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Institution

St Thomas' Hospital

HealthcareLondon, United Kingdom
About: St Thomas' Hospital is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Pregnancy. The organization has 12105 authors who have published 15596 publications receiving 624309 citations. The organization is also known as: St Thomas's Hospital & St. Thomas's.


Papers
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Journal ArticleDOI
TL;DR: Sildenafil was well tolerated by subjects and patients in all studies, with headache and other symptoms of vasodilation the most commonly reported adverse effects of treatment.
Abstract: Nitric oxide (NO) induces the formation of intracellular cyclic guanosine monophosphate (cGMP) by guanylate cyclase. Sildenafil, which selectively inhibits phosphodiesterase type 5 (PDE5) found predominantly in the corpora cavernosa of the penis, effectively blocks the degradation of cGMP and enhances erectile function in men with erectile dysfunction. The NO–cGMP pathway also plays an important role in mediating blood pressure. It is, therefore, possible that the therapeutic doses of sildenafil used to treat erectile dysfunction may have clinically significant effects on human hemodynamics. Three studies were undertaken to assess the effects of intravenously, intra-arterially, and orally administered doses of sildenafil on blood pressure, heart rate, cardiac output, and forearm blood flow and venous compliance in healthy men. A fourth study evaluated the hemodynamic effects of intravenous sildenafil in men with stable ischemic heart disease. In healthy men, significant (p

364 citations

Journal ArticleDOI
T. Ahmad1, R. A. Bouwman, Ioana Grigoras, Cesar Aldecoa  +2516 moreInstitutions (191)
TL;DR: Despite lower baseline risk, outcomes were similar in low- and middle-income compared with high-income countries and should also address the need for safe perioperative care.
Abstract: Background As global initiatives increase patient access to surgical treatments, there remains a need to understand the adverse effects of surgery and define appropriate levels of perioperative care. Methods We designed a prospective international 7-day cohort study of outcomes following elective adult inpatient surgery in 27 countries. The primary outcome was in-hospital complications. Secondary outcomes were death following a complication (failure to rescue) and death in hospital. Process measures were admission to critical care immediately after surgery or to treat a complication and duration of hospital stay. A single definition of critical care was used for all countries. Results A total of 474 hospitals in 19 high-, 7 middle- and 1 low-income country were included in the primary analysis. Data included 44 814 patients with a median hospital stay of 4 (range 2–7) days. A total of 7508 patients (16.8%) developed one or more postoperative complication and 207 died (0.5%). The overall mortality among patients who developed complications was 2.8%. Mortality following complications ranged from 2.4% for pulmonary embolism to 43.9% for cardiac arrest. A total of 4360 (9.7%) patients were admitted to a critical care unit as routine immediately after surgery, of whom 2198 (50.4%) developed a complication, with 105 (2.4%) deaths. A total of 1233 patients (16.4%) were admitted to a critical care unit to treat complications, with 119 (9.7%) deaths. Despite lower baseline risk, outcomes were similar in low- and middle-income compared with high-income countries. Conclusions Poor patient outcomes are common after inpatient surgery. Global initiatives to increase access to surgical treatments should also address the need for safe perioperative care.

364 citations

Journal ArticleDOI
TL;DR: Findings support both direct and mediational effects of social resources on adult depression and PTSD symptoms in women with histories of CMM, suggesting that resources are key factors in psychological adjustment of C MM victims.

361 citations

Journal ArticleDOI
TL;DR: The study data support the hypothesis that sex differences in anterior cruciate ligament tear rates are caused primarily by several interrelated intrinsic factors, most importantly, stiffness and muscular strength increase stress on the anterior cruiser ligament in female athletes.
Abstract: We performed a prospective study based on the hypothesis that physiologic differences exist between men and women in strength after adjustments for body weight; that the size of the anterior cruciate ligament is proportionate to the strength of its antagonists, the quadriceps muscles; and that women have a relatively small anterior cruciate ligament, thus predisposing them to a disproportionate number of anterior cruciate ligament injuries. One hundred matched high school basketball players, 50 male and 50 female, were evaluated with anthropometric measurements, body fat analysis, muscle strength evaluation, and magnetic resonance imaging measurements of the intercondylar notch and cross-sectional area of the anterior cruciate ligament at the outlet. The male players were taller and heavier than their female counterparts, although they had 11% less body fat. Male players had statistically greater quadriceps and hamstring muscle strength than female players, even when adjustments were made for body weight. With adjustments for body weight, the size of the anterior cruciate ligament in girls was found to be statistically smaller than in boys. There was no statistically significant difference in the notch width index between the sexes. The study data support our hypothesis that sex differences in anterior cruciate ligament tear rates are caused primarily by several interrelated intrinsic factors. Most importantly, stiffness and muscular strength increase stress on the anterior cruciate ligament in female athletes. The anterior cruciate ligament, when adjustments have been made for body weight, is smaller in female athletes, and therefore, probably does not compensate for the lack of stiffness and strength.

359 citations

Journal ArticleDOI
TL;DR: It is demonstrated for the first time in a prospective study that synovial membrane cytokine mRNA expression is predictive of joint damage progression in RA.
Abstract: OBJECTIVE The primary aim of this prospective 2-year study was to explain the wide variability in joint damage progression in patients with rheumatoid arthritis (RA) from measures of pathologic changes in the synovial membrane. METHODS Patients underwent clinical measurements and joint damage assessments by magnetic resonance imaging (MRI) and radiography at enrollment and at year 2. Synovial membrane was obtained by knee biopsy and assessed histologically by hematoxylin and eosin staining. Interleukin-1beta (IL-1beta), IL-10, IL-16, IL-17, RANKL, tumor necrosis factor alpha (TNFalpha), and interferon-gamma (IFNgamma) messenger RNA (mRNA) expression was determined by quantitative reverse transcription-polymerase chain reaction. The relationship of synovial measurements to joint damage progression was determined by multivariate analysis. RESULTS Sixty patients were enrolled. Histologic features had no relationship to damage progression. Multivariate analysis by several different methods consistently demonstrated that synovial membrane mRNA levels of IL-1beta, TNFalpha, IL-17, and IL-10 were predictive of damage progression. IL-17 was synergistic with TNFalpha. TNFalpha and IL-17 effects were most pronounced with shorter disease duration, and IL-1beta effects were most pronounced with longer disease duration. IFNgamma was protective. These factors explained 57% of the MRI joint damage progression over 2 years. CONCLUSION We have demonstrated for the first time in a prospective study that synovial membrane cytokine mRNA expression is predictive of joint damage progression in RA. The findings for IL-1beta and TNFalpha are consistent with results of previous clinical research, but the protective role of IFNgamma, the differing effects of disease duration, and IL-17-cytokine interactions had only been demonstrated previously by animal and in vitro research. These findings explain some of the variability of joint damage in RA and identify new targets for therapy.

358 citations


Authors

Showing all 12132 results

NameH-indexPapersCitations
David J. Hunter2131836207050
Rory Collins162489193407
Steven Williams144137586712
Geoffrey Burnstock141148899525
Nick C. Fox13974893036
Christopher D.M. Fletcher13867482484
David A. Jackson136109568352
Paul Harrison133140080539
Roberto Ferrari1331654103824
David Taylor131246993220
Keith Hawton12565755138
Nicole Soranzo12431674494
Roger Williams122145572416
John C. Chambers12264571028
Derek M. Yellon12263854319
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20237
202235
2021654
2020595
2019485
2018462