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S Basu

Publications and source records attributed to S Basu.

At least 19 recordsLinked to original sources
PubMed1995

Model-based estimation of population attributable risk under cross-sectional sampling.

The covariate-adjusted population attributable risk (PAR) measures the proportionate reduction in disease prevalence in the target population when the putative risk factor is removed, after adjusting for covariate effects. This paper extends the model-based approach developed for retrospective and cohort studies to the cross-sectional sampling design. An appropriate logit linear model is utilized to estimate the covariate-adjusted attributable risk. The asymptotic variance of this complex ratio estimate is obtained using Taylor series expansions which incorporate the sampling variation of the estimated model parameters and the appropriate estimates of risk factor prevalence. These methods are illustrated with cardiovascular disease risk factor data from the second National Health and Nutrition Examination Survey (NHANES II).

Adolescent↗
PubMed1995

Phosphorylation of Raf by ceramide-activated protein kinase.

The sphingomyelin pathway, initiated by hydrolysis of sphingomyelin to ceramide and stimulation of a Ser/Thr ceramide-activated protein (CAP) kinase, mediates tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta action. CAP kinase is membrane-bound and proline-directed, recognizing the minimal substrate motif Thr-Leu-Pro. TNF may use the sphingomyelin pathway to signal Raf1 to activate the MAP kinase cascade. Evidence shows that cytoplasmic Raf1 binds to GTP-ras upon cellular stimulation, is recruited to the plasma membrane, and activated. How membrane-bound Raf1 is activated is uncertain, but regulation of its kinase activity may involve its phosphorylation. Specific Raf kinases, however, have not hitherto been identified. Here we report that CAP kinase phosphorylates Raf1 on Thr 269, increasing its activity towards MEK (MAP kinase or ERK kinase). Moreover, in intact HL-60 cells, CAP kinase complexes with Raf1 and, in response to TNF and ceramide analogues, phosphorylates and activates Raf1, implicating CAP kinase as a link between the TNF receptor and Raf1.

Amino Acid Sequence↗
PubMed1995

Characterization of regions of herpes simplex virus type 1 glycoprotein E involved in binding the Fc domain of monomeric IgG and in forming a complex with glycoprotein I.

Glycoprotein E (gE) and glycoprotein I (gI) of herpes simplex virus type 1 form a molecular complex that binds the Fc domain of monomeric IgG. Two approaches were used to define regions of gE-1 involved in monomeric IgG binding and complex formation with gI-1. First, we constructed 22 in-frame gE-1 linker-insertion mutants and, in cotransfection experiments with gI-1, assayed each mutant for IgG monomer binding and the ability to complex with gI-1. Nine mutants with insertions between gE-1 amino acids 235 and 380 failed to bind IgG monomers, whereas mutants outside this region retained binding activity. Each mutant reacted with several gE-1 mAbs, was detected at the cell surface, and was fully processed. Only two gE-1 mutants with insertions at residues 235 and 264 lost the ability to co-immunoprecipitate with gI-1, which defines a region of gE-1 that complexes with gI-1. As an additional approach, we assayed 8 gE-1/gD-1 fusion proteins containing large overlapping gE-1 peptides inserted within the ectodomain of gD-1 for binding of IgG monomers and complex formation with gI-1. Three fusion proteins containing gE-1 peptides that overlap at residues 183-402 bound monomeric IgG. This region of gE-1 includes the Fc binding region defined by linker insertion mutagenesis. Five fusion proteins containing gE-1 peptides that overlap at residues 183-288 were co-immunoprecipitated with gI-1, confirming results of gE-1 linker insertion mutagenesis. These studies define two regions on gE-1 involved in Fc binding activity, one that interacts with gI-1, and another that binds IgG.

Amino Acid Sequence↗
PubMed1995

Enhanced tumor growth in brain dopamine-depleted mice following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment.

