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Biomedical subjects

S Ghosh

Publications and source records attributed to S Ghosh.

At least 955 records · Page 53Linked to original sources
PubMed1983

A quantitative study of muscle spindles and tendon organs in some intrinsic muscles of the hand in the bonnet monkey (Macaca radiata).

The number and density of muscle spindles and tendon organs have been determined in the following intrinsic muscles of the hand of bonnet monkeys: I lumbrical, II lumbrical, abductor digiti minimi, adductor pollicis, and I dorsal interosseous. All these muscles were found to be very rich in muscle spindles (17.6 to 42.31 per gram wet weight) but relatively poor in tendon organs (0.606 to 10.06 per gram wet weight). The lumbricals have very few tendon organs. The possible functional significance of these findings has been discussed.

Animals↗
PubMed1983

Ag-NOR staining in mouse sarcoma ascites cells.

In sarcoma cells, the nucleoli are small, ill-defined, and are present in large numbers making it difficult to stain them by classical staining procedures. A modified Ag-NOR technique has been applied to detect the nucleolus and the nucleolar-organizing region in the chromosome of a mouse sarcoma-180 ascites cell-line. The cells were found to have 8-14 nucleolar chromosomes. The nucleoli are present in varying numbers corresponding to the number of nucleolar chromosomes. Silver grains appear as dots at one end of the chromosome. This end is presumed to be the centromeric end as, in normal mice, the NORs are in association with the centromere. However, the centromeres are ATrich, whereas the NORs should be GCrich. This NORs in mouse chromosomes should be placed below the centromere as already shown by the nucleic acid hybridization technique.

Animals↗
PubMed1983

Mechanism of endotoxin-induced reduction in the number of beta-adrenergic receptors in dog livers: role of phospholipase A.

The role of phospholipase A on the endotoxin-induced reduction in the number of beta-adrenergic receptors in dog liver plasma membranes was investigated. The results show that digestion of control liver plasma membranes with exogenous phospholipase A2 (0.2 unit/200 micrograms protein) decreased the specific binding of (-)-[3H]dihydroalprenolol by 37.3% (P less than 0.01) and reduced the number of receptor sites by 31.7% (P less than 0.05). These decreases in the specific binding and the number of beta-adrenergic receptors were completely reversible by the addition of phosphatidylcholine (0.2 mM). Endotoxin administration (2 hr postendotoxin) decreased the specific binding by 36% (P less than 0.05) and reduced the number of beta-adrenergic receptors by 33% (P less than 0.05), and these decreases were completely reversible by the addition of 0.2 mM phosphatidylcholine. Digestion of control liver membranes with exogenous phospholipase A2 decreased phosphatidylcholine and phosphatidylethanolamine levels by 50.6 and 51.2%, respectively, but increased lysophosphatidylcholine and lysophosphatidylethanolamine levels by 12- and 8.4-fold, respectively. Endotoxin administration decreased phosphatidylcholine and phosphatidylethanolamine contents by 21.4 and 23.8%, respectively, but increased lysophosphatidylcholine and lysophosphatidylethanolamine contents by 2.1- and 1.4-fold, respectively. In addition, endotoxin administration increased endogenous phospholipase A activity by 73.5%. Based on these results, it is suggested that the decreases in the specific binding and the number of beta-adrenergic receptors in dog livers during endotoxic shock are a result of phospholipase A activation.

Animals↗
PubMed1983

Changes in alpha-adrenergic receptors in dog livers during endotoxic shock.

