St Bartholomew's Hospital

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.

Pursuit and practice of complementary therapies by cancer patients receiving conventional treatment

Abstract: Objectives: To determine what proportion of oncology patients receiving conventional medical treatment also use complementary treatments; to assess which complementary treatments are the most popular and to assess patients9 motivation for using them; to evaluate associated advantages and risks. Design: Postal screening questionnaire followed by semistructured interview. Setting: Two hospitals in inner London. Subjects—600 unselected oncology patients aged 18 or over who had known their diagnosis of cancer for at least three months. Main outcome measures: Prevalence and demography of use of complementary therapies; patients9 motivation and expectations of complementary therapies; areas of satisfaction and dissatisfaction associated with conventional and complementary therapies. Results: 415 (69%) patients returned the questionnaire. 16% had used complementary therapies. The most popular were healing, relaxation, visualisation, diets, homoeopathy, vitamins, herbalism, and the Bristol approach. Patients using complementary therapies tended to be younger, of higher social class, and female. Three quarters used two or more therapies. Therapies were mostly used for anticipated antitumour effect. Ill effects of diets and herb treatments were described. Satisfaction with both conventional and complementary therapies was high, although diets often caused difficulties. Patients using complementary therapies were less satisfied with conventional treatments, largely because of side effects and lack of hope of cure. Benefits of complementary therapies were mainly psychological. Conclusions: A sizeable percentage of patients receiving conventional treatments for cancer also use complementary therapies. Patient satisfaction with complementary therapies, other than dietary therapies, was high even without the hoped for anticancer effect. Patients reported psychological benefits such as hope and optimism.

The clinical significance of invasion of veins by rectal cancer.

Abstract: A histopathological study of 703 surgical specimens from patients with adenocarcinoma of the rectum revealed invasion of veins by primary growth in almost 52 per cent. Follow-up studies on the patients showed that the corrected 5-year survival rate was significantly worse and liver metastases developed more frequently when venous invasion was present. Invasion of extramural veins was particularly significant whereas spread confined to intramural veins was less important. Invasion of large (thick-walled) veins was of greater consequence than invasion of small (thin-walled) veins and spread into thick-walled extramural veins had the greatest adverse influence of all. Venous spread of tumour takes place in parallel with local spread as measured by the Dukes' stage but exerts an influence on prognosis independent of the Dukes' stage. Similarly, vein invasion parallels the number of lymph node metastases but appears to exert an independent influence on prognosis. Observation of venous spread provides a precise assessment of the likely behaviour of rectal carcinoma and supplements, but does not replace indices such as the Dukes' stage or the number of lymph node metastases in routine use. The implications for surgical technique and management are discussed.

Co-induction of nitric oxide synthase and cyclo-oxygenase: interactions between nitric oxide and prostanoids.