Brain dopamine influences immune functions and the role of immune functions in tumor growth is well established. Therefore, a study has been carried out to evaluate the correlation, if any, between brain dopamine and tumor growth. MPTP selectively destroys dopaminergic neurons in the brain. In the present study, Ehrlich carcinoma growth was evaluated in MPTP-treated mice. Results showed a correlation between depletion of striatal dopamine and enhanced tumor growth. Since in the present study striatal dopamine depletion in mice was associated with significantly decreased immune responses, the suggested correlation between brain dopamine and tumor growth was possibly mediated by the immune system.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

Dobutamine echocardiography and thallium-201 imaging predict functional improvement after revascularisation in severe ischaemic left ventricular dysfunction.

OBJECTIVES: To evaluate the concordance between thallium-201 uptake and echocardiographic wall thickening, which are both indicators of potentially reversible myocardial dysfunction, in patients with chronic ischaemic left ventricular failure and to assess their relative contribution to predicting improvement in regional function after revascularisation in a subgroup. PATIENTS AND METHODS: 45 patients with chronic ischaemic left ventricular dysfunction (mean (SD) ejection fraction 25 (8)%) underwent echocardiography before and after dobutamine infusion (10 micrograms/kg/min). Of these, 22 patients underwent rest echocardiography at a mean (SD) of 9 (1) weeks after revascularisation. 201Tl imaging was performed during dobutamine echocardiography and at rest, 1, and 4 h after treatment with sublingual glyceryl trinitrate on two separate days. Potentially reversible dysfunction was thought to be present when a myocardial segment contained a Tl score of > or = 3 (ascending score 1-4), or showed improved wall thickening of a dysynergic segment during dobutamine stimulation. RESULTS: Of the 201Tl protocols, the redistribution scan 1 h after treatment with glyceryl trinitrate best demonstrated myocardial viability. Concordance between 201Tl and dobutamine induced wall thickening was 82% (kappa = 0.59) for detecting potentially reversible myocardial dysfunction before revascularisation (n = 45). Regional function improved in 18 of 22 patients after revascularisation. There were 168 dysynergic segments before intervention. The sensitivity of echocardiography and 201Tl imaging for detecting "recoverable" or viable segments after revascularisation was 87% and 92% respectively and specificity was 82% and 78% respectively (P = NS). CONCLUSIONS: Dobutamine echocardiography and 201Tl imaging may be used to predict mechanical improvement in dysynergic segments after revascularisation in patients with chronic ischaemic left ventricular dysfunction.

Adult↗
PubMed1995

NIDDM is the major cause of diabetic end-stage renal disease. More evidence from a tri-ethnic community.

Diabetes is the single largest cause of end-stage renal disease (ESRD) in adults in the U.S. Insulin-dependent diabetes mellitus (IDDM) has been recognized for some time as an important cause of ESRD, but non-insulin-dependent diabetes mellitus (NIDDM) has been assumed, until recently, to rarely cause ESRD. The objective of this study is to determine the incidence of treatment of diabetic ESRD by diabetic type for three ethnic/racial groups: non-Hispanic whites, African-Americans, and Mexican-Americans. A population-based incidence cohort was assembled from all dialysis centers in Bexar (San Antonio) and Dallas counties in Texas. All patients with diabetic ESRD beginning dialysis between 1 December 1987 (Bexar) or 1 December 1988 (Dallas) and 31 July 1991 were identified. All non-hispanic whites and African-Americans and a 1/2 random sample of Mexican-Americans were approached for enrollment. Individuals were confirmed to have diabetes using the World Health Organization criteria. Diabetes typing was done using a computerized historical algorithm. Age-specific and age-adjusted incidence rates were obtained by diabetic type and ethnic/racial group. NIDDM causes the majority of diabetic ESRD: 59.5% for non-Hispanic whites, 92.8% for Mexican-Americans, and 84.3% for African-Americans. Mexican-Americans and African-Americans, respectively, have 6.1 and 6.5 times higher incidence of treatment for diabetic ESRD than non-Hispanic whites. NIDDM results in more ESRD than does IDDM. Minorities (African-Americans and Mexican-Americans) are at increased risk, and programs aimed at prevention of NIDDM-related ESRD must focus on them.

Adult↗
PubMed1995

Genetic marker profile of primitive Kutia Kondh tribal population of Phulbani district (Orissa).