The effects of endotoxin administration on alpha-adrenergic receptors in dog liver plasma membranes were studied using [3H]dihydroergocryptine as a radioactive ligand. The Scatchard analysis revealed a two-component binding characteristic both in control and endotoxin-injected dogs. The Kd (dissociation constant) of the high-affinity component was increased by 32.5% (0.4 +/- 0.04 nM for control vs 0.53 +/- 0.06 nM for endotoxic; P less than 0.05) with no significant change in the Kd for the low-affinity component (3.0 +/- 0.44 nM for control vs 3.4 +/- 0.44 nM for endotoxic) 2 hr following endotoxin administration. The maximum binding capacity of the high-affinity component was decreased by 38.1% (460 +/- 19.3 and 285 +/- 14.8 fmole/mg protein for control and endotoxic, respectively; P less than 0.01) and that of the low-affinity component was decreased by 34.2% (1050 +/- 66.4 and 690 +/- 44.6 fmole/mg protein for control and endotoxic, respectively; P less than 0.05) 2 hr after endotoxin injection. The competitive inhibition studies show that the apparent Kd values for (-)-epinephrine, (-)-norepinephrine, and prazosin were increased 15, 13, and 25 times, respectively, with no significant change in the apparent Kd values for yohimbine or phentolamine 2 hr postendotoxin. These data demonstrate that the binding affinity of the high-affinity component and the number of alpha-adrenergic receptor binding sites were decreased in endotoxic shock. A modification of the alpha-adrenergic receptors in dog livers induced by endotoxin administration may play an important role in the development of hepatic glucose dyshomeostasis during shock.

Animals↗
PubMed1983

Perinatal mortality--report of a hospital based study.

The perinatal mortality rate (PNMR) per 1000 births is reported in 27,394 consecutive births. It was 75.6, of which 40.0 were neonatal deaths and 35.6 were fetal losses. The PNMR was significantly higher at the two extremes of maternal age, in parity five and above, and with a previous history of fetal or neonatal loss. Other maternal contributing factors were antepartum haemorrhage, hydramnios and infections. One-third of the babies weighed 2500 g or less. The PNMR dropped precipitously from 340.48 in the birth weight group 1501 to 2000 g, to 46.6 in the group 2001 to 2500 g, indicating a cut-off point at 2000 g for a baby at high risk needing special care. The common necropsy causes of death were asphyxia (24.33%), pulmonary conditions (20.02%), congenital malformations (13.6%), and infections (6.19%). No cause of death could be detected at necropsy in 22.12% and no clinico-pathological cause of death could be assigned in 26.76% of deaths. A majority of deaths due to asphyxia could have been prevented by better antenatal and intranatal care. Low birth weight was an important cause of perinatal deaths, and better maternal nutrition and antenatal care could play an important role in reducing this.

Birth Weight↗
PubMed1983

Idiopathic autoantibody that inhibits fibrin monomer polymerization.

A 73-year-old female was found to have prolonged thrombin and reptilase times in the immediate post-operative period. These abnormalities were not corrected by the addition of normal plasma. They were subsequently shown to be due to an IgG immunoglobulin which inhibited fibrin monomer polymerization. The IgG immunoglobulin activity could be neutralized completely by prior incubation with either patient or normal fibrinogen, uncrosslinked fibrin monomers or IgG antisera. No inhibitory effect on thrombin activity, fibrinopeptide A release or on the fibrin cross-linking reaction of factor XIIIa could be detected. Purified patient fibrinogen was functionally normal as demonstrated by normal fibrinogen-fibrin polymerization and fibrinopeptide A release. No underlying cause for this phenomenon was found. The presence of the inhibitor was associated with excessive blood loss during the post-operative period.

Aged↗
PubMed1983

Quantitative quality control of antiglobulin reagents.

Double antibody radioimmunoassays have been developed for the quantification of anti-IgG, anti-C3, anti-C3c, anti-C3d and anti-C4 antibodies and for the determination of their binding constants. Assays were undertaken on 53 polyspecific antiglobulin reagents obtained from a variety of commercial and public sources. Concentrations of anti-IgG varied from 1.2 to 12.8 micrograms/ml in commercial products and from 0.4 to 6.0 micrograms/ml in public products. Concentrations of anti-C3 and anti-C3c varied from 0.1 to 1.0 micrograms/ml in most commercial products but in public products concentrations varied by more than 100-fold from 0.02 to 6.5 micrograms/ml. Concentrations of anti-C3d varied from 0.05 to 0.7 micrograms/ml in most commercial products and from less than 0.01 to 1.3 micrograms/ml in public products. Concentrations of anti-C4 varied from less than 0.01 to 0.18 micrograms/ml in commercial products and from less than 0.01 to 0.08 micrograms/ml in public products. Mean binding constants for commercial products were: anti-IgG 6.6 x 10(9) l/mol, anti-C3 4.6 x 10(9) l/mol, anti-C3c 5.3 x 10(9) l/mol, anti-C3d 0.4 x 10(9) l/mol and anti-C4 4.9 x 10(9) l/mol. Relationships were found between results obtained in quantitative assays of specific antibodies and independently performed serological assessments of potency. Anti-IgG was present in suboptimal concentrations for agglutination in several public products and anti-C3 and anti-C3c were in suboptimal concentrations for agglutination in many public and commercial products.

