Search PubMed⌕ Search

Biomedical subjects

S Gupta

Publications and source records attributed to S Gupta.

At least 901 records · Page 50Linked to original sources
PubMed1995

Possible role of Na(+)-K(+)-ATPase in the regulation of human corpus cavernosum smooth muscle contractility by nitric oxide.

1. This study was designed to determine the role of sodium-potassium adenosine triphosphatase (Na(+)-K(+)-ATPase) in the regulation of human corpus cavernosum smooth muscle contractility by nitric oxide (NO). In addition, we determined if the modulation of Na(+)-K(+)-ATPase activity by NO is dependent on the increase in intracellular cyclic GMP concentration. 2. The effect of NO donors, sodium-nitroprusside (SNP) and S-nitroso-glutathione (S-NO-Glu), and a permeable cyclic GMP analogue, 8-bromo-cyclic GMP, on Na(+)-K(+)-ATPase activity (measured as ouabain-sensitive 86Rb-uptake) was studied in human cultured corpus cavernosum smooth muscle cells (HCCSMC). In addition, the effect of the cyclic GMP lowering agent, methylene blue, on NO-induced increase in Na(+)-K(+)-ATPase activity was studied. 3. SNP (1 microM) caused time-dependent increases in ouabain-sensitive Rb-uptake (33-72%) over 2-20 min in HCCSMC. The stimulation of ouabain-sensitive Rb-uptake by SNP was concentration-dependent (30 and 102% with 0.1 and 1 microM SNP, respectively). Similarly, significant increases in ouabain-sensitive Rb-uptake were obtained with 1 and 10 microM S-NO-Glu. In contrast, incubation of HCCSMC with 8-bromo-cyclic GMP (100 microM) did not increase ouabain-sensitive Rb-uptake. 4. S-NO-Glu induced-increase in intracellular cyclic GMP synthesis, but not the increase in ouabain-sensitive Rb-uptake, was completely inhibited by methylene blue in HCCSMC. 5. The Na(+)-K(+)-ATPase inhibitor, ouabain, caused a concentration-dependent increase in tension (0.5 to 2 fold) in tissues contracted with 15 mM KCl. SNP and S-NO-Glu caused a concentration-dependent relaxation (concentration required to cause half maximal relaxation (ED50) = 0.04 and 0.2 microM, respectively) of HCC strips contracted with 15 mM K+. Ouabain (0.1 to 10 microM) inhibited the response to SNP and S-NO-Glu by shifting the concentration-response curves to the right and preventing full smooth muscle relaxation.6. These results indicate that the activity of Na+-K+-ATPase modulates the contractility of HCC smooth muscle, and that NO stimulates Na+-K+-ATPase activity in HCCSMC independently of its ability to increase the intracellular cyclic GMP concentration. They also suggest that stimulation of Na+-K+-ATPase activity plays an important role in NO-induced relaxation of HCC smooth muscle

Cells, Cultured↗
PubMed1995

Determination of MICs for Mycobacterium avium-M. intracellulare complex in liquid medium by a colorimetric method.

We investigated the potential of a rapid colorimetric microassay based on the reduction of dimethylthiazol-diphenyltetrazolium bromide (MTT) for determining the growth of Mycobacterium avium-M. intracellulare complex (MAC) and MICs of clofazimine, resorcinomycin A, and the quinolone PD 127391 against MAC. The reduction of MTT was directly proportional to the number of viable bacteria. A comparison of the MTT reduction test with the [3H]glycerol uptake assay showed the former to possess higher analytical sensitivity for detecting MAC growth in microtiter plates. The MIT reduction test avoids the use of radioisotopes and costly material and equipment; it is reliable, reproducible, and convenient for rapid routine susceptibility testing of MAC.

Anti-Bacterial Agents↗
PubMed1995

Activation-induced T-cell death is cell cycle dependent and regulated by cyclin B.

Developing thymocytes and some T-cell hybridomas undergo activation-dependent programmed cell death. Although recent studies have identified some critical regulators in programmed cell death, the role of cell cycle regulation in activation-induced cell death in T cells has not been addressed. We demonstrate that synchronized T-cell hybridomas, irrespective of the point in the cell cycle at which they are activated, stop cycling shortly after they reach G2/M. These cells exhibit the diagnostic characteristics of apoptotic cell death. Although p34cdc2 levels are not perturbed after activation of synchronously cycling T cells, cyclin B- and p34cdc2-associated histone H1 kinase activity is persistently elevated. This activation-dependent induction of H1 kinase activity in T cells is associated with a decrease in the phosphotyrosine content of p34cdc2. We also demonstrate that transient inappropriate coexpression of cyclin B with p34cdc2 induces DNA fragmentation in a heterologous cell type. Finally, in T cells, cyclin B-specific antisense oligonucleotides suppress activation-induced cell death but not cell death induced by exposure to dexamethasone. We therefore conclude that a persistent elevation of the level of cyclin B kinase is required for activation-induced programmed T-cell death.

Amino Acid Sequence↗
PubMed1995

The British Neurological Surveillance Unit: a nation-wide scheme for the ascertainment of rare neurological disorders.

