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排序方式: 共有972条查询结果,搜索用时 9 毫秒
1.
YS Nagar S Singh V Sawlani L Pal K Dimri P Lal 《Journal of Medical Imaging and Radiation Oncology》2005,49(2):160-162
A rare case of an advanced primary broad ligament carcinoma is discussed, with a review of the literature regarding its incidence, presentation and management. This patient showed a complete response to adjuvant cisplatin-based chemotherapy following panhysterectomy and is presently without any evidence of disease, 15 months after completion of her treatment. 相似文献
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对10名男性受试者单剂量po240mgVer缓释片药代动力学及心电图变化进行研究。血药浓度—时间数据用零级吸收过程的一室模型拟合,其药代动力学参数:Tmax5.9±1.6h;Cmax118.9±37.2μg·L-1;T1 5.4±1.5h;k030.5±17.5μg·L-1·h-1;T1/210.8±4.9h。PR间期延长有显著意义,血药浓度与PR间期变化满足S 型模型,其药效学参数:EC50 64.6±16.9μg·L-1; Emax54±11ms;s 1.68±0.66。 相似文献
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Hydrolysis of peptides within lumen of small intestine 总被引:2,自引:0,他引:2
7.
HLA and Thyrotoxicosis (Graves' Disease) in Chinese 总被引:1,自引:0,他引:1
S. H. Chan P. P. B. Yeo K. F. Lui G. B. Wee K. T. Woo P. Lim J. S. Cheah 《Tissue antigens》1978,12(2):109-114
HLA locus A and B typing was performed on 86 Chinese thyrotoxicosis (Graves' Disease) patients and 238 normal Chinese subjects. The frequency of HLA-Bw46 (Sin 2) was found to be significantly higher among the patients than controls (X2 = 26.15, corrected P <.003, relative risk = 3.74). The risk associated with Bw46 was reflected in the Bw46 heterozygotes. The relative risks of the joint occurrence of Bw46/B40 and Bw46/B13 were 8.74 and 5.88 respectively. 相似文献
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9.
Exclusion of the alpha 1(II) cartilage collagen gene as the mutant locus in type IA osteogenesis imperfecta. 总被引:5,自引:3,他引:5
B Sykes R Smith S Vipond C Paterson K Cheah E Solomon 《Journal of medical genetics》1985,22(3):187-191
Using two restriction site polymorphisms within the structural gene coding for human type II collagen we have examined the segregation of this gene in three pedigrees with dominantly inherited osteogenesis imperfecta (Sillence type IA). We have demonstrated that the gene does not segregate with clinical expression of the disease and cannot, therefore, contain the mutation responsible for osteogenesis imperfecta in these families. 相似文献
10.
Identification of two mutations in a compound heterozygous child with dihydrolipoamide dehydrogenase deficiency 总被引:1,自引:0,他引:1
Hong YS; Kerr DS; Craigen WJ; Tan J; Pan Y; Lusk M; Patel MS 《Human molecular genetics》1996,5(12):1925-1930
An infant girl with elevated blood lactate, pyruvate, and plasma
branched-chain amino acids was diagnosed with dihydrolipoamide
dehydrogenase (E3; dihydrolipoamide: NAD+ oxidoreductase, EC 1.8.1.4)
deficiency. Activities of the pyruvate dehydrogenase complex and E3 from
patient were 26 and 2% of controls in blood lymphocytes, and 11 and 14% in
cultured skin fibroblasts, respectively. Western blot analysis demonstrated
that the amount of E3 protein in fibroblasts from the patient and her
father was about half of controls, while Northern blot analysis showed
normal amounts of E3 RNA. DNA sequencing of cloned full-length E3 cDNAs
from the patient revealed two mutations in separate alleles. One is a
single base insertion of an extra adenine in the last codon of the leader
peptide sequence (TAC-->TAAC) leading to a nonsense mutation which
results in the premature termination of the precursor E3 polypeptide
(Y35X). The other is a missense mutation due to substitution of guanine for
adenine, causing an Arg-->Gly substitution at amino acid 460 of the
mature protein (R460G) which triggers the loss of E3 activity probably by
structural change in the E3 dimer. DNA sequencing of E3 cDNAs from the
parents demonstrated that the nonsense mutation was inherited from the
father and the missense mutation was inherited from the mother.
相似文献