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Institution

Clinical Trial Service Unit

About: Clinical Trial Service Unit is a based out in . It is known for research contribution in the topics: Population & Stroke. The organization has 428 authors who have published 1387 publications receiving 181920 citations.


Papers
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Journal ArticleDOI
TL;DR: Various diseases were major determinants of both global and age-comparative SRH, and cardiometabolic diseases had the strongest impact on both global SRH andAge-comparable SRH at the population level.
Abstract: Understanding the correlates of self-rated health (SRH) can help public health professionals prioritize health-promotion and disease-prevention interventions. This study aimed to investigate the association between multiple comorbidities and global SRH and age-comparative SRH. A total of 512,891 participants aged 30–79 years old were recruited into the China Kadoorie Biobank study from ten regions between 2004 and 2008. Multivariate logistic regression models were used to estimate the odds ratios (ORs) for the associations between comorbidities (including diabetes, hypertension, coronary heart disease, rheumatic heart disease, stroke, tuberculosis, emphysema/bronchitis, asthma, cirrhosis/chronic hepatitis, peptic ulcer, gallbladder disease, kidney disease, fracture, rheumatic arthritis, psychiatric disorders, depressive symptoms, neurasthenia, head injury and cancer) and SRH. Population attributable risks (PARs) were used to estimate the contribution of multiple comorbidities to poor global SRH and worse age-comparative SRH. After adjusting for covariates, suffering from various diseases increased the chance of reporting a poor global SRH [OR (95% CI) ranged from 1.10 (1.07, 1.13) for fracture to 3.21 (2.68, 3.83) for rheumatic heart disease] and a worse age-comparative SRH [OR (95% CI) ranged from 1.18 (1.13, 1.23) for fracture to 7.56 (6.93, 8.25) for stroke]. From the population perspective, 20.23% of poor global SRH and 45.12% of worse age-comparative SRH could attributed to the cardiometabolic diseases, with hypertension (7.84% for poor global SRH and 13.79% for worse age-comparative SRH), diabetes (4.35% for poor global SRH and 10.71% for worse age-comparative SRH), coronary heart disease (4.44% for poor global SRH and 9.51% for worse age-comparative SRH) and stroke (3.20% for poor global SRH and 10.19% for worse age-comparative SRH) making the largest contribution. Various diseases were major determinants of global and age-comparative SRH, and cardiometabolic diseases had the strongest impact on both global SRH and age-comparative SRH at the population level. Prevention measures concentrated on these conditions would greatly reduce the total burden of poor SRH and its consequences such as poor quality of life and use of health care services.

28 citations

Journal ArticleDOI
TL;DR: The trial demonstrates the feasibility of applying functional genomic and genetic approaches in randomized trials to assess molecular and individual level responses and differs from many previous studies and does not support a strong effect of vitamin D on long-term transcriptomic changes in blood or on plasma cytokine levels.