Blood samples from 330 Kutia Kondhs (a primitive tribal population of Orissa) were subjected to a battery of tests for genetic markers to find out the incidence of various blood group polymorphisms (ABO, MN, Duffy, JKa), serum proteins, sickling and G-6-PD deficiency. Predominance of O (39.09%) blood group for ABO, N blood group (53.44) for MN and Fya+b+ (55.72) for Duffy blood group, were observed. High incidence of Hp2-1 (39.33), SS (70.43) and CC (96.65) for haptoglobulin, C3 and transferrin respectively were seen. The overall frequency of sickling was observed to be 16.36 per cent. The sex-wise distribution of G-6-PD was 13.71 per cent for males and 1.84 for females.

Blood Group Antigens↗
PubMed1994

Mice lacking granulocyte colony-stimulating factor have chronic neutropenia, granulocyte and macrophage progenitor cell deficiency, and impaired neutrophil mobilization.

Mice lacking granulocyte colony-stimulating factor (G-CSF) were generated by targeted disruption of the G-CSF gene in embryonal stem cells. G-CSF-deficient mice (genotype G-CSF-/-) are viable, fertile, and superficially healthy, but have a chronic neutropenia. Peripheral blood neutrophil levels were 20% to 30% of wild-type mice (genotype G-CSF+/+) and mice heterozygous for the null mutation had intermediate neutrophil levels, suggesting a gene-dosage effect. In the marrow of G-CSF-/- mice, granulopoietic precursor cells were reduced by 50% and there were reduced levels of granulocyte, macrophage, and blast progenitor cells. Despite G-CSF deficiency, mature neutrophils were still present in the blood and marrow, indicating that other factors can support neutrophil production in vivo. G-CSF-/- mice had reduced numbers of neutrophils available for rapid mobilization into the circulation by a single dose of G-CSF. G-CSF administration reversed the granulopoietic defect of G-CSF-/- mice. One day of G-CSF administration to G-CSF-/- mice elevated circulating neutrophil levels to normal, and after 4 days of G-CSF administration, G-CSF+/+ and G-CSF-/- marrows were morphologically indistinguishable. G-CSF-/- mice had a markedly impaired ability to control infection with Listeria monocytogenes, with diminished neutrophil and delayed monocyte increases in the blood and reduced infection-driven granulopoiesis. Collectively, these observations indicate that G-CSF is indispensible for maintaining the normal quantitative balance of neutrophil production during "steady-state" granulopoiesis in vivo and also implicate G-CSF in "emergency" granulopoiesis during infections.

Animals↗
PubMed1994

Transfection of mu MDR 1 inhibits Na(+)-independent Cl-/-HCO3 exchange in Chinese hamster ovary cells.

We have used single-cell photometry to measure intracellular pH (pHi) for several MDR cell lines constructed by stably transfecting LR73 chinese hamster ovary fibroblasts with mutant and wild type murine MDR 1 genes. In addition, plasma membrane electrical potential (delta psi) has been measured for the same cells by the K+/valinomycin null point titration method using the ratiometric styryl probe di-4-ANEPPS. Both the untransfected, parental cell line and a cell line expressing substantial mutant MDR 1 protein (K432R/K1074R) that is unable to confer the MDR phenotype are found to have delta psi > or = -40 (+/- 5) mV and pHi < or = 7.16 (+/- 0.03) units. In contrast, MDR cell lines constructed by transfecting wild type mu MDR 1 cDNA are found to exhibit delta psi from 15 to 19 mV lower and pHi from 0.13 to 0.34 units higher. A cell line that overexpresses crippled MDR protein (S941F) that is not resistant to colchicine or doxorubicin, but which is resistant to vinblastine [Gros, P., Dhir, R., Croop, J., & Talbot, F. (1991) Proc. Natl. Acad. Sci. U.S.A. 88, 7289-7293], exhibits elevated pHi and slightly elevated delta psi, relative to LR73. Northern and western blot analyses confirm the substantial overexpression of the mu MDR genes and proteins in these lines, as well as the mild overexpression of endogenous hamster p-GP mRNA in some lines. In general agreement with previous studies that examined myeloma cells overexpressing hu MDR 1 protein [Roepe, P.D., Wei, L.-Y., Cruz, J., & Carlson, D. (1993) Biochemistry 32, 11042-11056] we find that overexpression of wild type mu MDR 1 protein inhibits Cl(-)- and -HCO3-dependent pHi homeostasis. Via single-cell photometry studies we now conclude that this is due to inhibition of Na(+)-independent Cl-/-HCO3 exchange (strict anion exchange or AE). As concluded previously for other MDR cells, decreased AE activity is not due to decreased expression of the exchanger; in fact, again similar to previous work [Roepe et al. (1993) Biochemistry 32, 11042-11056], we find increased levels of AE mRNA in some MDR cell lines. Models that may explain these data that are also consistent with the known physiology of cells that endogenously express MDR protein are suggested. These data are consistent with a model for MDR protein function wherein overexpression of the protein decreases delta psi and/or elevates pHi via Cl(-)- and -HCO3-dependent mechanisms.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Enhanced intracellular delivery of doxorubicin by scavenger receptor-mediated endocytosis for preferential killing of histiocytic lymphoma cells in culture.

