adenosine diphosphate/necrotisch

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Diabetes increases apoptosis and necrosis in both ischemic and nonischemic human myocardium: role of caspases and poly-adenosine diphosphate-ribose polymerase.

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OBJECTIVE Diabetes is an important predictor of morbidity and mortality after cardiac surgery, but the reason is unclear. The aims of these studies, therefore, were to elucidate whether cell death is greater in ischemic and nonischemic diabetic human myocardium than in nondiabetic myocardium and to

Poly(adenosine diphosphate ribose) polymerase inhibition prevents necrosis induced by H2O2 but not apoptosis.

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OBJECTIVE H2O2 causes DNA damage, which activates poly(adenosine diphosphate ribose) polymerase (PARP), a nuclear enzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate. When DNA strand breaks are extensive, consumption of NAD by PARP can cause adenosine triphosphate depletion. The

Effect of clopidogrel with and without eptifibatide on tumor necrosis factor-alpha and C-reactive protein release after elective stenting: results from the CLEAR PLATELETS 1b study.

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OBJECTIVE This study was performed to compare the effects of antiplatelet regimens on early inflammation and cardiac marker release after elective stenting. BACKGROUND Few data exist regarding the comparative effects of specific antiplatelet regimens on early inflammation marker release after

Biochemical pathways of apoptosis: nicotinamide adenine dinucleotide-deficient cells are resistant to tumor necrosis factor or ultraviolet light activation of the 24-kD apoptotic protease and DNA fragmentation.

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The function of nicotinamide adenine dinucleotide (NAD) and adenosine diphosphate (ADP) ribosylation reactions in the mechanism of apoptotic cell death is controversial, although one theory postulates an essential role for NAD depletion by poly-ADP-ribose polymerase. The present study examined the

Effects of inhibition of poly(adenosine diphosphate-ribose) synthase on acute cardiac allograft rejection.

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BACKGROUND Nitric oxide synthase (NOS)-2 is expressed during acute cardiac allograft rejection in association with death of heart muscle cells. The nuclear enzyme poly(adenosine diphosphate [ADP]-ribose) synthase (PARS) is activated by agonists such as NO and peroxynitrite, which cause single-strand

The poly(adenosine diphosphate-ribose) polymerase inhibitor PJ34 reduces pulmonary ischemia-reperfusion injury in rats.

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BACKGROUND Ischemia-reperfusion (I/R) injury after lung transplantation causes alveolar damage, lung edema, and acute rejection. Poly(adenosine diphosphate-ribose) polymerase (PARP) is a single-stranded DNA repair enzyme that induces apoptosis and necrosis after DNA damage caused by reactive oxygen

Oxyhemoglobin produces necrosis, not apoptosis, in astrocytes.

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OBJECTIVE Subarachnoid blood, resulting from traumatic brain injury or subarachnoid hemorrhage, has been linked with cell injury and stress gene induction. We investigated whether oxyhemoglobin (OxyHb), a major component in blood clots, exerts a cytotoxic effect on cultured astrocyte cells, and the

Growth inhibition and apoptosis induction by tumor necrosis factor-α in human urethral rhabdosphincter satellite cells.

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OBJECTIVE A decrease in the human urethral rhabdosphincter is reported with aging due to apoptosis, which may be a cause of urinary incontinence in the elderly population. To explore this mechanism we investigated the effects of tumor necrosis factor-alpha (Upstate, Temecula, California) on human

Isoproterenol Enhances Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand-Induced Apoptosis in Human Embryonic Kidney Cells through Death Receptor 5 up-Regulation.

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OBJECTIVE Chronic impairment of β-adrenergic receptor signaling increases cardiac apoptosis, hypertrophy and fibrosis. The aim of this study was to investigate whether isoproterenol (ISO), an agonist of the adrenergic receptor, can enhance tumor necrosis factor-related apoptosis-inducing ligand

Valsartan improves resting skin blood flow in type 2 diabetic patients and reduces poly(adenosine diphosphate-ribose) polymerase activation.

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OBJECTIVE To examine the effect of a 12-week daily treatment with 160 mg of valsartan, an angiotensin II receptor blocker, on the microcirculation and macrocirculation of type 2 diabetic patients (T2DM) and healthy subjects. METHODS This was a prospective, randomized, double-blind,

Tumor necrosis factor-alpha-induced dilatation of cerebral arterioles.

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OBJECTIVE In brain, several cell types produce tumor necrosis factor-alpha (TNFalpha) after injury or exposure to endotoxin. TNFalpha alone or in combination with endotoxin or other cytokines can cause expression of inducible nitric oxide (NO) synthase. We have previously demonstrated that endotoxin

Cholera toxin pretreatment protects against tumor necrosis factor lethality without compromising tumor response to therapy.

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Antitumor therapy with tumor necrosis factor is limited by systemic toxic effects. We studied whether cholera toxin, a bacterial exotoxin that adenosine diphosphate-ribosylates the alpha-subunit of Gs proteins, could separate the lethal from the antitumor effects of tumor necrosis factor. A single

Blocking Cyclic Adenosine Diphosphate Ribose-mediated Calcium Overload Attenuates Sepsis-induced Acute Lung Injury in Rats.

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BACKGROUND Acute lung injury (ALI) is a common complication of sepsis that is associated with high mortality. Intracellular Ca2+ overload plays an important role in the pathophysiology of sepsis-induced ALI, and cyclic adenosine diphosphate ribose (cADPR) is an important regulator of intracellular

Inhibition of poly (adenosine diphosphate-ribose) polymerase attenuates lung-kidney crosstalk induced by intratracheal lipopolysaccharide instillation in rats.

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BACKGROUND Acute respiratory distress syndrome (ARDS) is a severe form of lung injury that frequently occurs during pneumonia and sepsis. Lung inflammation in ARDS patients may have deleterious effects on remote organs such as the kidney. The nuclear enzyme poly(adenosine diphosphate-ribose)

Inhibition of poly(adenosine diphosphate-ribose) polymerase attenuates ventilator-induced lung injury.

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BACKGROUND Mechanical ventilation can induce organ injury associated with overwhelming inflammatory responses. Excessive activation of poly(adenosine diphosphate-ribose) polymerase enzyme after massive DNA damage may aggravate inflammatory responses. Therefore, the authors hypothesized that the

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