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Biomedical subjects

J Bhattacharya

Publications and source records attributed to J Bhattacharya.

At least 55 records · Page 3Linked to original sources
PubMed1999

Pressure is proinflammatory in lung venular capillaries.

Endothelial responses may contribute importantly to the pathology of high vascular pressure. In lung venular capillaries, we determined endothelial [Ca(2+)](i) by the fura-2 ratioing method and fusion pore formation by quantifying the fluorescence of FM1-43. Pressure elevation increased endothelial [Ca(2+)](i). Concomitantly evoked exocytotic events were evident in a novel spatial-temporal pattern of fusion pore formation. Fusion pores formed predominantly at vascular branch points and colocalized with the expression of P-selectin. Blockade of mechanogated Ca(2+) channels inhibited these responses, identifying entry of external Ca(2+) as the critical triggering mechanism. These endothelial responses point to a proinflammatory effect of high vascular pressure that may be relevant in the pathogenesis of pressure-induced lung disease.

Animals↗
PubMed1999

The design of Healthcare for Communities: a study of health care delivery for alcohol, drug abuse, and mental health conditions.

There is a shortage of data to inform policy debates about the quickly changing health care system. This paper describes Healthcare for Communities (HCC), a component of the Robert Wood Johnson Foundation's Health Tracking Initiative that was designed to fill this gap for alcohol, drug abuse, and mental health care. HCC bridges clinical perspectives and economic/policy research approaches, links data at market, service delivery, and individual levels, and features a household survey of nearly 9,600 individuals with an employer follow-back survey. Public use files will be available in late 1999.

Community Mental Health Services↗
PubMed1999

Binding of Escherichia coli heat-stable toxin and rise of guanylyl cyclase activity in the brush-border membranes of rabbit intestinal epithelial cells.

The study examines the age-related differences in the density of Escherichia coli heat-stable enterotoxin (STa) receptors in the small intestine of rabbits. The number of STa receptors was found to be 1.7 x 10(12) in 14-day old rabbits compared to 2.4 x 10(9) in 14-week old rabbits per milligram brush-border membrane protein. The STa-induced guanylyl cyclase activity in the intestinal brush-border membranes was found to be stimulated by 6.2 folds over the basal enzyme activity in 14-day old rabbits, whereas in the 14-week old rabbits, it was 4 folds over the basal activity. Moreover, the enzyme activity remained lower in the adult rabbits compared to the younger ones. Autoradiographic analysis of sodium dodecyl sulphate polyacrylamide gel electrophoresis showed two STa-binding proteins of apparent molecular weights of 140 and 38 kDa in the intestinal brush-border membranes of rabbits.

Age Factors↗
PubMed1998

Rise of intracellular free calcium levels with activation of inositol triphosphate in a human colonic carcinoma cell line (COLO 205) by heat-stable enterotoxin of Escherichia coli.

The heat-stable enterotoxin (STa) produced by Escherichia coli has been found to increase rapidly two potential intracellular signals, inositol triphosphate and cytosolic free calcium in a human colonic cell line, COLO 205. Addition of STa to COLO 205 cells prelabelled with myo-[2-3H]inositol resulted in a rapid rise of [3H]inositol triphosphate. Using fluorescent indicator, Fura-2AM, intracellular free Ca2+ has been found to increase 5.12-fold compared to control. Suspension of cells in calcium-free buffer demonstrated STa-induced rapid rise of cytosolic Ca2+. The same result was found when extracellular calcium was chelated with EGTA. This effect was not observed with cells that were pretreated with dantrolene which suggest that the intracellular calcium rise might be due to mobilization from intracellular stores. This study demonstrated for the first time a change in cytosolic calcium in cultured human colonic cells by STa, which is accompanied by inositol triphosphate activation.

Bacterial Toxins↗
PubMed1998

Rise of cytosolic Ca2+ and activation of membrane-bound guanylyl cyclase activity in rat enterocytes by heat-stable enterotoxin of Vibrio cholerae non-01.

The cytosolic calcium level ([Ca2+]i) and the membrane-bound guanylyl cyclase activity in the isolated rat intestinal epithelial cells were investigated. Heat-stable enterotoxin of Vibrio cholerae non-01 (NAG-ST) was found to increase both the [Ca2+]i and the enzyme activity. These changes occur similarly until 5 min of incubation with NAG-ST, indicating that these changes might be involved in NAG-ST induced signal transduction in rat enterocytes.