A conjugate of the antineoplastic drug doxorubicin (DXR) with maleylated bovine serum albumin (MBSA) was taken up by a human histiocytic lymphoma cell line (U937) through the high efficiency process of scavenger receptor-mediated endocytosis resulting in a sixfold higher intracellular concentration of the drug compared to that obtained when the free drug was administered. Compared to the free drug, the drug conjugate showed significantly higher cytotoxicity towards U937 cells presumably because of intracellular availability of a pharmacologically active form of the drug. The intracellular product released after lysosomal degradation of the drug conjugate was chromatographically identical to free DXR. These findings merit serious consideration in the development of new chemotherapeutic agents for the treatment of histiocytic malignancies.

Albumins↗
PubMed1994

Structure of the O-specific side chain of the lipopolysaccharide from Escherichia coli O126.

The polysaccharide isolated from Escherichia coli O126 lipopolysaccharide contains D-galactose, D-mannose, L-fucose, and 2-acetamido-2-deoxy-D-glucose in the molar ratios 1:1:1:1. The structure of the O-antigen of the lipopolysaccharide from E. coli O126 was established by compositional analysis, partial degradation, methylation analysis, and nuclear magnetic resonance spectroscopy. These studies revealed that the O-antigen is branched and built up of tetrasaccharide repeating units having the following structure: [formula: see text]

Carbohydrate Conformation↗
PubMed1994

Analysis of glycosphingolipids by fluorophore-assisted carbohydrate electrophoresis using ceramide glycanase from Mercenaria mercenaria.

Polyacrylamide gel electrophoresis of fluorophore-labeled saccharides is a simple and sensitive separation method for glycan analysis. This method requires an aldehydic reducing carbon on the saccharide in order to react with the amine group of the fluorophore (8-aminonaphthalene-1,3,6-trisulfonic acid or 2-aminoacridone). We have used exoglycosidase-free ceramide glycanase from hard-shelled clam to expose the reducing terminal of the glycan in glycosphingolipid by cleaving the linkage between the glycan and the ceramide. The released glycan was used for fluorophore-assisted carbohydrate electrophoresis, in order to qualitatively determine its monosaccharide composition, chain length, and glycosidic linkages using linkage-specific glycosidases, including a beta 1-3,4 galactosidase from clam.

Animals↗
PubMed1994

Reverse redistribution of thallium-201 represents a low-risk finding in thrombolysed patients following myocardial infarction.

