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biotin/emorragia

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Pagina 1 a partire dal 171 risultati
Attenuation of blood-brain barrier (BBB) disruption is one of the therapeutic candidates for treatment of subarachnoid hemorrhage (SAH). In this study, the protective effect of sodium orthovanadate (SOV) on BBB disruption was investigated in SAH using the endovascular perforation model. Fifty-five
OBJECTIVE To investigate the relationship between inflammatory response and cell apoptosis in the perihematoma region in patients with intracerebral hemorrhage (ICH). METHODS Surgical specimens were obtained from the area 1 cm adjacent to the hematoma. Thirty patients with ICH were divided into five
OBJECTIVE Granulocyte colony-stimulating factor (G-CSF) plays a role in regulating phosphatidylinositol-3-kinase/serine/threonine kinase (PI3K/AKT) pathway, affecting cell proliferation and apoptosis, and inducing vascular endothelial growth factor (VEGF) expression. This study investigated the
A modified sandwich enzyme-linked immunosorbent assay using biotin-streptavidin system (BS-ELISA) was developed to determine levels of tumor necrosis factor-alpha (TNF-alpha) in serum samples of children infected with dengue virus (n=99) and healthy controls (n=41). The minimum detectable

The role of aquaporin 4 in apoptosis after intracerebral hemorrhage.

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BACKGROUND We previously reported that aquaporin-4 deletion (AQP4-/-) in mice increased edema and altered blood-brain barrier integrity following intracerebral hemorrhage (ICH). To date, little is known about the role of AQP4 in apoptosis after ICH. The purpose of this study was to examine the role
BACKGROUND This study aimed to investigate the potential neuroprotective effect of recombinant osteopontin (r-OPN) on apoptotic changes via modulating phosphoinositide-3-kinase/Akt/glycogen synthase kinase 3 beta (PI3K/Akt/GSK-3β) signaling in a rat model of intracerebral hemorrhage (ICH). MATERIAL
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

Effects of low-dose unfractionated heparin on early brain injury after subarachnoid hemorrhage in mice.

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Sphingosine kinase (SphK) 1 has been reported as an important signaling node in anti-apoptotic signaling. Heparin is a pleiotropic drug that antagonizes many pathophysiological mechanisms. In this study, we evaluated if heparin prevents early brain injury (EBI) after subarachnoid
OBJECTIVE Progranulin has been reported to have neuroprotective actions in cultured neurons. This study investigated the effect of recombinant rat progranulin on early brain injury after subarachnoid hemorrhage. METHODS Controlled in vivo laboratory study. METHODS Animal research

Apoptotic epithelial cells in biopsy specimens from infants with streaked rectal bleeding.

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BACKGROUND Histologic studies of rectosigmoidal mucosal biopsies of infants with isolated blood-streaked stool have shown many eosinophils and revealed aggregates of small dark granules (nuclear dust). However, no description of the nuclear dust has been made for this condition and the nature of the

Brisk production of nitric oxide and associated formation of S-nitrosothiols in early hemorrhage.

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The results of previous inhibitor studies suggest that there is some increase in nitric oxide (NO) production from constitutive NO synthase in early hemorrhage (H), but the magnitude of NO production early after H has not been previously assessed. It is generally believed that only modest production
OBJECTIVE To investigate the association of hypoxia-inducible factor-1α (HIF-1α) expression and apoptosis in the cerebral cortex following subarachnoid hemorrhage (SAH). METHODS Subarachnoid hemorrhage was induced by modified monofilament puncture method in rats. Thirty-five adult male
Oxidative stress and neuronal apoptosis are considered crucial therapeutic targets against early brain injury (EBI) after subarachnoid hemorrhage (SAH). Emerging evidence indicates that mitochondrial dysfunction is the main reason for oxidative stress and neuronal apoptosis. MitoNEET, an outer

Pathogenesis of hemorrhagic enteritis virus infection in turkeys.

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The pathogenesis of hemorrhagic enteritis was investigated in 4-week-old specific-pathogen-free (SPF) turkeys after oral administration of hemorrhagic enteritis virus. The virus antigen was detected and quantified in tissues at various days post-infection (DPI) by an avidin-biotin-enhanced enzyme

Correlation of free radical level and apoptosis after intracerebral hemorrhage in rats.

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OBJECTIVE To investigate the correlation of perihematomal free radical level and neuronal apoptosis following the intracerebral hemorrhage (ICH). METHODS Animals were randomly divided into 4 groups: sham operation group, model group, 1 mg/kg edaravone group, and 3 mg/kg edaravone group. Each group
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