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xeroderma pigmentosum/fever

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文章临床试验专利权
7 结果
Human xeroderma pigmentosum (XP) or Fanconi anemia (FA) fibroblasts displayed shouldered 45 degrees C heat survival curves not significantly different from normal fibroblasts, a result similar to that previously found for ataxia telangiectasia (AT) cells, indicating heat resistance is not linked to

Hyperthermia and host-cell reactivation of adenovirus 12.

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Exposure of cultured human fibroblasts to hyperthermia delayed the host-cell reactivation of UV-irradiated human adenovirus type 12 (AD12). The experimental design consisted of irradiating human AD12 with UV doses ranging from 180 to 1800 ergs/mm2, infecting human cell populations at 37 degrees C,
Hyperthermia specifically inhibits the repair of UV-induced DNA photolesions in transcriptionally active genes. To define more precisely which mechanisms underlie the heat-induced inhibition of repair of active genes, removal of cyclobutane pyrimidine dimers (CPDs) was studied in human fibroblasts
BACKGROUND Xeroderma pigmentosum (XP) is an autosomal recessive disease caused by mutations in DNA repair genes. Clinical manifestations include extreme sensitivity to ultraviolet (UV) rays, freckle-like pigmentation, ocular abnormalities, and an increased risk of developing neoplasms in sun-exposed
Emir S, Hacısalihoğlu Ş, Özyörük D, Kaçar D, Erdem A, Karakuş E. Squamous cell carcinoma associated with Xeroderma pigmentosum: an unusual presentation with a tremendously huge mass over the face and paraneoplastic hypercalcemia-hyperleukocytosis. Turk J Pediatr 2017; 59: 711-714. Xeroderma
Amifostine is a broad-spectrum cytoprotective agent approved for protection against cisplatin toxicities and radiation-induced xerostomia; strong clinical evidence exists that amifostine protects normal mucosa and lung from radiation damage. Hypotension, nausea/vomiting, fatigue and fever/rash are

A temperature-sensitive disorder in basal transcription and DNA repair in humans.

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The xeroderma pigmentosum group D (XPD) helicase subunit of TFIIH functions in DNA repair and transcription initiation. Different mutations in XPD give rise to three ultraviolet-sensitive syndromes: the skin cancer-prone disorder xeroderma pigmentosum (XP), in which repair of ultraviolet damage is
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