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We have examined the contributions of O6-alkylguanine-DNA alkyl-transferase (AGT) and nucleotide excision repair to the protection of human cells from the toxic and mutagenic effects of ethylnitrosourea. Three human lymphoblastoid cell lines were used: one which possesses both of these DNA repair pathways; one derived from a xeroderma pigmentosum complementation group A patient, which expresses AGT but is deficient in nucleotide excision repair; and a third which does not express AGT but is capable of excision repair. The level of active AGT in the cells was further modulated with the use of the AGT inhibitor, O6-benzylguanine. These cells were exposed to ethylnitrosourea in both the presence and absence of O6-benzylguanine, and population survival, growth, and mutagenesis at the hypoxanthine-guanine phosphoribosyl-transferase locus were measured. The results for all three measurements indicated that the lack of either AGT or nucleotide excision repair significantly impairs the ability of human cells to withstand DNA ethylation damage. Furthermore, the inhibition of AGT in xeroderma pigmentosum group A cells did not increase toxicity or mutagenicity, suggesting that AGT and nucleotide excision repair cooperate in the removal of DNA ethyl adducts. Related studies in our laboratory have shown that AGT and nucleotide excision repair are both necessary for the efficient removal of O6-ethyldeoxyguanosine.  相似文献   
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Although social work participation on interdisciplinary teams is long-standing, little research has been done to examine its effectiveness. This study used the Index of Interdisciplinary Collaboration to explore relationships between selected variables and teamwork in the hospice setting.The findings indicate that hospice social workers report a high level of interdisciplinary collaboration with colleagues. Whereas education, hospice census, the presence of other social workers, and quality of care were found to be unrelated to overall levels of collaboration, individual items measuring collaboration proved to be linked with hospice census, the presence of other social workers on the team, and quality of care. Further research is required to investigate other possible related variables and their impact on successful interdisciplinary collaboration and service delivery.  相似文献   
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There is scant information pertaining to airborne ammonia exposures from either spills or common household uses of ammonia-containing floor and tile cleaners or from spray-on glass cleaners. We assessed instantaneous and event-specific time-weighted average (TWA) exposures to airborne ammonia during spills and use (per label directions) of a household floor and tile cleaner and two spray-on window cleaners. Airborne ammonia levels measured at breathing zone height (BZH) above the spilled floor and tile cleaner product reached 500 p.p.m. within 5 min, while levels for spilled window cleaner were below 8 p.p.m. TWA exposures were assessed while tile walls and floors were cleaned in three different bathrooms of a residence, and during use of a spray-on glass cleaner while washing several large windows in an office setting. NIOSH Method 6015 was utilized with concurrent field measurements every 60 s using a Drager PAC III monitor with an electrochemical cell detector. Peak ammonia levels ranged from 16 to 28 p.p.m. and short-term TWA concentrations ranged from 9.4 to 13 p.p.m. during mixing (0.1% ammonia) and cleaning tiles in the three bathrooms. Ammonia exposures while using spray-on window cleaner were over 10-fold lower (TWA=0.65 p.p.m.). Use of the floor and tile cleaner mixed at 0.2% ammonia led to peak airborne ammonia levels within 3-5 min at 36-90 p.p.m., and use of full strength cleaner (3% ammonia) led to peak ammonia levels of 125 to >200 p.p.m. within 2-3 min. Spillage or intentional use of the full strength floor and tile cleaner led to airborne ammonia concentrations that exceed occupational short-term exposure limits, while spillage or use of the spray-on window cleaner did not approach potentially hazardous airborne ammonia levels and likely represents a minimal inhalation health hazard. We conclude that routine household uses of ammonia are unlikely to produce significant exposures when using standard cleaning solutions (0.1-0.2%), but spillage or use of concentrated ammonia solutions (e.g., 3%) in poorly ventilated areas can lead to potentially hazardous airborne ammonia exposures.  相似文献   
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Varicella-like rash after immunization with the live attenuated varicella vaccine is relatively common. Such vaccine-associated rashes generally consist of fewer lesions than occur in chickenpox. We describe a 15-month-old girl who experienced the onset of recurring papular urticaria after varicella immunization. The rash was varicella-like and thought by us to be caused by vaccine virus.  相似文献   
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We report here the genetic findings of a new isolated familial somatotropinoma (IFS) kindred in which the mother (subject I:2) and one daughter (subject II:2) are affected; their ages at diagnosis were 25 and 14 years respectively. Additionally, patient I:2 developed virilization due to an androgen-secreting adrenocortical mass, presenting clinical and molecular features of sporadic adrenal carcinoma. To genotype this family and to narrow down the candidate interval of the putative IFS gene at 11q13, we performed haplotyping on the DNA from all five members of the family and allelotyping of one available somatotropinoma using polymorphic microsatellite markers from chromosome region 11q12.1-11q13.5. Results indicated that the disease haplotype, between markers D11S956 and D11S527, was transmitted from subject I:2 only to subject II:2. A meiotic recombination event was detected in the fraternal twin sister of II:2 (subject II:1), but her disease status is unknown. Since she is only 18 years old this genetic event cannot yet narrow down the area involved in the pathogenesis of IFS. Allelotyping of the somatotropinoma from II:2 revealed loss of the chromosome carrying the wild-type copy of the putative IFS gene inherited from her father. These results support the involvement of a tumor suppressor gene at 11q13.1-q13.3 in the pathogenesis of IFS.  相似文献   
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