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Biomedical subjects

B Patel

Publications and source records attributed to B Patel.

At least 199 records · Page 11Linked to original sources
PubMed1983

Capping of cholera toxin-ganglioside GM1 complexes on mouse lymphocytes is accompanied by co-capping of alpha-actinin.

We used cholera toxin, which binds exclusively and with a high affinity to the ganglioside GM1, as a probe to investigate the distribution of this glycolipid on the surface of mouse lymphocytes. When lymphocytes are incubated with cholera toxin (or its B subunit) and then sequentially with horse anti-toxin and FITC-swine anti-horse Ig at 37 degrees C, the cholera toxin-ganglioside GM1 complex is redistributed to a cap at one pole of the cell. The capping of cholera toxin-GM1 complexes is slower than the capping of surface-Ig complexes, requires two antibodies, and is inhibited at high toxin concentrations. Cholera toxin-GM1, like surface-Ig capping, is an energy-dependent process and is inhibited by sodium azide, low temperatures, or cytochalasin B, but is unaffected by demecolcine. An affinity-purified antibody against alpha-actinin was used to examine the distribution of this cytoskeletal component during the capping process. 88% of the cells that had a surface Ig cap displayed a co-cap of alpha-actinin, and 57% of the cells that had a cholera toxin-GM1 cap displayed a co-cap of alpha-actinin. Time course studies revealed similar kinetics of external ligand cap formation and the formation of alpha-actinin co-caps. We conclude that capping of a cell-surface glycolipid is associated with a reorganization of the underlying cytoskeleton. The implications of such an association are discussed in the context of current models of the mechanism of capping.

Actinin↗
PubMed1982

Characterization of the cholera toxin receptor on Balb/c 3T3 cells as a ganglioside similar to, or identical with, ganglioside GM1. No evidence for galactoproteins with receptor activity.

Balb/c 3T3 cells contain a large number [(0.8-1.6) x 10(6)] of high-affinity (half-maximal binding at 0.2 nM) binding sites for cholera toxin that are resistant to proteolysis, but are quantitatively extracted with chloroform/methanol. The following evidence rigorously establishes that the receptor is a ganglioside similar to, or identical with, ganglioside GM1 by the galactose oxidase/NaB3H4 technique on intact cells was inhibited by cholera toxin. (2) Ganglioside GM1 was specifically adsorbed from Nonidet P40 extracts of both surface- (galactose oxidase/NaB3H4 technique) and metabolically ([1-14C]palmitate) labelled cells in the presence of cholera toxin, anti-toxin and Staphylococcus aureus. (3) Ganglioside GM1 was the only ganglioside labelled when total cellular gangliosides separated on silica-gel sheets were overlayed with 125I-labelled cholera toxin, although GM3 and GD1a were the major gangliosides present. In contrast no evidence for a galactoprotein with receptor activity was obtained. Cholera toxin did not protect the terminal galactose residues of cell-surface glycoproteins from labelling by the galactose oxidase/NaB3H4 technique. No toxin-binding proteins could be identified in Nonidet P40 extracts of [35S]-methionine-labelled cells by immunochemical means. After sodium dodecyl sulphate/polyacrylamide-gel electrophoresis none of the major cellular galactoproteins identified by overlaying gels with 125I-labelled ricin were able to bind 125I-labelled cholera toxin. It is concluded that the cholera toxin receptor on Balb/c 3T3 cells is exclusively ganglioside GM1 (or a related species), and that cholera toxin can therefore be used to probe the function and organisation of gangliosides in these cells as previously outlined [Critchley, Ansell, Perkins, Dilks & Ingram (1979) J. Supramol. Struct. 12, 273-291].

Animals↗
PubMed1981

CT diagnosis of venous pseudotumors in the chest and abdomen.

