one of the human NSC lines, expresses a normal human karyotype of 46, XX, and nestin, a cell type-specific marker for NSCs. F3 has the
Short-term correction of factor VIII deficiency in a murine model of hemophilia A after delivery of adenovirus murine factor VIII in utero.
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Development of in utero gene transfer approaches may provide therapies for genetic disorders with perinatal morbidity. In hemophilia A, prenatal and postnatal bleeding may be catastrophic, and modest increments in factor VIII (FVIII) activity are therapeutic. We performed transuterine i.p. gene
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