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Biomedical subjects

R Qureshi

Publications and source records attributed to R Qureshi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Diabetes in pregnancy in Pakistani women: prevalence and complications in an indigenous south Asian community.

The aim of this study was to determine the prevalence and complications as well as to correlate maternal and fetal outcome with glycaemic control, in a community of Pakistani women. This was a retrospective study of 6830 deliveries over a 5-year period in a tertiary care hospital in Karachi. Either a 75 g glucose tolerance test or a screening 50 g glucose challenge was administered depending on risk factors for Gestational Diabetes Mellitus (GDM). Case records of deliveries during this period were analysed for presence of GDM or pre-existing diabetes; glycaemic control and complications were ascertained for those with diabetes. During this period 267 (3.9%) of the 6380 deliveries were identified as diabetic pregnancies. Of these 223 (3.3%) had GDM and 44 (0.6%) women had pre-existing diabetes mellitus. Overall maternal complications were high; pre-eclampsia (19%), polyhydramnios (4.6%), and threatened abortion (3.4%). Fetal complications of macrosomia (13.1%), intrauterine growth retardation (7.1%), intrauterine deaths (5.3%) were noted. Complications were higher in poorly controlled groups. We conclude that the prevalence of GDM in Pakistani women in our study was comparable to their Western counterparts but complication rates were higher, possibly due to poorer glycaemic control.

Adult↗
PubMed1991

Mast cells are critical for the production of leukotrienes responsible for neutrophil recruitment in immune complex-induced peritonitis in mice.

Mast cells are secretory cells strategically located in the vicinity of blood vessels where they can readily initiate and modulate various inflammatory processes, including plasma exudation and leukocyte infiltration. We have previously shown that 50% of the neutrophil influx during immune complex peritonitis in mice is due to mast cells. Eicosanoids are important mediators of various inflammatory processes including neutrophil infiltration. The possibility that mast cells are essential for the production of leukotrienes (LT) involved in the elicitation of neutrophils in immune complex peritonitis was investigated in mast cell-deficient, WBB6F1-W/WV, and normal, WBB6F(1-)+/+, mice. The time course and amounts of immunoreactive PGE2, 6-keto-PGF1 alpha, and TX3B2 released into the peritoneal exudates were similar in both sets of mice. LTB4 and LTC4 levels, however, were twofold higher in +/+ than in W/WV mice 2 h after stimulation. HPLC analysis of the peritoneal exudate confirmed the presence of leukotrienes. The 5-lipoxygenase inhibitor A-63162 blocked leukotriene production in a dose-dependent manner in both sets of mice. However, this compound caused a significant reduction (60%) of neutrophil infiltration only in WBB6F(1-)+/+ but not in the mast cell-deficient mice. Mast cell reconstitution of WBB6F1-W/WV mice restored the effect of A-63162 on PMN recruitment. These data suggest that mast cells in the vicinity of blood vessels are important for the synthesis of leukotrienes responsible for PMN recruitment.

Acetamides↗
PubMed1990

The importance of mast cells for the neutrophil influx in immune complex-induced peritonitis in mice.

The role of mast cells in polymorphonuclear leukocyte (PMN) influx in Ag-antibody complex-induced peritonitis was evaluated in mast cell-deficient WBB6F1-W/Wv (W/Wv) mice and their normal littermates, WBB6F1-+/+ (+/+). Peritoneal cell influx was evaluated after i.p. injection of preformed immune complexes. The first significant elevation in the PMN count over PBS-treated controls in +/+ mice was observed 2 h after stimulation. During the period of maximum leukocyte concentrations (6 to 10 h), the increase in total cell count was 5-fold and in PMN 25-fold. In W/Wv mice the PMN influx started 2 h later than in the +/+ mice, and the maximum response (8 to 10 h) was only 50% of that in controls. Reconstitution of mast cells in W/Wv mice for 2 wk or more restored the PMN response to immune complexes. Mast cell release due to AG-antibody complexes was evaluated by measuring fluorescence intensity after berberine sulfate staining for heparin in mast cells from unstimulated as well as stimulated +/+ mice. There was a significant decrease in fluorescence intensity as early as 15 min after stimulation. By 30 min the fluorescence intensity had declined by 65%. This indicates extensive mast cell release that started before PMN mobilization. These experiments demonstrate that mast cells make a significant contribution to immune complex-induced inflammation.

