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 published on a yearly basis
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TL;DR: Marrow smears from entrants to the Medical Research Council trial UKALL VIII, other than those from children with B‐ALL, were studied prospectively for the presence or absence of blast cell vacuoles and for any clinical or biological relevance this feature might have.
Abstract: As part of a central review of cell morphology in childhood lymphoblastic leukaemia (ALL), marrow smears from entrants to the Medical Research Council trial UKALL VIII, other than those from children with B-ALL, were studied prospectively for the presence or absence of blast cell vacuoles and for any clinical or biological relevance this feature might have. Adequate slides were available from 733 patients (88% of the trial entrants) after five with B ALL were excluded. Vacuolated blast cells (greater than 10%) were present in 204 (28%). The presence of vacuoles was associated with PAS positivity (chi 2 = 27.8; P less than 0.0001), a diagnostic white cell count (WBC) less than 50 x 10(9)/l (chi 2 = 13.1; P less than 0.0001), and the immunophenotype of 'common' ALL (CD10 positive) (chi 2 = 9.1; P less than 0.01). There was no clear association with French-American-British (FAB) type L1 or L2. The 204 patients with vacuoles had a significantly superior disease free survival compared to the remainder (2P = 0.01), a difference which remained significant when the analysis was stratified by FAB type (2P = 0.01), age (2P = 0.02) or sex (2P = 0.02), but which was lost when stratified by WBC (2P = 0.06). These findings provide further evidence that, outside the context of B-ALL, vacuoles are indicative of a relatively benign disease which responds well to therapy. The French-American-British (FAB) classification should be modified to take this into account.
20 citations
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TL;DR: Prolonged moderate tea consumption benefited bone health in women but not in men, and for stronger tea consumption with more tea leaves added, neither benefit nor harm to bone health was observed.
Abstract: Tea is a worldwide drink with controversial effect on bone health. The sex-specific associations are unrevealed among general population. This study showed that prolonged moderate tea consumption benefited bone health in women, while no additional benefit with stronger tea. However, tea consumption was not associated with bone health in men. Tea consumption has been shown a potentially beneficial effect on bone health in postmenopausal women. However, little is known about such association in men, and whether stronger tea instead harms bone health due to elevated urinary excretion of calcium associated with caffeine in the tea. The aim of this study was to examine the association between various metrics of tea consumption and bone health. The present study included 20,643 participants from the China Kadoorie Biobank (CKB), who have finished both baseline survey (2004–2008) and a re-survey (2013–2014). They were aged 38–86 years at re-survey. Tea consumption was self-reported at both baseline and re-survey. Bone mineral density (BMD) was measured using calcaneal quantitative ultrasound once at re-survey. Compared with non-consumers, prolonged weekly tea consumers in women was associated with higher calcaneus BMD measures, with β (95% CI) of 0.98 (0.22, 1.74) for BUA, 4.68 (1.74, 7.61) for SOS, and 1.95 (0.81, 3.10) for SI. Among prolonged weekly tea consumers, no linear increase in BMD measures with the amount of tea leaves added was observed. The SOS and SI were higher in consumers with tea leaves 3.0–5.9 g/day than in those with < 3.0 g/day, but were reduced to non-significant for those with ≥ 6.0 g/day. Tea consumption was not associated with calcaneus BMD measures in men. Prolonged moderate tea consumption benefited bone health in women but not in men. For stronger tea consumption with more tea leaves added, neither benefit nor harm to bone health was observed.
20 citations
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TL;DR: This placebo-controlled trial does not indicate any adverse effects of prolonged treatment with simvastatin on systematically sought measures of sleep disturbance.
Abstract: 1It has been suggested that lipophilic HMG CoA reductase inhibitors, like lovastatin and simvastatin, may cause sleep disturbance.
2Six hundred and twenty-one patients at increased risk of coronary heart disease were randomized in a single centre to receive 40mg daily simvastatin, 20mg daily simvastatin or matching placebo. To assess the effects of prolonged use of simvastatin on nocturnal sleep quality and duration, a sleep questionnaire was administered to 567 patients (95% of 595 survivors) at an average of 88 weeks (range: 44–129 weeks) after randomization.
3The main outcome measures were sleep-related problems and use of sleep-enhancing medications reported during routine study follow-up visits, and responses to the sleep questionnaire about changes in sleep duration and about various sleep events during the preceding month.
4No differences were observed between the treatment groups in the frequency of sleep-related problems reported, in the proportion of follow-up visits at which such problems were reported, or in the use of sleep-enhancing medications. The numbers who stopped study treatment were similar in the different treatment groups, and no patient stopped principally because of insomnia. In response to the sleep questionnaire, there were no significant differences between the treatment groups in reports of various sleep events during the preceding month, except that slightly fewer patients allocated simvastatin reported waking often. No differences in sleep duration were observed.
5This placebo-controlled trial does not indicate any adverse effects of prolonged treatment with simvastatin on systematically sought measures of sleep disturbance.
