Institution
St Bartholomew's Hospital
Healthcare•London, United Kingdom•
About: St Bartholomew's Hospital is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Cancer. The organization has 11054 authors who have published 13229 publications receiving 501102 citations. The organization is also known as: St. Bartholomew's Hospital & The Royal Hospital of St Bartholomew.
Topics: Population, Cancer, Transplantation, Diabetes mellitus, Pregnancy
Papers published on a yearly basis
Papers
More filters
••
TL;DR: Severe weakness requiring prolonged rehabilitation and abnormal clinical neurologic findings are extremely common in survivors of protracted critical illness, and can be found up to 5 yrs after intensive care unit discharge in >90% of these long-stay patients.
Abstract: ObjectiveTo establish the prevalence, clinical characteristics, and electrophysiologic features of residual neuromuscular dysfunction after prolonged critical illness.DesignProspective follow-up study of survivors of prolonged critical illness.SettingA university hospital and two district general ho
381 citations
••
TL;DR: In this paper, a pixel-by-pixel linear regression was performed to remove differences in global CBF between subjects, and pixels at which rCBF then showed a significant negative correlation with age were identified.
Abstract: Positron emission tomographic (PET) images of regional cerebral blood flow (rCBF) from 30 normal, resting volunteers aged 30 to 85 years were analysed to identify areas where rCBF fell with age. Images were anatomically normalised, and a pixel-by-pixel linear regression was performed to remove differences in global CBF between subjects. Pixels at which rCBF then showed a significant (p less than 0.01) negative correlation with age were identified. They were displayed as a statistical parametric map (SPM) of correlations. We demonstrate an age-related decrease in adjusted rCBF in the cingulate, parahippocampal, superior temporal, medial frontal, and posterior parietal cortices bilaterally, and in the left insular and left posterior prefrontal cortices (omnibus significance, chi 2 = 2,291, p less than 0.0001, df = 1). Decreases in rCBF suggest a regionally specific loss of cerebral function with age. The affected areas were all limbic, or association, cortices. Therefore, these decreases may constitute the cerebral substrate of the cognitive changes that occur during normal aging.
380 citations
••
TL;DR: Rising airway bacterial load and species changes are associated with greater airway inflammation and accelerated decline in FEV1, an important factor in disease progression.
Abstract: Chronic obstructive pulmonary disease (COPD) is characterized by an accelerated decline in lung function and progressive airway inflammation. Bacteria have been isolated from the lower airway of stable COPD patients, and airway inflammation has been related to bacterial load and type. The relationship between bacterial colonization, airway inflammation, and lung function decline remains uncertain. We studied 30 patients with COPD, mean (SD) FEV1 0.947 (0.329), 34.8% (13.6%) predicted, for 12 months. Sputum collected at recruitment and the end of the study was analyzed for cytokines and for quantitative bacteriology. The decline in FEV1 was 57.6 (137.6) ml year-1. Bacterial growth was identified in all subjects, with an initial count of 107.47(0.91) cfu ml-1 rising to 107.93(0.81) cfu ml-1 at the end of the study (p = 0.019). FEV1 decline was related to this increase in airway bacterial load (r = 0.59, p = 0.001). FEV1 decline was greater in subjects who exhibited a change in the colonizing bacterial type compared with those with persistence of a single bacterial species over the study period (p = 0.017). Higher sputum interleukin (IL-8) was associated with greater declines in FEV1 (p = 0.03). Rising airway bacterial load and species changes are associated with greater airway inflammation and accelerated decline in FEV1. Bacterial colonization in COPD is an important factor in disease progression.
380 citations
••
TL;DR: The CBD tau association suggests that PSP and CBD share a similar cause, although the pathogenic mechanism behind the two diseases leads to a different clinical and pathologic phenotype.
Abstract: OBJECTIVE:
To analyze the association of polymorphisms in the tau gene with pathologically confirmed corticobasal degeneration (CBD).
