Stephen J. O'Brien

Bio: Stephen J. O'Brien is an academic researcher from Saint Petersburg State University of Information Technologies, Mechanics and Optics. The author has contributed to research in topics: Population & Gene. The author has an hindex of 153, co-authored 1062 publications receiving 93025 citations. Previous affiliations of Stephen J. O'Brien include University College Cork & QIMR Berghofer Medical Research Institute.

Return to Sport After Bone-Patellar Tendon-Bone Autograft ACL Reconstruction in High School-Aged Athletes.

Abstract: Background:Anterior cruciate ligament (ACL) injuries are occurring with increasing frequency in the adolescent population. Outcomes after ACL reconstruction (ACLR) are inconsistently reported in ho...

Expression of feline leukaemia virus antigens on cat lymphoma cells: kinetics of biosynthesis.

Abstract: Summary Cultured feline lymphoma cells (FL-74), productively infected with a feline leukaemia virus (FeLV) were quantitatively examined with a radioimmune assay for cell membrane associated FeLV-p27 and total FeLV associated cell surface antigens (FeLV-CSA) using a monospecific antiserum and a broadly reactive antiserum respectively. The infected cells bound 5.6 × 105 anti-FeLV-p27 IgG molecules/cell, representing 40% of the total FeLV-CSA detected. The kinetics of synthesis of surface associated p27 and total FeLV-CSA was determined following their removal by treatment of intact cells with trypsin. Both p27 and the total FeLV-CSA population reappeared on the cell surface within 6 to 8 h following trypsin digestion. Antigen re-expression was blocked by cycloheximide but not by actinomycin D or cordycepin. The time course of antigen decay with these same antimetabolites indicated that the average turnover rate of cell surface p27 and FeLV-CSA was 6 to 8 h while the mRNAs which specify these antigens have a lifetime of at least 10 h. Virus production was blocked in less than 2 h by cycloheximide, and within 2 to 4 h by actinomycin D. Virus production continued at a reduced rate for at least 6 h in the presence of cordycepin. The difference in sensitivity to inhibitors of RNA synthesis of p27 and FeLV-CSA production (blocked in 9 to 10 h) and of virus production (blocked in 2 to 4 h) supports the proposition of two non-equilibrating pools of intracellular virus RNA molecules with different half-lives: one associated with polyribosomes, and another which becomes encapsulated in the completed virion.

The cemented custom femoral stem - a 10 year review

Abstract: We report a series of 706 patients (759 hip implants) with an average follow up of 10.5 years (range, 10 - 11 years) following total hip replacement (THR) using a cemented custom-made femoral stem ...

Initial sequencing and analysis of the human genome.

Abstract: The human genome holds an extraordinary trove of information about human development, physiology, medicine and evolution. Here we report the results of an international collaboration to produce and make freely available a draft sequence of the human genome. We also present an initial analysis of the data, describing some of the insights that can be gleaned from the sequence.

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls

Abstract: There is increasing evidence that genome-wide association ( GWA) studies represent a powerful approach to the identification of genes involved in common human diseases. We describe a joint GWA study ( using the Affymetrix GeneChip 500K Mapping Array Set) undertaken in the British population, which has examined similar to 2,000 individuals for each of 7 major diseases and a shared set of similar to 3,000 controls. Case-control comparisons identified 24 independent association signals at P < 5 X 10(-7): 1 in bipolar disorder, 1 in coronary artery disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 in type 1 diabetes and 3 in type 2 diabetes. On the basis of prior findings and replication studies thus-far completed, almost all of these signals reflect genuine susceptibility effects. We observed association at many previously identified loci, and found compelling evidence that some loci confer risk for more than one of the diseases studied. Across all diseases, we identified a large number of further signals ( including 58 loci with single-point P values between 10(-5) and 5 X 10(-7)) likely to yield additional susceptibility loci. The importance of appropriately large samples was confirmed by the modest effect sizes observed at most loci identified. This study thus represents a thorough validation of the GWA approach. It has also demonstrated that careful use of a shared control group represents a safe and effective approach to GWA analyses of multiple disease phenotypes; has generated a genome-wide genotype database for future studies of common diseases in the British population; and shown that, provided individuals with non-European ancestry are excluded, the extent of population stratification in the British population is generally modest. Our findings offer new avenues for exploring the pathophysiology of these important disorders. We anticipate that our data, results and software, which will be widely available to other investigators, will provide a powerful resource for human genetics research.