Animals↗
PubMed1990

Serum cholesterol in neonates and their mothers. A pilot study.

Reports from the Aga Khan University indicate that 58% of 400 school children studied had undesirably high serum cholesterol levels. The present study was undertaken to determine whether the high cholesterol levels are present at birth and to determine the relationship between cord blood, maternal blood cholesterol and maternal diet. Cord blood from 58 neonates and fasting venous blood from 45 mothers were analyzed from total serum cholesterol. Mothers were interviewed regarding their usual diet during pregnancy. Mean cord blood cholesterol was 56.90 mg/dl (range 26 to 123 mg/dl). Mean maternal blood cholesterol was 232.4 mg/dl (range 141-382 mg/dl). Mean maternal intake of cholesterol was 457 mg (recommended level less than or equal to 300 mg/day). There was no significant co-relation between cord blood cholesterol and maternal blood cholesterol or maternal intake of cholesterol. Eighteen percent of the mothers reported a strong family history of hypercholesterolemia and/or heart disease, but this genetic tendency was not observed in the blood cholesterol level at birth indicating that environmental factors namely diet may have a prime role in determining serum cholesterol levels in childhood.

Cholesterol↗
PubMed1988

The role of mast cells in thioglycollate-induced inflammation.

The possible role of mast cells in the initiation of inflammation was studied in genetically mast cell-deficient mice, WBB6F1-W/Wv. Inflammation was induced by i.p. injection of thioglycollate. The influx of neutrophils was markedly delayed in WBB6F1-W/Wv mice as compared to the WBB6F1-+/+, mice (congeneic controls). At the time (14 h) of maximum influx of neutrophils in WBB6F1-+/+ mice, thioglycollate caused a 3-fold increase in the total cell number in the peritoneal lavage fluid, and the neutrophil count was elevated 14-fold. At the same time point in W/Wv mice, the total cell number in the peritoneal lavage fluid was not increased significantly and the neutrophils were increased only three- to four-fold. Not only was the neutrophil influx in WBB6F1-W/Wv mice delayed, but the length of time during which the neutrophil count was elevated in the peritoneal fluid was significantly shortened. Transfer (i.p.) of mast cells cultured from the bone marrow of congeneic controls corrected the delay in the neutrophil influx. The magnitude of the neutrophil influx in WBB6F1-W/Wv mice was equivalent to that of congeneic controls 9 days after mast cell repletion. Histologic studies were performed to follow the migration and differentiation of mast cells after adoptive transfer into WBB6F1-W/Wv mice. No connective tissue mast cells could be identified on day 9 when the inflammatory reaction was restored. Migration of mast cells into the tissue, as studied in the cecum, progressed steadily. On day 9 after adoptive transfer, the mast cell number was 38% of congeneic controls. Therefore, the increase in thioglycollate-induced neutrophil influx in WBB6F1W/Wv mice after mast cell repletion seemed to be correlated, at least to some extent, with the migration of mast cells into tissues and not with differentiation into connective tissue mast cells. However, a certain maturation and differentiation may have occurred. These results suggest that mast cells play an important role, although they do not seem to be the only cell type responsible for the initiation of inflammation.

Animals↗
PubMed1988

Role of leukotrienes in vascular changes in the rat mesentery and skin in anaphylaxis.

