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Pagina 1 a partire dal 563 risultati
Determination of tumor necrosis factor-alpha levels in dengue virus infected patients by sensitive biotin-streptavidin enzyme-linked immunosorbent assay.
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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
Familial infantile bilateral striatal necrosis: clinical features and response to biotin treatment.
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BACKGROUND
Infantile bilateral striatal necrosis (IBSN) encompasses several syndromes of bilateral symmetric, spongy degeneration of the caudate nucleus, putamen, and globus pallidus. The familial form of IBSN is rare, and inheritance is either autosomal recessive or maternal.
METHODS
The authors
Immunological evidence for a human ovarian tumor necrosis factor-alpha.
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Tumor necrosis factor-alpha (TNF alpha) was localized to follicular and luteal compartments of the human ovary using a biotin strept-avidin immunocytochemical technique with polyclonal antibodies to human recombinant TNF alpha. Immunoreactive TNF alpha (I-TNF) was observed in granulosa cells of
Tumor necrosis factor-alpha (TNF-alpha) in loosening of total hip replacement (THR).
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OBJECTIVE
The initially well-fixed implants of total hip replacement (THR) are in the long-term subject to aseptic loosening. Many cytokines can contribute to osteolysis due to osteoclast recruitment and/or activation. However, in this respect tumor necrosis factor-alpha (TNF-alpha) plays a pivotal
Jurkat cells respond to biotin deficiency with increased nuclear translocation of NF-kappaB, mediating cell survival.
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Members of the NF-kappaB family of transcription factors cause transcriptional activation of anti-apoptotic genes. Here we determined whether survival of biotin-deficient cells is mediated by nuclear translocation of NF-kappaB. Human T (Jurkat) cells were cultured in biotin-deficient or
Rapid and sensitive detection of infectious spleen and kidney necrosis virus by loop-mediated isothermal amplification combined with a lateral flow dipstick.
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Loop-mediated isothermal amplification (LAMP) allows rapid amplification of nucleic acids under isothermal conditions. In this report, a 20-min LAMP amplification of the DPOL gene of infectious spleen and kidney necrosis virus (ISKNV) using a biotin-labeled primer was combined with lateral flow
Asbestos and cigarette smoke cause increased DNA strand breaks and necrosis in bronchiolar epithelial cells in vivo.
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Coexposures to asbestos and cigarette smoke cause increased risks of lung cancer in asbestos workers. Although these carcinogens cause DNA damage to epithelial cells in vitro via generation of reactive oxygen species (ROS), it is unclear whether they cause injury to bronchiolar epithelial cells
Role of tumor necrosis factor alpha in disease using a mouse model of Shiga toxin-mediated renal damage.
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Mice have been extensively employed as an animal model of renal damage caused by Shiga toxins. In this study, we examined the role of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) in the development of toxin-mediated renal disease in mice. Mice pretreated with TNF-alpha and
Regulation of tumor necrosis factor-like weak inducer of apoptosis receptor protein (TWEAKR) expression by Kaposi's sarcoma-associated herpesvirus microRNA prevents TWEAK-induced apoptosis and inflammatory cytokine expression.
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Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is the causative agent of KS, the second most common AIDS-associated malignancy. KSHV expresses at least 18 different mature microRNAs (miRNAs) during latency. To identify cellular targets of KSHV miRNAs, we have analyzed a previously reported
Differential effects of heparin on NO and tumor necrosis factor-alpha production in bovine blood mononuclear cells stimulated with Salmonella typhimurium lipopolisaccharide.
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We investigated the influence of heparin, one of the extracellular matrix (ECM) components, on nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) production by bovine peripheral blood mononuclear cells (PBMC) and monocytes left to adhere for 2 (freshly adherent monocytes) and 48 h
Activation of the CED3/ICE-related protease CPP32 in cerebellar granule neurons undergoing apoptosis but not necrosis.
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Neuronal apoptosis occurs during nervous system development and after pathological insults to the adult nervous system. Inhibition of CED3/ICE-related proteases has been shown to inhibit neuronal apoptosis in vitro and in vivo, indicating a role for these cysteine proteases in neuronal apoptosis. We
Detection of the infectious hematopoietic necrosis virus directly from infected fish tissues by dot blot hybridization with a non-radioactive probe.
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A method was developed for the rapid diagnosis of the infectious hematopoietic necrosis virus (IHNV) based on dot blot hybridization with a non-radioactive probe. When the assay was developed through a color reaction both biotin- and alkaline phosphatase-labeled probes were highly specific for IHNV
Oocytic tumor necrosis factor alpha: localization in the neonatal ovary and throughout follicular development in the adult rat.
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Tumor necrosis factor alpha (TNF alpha) has previously been immunolocalized within mouse oocytes. Our first objective was to examine TNF alpha immunolocalization in ovaries of adult, fetal, and neonatal rats. Our second objective was to examine TNF alpha mRNA in ovaries by Northern blot analysis and
Significant damage of the conduction system during cardioplegic arrest is due to necrosis not apoptosis.
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OBJECTIVE
Ventricular conduction disturbances following cardioplegic arrest remains a serious, yet unsolved problem. In the present study we examined whether myocardial conduction cells (MCC, Purkinje fibers) are more vulnerable to ischemia/reperfusion injury than working myocardial cells and
Immunomagnetic isolation of tumor necrosis factor receptosomes.
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Internalized tumor necrosis factor (TNF) receptor-1 (TNF-R1) recruits the adaptor proteins TRADD and FADD, as well as caspase-8, to establish the "death-inducing signaling complex" (DISC). DISC formation and apoptosis depend strictly on TNF-R1 internalization, whereas recruitment of TRAF-2 and RIP-1
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