BACKGROUND:
The authors previously described an extended tau haplotype (H1) that covers the human tau gene and is associated with the development of progressive supranuclear palsy (PSP). The authors now extend this analysis to CBD, a neurodegenerative condition with clinical and neuropathologic similarities to PSP. Like PSP, CBD is associated with accumulation of aggregates containing the 4-repeat isoforms of tau. Because of difficulty in diagnosis of CBD, the authors only analyzed cases with pathologically confirmed CBD.
METHODS:
The authors collected 57 unrelated, neuropathologically confirmed cases of CBD. Tau sequencing in these cases failed to show the presence of pathogenic mutations. Polymorphisms that spanned the tau gene were analyzed in all CBD cases and controls.
RESULTS:
Analyzing tau polymorphisms in CBD cases showed that the frequency of H1 and H1/H1 was significantly increased when analyzing all cases and when separating by country of origin. H1 frequency in all CBD cases was 0.921, compared with a control frequency of 0.766 (X(2) = 9.1, p = 0.00255 [1df], OR 3.56 [8.43 > CI 95% > 1.53]). The H1/H1 frequency was also significantly higher at 0.842 compared with 0.596 in age-matched controls (X(2) = 17.42, p = 0.00016, 2df), OR 3.61 [7.05 > CI 95% > 1.85]).
CONCLUSIONS:
The CBD tau association described here suggests that PSP and CBD share a similar cause, although the pathogenic mechanism behind the two diseases leads to a different clinical and pathologic phenotype.
380 citations
••
TL;DR: A consensus document on the diagnosis and management of C1 inhibitor deficiency, a syndrome characterized clinically by recurrent episodes of angio‐oedema, which can cause fatal laryngeal oedema and features indistinguishable from gastrointestinal tract obstruction is presented.
Abstract: Summary We present a consensus document on the diagnosis and management of C1 inhibitor deficiency, a syndrome characterized clinically by recurrent episodes of angio-oedema. In hereditary angio-oedema, a rare autosomal dominant condition, C1 inhibitor function is reduced due to impaired transcription or production of non-functional protein. The diagnosis is confirmed by the pres- ence of a low serum C4 and absent or greatly reduced C1 inhibitor level or function. The condition can cause fatal laryngeal oedema and features indis- tinguishable from gastrointestinal tract obstruction. Attacks can be precipi- tated by trauma, infection and other stimulants. Treatment is graded according to response and the clinical site of swelling. Acute treatment for severe attack is by infusion of C1 inhibitor concentrate and for minor attack attenuated androgens and/or tranexamic acid. Prophylactic treatment is by attenuated androgens and/or tranexamic acid. There are a number of new products in trial, including genetically engineered C1 esterase inhibitor, kal- likrein inhibitor and bradykinin B2 receptor antagonist. Individual sections provide special advice with respect to diagnosis, management (prophylaxis and emergency care), special situations (childhood, pregnancy, contracep- tion, travel and dental care) and service specification.
379 citations
Authors
Showing all 11065 results
Name | H-index | Papers | Citations |
---|---|---|---|
Philippe Froguel | 166 | 820 | 118816 |
Geoffrey Burnstock | 141 | 1488 | 99525 |
Michael A. Kamm | 124 | 637 | 53606 |
David Scott | 124 | 1561 | 82554 |
Csaba Szabó | 123 | 958 | 61791 |
Roger Williams | 122 | 1455 | 72416 |
Derek M. Yellon | 122 | 638 | 54319 |
Walter F. Bodmer | 121 | 579 | 68679 |
John E. Deanfield | 120 | 497 | 61067 |
Paul Bebbington | 119 | 583 | 46341 |
William C. Sessa | 117 | 383 | 52208 |
Timothy G. Dinan | 116 | 689 | 60561 |
Bruce A.J. Ponder | 116 | 403 | 54796 |
Alexandra J. Lansky | 114 | 632 | 54445 |
Glyn Lewis | 113 | 734 | 49316 |