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.

Metabolic syndrome biomarkers and prostate cancer risk in the UK Biobank.

Abstract: We investigated the association between metabolic syndrome (MetS) and its components and risk of prostate cancer (PCa) in a cohort of men enrolled in the UK Biobank. Our study cohort included 220 622 PCa-free men with baseline measurements of triglycerides (TGs), HDL-cholesterol (HDL), glycated hemoglobin (HbA1c), blood pressure (BP), and waist circumference (WC). Multivariable Cox proportional hazards regression was used to analyze associations with PCa for: individual metabolic components (TG, HDL, HbA1c, BP, WC), combinations of two and three components, and MetS overall (three or more components). We conducted mediation analyses to examine potential hormonal and inflammatory pathways (total testosterone [TT], C-reactive protein [CRP], insulin-like growth factor 1 [IGF-1]) through which MetS components may influence PCa risk. A total of 5409 men in the study developed PCa during a median follow-up of 6.9 years. We found no significant association between MetS and PCa risk (hazard ratio [HR] = 0.99, 95% confidence interval [CI] = 0.92-1.06). No associations were found with PCa risk and individual measurements of TG, HDL, BP, or WC. However, an inverse association was observed with elevated HbA1c (≥42 mmol/mol) (HR = 0.89, 95% CI = 0.79-0.98). Consistent inverse associations were observed between HbA1c and risk of PCa. Mediation analysis revealed TT, CRP, and IGF-1 as potential mediating factors for this association contributing 10.2%, 7.1%, and 7.9% to the total effect, respectively. Overall MetS had no association with PCa risk. However, a consistent inverse association with PCa risk was found for HbA1c. This association may be explained in part through hormonal and inflammatory pathways.

Increasing the use of mobile technology-derived endpoints in clinical trials.

Abstract: Mobile technology can be used in clinical trials to generate novel endpoints that provide information that was previously difficult or impossible to obtain. Technology-derived novel endpoints could also make clinical trials more efficient and less burdensome to trial participants while contributing to a meaningful and real-world understanding about patient experiences beyond the brief data ‘‘snapshots’’ typically gathered in clinical care or research settings. This research letter summarizes the recommendations provided by the Clinical Trials Transformation Initiative (CTTI) which are intended to support the selection, development and inclusion of such technology-derived novel endpoints in future clinical trials.

Helicobacter pylori and gastric cancer: time for mega-trials?

Abstract: The first report of an association between chronic infection Helicobacter pylori, a spiral bacterium of the stomach, and gas cancer appeared in 1991 and in 1994 the International Agenc Research of Cancer declared H. pylori a human ‘carcinogen (IARC Working Group, 1994). Five years after that rep however, the causal role of H. pylori in gastric cancer remain controversial, with risk estimates ranging from ninefold (We and Forman, 1996) to no important association at all (Cresp Citarda, 1996). Recent quantitative reviews, by contrast, sug that H. pylori infection is likely to be only a moderate risk fact for gastric cancer (Danesh, 1999 a, 1999b). Reliable epidemiological evidence on H. pylori and gastric cancer is still relatively sparse. Although the number of c reported in prospective studies has increased by threefold 1994, there are now a total of only about 800 cases in ten pub prospective studies. A synthesis of these studies indicates th H. pylori is two or three times more common in people with gas cancer than in others (Figure 1). Doubts persist, however, abo extent to which inadequate adjustment for possible confoun factors, such as smoking and markers of poverty, and the pre tial publication of studies with more extreme results might have to exaggerated estimates. The biological plausibility of a ca association is suggested by strong correlations reported betwe H. pylori infection and putatively precancerous gastric lesions (suc atrophic gastritis and intestinal metaplasia) (Kuipers et al, 1 Sakaki et al, 1995) and by the production of lesions that rese human gastric cancer in Mongolian gerbils following long-te experimental infection (Watanabe et al, 1998). Even if a two threefold relative risk were established, however, it would explain the sharp variations in gastric cancer mortality betw populations (e.g. 20-fold higher in certain parts of China than in USA) (Peto, 1990) or between past and present (e.g. the fiv decrease in Scotland between 1950 and 1990) (Swerdlow 1998). Moreover, although H. pylori infects men and women abo equally and is strongly associated with duodenal ulceration, ga cancer is twice as common in men and may be inversely asso with duodenal ulceration (Howson et al, 1986; Hansson e 1996). Clearly, if H. pylori is a cause of gastric cancer, there m be some other major cause(s) of the disease. To assess the role of the infection in gastric cancer m precisely would require larger studies than hitherto, especial