The aim of the study was to evaluate the prevalence and clinical significance of reverse redistribution on thallium-201 imaging in post-myocardial infarction patients who have undergone thrombolytic therapy. Sixty-two patients aged 35-79 (mean 60) years with proven myocardial infarction who had undergone thrombolysis were studied 6 weeks post infarction. Standard stress and 4-h redistribution imaging was performed with 201Tl following treadmill exercise. Separate day rest injection of 201Tl was given after sublingual nitroglycerine; imaging was performed at 1 h. Planar images were acquired in three standard views and semiquantitative segmental analysis of the images was performed from the unprocessed images. All patients had radionuclide ventriculography for the assessment of left ventricular ejection fraction and wall motion abnormality. Thirty-three patients also had coronary angiography. 201Tl scintigraphy revealed fixed defects in 19 patients, reversible defects in 22, and reverse redistribution in 21. Those with reverse redistribution had a significantly higher exercise capacity (P < 0.01). Mean (SD) left ventricular ejection fraction was 46 (12)% for those with fixed defects, 47 (9)% for those with reversible defects and 45 (15)% for patients with reverse redistribution (P = NS). The regional wall motion abnormality score was 8 (5), 11.8 (2.2) and 14.2 (6) respectively in patients with reverse redistribution, redistribution alone and fixed defects. Regions with reverse redistribution revealed less regional wall motion abnormality compared to the other two groups (P < 0.01). Fifteen patients demonstrated significant 201Tl uptake in the region showing reverse redistribution, with rest injection of 201Tl following sublingual nitroglycerine, suggesting viable myocardium in that region.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1994

Corneal permeability to and ocular metabolism of phenyl substituted prostaglandin esters in vitro.

The corneal permeability to and metabolism of four phenyl substituted prostaglandin analogues have been studied in vitro. Porcine corneas were mounted in incubation chambers dividing each chamber into an epithelial and endothelial side compartment. The analogues were added to incubation medium on the epithelial side. The permeability coefficients of 17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhDH100A), 15-keto-17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhXA12), 13,14-dihydro-15-hydroxy (R, S)-17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhXA34) and 13,14-dihydro-17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhXA41) were determined to be in the range of 5.1-11.0 x 10(-6) cm x s-1. All analogues in the endothelial compartment had been hydrolysed to corresponding acids but any other metabolism of PhDH100A, PhXA34 and PhXA41 after 4 h of incubation was minimal. In contrast, PhXA12 free acid was extensively metabolised to the 13,14-dihydro metabolite. To investigate whether the porcine ocular tissues contain 15-hyroxyprostaglandin dehydrogenase (15-PGDH) activity, prostaglandin F2 alpha (PGF2 alpha) and PhDH100A were used as substrates. PGF2 alpha and the phenyl-substituted analogues were also tested for their capacity as substrate to 15-PGDH in general. The 15-PGDH activity was low in all ocular tissues. The capacity of various ocular tissues or purified 15-PGDH to metabolise PhDH100A was lower than with PGF2 alpha as substrate. PhXA34 and PhXA41 were found not to be metabolised by 15-PGDH. Thus, the phenyl substituted PG esters penetrated the cornea and in the process were hydrolysed to their corresponding acids. No appreciable further metabolism occurred except for PhXA12 which was reduced by delta 13-reductase.

Animals↗
PubMed1994

Anti-ischaemic and haemodynamic effects of elgodipine, a potent new generation calcium antagonist, in chronic stable angina.

The effects of oral elgodipine, a new dihydropyridine calcium antagonist on ischaemia and left ventricular function were assessed by a single blind placebo controlled study in 12 patients with chronic stable angina. Graded treadmill exercise and echocardiography/Doppler were performed before and 90 min after single oral doses of elgodipine of 20 mg, 40 mg and 60 mg, or placebo, given at weekly intervals. Elgodipine significantly increased exercise time by 1.1, 2.0 and 2.4 min, (P < 0.001 in each case) and time to onset of angina by 1.1 (P < 0.01), 1.9 (P < 0.001) and 2.6 min (P < 0.001) with increasing doses of the drug. Angina was abolished in 50% of patients with significant improvement in ST depression at peak exercise (P < 0.001) with the 60 mg dose. Blood pressure fell significantly at rest and peak exercise with a corresponding significant increase in heart rate. Ejection fraction was increased by 7.8% (P < 0.001) and 8.4% (P < 0.001) as was the stroke volume by 9.3 ml (P < 0.001) and 12.5 ml (P < 0.001) at 40 mg and 60 mg respectively. Peak mitral A to E velocity ratio and total peripheral resistance decreased significantly in a dose related linear trend. Only minor side effects were noted and no patient required withdrawal from the study. The results demonstrate that oral elgodipine is a potent anti-ischaemic agent. An improvement in the echocardiographic parameters of left ventricular systolic and diastolic function was also seen.

Aged↗