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hydantoin/atrophie

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ArtikelKlinische VersuchePatente
13 Ergebnisse

[Hydantoin atrophy (degeneration) of the cerebellum].

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Ultrastructural studies on hydantoin induced lymphomas in mice.

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Ultrastructural studies were done on cells from original tumors and from short time cultures of mouse thymic lymphomas experimentally induced by chronic exposure to diphenyl-hydantoin. The tumors appeared in mouse strains with low (C57Bl) and high (SJL/J) susceptibility to spontaneous lymphoma

Blepharoptosis and central nervous system abnormalities in combined valproate and hydantoin embryopathy.

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OBJECTIVE To report a case of intrauterine anticonvulsant exposure with subsequent ocular adnexal manifestations. METHODS Case report. RESULTS An 18-month-old child with known anticonvulsant embryopathy was referred for the management of bilateral congenital blepharoptosis. Physical examination

Structural basis for the stabilization of amyloidogenic immunoglobulin light chains by hydantoins

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Misfolding and aggregation of immunoglobulin light chains (LCs) leads to the degeneration of post-mitotic tissue in the disease immunoglobulin LC amyloidosis (AL). We previously reported the discovery of small molecule kinetic stabilizers of the native dimeric structure of full-length LCs, which

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

Phenytoin as a novel anti-vitiligo weapon.

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Vitiligo is a psychologically devastating clinical conundrum which affects approximately 1% of the general population. The exact cause of the illness is an enigma, but several hypotheses about its pathogenesis are advanced. The autoimmune hypothesis proposes an autoimmune attack against melanocytes.

Spectrum of epilepsy in tuberous sclerosis.

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Tuberous sclerosis (TS) is an autosomal dominant disease that affects the brain, skin, eye, heart and kidney. The diagnostic criteria for tuberous sclerosis complex (TSC) have recently been revised. There are relatively few Indian studies on this disorder. Twenty-six patients diagnosed as having TS
Nitrofurantoin was studied and evaluated because of its widespread use as a drug for treating urinary tract infections in humans, its structural relationship to known carcinogenic 5-nitrofuran compounds, and the lack of adequate studies to assess its carcinogenicity. Toxicology and carcinogenesis
Two degenerate primers established from the alignment of highly conserved amino acid sequences of bacterial dihydropyrimidinases (DHPs) were used to amplify a 330-bp gene fragment from the genomic DNA of Bacillus sp. TS-23 and the amplified DNA was successfully used as a probe to clone a dhp gene

Corticosteroid-induced dendrite loss and behavioral deficiencies can be blocked by activation of Abl2/Arg kinase.

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Stressor exposure induces neuronal remodeling in specific brain regions. Given the persistence of stress-related illnesses, key next steps in determining the contributions of neural structure to mental health are to identify cell types that fail to recover from stressor exposure and to identify

[Erythematodes and nervous system (author's transl)].

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Lupus erythematodes is related to the vegetative nervous system in Raynaud's disease, the butterfly distribution in the face, the involvement of the lateral part of the eyebrows (Hertoghe) and in cerebral attacks. Involvement of peripheral and central animal nervous systems is common and produces

[Pharmacotherapy in pregnancy].

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Between 1958 and 1961 approximately 10,000 children with severe limb defects were born, whose mothers had taken the somnifacient thalidomid. Since then, pharmaceutical agents in pregnancy are applied with legitimate caution by the pharmaceutical industry, physicians and patients, although often

Hippocampal adult neurogenesis is maintained by Neil3-dependent repair of oxidative DNA lesions in neural progenitor cells.

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Accumulation of oxidative DNA damage has been proposed as a potential cause of age-related cognitive decline. The major pathway for removal of oxidative DNA base lesions is base excision repair, which is initiated by DNA glycosylases. In mice, Neil3 is the main DNA glycosylase for repair of
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