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diphenyl/atrophie

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Effects of two-photon absorption on degenerate four-wave mixing in solutions of diphenyl polyenes.

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We have observed double-peaked phase-conjugate pulses in the degenerate four-wave mixing of nanosecond laser pulses in solutions of diphenyl polyenes. We attribute this to the superposition of fast and slow gratings, where the slow grating is due to two-photon absorption. This is supported by the
In this study, waste edible oil was prepared by both heat and aeration treatment, and the increasing inhibitive effect of tocopherol treatment on the acid value (AV) and carbonyl value (CV) of the oil was investigated. The AV and CV of waste edible oil treated with tocopherol were 0.1-1.0% lower
Short-term inhalation toxicity studies with respirable polymeric methylene diphenyl diisocyanate (polymeric MDI) aerosol were performed in rats. The 4-hr LC50 was found to be 490 mg polymeric MDI/m3 (95.5% < 4.3 microns). Exposure of (4-week-old) rats to 0, 2.2, 4.9, or 13.6 mg polymeric MDI/m3 (95%

[Effect of exposure to higher decabrominated diphenyl ether (PBDE-209) on learning and memory functions of BALB/c mice].

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OBJECTIVE To investigate the effects of exposure to decabrominated diphenyl ether (PBDE-209) on learning and memory of BALB/c mice. METHODS Eighteen female BALB/c mice were randomized divided into 3 groups and gavaged with peanut oil in the control groups and 300, 1500 mg x kg(-1)xd(-1) PBDE-209 in
Four groups of 60 Wistar rats of each sex were exposed by inhalation to 0, 0.2, 1.0, or 6.0 mg/m3 respirable polymeric methylene diphenyl diisocyanate (polymeric MDI) aerosol (93.5% < 4.2 microns) for 6 hr a day, 5 days a week for up to 24 months. In addition, satellite groups of 10 rats/sex/group

Plasma membrane fluidity during regeneration and atrophy of the rat liver following portal branch ligation.

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Dynamic changes in liver plasma membrane fluidity caused by regeneration and atrophy were assessed in rats following portal branch ligation (PBL). The portal branch, which perfuses 70% of the liver, was ligated with 5-0 prolene, and liver plasma membranes were isolated by ultracentrifugation. The

Electrophysiological findings in diphenyl poisoning.

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The fungistatic agent diphenyl caused fatal poisoning with signs of neurotoxicity in a worker in a Finnish paper mill. This initiated a neurophysiological study of 24 workers occupationally exposed to diphenyl. Ten men showed EEG abnormalities, mainly diffuse or generalized ones. The abnormalities

Diphenyl ditelluride intoxication triggers histological changes in liver, kidney, and lung of mice.

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Tellurium compounds may be cytotoxic to different cells types. Thus, this work evaluated the effect of diphenyl ditelluride ((PhTe)2), an organotellurium commonly used in organic synthesis, on the morphology of liver, kidney, and lung. Adult mice were acutely (a subcutaneous single dose: 250

Chronic diphenyl hydantoin encephalopathy in mentally retarded children and adolescent with severe epilepsy.

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An account is given of chronic diphenyl hydantion (DPH) encephalopathy in 21 mentally retarded epileptics with increasing psychomotor deterioration, choreiform hyperkinesia, deposits of immunoglobulins in the skin, and changes in serum immunoglobulins. Three months after withdrawal of DPH the

Photoinduced C-N bond cleavage in 2-azido-1,3-diphenyl-propan-1-one derivatives: photorelease of hydrazoic acid.

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Photolysis of 3-azido-1,3-diphenyl-propan-1-one (1a) in toluene yields 1,3-diphenyl-propen-1-one (2), whereas irradiation of 3-azido-2,2-dimethyl-1,3-diphenyl-propan-1-one (1b) results in the formation of mainly 2,2-dimethyl-1,3-diphenyl-propan-1-one. Laser flash photolysis (308 nm) of 1a,b in

Survival motor neuron protein regulates apoptosis in an in vitro model of spinal muscular atrophy.

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Progressive spinal muscular atrophy (SMA), the most prevalent hereditary lower motor neuron disease, is caused by mutations in the telomeric copy of the survival of motor neuron (SMN1) gene. Unlike other cells, lower motor neurons cannot tolerate low levels of smn protein. However, it is unclear as
Glutaryl-CoA dehydrogenase deficiency is an inherited metabolic disease characterized by elevated concentrations of glutaric acid (GA) and its metabolites glutaconic acid (GC) and 3-hydroxy-glutaric acid (3-OH-GA). Its hallmarks are striatal and cortical degeneration, which have been linked to

Acute Liver Toxicity Induced by 1,1-Diphenyl-2-picryl-hydrazyl (DPPH) in ICR Mice.

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ABSTRACT The hepatotoxic effects of 1,1-diphenyl-2-picryl-hydrazyl (DPPH) in ICR mice were examined. Acute liver injury was induced by a single dose of DPPH (100 mg/kg) intraperitoneally. At 12, 24, 48, and 72 h after treatment, mice were sacrificed for serum and liver. To assess hepatotoxicity, the
The mixed CCK antagonist N-(3-oxo- 2,3-dihydro-1H-pyrazol-4-yl)-indole-carboxamide MPP with a binding affinity of 25nM /20nM and the CCK1 selective 3-oxo-1,2-diphenyl-2,3-dihydro-1Hpyrazol- 4-yl)-N'-phenyl-urea MPM (IC50 = 25nM) represent the best two compounds of an amide and a urea pyrazoline
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