28 citations

Journal ArticleDOI
TL;DR: In this paper, the authors investigated the presence of the H. pylori genome in buffy coat samples and in diseased arterial segments and used a PCR that involved nested primers specific for the 16S rRNA gene.
Abstract: A number of epidemiological studies have suggested associations between Helicobacter pylori seropositivity and coronary heart disease (2). High concentrations of immunoglobulin G antibody to H. pylori are fairly reliable indicators of chronic gastric infection, but the presence of antibodies in serum does not necessarily indicate persistent exposure of the coronary arteries to any type of insult. Although a number of pathological studies have reported the presence of Chlamydia pneumoniae DNA, antigens, or elementary bodies in diseased arterial specimens (3), there is little direct evidence available on the possible presence of H. pylori in the bloodstream or in vascular tissue. Hence, we investigated the presence of the H. pylori genome in buffy coat samples and in diseased arterial segments. We used a PCR that involved nested primers specific for the 16S rRNA gene of H. pylori, optimized to detect as little as 0.01 pg of genomic DNA (or about a dozen organisms) (6). DNA had been extracted from the buffy coat samples of 77 healthy individuals for a genetic study of myocardial infarction; 52 of these individuals were known to be strongly seropositive for immunoglobulin G antibodies to H. pylori, and 25 were chosen as seronegative controls. Samples of carotid atheroma were taken from another 39 individuals at carotid endarterectomy. DNA was extracted from the tissue by using a commercial kit (Puregene; Flowgen Ltd.) and analyzed by operators unaware of the tissue source. PCR products of samples appearing positive on gel electrophoresis were probed by Southern hybridization and autoradiographed for 1 week. Only 1 of the 77 buffy coat samples tested positive, and it belonged to a seropositive individual. Only 1 of the 39 atheromatous specimens collected at carotid surgery tested positive. A number of standard precautions were taken in the present study to protect against spurious results due to contamination, including the use of dedicated laboratory space, reagents, and instruments for pre- and post-PCR work and the testing of positive controls and negative controls in parallel with the test samples. Despite these precautions, the possibility of contamination in the two samples that tested positive for H. pylori DNA cannot be definitely excluded, nor can we exclude the possibility that a low-copy-number infection was actually present but undetected by our highly sensitive assay. Still, the present study adds to the sparse data that exists on H. pylori DNA in the bloodstream and in vascular tissue, being the first reported detection of H. pylori markers in human vascular tissue. It, however, does not support the likelihood of a high prevalence of the organism in buffy coat samples or in carotid atheroma. The only available report of H. pylori bacteremia involved positive blood cultures in a patient with gastric perforation due to malignancy (7), but in vitro studies suggest that any organisms penetrating beyond the gastric mucosa should be killed rapidly by complement proteins (5). Whereas a large number of studies have reported on the presence of markers of C. pneumoniae and cytomegalovirus in vascular lesions (2), there is only one previously reported study of H. pylori and atheroma (1). That study did not detect H. pylori DNA in any of the atherosclerotic plaques of 50 patients with abdominal aortic aneurysms, although about one-half of these samples tested positive for C. pneumoniae DNA (1). If H. pylori is relevant to the causation of vascular disease, it remains unclear how its effects are mediated. This suggests the need for further studies of coronary atheroma and comparisons of concentrations in plasma of vascular risk factors in seropositive and in seronegative individuals (4), as well as before and after H. pylori eradication treatment.

28 citations

Journal ArticleDOI
TL;DR: The objectives of this study were to compare the risks of Parkinson's disease among those with versus those without prior stroke or heart disease at baseline in a prospective study of 0.5 million adults in China, and to examine associations of cardiovascular disease risk factors with risk of Parkinson't disease.
Abstract: Objective The objectives of this study were to compare the risks of Parkinson's disease among those with versus those without prior stroke or heart disease at baseline in a prospective study of 0.5 million adults in China, and to examine associations of cardiovascular disease risk factors (cigarette smoking, hypertension, diabetes, obesity) with risk of Parkinson's disease. Methods During an average of 11.5 years of follow-up of 503,497 middle-aged participants in the China Kadoorie Biobank study, 603 incident cases were hospitalized with a diagnosis of Parkinson's disease. Cox proportional hazards models were used to assess associations of history of heart disease or stroke with Parkinson's disease in all participants, and of cardiovascular disease risk factors with Parkinson's disease in a subset without prior cardiovascular disease. Results In this population the incidence rate of Parkinson's disease (mean [SD] age of cases, 61 [10] years) was 13.3 (95% confidence interval: 12.3-14.4) per 100,000 person-years. Incidence increased with age, and was higher in men than in women, and in urban than in rural residents. Prior stroke was associated with about twofold higher risk of Parkinson's disease (hazard ratio 1.94; 1.39-2.69). After adjustment for confounders in those without prior cardiovascular disease, a 5 kg/m2 higher body mass index was associated with 17% (1.17; 1.03-1.34: P = 0.019) higher risk of Parkinson's disease, but neither hypertension, diabetes, nor current cigarette smoking was significantly associated with Parkinson's disease. Interpretation Prior stroke and adiposity were each associated with higher risks of Parkinson's disease, but none of the other cardiovascular disease risk factors were significantly associated with Parkinson's disease in this population.

27 citations


Authors

Showing all 428 results

NameH-indexPapersCitations
Salim Yusuf2311439252912
Richard Peto183683231434
Cornelia M. van Duijn1831030146009
Rory Collins162489193407
Naveed Sattar1551326116368
Timothy J. Key14680890810
John Danesh135394100132
Andrew J.S. Coats12782094490
Valerie Beral11447153729
Mike Clarke1131037164328
Robert Clarke11151290049
Robert U. Newton10975342527
Richard Gray10980878580
Braxton D. Mitchell10255849599
Naomi E. Allen10136437057
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2021136
2020116
2019122
201894
2017106
201688