Antibodies, Anti-Idiotypic↗
PubMed1983

Changes in beta-adrenergic receptors in dog livers during endotoxic shock.

The effects of endotoxin administration on beta-adrenergic receptors in dog liver plasma membranes were studied using [3H]dihydroalprenolol as a radioactive ligand. The Scatchard analysis revealed a one-component binding characteristic both in control and endotoxin-injected dogs. The Kd (dissociation constant) value was increased by 60% (4.2 +/- 0.5 nM for control vs. 6.7 +/- 0.5 nM for endotoxic; P less than 0.01) and the Bmax (maximum binding capacity) was decreased by 38% (600 +/- 60 and 370 +/- 70 fmol/mg protein for control and endotoxic, respectively; P less than 0.01) 2 h following endotoxin administration. The competitive inhibition studies show that the apparent Kd values for (-)-isoproterenol, (-)-epinephrine, and (-)-norepinephrine were increased by 14, 51, and 5 times, respectively, 2 h postendotoxin. In addition, endotoxin in vitro had a dose-dependent inhibitory effect on the specific binding of [3H]dihydroalprenolol, and it also reduced the number of beta-receptors. These data demonstrate that endotoxin, both in vivo and in vitro, decreased the binding affinity and the number of beta-adrenergic receptors in dog liver plasma membranes. A modification of the beta-adrenergic receptors in dog livers induced by endotoxin administration may play an important role in the development of hepatic glucose dyshomeostasis during shock.

Animals↗
PubMed1983

Decrease in adenylate cyclase activity in dog livers during endotoxic shock.

The effects of endotoxin administration on adenylate cyclase in dog liver plasma membranes were studied. The basal, fluoride-, guanine nucleotide-, isoproterenol-, and glucagon-stimulated adenylate cyclase activities were decreased by 61, 62, 69, 83, and 63%, respectively, 2 h after in vivo administration of endotoxin. Endotoxin (100 micrograms/ml) in vitro decreased the guanine nucleotide-, isoproterenol-, and glucagon-stimulated adenylate cyclase activities by 24, 25, and 21%, respectively. These data demonstrate that endotoxin administered in vivo or in vitro had an inhibitory effect on the adenylate cyclase enzyme system in dog liver plasma membranes. Because of the involvement of the adenylate cyclase-adenosine 3',5'-cyclic monophosphate (cAMP) system in the regulation of hepatic carbohydrate metabolism, the finding that endotoxin administration decreased adenylate cyclase activity in the liver should contribute to the understanding of the pathophysiology of altered hepatic glucose homeostasis during shock.

Adenylyl Cyclases↗
PubMed1983

Chronic inflammatory bowel disease, deep-venous thrombosis and antithrombin activity.

Of 34 patients with chronic inflammatory bowel disease (CIBD), 4 developed well-documented episodes of deep-venous thrombosis. All 4 patients had active disease at the time of thrombosis. This group was studied to determine if the tendency to deep-venous thrombosis in patients with CIBD was associated with reduced antithrombin activity by measuring the concentration of three thrombin inhibitors, antithrombin III (AT III), alpha 2-macroglobulin (alpha 2 M) and alpha 1-antitrypsin. 2 patients had low AT III levels and 10 had low alpha 2 M levels. 2 patients who developed deep-venous thrombosis had significantly low levels of both AT III and alpha 2 M. It is suggested that in patients with diseases predisposing to thrombosis and associated with low AT III levels, the measurement of alpha 2 M in addition to AT III may predict those particularly at risk.

Antithrombin III↗