adenyl cyclase/nekrozė

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The molecular action of tumor necrosis factor-alpha.

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Tumor necrosis factor-alpha (TNF-alpha) is a polypeptide hormone newly synthesized by different cell types upon stimulation with endotoxin, inflammatory mediators (C5a anaphylatoxin), or cytokines such as interleukin-1 and, in an autocrine manner, TNF itself. The net biological effect of TNF-alpha

Increased expression of resistin and tumour necrosis factor-alpha in pig adipose tissue as well as effect of feeding treatment on resistin and cAMP pathway.

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OBJECTIVE Resistin, a novel hormone, is expressed in mouse, rat and human adipose tissue. Its resistance to insulin is controversial. We hypothesized that resistin has the similar roles like those of tumour necrosis factor-alpha (TNF-alpha), a putative mediator of insulin resistance, and they are in

[The change of adrenergic receptor-adenyl cyclase system on myocardial ischemic preconditioning in rats].

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OBJECTIVE To study the varies and effects of ischemic preconditioning of myocardium on every part of adrenergic receptor-adenyl cyclase system in rats in vivo. METHODS SD rats were randomly divided into three groups: CON group (n = 6), IP group (n = 12) and I/R group (n = 12). Surgical procedure

Prostaglandin I2 analogs suppress tumor necrosis factor α production and the maturation of human monocyte-derived dendritic cells.

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BACKGROUND Dendritic cells (DCs) are professional antigen-presenting cells and have critical roles in regulating immune responses. Prostaglandin I2 (PGI2) analogs are considered to be potential treatments for asthma. However, the effect of PGI2 analogs on human monocyte-derived DCs (MDDCs) is still

The effect of anti-lipolytic agents on isoprenaline-induced myocardial necrosis in the rat.

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The effect of inhibiting isoprenaline-induced lipolysis on the degree of damage produced in the rat myocardium by this amine has been investigated by pre-dosing rats with the anti-lipolytic agent 5-fluoro-nicotinic acid. The degree of myocardial necrosis produced in animals given isoprenaline alone

Interleukin 1 and tumor necrosis factor inhibit cardiac myocyte beta-adrenergic responsiveness.

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Reversible congestive heart failure can accompany cardiac allograft rejection and inflammatory myocarditis, conditions associated with an immune cell infiltrate of the myocardium. To determine whether immune cell secretory products alter cardiac muscle metabolism without cytotoxicity, we cultured

C-reactive protein decreases interleukin-10 secretion in activated human monocyte-derived macrophages via inhibition of cyclic AMP production.

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OBJECTIVE C-Reactive protein (CRP), a cardiovascular risk marker, could also participate in atherosclerosis. Atherosclerotic plaques express CRP and interleukin (IL)-10, a major antiinflammatory cytokine. IL-10 deficiency results in increased lesion formation, whereas IL-10 delivery attenuates

Molecular pharmacology of the beta-adrenergic receptor on THP-1 cells.

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The beta-adrenergic receptor, its occupancy and subsequent modulation of intracellular cAMP, and mRNA expression were characterized for the promonocytic leukemia cell line THP-1. We report that THP-1 cells appear to express a beta-1 receptor with a Kd of 1.8 +/- 0.3 x 10(-11) microM and a B max of

Molecular mechanisms underlying cyclic AMP inhibition of macrophage dependent TNF-alpha production and neurotoxicity in response to amyloidogenic C-terminal fragment of Alzheimer's amyloid precursor protein.

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In the present study, we characterized the intracellular pathway involved in the macrophage production of tumor necrosis factor-alpha (TNF-alpha) and the molecular mechanisms by which cyclic AMP (cAMP) regulates the neurotoxic inflammatory signaling cascade in response to the 105 amino acid

Rabbit pigmented ciliary epithelium produces interleukin-6 in response to inflammatory cytokines.

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Interleukin-6 is a multifunctional cytokine that is found in high concentrations in intraocular fluids during the uveitic response. Although monocytic cells are a major source of interleukin-6, resident intraocular cells may also contribute to its accumulation in intraocular fluids during uveitis.

Cytokines increase neutral endopeptidase activity in lung fibroblasts.

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Fibroblasts of the pulmonary interstitium are intimately involved in the response of the lung to inflammation as well as in repair of injured tissues. The response of fibroblasts within an inflammatory site appears to be directed, in part, by peptide mediators. Neutral endopeptidase (NEP), a

Bacillus anthracis-derived edema toxin (ET) counter-regulates movement of neutrophils and macromolecules through the endothelial paracellular pathway.

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BACKGROUND A common finding amongst patients with inhalational anthrax is a paucity of polymorphonuclear leukocytes (PMNs) in infected tissues in the face of abundant circulating PMNs. A major virulence determinant of anthrax is edema toxin (ET), which is formed by the combination of two proteins

Cell coupling and impulse propagation in the failing heart.

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Cell coupling and impulse propagation were investigated in the ventricle of cardiomyopathic hamsters at an advanced stage of heart failure. An appreciable decline in junctional conductance was found, a phenomenon in part related to activation of the plasma and cardiac renin-angiotensin systems.

Hypocapnic hypothesis of Leigh disease.

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Leigh syndrome (LS) is a neurogenetic disorder of children caused by mutations in at least 75 genes which impair mitochondrial bioenergetics. The changes have typical localization in basal ganglia and brainstem, and typical histological picture of spongiform appearance, vascular proliferation and

Pepsinogens: physiology, pharmacology pathophysiology and exercise.

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Human gastric mucosa contains aspartic proteinases that can be separated electrophoretically on the basis of their physical properties into two major groups: Pepsinogen I (PGA, PGI); and Pepsinogen II (PGC, PGII). Pepsinogens consist of a single polypeptide chain with molecular weight of

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