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Effect of hyperthermia on poly(adenosine diphosphate-ribose) glycohydrolase.

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The effects of supranormal temperature on the activity of poly(ADP-ribose) glycohydrolase were studied by assaying the enzyme in cell extracts derived from cells subjected to hyperthermia and comparing with extracts that were heated in vitro. The enzyme activity was reduced by both hyperthermic

Mechanism of alteration of poly(adenosine diphosphate-ribose) metabolism by hyperthermia.

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The effects of hyperthermia on adenine nucleotide metabolism including NAD and poly(ADP-ribose) have been studied in confluent cultures of C3H10T1/2 cells. Cells replated immediately following hyperthermic treatment showed only 9% survival relative to controls while after a 24-h recovery period at

Halothane-induced ATP depletion in platelets from patients susceptible to malignant hyperthermia and from controls.

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Since the cellular defect of malignant hyperthermia (MH) may occur in tissues other than muscle and since platelets share certain contractile characteristics with muscle cells, testing platelets has been suggested as a way to diagnose susceptibility to MH. In analogy to the in vitro depletion of

Effect of hyperthermia in vitro and in vivo on adenine and pyridine nucleotide pools in human peripheral lymphocytes.

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Hyperthermia has been shown in vitro and in vivo to potentiate the effects of ionizing irradiation. Previous studies found that hyperthermia alters the metabolism of adenosine diphosphate (ADP)-ribose polymers required for recovery from DNA damage and that poly(ADP-ribose) polymerase activity is

Modulation of hyperthermia-induced platelet aggregation inhibition in the presence of urea.

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OBJECTIVE This study has been conducted to evaluate the effect of urea on aggregation responses of heat-treated platelets. METHODS The urea was added to platelet-rich plasma (PRP) samples in final concentrations of 50 and 100 mM. PRP samples, with or without exogenous urea, were incubated at 37 °C,

Whole-body hyperthermia and ADPRT inhibition in experimental treatment of brain tumors.

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Malignant primary brain tumors have hitherto been incurable. One reason for this may be the migrating tumor cells that spread into the surrounding normal brain, creating the basis for inevitable recurrences. Therefore, local therapy may have a temporary effect, but for a cure, the treatment must

Cyclic ADP-ribose induces a larger than normal calcium release in malignant hyperthermia-susceptible skeletal muscle fibers.

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Malignant hyperthermia (MH) is associated with abnormal regulation of intracellular calcium in skeletal muscle fibers. Cyclic adenosine diphosphate-ribose (cADPR) is an endogenous metabolite of beta-NAD+ that induces Ca2+ release from intracellular stores in many tissues. Microinjection of cADPR

A plasma inhibitor of platelet aggregation in patients with Argentine hemorrhagic fever.

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Hemorrhage in patients with Lassa fever is associated with the presence of a circulating plasma inhibitor of platelet aggregation. This study was to determine whether patients with Argentine hemorrhagic fever (AHF) develop a similar inhibitor. Normal platelets showed significantly weaker aggregation

Hemostatic and platelet kinetic studies in dengue hemorrhagic fever.

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In an attempt to reveal certain aspects of the pathogenesis of the bleeding disorder in dengue hemorrhagic fever, hemostatic and platelet kinetic studies were carried out in 61 children with this disease. As has been shown by others, thrombocytopenia and hypofibrinogenemia were the two most

Characterization of polymers of adenosine diphosphate ribose generated in vitro and in vivo.

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Methods have been developed and applied to determine the size and branching frequency of polymers of ADP-ribose synthesized in nucleotide-permeable cultured mouse cells and in intact cultured cells. Polymers were purified by affinity chromatography with a boronate resin and were fractionated

[Clinical features and laboratory findings of thrombotic thrombocytopenic purpura associated with ticlopidine].

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Ticlopidine is an antiplatelet agent that interferes with platelet membrane function by inhibiting adenosine diphosphate-induced platelet activation. It is used in an increasing number of cases of cerebrovascular disease, unstable angina, coronary artery stenting, and peripheral vascular diseases.

Severe aplastic anemia induced by ticlopidine: report of a case.

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Ticlopidine is a powerful antiplatelet activator that inhibits adenosine diphosphate (ADP)-induced platelet aggregation. Its most common side-effects are skin rashes, diarrhea and neutropenia. Aplastic anemia is rare. This paper reports a patient with severe aplastic anemia that developed after the

Synthesis and pharmacological screening of novel non-acidic gastroprotective antipyretic anti-inflammatory agents with anti-platelet properties. 5-Alkyl/cycloalkylamino substituted 2-amino-5H-[1]benzopyrano[4,3-d] pyrimidines.

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The preparation and screening of antipyretic, anti-inflammatory, analgesic, gastroprotective and antiplatelet activities of original non-acidic aminobenzo-pyranopyrimidine derivatives are described. Major and dose-dependent analgesic and antipyretic properties were detected in all the compounds

Antipyretic and platelet antiaggregating effects of nimesulide.

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Nimesulide strongly inhibited ex vivo platelet aggregation in guinea-pigs after both single and repeated (once daily for 5 days) oral dosing, irrespective of the aggregating agent used (adenosine diphosphate, arachidonic acid or collagen). Its potency was consistently greater than that shown by

Poly(ADP-ribose)polymerase-activity of chicken embryo cells exposed to nucleotoxic agents.

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Poly(ADP-ribose)polymerase (PARP)-activity was assessed in vitro from the incorporation of the adenosine-diphosphate-ribose moiety of 14C-NAD+ in the acid-insoluble cell fraction. When compared to mammalian (rat) cells, chicken embryo cells exhibit an almost three- to fourfold higher constitutive

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