20 citations
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TL;DR: Karim et al. as mentioned in this paper compared the genetic profiles of over 30,000 COVID-19 patients and a million healthy individuals and found that nine proteins were found to have an impact on infection and disease severity.
Abstract: Individuals who become infected with the virus that causes COVID-19 can experience a wide variety of symptoms. These can range from no symptoms or minor symptoms to severe illness and death. Key demographic factors, such as age, gender and race, are known to affect how susceptible an individual is to infection. However, molecular factors, such as unique gene mutations and gene expression levels can also have a major impact on patient responses by affecting the levels of proteins in the body. Proteins that are too abundant or too scarce may mean the difference between dying from or surviving COVID-19. Identifying the molecular factors in a host that affect how viruses can infect individuals, evade immune defences or trigger severe illness, could provide new ways to treat patients with COVID-19. Such factors are likely to remain constant, even when the virus mutates into new strains. Hence, insights would likely apply across all virus strains, including current strains, such as alpha and delta, and any new strains that may emerge in the future. Using such a ‘natural experiment’ approach, Karim et al. compared the genetic profiles of over 30,000 COVID-19 patients and a million healthy individuals. Nine proteins were found to have an impact on COVID-19 infection and disease severity. Four proteins were ranked as top priorities for potential treatment targets. One protein, called CD209 (also known as DC-SIGN), is involved in how the virus enters the host cells, and had one of the strongest associations with COVID-19. Two proteins, called IL-6R and FAS, were involved in the immune response and could be responsible for the immune over-activation often seen in severe COVID-19. Finally, one protein, called OAS1, formed part of the body’s innate antiviral defence system and appeared to reduce susceptibility to COVID-19. Knowing more about the proteins that influence the severity of COVID-19 opens up new ways to predict, protect and treat patients who may have severe or fatal reactions to infection. Indeed, one of the identified proteins (IL-6R) had already been targeted in recent clinical trials with some encouraging results. Considering CD209 as a potential receptor for the virus could provide another avenue for therapeutics, similar to previously successful approaches to block the virus’ known interaction with a receptor protein. Ultimately, this research could supply an entirely new set of treatment options to help combat the COVID-19 pandemic.
19 citations
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Clinical Trial Service Unit1, Leiden University Medical Center2, Université catholique de Louvain3, University of Hasselt4, Leipzig University5, Uppsala University6, Johnson & Johnson7, European Society of Cardiology8, University of London9, Medicines and Healthcare Products Regulatory Agency10, Pharmaceuticals and Medical Devices Agency11, Katholieke Universiteit Leuven12, National Cancer Research Institute13, GlaxoSmithKline14, Health Sciences North15, European Medicines Agency16, National Institute for Health Research17, John Radcliffe Hospital18
TL;DR: This paper summarizes the key insights and discussions from the workshop, highlights subsequent progress, and identifies next steps to produce meaningful change in the conduct of cardiovascular clinical research.
Abstract: Evidence generated from randomized controlled trials forms the foundation of cardiovascular therapeutics and has led to the adoption of numerous drugs and devices that prolong survival and reduce morbidity, as well as the avoidance of interventions that have been shown to be ineffective or even unsafe. Many aspects of cardiovascular research have evolved considerably since the first randomized trials in cardiology were conducted. In order to be large enough to provide reliable evidence about effects on major outcomes, cardiovascular trials may now involve thousands of patients recruited from hundreds of clinical sites in many different countries. Costly infrastructure has developed to meet the increasingly complex organizational and operational requirements of these clinical trials. Concerns have been raised that this approach is unsustainable, inhibiting the reliable evaluation of new and existing treatments, to the detriment of patient care. These issues were considered by patients, regulators, funders, and trialists at a meeting of the European Society of Cardiology Cardiovascular Roundtable in October 2015. This paper summarizes the key insights and discussions from the workshop, highlights subsequent progress, and identifies next steps to produce meaningful change in the conduct of cardiovascular clinical research.
19 citations
Authors
Showing all 428 results
Name | H-index | Papers | Citations |
---|---|---|---|
Salim Yusuf | 231 | 1439 | 252912 |
Richard Peto | 183 | 683 | 231434 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Rory Collins | 162 | 489 | 193407 |
Naveed Sattar | 155 | 1326 | 116368 |
Timothy J. Key | 146 | 808 | 90810 |
John Danesh | 135 | 394 | 100132 |
Andrew J.S. Coats | 127 | 820 | 94490 |
Valerie Beral | 114 | 471 | 53729 |
Mike Clarke | 113 | 1037 | 164328 |
Robert Clarke | 111 | 512 | 90049 |
Robert U. Newton | 109 | 753 | 42527 |
Richard Gray | 109 | 808 | 78580 |
Braxton D. Mitchell | 102 | 558 | 49599 |
Naomi E. Allen | 101 | 364 | 37057 |