Animals↗
PubMed1997

Binding of Escherichia coli heat-stable enterotoxin and rise of cyclic GMP in COLO 205 human colonic carcinoma cells.

Escherichia coli heat-stable enterotoxin (STa) was found to bind on the surface of human colonic (COLO 205) cells. The binding of [125I]STa to cell membranes was found to be specific, reversible and saturable. Scatchard analysis of the equilibrium binding demonstrated a single class of binding sites with a Kd of 0.5 x 10(-10) M. Autoradiographic analysis of polyacrylamide gel electrophoresis revealed the specific incorporation of [125I]STa into a single STa binding protein with a molecular mass of 95 kDa. Following incubation of COLO 205 cells with STa, a rise of intracellular cGMP was also evident.

Bacterial Toxins↗
PubMed1997

Barrier effects of hyperosmolar signaling in microvascular endothelium of rat lung.

We determined the effects of hyperosmolarity on lung microvascular barrier properties by means of the split-drop technique in single venular capillaries of the isolated, blood-perfused rat lung. Using isosmolar and hyperosmolar test solutions (colloid osmotic pressure = 21 cm H2O), we quantified transcapillary flux at a fixed absorptive capillary pressure, and the capillary hydraulic conductivity (Lp). Loss of barrier function was indicated in flux reversal from isosmolar absorption to hyperosmolar filtration (P < 0. 01), and by hyperosmolarity-induced Lp increase (P < 0.01). Barrier recovery after a 1-min hyperosmolar exposure was delayed > 25 min. The flux reversal was blocked by the tyrosine kinase inhibitors genistein and MDC (P < 0.01). Genistein also inhibited the Lp increase (P < 0.01). Immunoblots of hyperosmolarity-exposed, cultured rat lung microvascular endothelial cells (RLMEC) and of endothelial cells freshly harvested from lungs given hyperosmolar infusions indicated a genistein-inhibitable enhancement of protein tyrosine phosphorylation. Immunoprecipitation studies indicated tyrosine phosphorylation of the mitogen activated protein kinases (MAPK) ERK1 and ERK2 and the adaptor protein Shc in lysates of RLMEC exposed to hyperosmolar conditions. We conclude that in lung venular capillaries hyperosmolarity deteriorates barrier properties, possibly by inducing tyrosine phosphorylation of endothelial proteins.

Animals↗
PubMed1997

The role of plain radiography in the management of suspected orbital blow-out fractures.

We reviewed the indications for radiography and its impact on management in 100 consecutive patients referred to the Radiology Department from the Accident and Emergency Department of a large eye hospital in order to assess the utility of orbital plain radiographs in patients suspected of having blow-out fractures. We assessed whether administration of antibiotics or referral for surgical or orthoptic treatment was influenced by clinical features, radiographic findings or both. Ophthalmologists interpreting the radiographs appeared to be guided by the presence or absence of physical signs. No patient in whom they overlooked a fracture which was not evident clinically was subsequently referred for surgery. All patients who did have surgery for complications of a blow-out fracture underwent pre-operative computed tomography. Neither referral for orthoptic treatment nor administration of systemic antibiotics was consistently influenced by the presence or absence of a fracture. Given these findings, and the observation that the decision to operate was guided exclusively by clinical rather than radiological criteria, we recommend that only patients with well-defined indications for surgery (enophthalmos of more than 2 mm at any time within the first 6 weeks following the injury, and/or diplopia in the primary and/or downgaze reading positions not showing evidence of resolving within 2 weeks of the injury) should undergo radiography.

Adolescent↗
PubMed1996

Ca2+ waves in lung capillary endothelium.