Appearances simulating neoplastic masses were found in five patients undergoing computed tomographic (CT) scanning of the chest and abdomen for a variety of indications. In each case the appearance was shown to be due to dilated collateral venous channels in association with portal hypertension or interruption of the inferior vena cava. The vascular origin of the masses was confirmed by CT scanning during intravenous bolus injection of contrast. Angiographic confirmation was obtained in three subjects. Enlarged collateral veins should be considered in the differential diagnosis of appearances suggesting mediastinal or abdominal lymphadenopathy at CT scanning.

Abdominal Neoplasms↗
PubMed1981

Glenn shunt: long-term results and current role in congenital heart operations.

Fifty cyanotic patients (aged 2 days to 22 years) underwent Glenn shunts for tricuspid atresia and other cyanotic heart defects. Thirteen of 15 operative deaths occurred in infants less than 4 months old, and only 1 death has occurred in the last 9 years. Results were poor in patients with Ebstein's anomaly, truncus arteriosus, transposition of the great vessels, and complex defects other than tricuspid atresia and univentricular heart. Of the 35 patients followed from 0.9 to 14.8 years, 12 were followed for more than 10 years. None of the 11 late deaths could be attributed to complications of the shunt. Minimal evidence of intrapulmonary shunting was found by angiography, pulmonary venous oximetry, or radioisotopic studies. Late deterioration due to venous collaterals and decreased flow to the opposite lung necessitated Blalock-Taussig shunts in 6 and Fontan procedures in 10. All survived the Fontan procedures with minimal morbidity. These data support the concept that Glenn shunts do not necessarily result in pulmonary abnormalities and may be indicated as a staged procedure in a few selected patients prior to a Fontan procedure.

Adolescent↗
PubMed1981

Superior gluteal artery haemorrhage following pelvic features controlled by embolisation.

Successful embolisation of active bleeding from the superior gluteal artery seen in two patients within the last 12 months is described. Both patients had extensive abdominal and pelvic injuries. One patient eventually died from renal failure and a perforated colon. The other patient is mobile and has been periodically seen in the out-patient department over the past nine months. In both instances, haemorrhage was at the sacrosciatic notch. Early angiography, in patients with extensive pelvic trauma and major blood requirements, with intent to embolise any identifiable bleeding source would appear to be the best initial manoeuvre to prevent exsanguination.

Adolescent↗
PubMed1980

Development of growth hormone receptors in rabbit and lamb liver after hypophysectomy.

The prolactin receptors of rat liver are pituitary-dependent, and previous studies have shown that prolactin itself plays a role in inducing and maintaining their presence. This study tried to determine if hepatic growth hormone (GH) receptors are comparably dependent on the pituitary. Young 47-day and older 116-day old rabbits were either hypophysectomized (H) or sham-operated (S). Hypophysectomy completely arrested the growth of the older rabbits but only reduced it by 50 p. 100 in the young ones. After 21 days, the specific binding (sb) of 125I-labelled human GH (hGH) to liver membranes was measured in H and S animals. The sb of hGH in H rabbits compared to S animals (older, young) was 14.9 p. 100 in older H rabbits and 45.5 p. 100 in young H animals. Similar studies in lambs showed that the sb of hGH in H lambs (compared to S animals) was 23.9 p. 100. When some H lambs were treated with 1 mg/kg of oGH or bGH 3 times per week, the sb of hGH was significantly increased to 56.1 p. 100 of the S levels. All changes in sb reflected changes in receptor number, as shown by the dose response binding curves. This study demonstrates that hepatic GH receptors in both the rabbit and the lamb are pituitary-dependent. The level in rabbits is correlated with the growth rate. Since GH receptor levels were partially restored in GH-treated lambs, it is possible that GH plays a role in inducing its own receptors.

Animals↗
PubMed1980

Secondary amenorrhoea due to autoimmune ovarian failure.

A case of spontaneous premature menopause due to autoimmune ovarian failure is described. This report emphasises that this uncommon condition is important to diagnose because of its association with other autoimmune endocrine disorders including Addison's disease. In addition, in the present case, the marked increase in luteinizing hormone with relatively normal follicle stimulating hormone raises the possibility of a non-steroidal inhibitory feedback of follicle stimulating hormone.

Addison Disease↗