The role of leukotrienes and other mediators of vascular changes in anaphylaxis were studied in rats sensitized with monoclonal anti-DNP IgE and challenged with DNP-BSA. Microvascular changes in the mesentery were followed by intravital fluorescent microscopy and in the skin by exudation of Evans blue dye. Administration of Ag i.v. caused a marked increase in the peristaltic movement of the intestine, plasma exudation, and arteriolar constriction in the mesentery. The microvascular changes were accompanied by a profound fall in blood pressure, which was biphasic. The first phase lasted for approximately 2 min. The second phase was very prolonged and the hypotension was still maintained 40 min after Ag challenge. The changes observed were dose dependent with regard to Ag. Intradermal application of Ag resulted in dose-dependent extravasation of Evans blue dye in the skin. Plasma exudation was partially inhibited by pyrilamine and methysergide. However, their effect seemed to be more pronounced in the skin than in the mesentery. The leukotriene D4-R antagonist L-649,923 and the 5-lipoxygenase inhibitor ONO-LP-049, alone or in combination with other inhibitors, did not alter the plasma leakage in the skin. In the mesentery, the leukotriene antagonists alone had a moderate effect on vascular permeability. However, the combination of these agents with pyrilamine completely inhibited macromolecular extravasation. The hypotension was modulated by the antihistamines as well as the leukotriene and serotonin antagonists. Pyrilamine inhibited the first phase and the second phase. The major effect of methysergide was a decrease in the duration of the hypotension. This was especially evident when it was administered in combination with other inhibitors. The leukotriene antagonists when given alone had moderate effects on the blood pressure changes. However, in combination with pyrilamine, the hypotension was substantially reduced. Leukotrienes appeared to be important mediators of the vascular changes in the mesentery but not in the skin (passive cutaneous anaphylaxis). They markedly potentiated the action of histamines.

Animals↗
PubMed1985

Neutral and acidic species of human intestinal mucin. Evidence for different core peptides.

Highly purified human mucins from postmortem intestinal tissue were fractionated on anion exchange columns to generate separate neutral and acidic species. The neutral mucin (less than 1.0 mol % sialic acid) was the major species (greater than 80% by weight) and contained a higher molar proportion of fucose, galactose, and N-acetylglucosamine, and a lower proportion of sialic acid and N-acetylgalactosamine than the acidic species (greater than 10 mol % sialic acid). Amino acid analyses revealed a highly significant enrichment in serine, aspartate, and alanine in the neutral species and proline, threonine, and glycine in the acidic species. Thiol reduction of each species to remove their integral 118,000-dalton component did not alter the essential interspecies differences. Differences in threonine, proline, and serine also remained after removal of all "naked" or pronase-susceptible peptide regions from each species. These results indicate that neutral and acidic mucins contain glycopeptide segments exclusive of their 118,000-dalton and naked peptide components, which differ in amino acid composition. The key amino acid markers are similar to those observed for fuco- and sialoglycopeptides obtained after proteolytic digestion of human colonic mucin by Gold et al. (Gold, D.V., Schochat, D., and Miller, F. (1981) J. Biol. Chem. 256, 6354-6358). The oligosaccharide composition of small intestinal and colonic mucin may therefore depend upon transcriptional control of the synthesis of specific mucin peptides as well as the post-translational activity of glycosyltransferases. These findings may have significance for the quality and functions of mucus produced in a variety of pathological states.

Amino Acids↗
PubMed1984

Meptazinol activity on morphine-naive and morphine-dependent guinea-pig ileum: correlation with in vivo studies.

The effects of meptazinol and some opioid agonists and antagonists were studied on opioid-naive guinea-pig ileum (GPIN) and ileum taken from morphine-dependent guinea-pigs (GPID). Meptazinol produced a biphasic effect in GPIN and GPID with a depression of the electrically induced twitch response at lower concentrations and contractural potentiation at higher concentrations. The effects of meptazinol in both GPIN and GPID were similar, thus distinguishing it from the other opioid agonists and antagonists which produced differential effects on these tissues. In morphine-pelletted rats, meptazinol (5 mg/kg i.p.) did not produce notable withdrawal as measured by behavioural observation. However, meptazinol (30 mg/kg i.p.) enhanced the signs associated with cholinergic activation. It is suggested that meptazinol possesses a cholinergic component and that the morphine-withdrawal signs observed to the higher meptazinol dose were more probably attributable to cholinergic stimulation rather than any underlying opioid-precipitated withdrawal.

