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Institution

St Bartholomew's Hospital

HealthcareLondon, 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.


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Journal ArticleDOI
TL;DR: It is demonstrated that rat mast cells release a factor with the same pharmacological profile as NO, and that this NO-like factor is derived from L-arginine.

145 citations

Journal ArticleDOI
TL;DR: The illness biographies and daily lives of HIV-positive African women receiving treatment in London are explored, revealing marked similarities and differences which need to be properly understood by health and social care professionals to offer the most appropriate care for this growing population of patients.
Abstract: There are no studies that have examined the particular needs and experiences of African women living with HIV in the UK at a time when they represent an increasingly large proportion of the UK HIV epidemic. This study explores the illness biographies and daily lives of HIV-positive African women receiving treatment in London. Sixty-two women from 11 African countries attending HIV specialist clinics in five London hospitals participated in self-completion questionnaires and in depth semi-structured interviews. Using a narrative approach, women were asked to talk about their HIV status in the broader context of their life history. Important differences exist within this group based mainly on nationality, income, education level and legal status in the UK. However, marked similarities also emerged which were related in part to their situation as migrants and were compounded by their illness. Stigma, both actual and perceived, had a profound impact on women's lives, making control of information about their situation a matter of acute concern. This had an effect on how women accessed health services and voluntary sector agencies. The resilience of women in dealing with difficulties in their lives was strengthened by religious belief. Such similarities and differences need to be properly understood by health and social care professionals if they are to offer the most appropriate care for this growing population of patients.

144 citations

Journal ArticleDOI
TL;DR: It appears possible that PGE1 acts as a direct inhibitor of osteoclastic bone resorption but has an additional effect on other cells in bone, which are induced by P GE1 to cause osteoclast stimulation.
Abstract: Cells were disaggregated from osteoclastomas, and the response of the giant cells to calcium-regulating hormones, prostaglandin (PG)E1 and dibutyryl cyclic AMP (dbcAMP) was observed by phase-contrast time-lapse video microscopy. The pattern and nature of their response was very similar to that previously found to be characteristic of osteoclasts: calcitonin (CT), PGE1 and dbcAMP induced cytoplasmic quiescence, while parathyroid hormone (PTH) showed no influence on cytoplasmic motility or behaviour. The cells were also cultured on slices of devitalized cortical bone for 5 or 18 h. After this time the giant cells were associated with the appearance in the scanning electron microscope of characteristic resorption pits, the volume of which was calculated by computer-assisted morphometric and stereophotogrammetric techniques after removal of cells. Calcitonin caused a dramatic reduction in the volume of bone resorbed by these isolated cells compared with control cultures, while PTH was without significant effect. This result supports the view that PTH does not increase bone resorption in intact bone through a direct effect on osteoclasts. PGE1, which stimulates bone resorption when added to intact bone, paradoxically reduced resorption in our cultures. It thus appears possible that PGE1 acts as a direct inhibitor of osteoclastic bone resorption but has an additional effect on other cells in bone, which are induced by PGE1 to cause osteoclastic stimulation.

144 citations

Journal ArticleDOI
TL;DR: The data suggest that normal or enhanced responses of hypercortisolaemic patients with Cushing's syndrome contrast with the complete inhibition of the responses to CRF‐41 in normal subjects given dexamethasone, suggesting these patients have a functional defect of ACTH secretion due to the failure of CRF to reach the corticotroph.
Abstract: Synthetic CRF-41 has been given to 43 patients with hypothalamic, pituitary or adrenal diseases and contrasted with the responses in 20 normal subjects. In the normal subjects the mean increment in serum cortisol (+/- SE) was 276 +/- 38 nmol/l; the increments showed a significant negative correlation with the basal serum cortisol levels (r = -0.56; P less than 0.02). The mean peak serum cortisol was 662 +/- 34 nmol/l and the mean peak corticosterone was 28.6 +/- 3.8 nmol/l. There was a significant positive correlation between the peak serum corticosterone and cortisol concentrations (r = 0.84; P less than 0.0001). Dexamethasone pretreatment abolished the rise in cortisol in response to CRF-41. The peak serum cortisol following CRF-41 was not significantly different between the normal subjects and those patients with pituitary disease who had normal cortisol responses to insulin-induced hypoglycaemia. However, in individual patients the peak cortisol levels induced by hypoglycaemia were greater than, but significantly correlated with, those induced by 100 micrograms of CRF-41. Seven patients were ACTH deficient in response to hypoglycaemia, and of these six responded normally to CRF-41. Only one of these patients had a lesion clearly originating in the hypothalamus; four had pituitary tumours with suprasellar extensions and the remaining patient had idiopathic GH and ACTH deficiency. Our data suggest that these patients have a functional defect of ACTH secretion due to the failure of CRF to reach the corticotroph. Of the four patients with pituitary-dependent Cushing's disease who were on no treatment at the time of testing, three showed an exaggerated and one a normal response to CRF-41. These normal or enhanced responses of hypercortisolaemic patients with Cushing's syndrome contrast with the complete inhibition of the responses to CRF-41 in normal subjects given dexamethasone. In the treated patients with Cushing's syndrome and normal serum cortisol levels, those with pituitary-dependent disease showed an enhanced ACTH response to CRF-41 as compared with the ectopic ACTH group, but there was some overlap between the two groups. Acromegalic patients did not show a GH response to CRF-41. We conclude that administration of CRF-41 is a safe new method for investigating disorders of the hypothalamo-pituitary axis.

144 citations

Journal ArticleDOI
TL;DR: The combination of normal unbound-plasma- œstradiol and reduced unbound androgen levels of hypo- gonadism in chronic liver disease and increased hepatic S.B.H.G. production is suggested.

144 citations


Authors

Showing all 11065 results

NameH-indexPapersCitations
Philippe Froguel166820118816
Geoffrey Burnstock141148899525
Michael A. Kamm12463753606
David Scott124156182554
Csaba Szabó12395861791
Roger Williams122145572416
Derek M. Yellon12263854319
Walter F. Bodmer12157968679
John E. Deanfield12049761067
Paul Bebbington11958346341
William C. Sessa11738352208
Timothy G. Dinan11668960561
Bruce A.J. Ponder11640354796
Alexandra J. Lansky11463254445
Glyn Lewis11373449316
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20232
202216
2021390
2020354
2019307
2018257