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fluoride/nécrose

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Phenylmethylsulfonyl fluoride (PMSF) administration to rats, was effective in partially preventing liver necrosis induced by thioacetamide, dimethylnitrosamine or galactosamine, when given 6 hr after the hepatotoxins. In the case of galactosamine but not of the other necrogenic chemicals, protection

(18)F-fluoride PET/CT in avascular necrosis of the femoral head.

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Avascular necrosis (AVN) of the femoral head is a devastating disease in young adults. Magnetic resonance imaging is considered the most sensitive and specific technique in the diagnosis of this condition. The authors present an interesting image of bilateral AVN of the femoral heads diagnosed on
OBJECTIVE Femoral head avascular necrosis (FHAVN) is one of the increasingly common causes of musculoskeletal disability and poses a major diagnostic and therapeutic challenge. Although radiography, scintigraphy, computed tomography (CT), and magnetic resonance imaging (MRI) have been widely used in

Tissue necrosis after subgingival irrigation with fluoride solution.

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Irrigation of periodontal pockets with fluoride solution after scaling and root planing is occasionally recommended to inhibit the growth of pathogenic bacteria in the periodontal pocket. At the same time, irrigation enables mechanical removal of loosely adhering plaque and debris. Due to its

Further studies on the mechanism of the late protective effects of phenylmethylsulfonyl fluoride on carbon tetrachloride-induced liver necrosis.

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We previously reported that phenylmethylsulfonyl fluoride (PMSF) administration to rats (100 mg/kg, ip in olive oil) as late as 6 or 10 hr after CCl4 (1 ml/kg, ip as a 20% v/v solution in olive oil) can partially prevent the necrogenic response to the hepatotoxin at 24 hr. Here we confirm that

4-(2-Aminoethyl)benzenesulfonyl fluoride attenuates tumor-necrosis-factor-alpha-induced blood-brain barrier opening.

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The effect of serine protease inhibitor 4-(2-aminoethyl)benzenesulfonyl fluoride (AEBSF) was investigated on the prevention of tumor-necrosis-factor-alpha (TNF-alpha)-induced blood-brain barrier opening. TNF-alpha (10,000 IU) was injected intracarotidly to newborn pigs pretreated with 0, 2.4, 4.8,

Late preventive effects of phenylmethylsulfonyl-fluoride on carbon tetrachloride-induced liver necrosis.

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The administration to rats of phenylmethylsulfonylfluoride (PMSF) 6 or 10 h after tetrachloride (CCl4) significantly prevented liver necrosis induced by this hepatotoxin at 24 h but not at 72 h. Preventive effects of PMSF were not due to interference with CCl4 absorption from the peritoneum since

Bone formation in ankylosing spondylitis during anti-tumour necrosis factor therapy imaged by 18F-fluoride positron emission tomography.

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Excessive bone formation is an important hallmark of AS. Recently it has been demonstrated that axial bony lesions in AS patients can be visualized using 18F-fluoride PET-CT. The aim of this study was to assess whether 18F-fluoride uptake in clinically active AS patients is related to focal bone

Bone formation in ankylosing spondylitis during anti-tumour necrosis factor therapy imaged by 18F-fluoride positron emission tomography.

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Nephrotoxicity of uranyl fluoride in uninephrectomized and sham-operated rats.

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The aim of the present study was to determine whether the nephrotoxicity of the uranium-containing compound uranyl fluoride (UO2F2) is enhanced after unilateral nephrectomy. Unilaterally nephrectomized (NPX) and sham-operated (SO) rats were given single intravenous injections of UO2F2 at doses
The native lipooligosaccharide (LOS) from Neisseria meningitidis strain 89I was analyzed by matrix-assisted laser desorption ionization (MALDI) time-of-flight (TOF) mass spectrometry and the spectrum compared with that of the LOS after O-deacylation and hydrogen fluoride treatment. The data are

Interleukin-1 and tumor necrosis factor are not synergistic for human synovial fibroblast PLA2 activation and PGE2 production.

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Patterns of arachidonic acid release and metabolism were altered in human synovial fibroblasts following exposure to cytokines. Recombinant interleukin-1 induced an approximate 3-fold increase in [3H]-AA release, a 7-fold increase in PGE2 production and a 2-fold increase in PLA2 activity in human

Superphosphate poisoning of sheep: the role of fluoride.

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Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep

Sodium fluoride/copper naphthenate toxicosis in cattle.

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Fourteen cattle on a Kansas pasture died from ingestion of a wood preservative compound containing sodium fluoride and copper naphthenate. Clinical signs included depression, anorexia, ataxia, diarrhea, and recumbency. Grossly visible lesions included perirenal edema, pale kidneys, and forestomach

Soil fluoride spiking effects on olive trees (Olea europaea L. cv. Chemlali).

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A pot experiment under open air conditions was carried out to investigate the uptake, accumulation and toxicity effects of fluoride in olive trees (Olea europaea L.) grown in a soil spiked with inorganic sodium fluoride (NaF). Six different levels (0, 20, 40, 60, 80 and 100mM NaF) of soil spiking
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