Although cytosolic Ca2+ importantly regulates organ function, lung microvascular [Ca2+]i regulation remains poorly understood because of the lack of direct in situ quantification. In the present study, we report the first endothelial [Ca2+]i quantification by the fura 2 method in microscopically imaged venular capillaries of the isolated blood-perfused rat lung. Sequential images indicated the presence of intercellular Ca2+ waves that spontaneously originated from pacemaker endothelial cells and then spread for short distances along the capillary wall, inducing synchronous endothelial [Ca2+]i oscillations. Fast Fourier analyses of the oscillations revealed a dominant wave component with an amplitude of 37 nmol/L, frequency of 0.4 min-1, and velocity of 5 microns/s. The intracellular Ca2+ wave was unaffected by blood flow stoppage or by infusions of Ca(2+)-containing or Ca(2+)-free dextran. Inhibition of the wave by thapsigargin in Ca(2+)-free dextran and by the gap junction uncoupler, heptanol, indicated that it was generated by endosomal Ca2+ release in the pacemaker cell and was propagated by gap junctional communication. In the presence of histamine, enhancement of the wave accounted for a significant component of the coordinated [Ca2+]i increase in the capillary segment. No intercellular Ca2+ waves were evident in adjoining alveolar epithelial cells. Our findings indicate a novel mechanism of [Ca2+]i regulation in the lung capillary under both resting and stimulated conditions. Pacemaker-induced Ca2+ waves, generated intracellularly by unknown initiating mechanisms, communicated to adjoining cells to determine [Ca2+]i profiles in short interbranch segments of capillary walls.

Animals↗
PubMed1995

Soluble ligands of the alpha v beta 3 integrin mediate enhanced tyrosine phosphorylation of multiple proteins in adherent bovine pulmonary artery endothelial cells.

Binding of substrate-bound extracellular matrix proteins to cell surface integrins results in a variety of cellular responses including adhesion, cytoskeletal reorganization, and gene expression. We have previously shown that addition of soluble SC5b-9, the complement-vitronectin complex, resulted in an RGD-dependent increase in lung venular hydraulic conductivity (Ishikawa, S., Tsukada, H., and Bhattacharya, J. (1993) J. Clin. Invest. 91, 103-109). To identify specific integrin(s) and signal transduction pathways that are responsive to soluble vitronectin-containing ligands, we exposed confluent bovine pulmonary artery cells to purified soluble human mono- or multimeric vitronectin, or SC5b-9, and determined the extent of endothelial cell protein tyrosine phosphorylation. Monomeric vitronectin (Vn) did not induce enhanced protein tyrosine phosphorylation. However, multimeric Vn and SC5b-9 elicited time- and concentration-dependent increases in tyrosine phosphorylation of numerous proteins. Antiserum against vitronectin, RGD peptides, and monoclonal and polyclonal antibodies against the alpha v beta 3 integrin blocked the vitronectin- or SC5b-9-induced enhanced accumulation of tyrosine phosphoproteins, while antibodies against beta 1 integrins and the alpha v beta 5 integrin did not. Clustering of the alpha v beta 3 integrin using monoclonal antibody LM609 caused a pattern of enhanced tyrosine phosphorylation similar to that caused by multimeric Vn and SC5b-9, suggesting that aggregation of alpha v beta 3 was critical for signaling. Among the proteins that underwent enhanced tyrosine phosphorylation in response to vitronectin were the cytoskeletal proteins paxillin, cortactin, and ezrin, as well as the SH2 domain-containing protein Shc, and p125FAK. We conclude that ligation of the alpha v beta 3 integrin by soluble ligands promotes enhanced phosphorylation of several proteins implicated in tyrosine kinase signaling and suggest that this pathway may be important in inflammatory states which are accompanied by accumulation of SC5b-9.

Animals↗
PubMed1995

Role of outer membrane proteins on the adherence of Vibrio parahaemolyticus to rabbit intestinal epithelial cell in vitro.

Antiserum against outer membrane preparation of a Kanagawa phenomenon-positive strain of Vibrio parahaemolyticus were raised in rabbits and absorbed with their lipopolysaccharide. The anti-outer membrane protein serum and its Fab (IgG) fragment inhibited the adherence of Kanagawa-positive strains to rabbit intestinal epithelial cells in vitro. Preincubation of rabbit intestinal epithelial cells with outer membrane preparation also inhibited the adherence of these bacteria. Anti-lipopolysaccharide serum or its Fab (IgG) fragment did not inhibit adherence of V. parahaemolyticus. Moreover, pre-treatment of rabbit intestinal epithelial cells with lipopolysaccharide did not inhibit adherence of these strains. These results suggest that outer membrane proteins of V. parahaemolyticus play an important role in the adherence of Kanagawa-positive strains to rabbit intestinal epithelial cells.