Abstract: 1. Lipopolysaccharide (LPS) co-induces nitric oxide synthase (iNOS) and cyclo-oxygenase (COX-2) in J774.2 macrophages. Here we have used LPS-activated J774.2 macrophages to investigate the effects of exogenous or endogenous nitric oxide (NO) on COX-2 in both intact and broken cell preparations. NOS activity was assessed by measuring the accumulation of nitrite using the Griess reaction. COX-2 activity was assessed by measuring the formation of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) by radioimmunoassay. Western blot analysis was used to determine the expression of COX-2 protein. We have also investigated whether endogenous NO regulates the activity and/or expression of COX in vivo by measuring NOS and COX activity in the lung and kidney, as well as release of prostanoids from the perfused lung of normal and LPS-treated rats. 2. Incubation of cultured murine macrophages (J774.2 cells) with LPS (1 microgram ml-1) for 24 h caused a time-dependent accumulation of nitrite and 6-keto-PGF1 alpha in the cell culture medium which was first significant after 6 h. The formation of both 6-keto-PGF1 alpha and nitrite elicited by LPS was inhibited by cycloheximide (1 microM) or dexamethasone (1 microM). Western blot analysis showed that J774.2 macrophages contained COX-2 protein after LPS administration, whereas untreated cells contained no COX-2. 3. The accumulation of 6-keto-PGF1 alpha in the medium of LPS-activated J774.2 macrophages was concentration-dependently inhibited by chronic (24 h) exposure to sodium nitroprusside (SNP; 1-1000 microM). Sodium nitroprusside (1-1000 microM) also acutely (30 min) inhibited COX-2 activity in broken cell preparations of LPS-activated (12 h) J774.2 macrophages, in a similar concentration dependent manner. Addition of adrenaline (5 mM) and glutathione (0.1 mM) increased the activity of COX-2 in broken cell preparations. In the presence of these co-factors, SNP inhibited prostanoid production only at the highest concentration used (1 mM). When J774.2 cells were incubated in the presence of LPS (1 microg ml-1) and NG-monomethyl-L-arginine (L-NMMA: 1 mM) for 12 h, SNP at the highest concentration used (1 mM) acutely (30 min) inhibited the activity of COX-2 in cell homogenates with co-factors. However, when J774.2 macrophages were incubated for 24 or 12 h with LPS (1 microg ml-1)and L-NMMA (1 mM), the addition of SNP (0.001-1I000 microM) increased in a concentration-dependent manner the accumulation of 6-keto-PGF1a in intact cells (measured at 24 h) and COX-2 activity in cell homogenates in the presence of co-factors (determined at 12 h). SNP (1 mM; together with LPS for 12 h)decreased the amount of COX-2 protein induced by LPS in J774.2 macrophages.4. Indomethacin (30 1AM) abolished the formation of 6-keto-PGFa by LPS-activated macrophages, but had no effect on the release of nitrite. Conversely, L-NMMA, at the highest concentrations used (1 and 10 mM), increased the release of 6-keto-PGFIa an effect which was reversed by excess L-arginine (3 mM)but not by D-arginine. Similarly, the decrease in nitrite formation caused by L-NMMA was partially reversed by L-arginine (3 mM), but not by D-arginine. L-NMMA (10 mM; together with LPS for 12 h)increased the amount of COX-2 protein induced by LPS in J774.2 macrophages.5. In separate experiments, J774.2 macrophages were activated with LPS (1 microg ml-1), and L-NMMA(10 mM) was added for various times (0.5-24 h) before the collection of mediun at 24 h. L-NMMAenhanced the release of 6-keto-PGFI,, in a time-dependent manner, with the maximal enhancement seen when the NOS inhibitor was incubated with the cells for 24 h. 6. In experiments on male Wistar rats, we investigated the effect of L-NMMA on the release of prostanoids (6-keto-PGF1a prostaglandin E2, thromboxane B2) elicited by arachidonic acid (AA,30nmol) from ex vivo perfused kidneys and lungs. The release from the organs from normal and LPS-treated rats was unaffected by L-NMMA intraperitoneally (30 mg kg-1) for 6 h together with LPS(5 mg kg-1) or LPS vehicle. Similarly, acute (5 min) in vitro exposure to L-NMMA (1 mM) of the perfused organs from control and LPS-treated animals did not change the release of prostanoids elicited by AA (30 nmol).7. These results show that LPS causes the induction of iNOS and COX-2 in J774.2 macrophages. The co-release of NO and PGI2 induced by LPS is dependent on protein synthesis and occurs after a lag-time of 6-12 h. The formation of COX metabolites has no effect on NOS activity whereas NO inhibits both COX-2 activity and induction. These results demonstrate that NOS and COX can be co-induced in vitro and that under these conditions large amounts of NO inhibit the degree of COX expression and activity.In the absence of endogenous NO, lesser amounts of exogenous NO increase the activity of COX-2. In those situations in vivo when the level of NO induction is relatively low, NO does not regulate the increased activity of COX.