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41.
A case-control study using logistic regression included 500 employees of the nuclear works (162 patients with lung carcinoma and 338 healthy controls). After examination of radiation and nonradiation causative factors 5 proved statistically significant. For them the following chance proportions were obtained: smoking 6.6, plutonium pneumosclerosis 4.6, plutonium incorporation 3.1, chronic nonspecific pulmonary diseases 2.1, external gamma-radiation 1.6. Attributive risk for the total of the radiation factors makes up 25% at the most while of the nonradiation factors at least 70%. 相似文献
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Popov V. S. Brykov N. N. Andrushchenko M. I. Dmitrichenko N. S. Pristupa P. G. Zakaryan N. A. Chegonenko V. D. Godlevskii A. R. Makarova M. N. Poskotinov V. V. Veres A. V. Chupyatov V. M. 《Refractories and Industrial Ceramics》1983,24(7-8):349-352
Refractories and Industrial Ceramics - 相似文献
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P. G. Pristupa 《Refractories and Industrial Ceramics》1979,20(7-8):400-401
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We reported a patient in whom slight congestive heart failure gradually developed 20 years after mitral valve replacement with a Delrin disc Bj?rk-Shiley valve prosthesis. Although no evident cause of prosthetic valve malfunction could be detected preoperatively, the mitral prosthesis was excised and replaced uneventfully with a 29 mm St. Jude Medical valve prosthesis. At gross inspection, marked wears of the Delrin disc surface and strut shaped indentations were present. These disc variance, occurred much earlier than initially predicted by Dr. Bj?rk, allowed prosthetic valve malfunction. The patient with this specific model should be carefully followed-up, if necessary, performed reoperation. 相似文献
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A 9-yr-old African-American male presenting with severe recurrent pyogenic infections was found to have C2 deficiency (C2D). Analysis of his genomic DNA demonstrated that he carried one type I C2D allele associated with the HLA-A25, B18, DR15 haplotype. Screening all 18 exons of the C2 gene by exon-specific PCR/single-strand conformation polymorphism indicated abnormal bands in exons 3, 7, and 6, the latter apparently caused by the 28-bp deletion of the typical type I C2D allele. Nucleotide (nt) sequencing of the PCR-amplified exons 3 and 7 revealed a heterozygous G to A transition at nt 392, causing a C111Y mutation, and a heterozygous G to C transversion at nt 954, causing a E298D mutation and a polymorphic MaeII site. Cys111 is the invariable third half-cystine of the second complement control protein module of C2. Pulse-chase biosynthetic labeling experiments indicated that the C111Y mutant C2 was retained by transfected COS cells and secreted only in minimal amounts. Therefore, this mutation causes a type II C2D. In contrast, the E298D mutation affected neither the secretion of C2 from transfected cells nor its specific hemolytic activity. Analysis of genomic DNA from members of the patient's family indicated that 1) the proband as well as one of his sisters inherited the type I C2D allele from their father and the novel type II C2D allele from their mother; 2) the polymorphic MaeII site caused by the G954C transversion is associated with the type I C2D allele; and 3) the novel C111Y mutation is associated in this family with the haplotype HLA-A28, B58, DR12. 相似文献
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ZB Niazi 《Canadian Metallurgical Quarterly》1998,101(1):248-249