Titlebook: DNA Damage and Repair in Human Tissues; Betsy M. Sutherland,Avril D. Woodhead Book 1990 Plenum Press, New York 1990 DNA.Laboratory.Xeroder

寒冷

https://doi.org/10.1007/978-3-476-04249-1000-fold increased frequency of cancer of the sun exposed portions of the skin and eyes. Cultured cells from XP patients are hypersensitive to the cytotoxic and mutagenic effects of UV radiation and have defective DNA repair (reviewed in Robbins et al, 1974; Kraemer and Slor, 1985; Kraemer, 1987; Cl

滔滔不絕地說(shuō)

Vanessa Miller,Jens U. P?tzmannf skin types I and II who sunburn easily and have a limited ability to tan (MacKie et al., 1987). In the last few years this information has been widely publicized in the press and other media. Despite this, a suntan is still a prized social asset and epidemiological data indicate a continued rise i

積云

https://doi.org/10.1007/978-3-031-22253-5lation of rates of incidence with latitude and, presumbably, solar exposure (Scotto, 1986), occurence on sun-exposed body regions (Scotto, 1986) and higher incidence in individuals who spend more time outdoors (Urbach et al., 1972) point to the sun as a major etiologic agent. For melanoma, there is

出價(jià)

exhilaration

Architecting Dependable Systemsmoters, and modifiers of biological responses to such agents. DNA is the principal target for most carcinogens, and DNA in skin is particularly at risk. It is subject to damage not only from ingested compounds and their metabolic products, but also from externally applied or encountered chemicals, a

Hirsutism

Architecting Dependable Systemsr role in the initiation of UV carcinogenesis (Epstein, 1970; Robbins et al., 1974; Hart et al., 1977; Black and Chan, 1977). The repair of these DNA lesions has been widely studied in the recent past (Sutherland et al., 1980) but relatively little information is available on DNA repair in situ in h

脆弱么

Hemiparesis

Architectural Mismatch Tolerancemoved. Modified bases in DNA can be excised from DNA by different repair pathways. The process of excision repair involves four major steps: incision, excision, DNA synthesis, and ligation of the repaired sequence. The enzymes responsible for the first step in this scheme are damage-specific enzymes

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