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Concomitant acral necrosis and haemolytic uraemic syndrome following ingestion of quinine.
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Thrombotic microangiopathy, which broadly includes thrombotic thrombocytopaenic purpura (TTP) and haemolytic uraemic syndrome (HUS), is a multisystemic disorder that is characterised by thrombocytopaenia, microangiopathic haemolytic anemia and ischaemic manifestations, resulting from platelet
Quinine inhibits release of tumor necrosis factor, apoptosis, necrosis and mortality in a murine model of septic liver failure.
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We investigated the effect of quinine on liver injury induced by lipopolysaccharide in mice sensitized with D-galactosamine. This model is characterized by high systemic release of tumor necrosis factor, which mediates hepatic apoptosis and necrosis. Pretreatment with quinine, a K+ channel blocker,
The effects of quinine and artesunate treatment on plasma tumor necrosis factor levels in malaria-infected patients.
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Tumor necrosis factor-alpha (TNF-alpha) is an endogenous mediator of shock and inflammation including malaria. Many lines of evidence suggest that cytoadherence, the life-threatening pathology associated with complicated and cerebral malaria, results from the overproduction of TNF in response to
Quinine inhibits production of tumor necrosis factor-alpha from human alveolar macrophages.
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Although tumor necrosis factor-alpha (TNF-alpha) produced by alveolar macrophages plays a key role in acute and chronic inflammatory states of the lung, the regulation of TNF-alpha synthesis remains to be elucidated. Recently, a K channel blocker, quinine, has been reported to inhibit cell
[Quinine-induced renal bilateral cortical necrosis].
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Acute bilateral renal cortical necrosis is a rare cause of renal failure frequently induced by disseminated intravascular coagulation (Dic) following obstetrical complications, sepsis and drugs. We describe a case of Dic with bilateral cortical necrosis after ingestion of only one tablet of quinine.
Suppression of tumor cell proliferation by quinine via the inhibition of the tumor necrosis factor receptor‑associated factor 6‑AKT interaction.
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Protein kinase B (AKT), is a pivotal component of pathways associated with cell survival, metabolism, invasion and metastasis. AKT mediates anti‑apoptotic and proliferative signaling in response to essential cytokines. Tumor necrosis factor receptor‑associated factor (TRAF)6, an E3 ubiquitin ligase,
Prevention of pancreatic fat necrosis by enzyme inhibitors. III. Quinine.
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Necrosis, and Strong Solutions of Quinine.
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[Diluted injectable quinine in the intramuscular and intrarectal route: comparative efficacity and tolerance in malaria treatment for children ].
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The intramuscular (i.m.) route is generally used for treatment of childhood falciparum malaria in outlying health care units in Togo. The purpose of this randomized therapeutic trial was to compare the efficacy and tolerance of diluted injectable quinine administered by the i.m. versus intrarectal
Activation of potassium and chloride channels by tumor necrosis factor alpha. Role in liver cell death.
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Despite abundant evidence for changes in mitochondrial membrane permeability in tumor necrosis factor (TNF)-mediated cell death, the role of plasma membrane ion channels in this process remains unclear. These studies examine the influence of TNF on ion channel opening and death in a model rat liver
[Acral necroses after therapy with quinine sulfate for calf cramps].
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The most common cause of acral cyanosis is vascular spasm which can be induced by several drugs. An 87-year-old woman developed red and livid skin lesions on the fingers of both hands and several toes one month after beginning treatment with quinine sulfate 200 mg daily. The skin lesions progressed
Serum levels of quinine following intramuscular administration to children.
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The serum quinine level was assayed in 31 children four hours after receiving an intramuscular injection of quinine dihydrochloride; in 14 children the level was also assayed 2 hours after the injection. The quinine was quickly absorbed from muscle, with serum quinine levels being significantly
Ultrastructural changes and olfactory deficits during 3-methylindole-induced olfactory mucosal necrosis and repair in mice.
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Olfactory mucosa from C57BL/6N mice was examined by transmission electron microscopy at 0.5, 1, 2, 4, 6, 24, 48, and 72 h after 400 mg 3-methylindole (3MI)/kg ip, and at 7, 14, and 21 days after 300 mg 3MI/kg or vehicle. Degeneration was evident in epithelial cells of Bowman's glands and olfactory
Ibuprofen does not affect levels of tumor necrosis factor alpha and soluble tumor necrosis factor receptor types I and II in Gabonese children with uncomplicated Plasmodium falciparum malaria.
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We assessed the ability of ibuprofen to modulate tumor necrosis factor alpha (TNF-alpha), soluble tumor necrosis factor receptor type I (sTNFR-I), and soluble tumor necrosis factor receptor type II (sTNFR-II) responses during the treatment of fever in uncomplicated Plasmodium falciparum malaria, in
Membrane potential modulates release of tumor necrosis factor in lipopolysaccharide-stimulated mouse macrophages.
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Lipopolysaccharide (LPS)-mediated synthesis of macrophage gene products such as tumor necrosis factor (TNF) is controlled by different signaling pathways. We investigated intracellular free Ca2+ (Ca2+ic) and the membrane potential as early cellular responses to LPS and their role in the synthesis
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