Animals↗
PubMed1995

Ligation of endothelial alpha v beta 3 integrin increases capillary hydraulic conductivity of rat lung.

Complement-mediated pulmonary edema results from increases in lung capillary hydraulic conductivity (Lp), possibly by receptor-mediated mechanisms. We considered the Lp effects of vitronectin and the vitronectin-containing complement complex SC5b-9, which ligate the integrin alpha v beta 3. Vitronectin, SC5b-9, and SC5b-9-enriched zymosan-activated serum all rapidly increased Lp, as determined by the split-drop technique in single lung capillaries of rat lung. The Lp increases were inhibited by a monospecific (LM609) and a polyclonal (R838) antibody against the alpha v beta 3 integrin but not by an irrelevant monoclonal antibody isotype matched with LM609, by a monoclonal antibody against the alpha v beta 5 integrin, or by preimmune rabbit serum. Vitronectin monomers failed to increase Lp. The tyrosine kinase blockers genistein and methyl 2,5-dihydroxycinnamate caused significant concentration-dependent inhibitions of Lp increases due to vitronectin and zymosan-activated serum. By contrast, the protein kinase C blocker calphostin C had no major effect. We conclude that (1) multivalent ligation of the luminally located alpha v beta 3 integrin of lung capillary endothelium increases transcapillary liquid flux, and (2) the dominant signal transduction pathway for this effect occurs through tyrosine kinase activation.

Animals↗
PubMed1995

Susceptibility status of Phlebotomus argentipes to DDT, dieldrin and malathion in Hoogly, West Bengal.

Susceptibility tests were carried out with DDT (4%), dieldrin (0.4%) and malathion (5%) using the WHO test kits against Phlebotomus argentipes sandflies collected from Dankuni, situated in Hoogly district, 21 km from Calcutta, West Bengal. P. argentipes was found to be susceptible to all the three insecticides tested. LT 50 was calculated to be 10.6 minutes, 10.2 minutes and 2.8 minutes for DDT, dieldrin and malathion against the flies.

Animals↗
PubMed1994

Endometrial ossification: a cause of secondary infertility. Report of two cases.

Two cases of endometrial ossification with secondary infertility are reported; pelvic ultrasonography suggested an intrauterine foreign body in one case. Hysteroscopy was necessary to make the correct diagnosis and to remove the bony fragments from the two cases. One patient conceived naturally after the bony fragments were removed.

Abortion, Induced↗
PubMed1994

Diameters of juxtacapillary venules determined by oil-drop method in rat lung.

We report a new method for precise quantification of lung microvascular diameter. Isolated blood-perfused rat lungs (500-g Sprague-Dawley rats) at constant inflation pressure [alveolar pressure (PA)] and stopped blood flow were viewed by microscopy and video. Subpleural venules of the second and third postcapillary generations were microinjected with oil colored with Sudan Black. Vascular pressure (Pvas) was varied in steps, and at each step the horizontal diameter (DH) and the length of the oil-filled segment were determined by microcaliper measurements of the replayed video image. At PA = 5 cmH2O, a decrease in Pvas from 25 to 0 cmH2O decreased DH in the second-generation venules from 55 +/- 2 (SE) to 41 +/- 1 microns (n = 13) and in the third-generation venules from 96 +/- 6 to 73 +/- 6 microns (n = 6). The constant-volume oil-filled segment conformed to the cylinder formula in that decreases in DH correlated linearly with 1/ square root of length, thereby indicating that at all Pvas values venular geometry was constant and probably circular in cross section. The decrease in Pvas to -5 cmH2O did not further decrease DH. At Pvas = 10-25 cmH2O, an increase in PA to 15 cmH2O did not significantly increase DH, although the increase in PA did diminish the slope (compliance) of the DH-Pvas relationship in second- but not third-generation venules. We conclude that 1) lung expansion decreases compliance of juxtacapillary venules, 2) venules retain circular cross sections at Pvas between -5 and 25 cmH2O, and 3) venules are patent at subzero Pvas.

Animals↗