Animals↗
PubMed1983

Human intestinal mucin in cystic fibrosis.

Human intestinal mucins from six subjects with Cystic Fibrosis (CF) and eight subjects without CF were prepared from tissue obtained at surgery (one case) and postmortem. Subjects were not age-matched, but the nonCF mucin was obtained from subjects with ages which bracketed those of the CF subjects. Cesium chloride analytical gradient ultracentrifugation showed that CF mucins were generally denser than nonCF mucins. Sedimentation coefficients were also higher in the CF samples. CF mucins were enriched in fucose, galactose, N-acetylglucosamine and total carbohydrate per mg protein and per oligosaccharide chain (mole/mole GalNAc). Fucose/sialic acid molar ratios were significantly higher in CF mucins, and the average oligosaccharide chain length was approximately three residues greater in CF as compared with nonCF mucins. There was no difference in amino acid profiles or the number of side chains per molecule. The mean sulfate content was higher in the CF mucins but not to a level of significance; however, in the eight mucins, sulfate content correlated positively with total carbohydrate, N-acetylglucosamine and galactose, and therefore increased with oligosaccharide chain length. CF intestinal mucin was therefore denser and more highly glycosylated than nonCF musin and probably contained more sulfate. The increase in glycosylation resulted from a rise in fucose, galactose, and N-acetylglucosamine without a concomitant rise in sialic acid.

Acetylglucosamine↗
PubMed1979

The role of disulphide bonds in human intestinal mucin.

Goblet-cell mucin (mucin 1) was isolated and purified from human small-intestinal scrapings. After application of mucin 1 to DEAE-Bio-Gel (A) columns, most of the glycoprotein (76-94% of hexoses) was eluted in the first peak (designated mucin 2). Minor amounts of acidic glycoproteins were eluted with 0.2m- and 0.4m-NaCl in later peaks. Analyses of mucin 1 and mucin 2 revealed mucin 2 to be a monodisperse highly glycosylated glycoprotein containing 6.3% by wt. of protein, N-acetylgalactosamine, N-acetylglucosamine, galactose and fucose. Mucin 1 was similar in composition, but was polydisperse and contained more protein (12.3% by wt.) as well as N-acetylneuraminic acid. Analytical CsCl-gradient ultracentrifugation showed both mucin 1 and mucin 2 to have a major component with an average buoyant density of 1.47000g/ml. Mucin 1 also contained a slightly less-dense minor glycoprotein component. After exhaustive reduction and alkylation mucin 1 retained its major component, but partly dissociated into two lighter glycoprotein components. Mucin 2, in contrast, did not change its density distribution after reduction. Band ultracentrifugation in (2)H(2)O-containing iso-osmotic buffers showed that mucin 1 contained a major fast-sedimenting component (s(o)=37+/-2S), and a minor amount of a slower-sedimenting component. After reduction there was an increased quantity of the latter component, for which an s(o) value of 14.5S was calculated. In contrast, mucin 2 was unaltered by reduction (s(o)=33+/-2S). These findings indicate that the major component of goblet-cell mucin (mucin 2) does not dissociate after S-S-bond reduction, and thus does not apparently rely for its polymeric structure on the association of subunits through covalent disulphide bonds. However, the effects of reduction on mucin 1 suggest that in the native mucin intramolecular disulphide bonds in the minor glycoproteins may stabilize their structure, permitting secondary non-covalent interactions to develop with the major dense mucin (mucin 2) protein.

Amino Acids↗