The British Neurological Surveillance Unit was set up in January 1993 with the aim of co-ordinating and improving the ascertainment of rare neurological disorders in the United Kingdom by using a system of nation-wide active surveillance. The unit provides a service for individual investigators who must first submit possible studies to a scientific advisory committee. Once accepted the condition is listed on a report card which is sent to every member of the British neurological community every month. The cards are easy to use, and all the reporting neurologist has to do is tick a box indicating whether a case has (or has not been) seen. At the end of every month the individual investigators then initiate further follow-up by contacting the reporting neurologists. In the first year of operation the scheme has assisted in the surveillance of 6 disorders and the following number of verified cases have so far been ascertained: polio in adults (n = 0); acute psychological disorders in patients with epilepsy (n = 75); Guillain-Barré syndrome in the south of England (n = 32); epilepsia partialis continua (n = 40); amyloid neuropathy (n = 12), and agenesis of the corpus callosum (n = 24). The monthly response rates are between 65 and 75%, with the eventual aim of achieving over 90% after the scheme has become more established.

Amyloid Neuropathies↗
PubMed1995

Polyarteritis nodosa presenting as perirenal hemorrhage.

Though renal involvement with microaneurysm formation is common in polyarteritis nodosa (PAN), spontaneous perirenal hematoma (SPH) is rare. We report a patient in whom SPH was the presenting manifestation of PAN. SPH is a potential life-threatening complication of PAN and its early recognition is emphasized.

Adult↗
PubMed1995

Neurological soft signs in neuroleptic-naive and neuroleptic-treated schizophrenic patients and in normal comparison subjects.

OBJECTIVE: The goal of this study was to assess neurological soft signs and developmental reflexes in schizophrenic patients who had never received neuroleptic medication and those who were receiving neuroleptic medication. METHOD: Neurological soft signs and developmental reflexes were examined in 26 schizophrenic patients who had never received a neuroleptic, 126 schizophrenic patients who were currently receiving neuroleptics, and 117 normal subjects. RESULTS: Soft signs were present in 23% of the neuroleptic-naive and 46% of the medicated schizophrenic patients. Developmental reflexes were present in 19% of the neuroleptic-naive and 12% of the medicated patients. Both soft signs and developmental reflexes were absent in the normal subjects. There were significant differences between patients and normal subjects in neurological soft signs and developmental reflexes. The possibly confounding variables of age, age at onset, duration of illness, number of hospitalizations, Abnormal Involuntary Movement Scale (AIMS) scores, and Simpson-Angus Scale extrapyramidal symptom scores were assessed by using logistic regression in the patients who were receiving neuroleptics. AIMS scores and Simpson-Angus Scale scores correlated with soft signs in these patients. CONCLUSIONS: The presence of neurological soft signs in schizophrenic patients who had never received neuroleptics indicates that these signs are present independent of medication effects, but it is possible that neuroleptics contribute to the prevalence of these abnormalities, as demonstrated by the patients who were receiving neuroleptics.

Adult↗
PubMed1995

Lipid profile in the first-degree relatives of patients with precocious coronary heart disease in Rohtak area (Northern India).

Twenty-five patients with precocious coronary heart disease (CHD) (aged forty years or less) and 82 first-degree relatives were studied for lipid profile. Eighty-eight age- and sex-matched controls were also studied. The mean serum cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, and total cholesterol/high density lipoprotein cholesterol of patients and their first-degree relatives were significantly higher as compared with normal controls. High density lipoprotein cholesterol values were found to be almost identical in the patient group, their first-degree relatives, and normal controls. Hyperlipidemia was found in 68% of patients with CAD, of their first-degree relatives, and 24% of controls. Almost all lipid fractions in relatives of hyperlipidemic patients paralleled those of the patients suffering from CHD. Of 25 families studied, 16 had hyperlipidemia. In conclusion, it can be stated that there is a statistically significant hyperlipidemia in young patients with CHD that has a significant familial clustering, thus delineating a group of high-risk individuals (first-degree relatives of young coronary patients) for possible primary prevention of CHD. This familial clustering could be due to genetic or environmental factors; however, the relative contribution of these two factors requires further investigation.

Adolescent↗
PubMed1995

Role of protein kinase beta isozyme in multidrug resistance in murine leukemia P388/ADR cells.

To define a role of protein kinase C (PKC) in multidrug resistance (MDR), we examined the influence of PKC isozyme specific antibodies delivered intracellularly, on drug sensitivity and drug accumulation in P388/ADR cells. Drug sensitive (P388) and drug resistant (P388/ADR) cells were permeabilized at 4 degrees C with L-lysolecithin and were incubated with rabbit anti-PKC, alpha, beta antibodies, or normal rabbit serum for 10 minutes at 37 degrees C. Daunorubicin (DNR) accumulation and drug sensitivity were studied by flow cytometry and MTT assay, respectively. Anti-PKC beta antibody partially corrected drug accumulation defect and completely reversed resistance to DNR. Anti-PKC alpha antibody had no effect on either parameter of MDR. These results suggest that PKC beta plays an important role in MDR in P388/ADR cells. Furthermore, the technique of intracellular delivery of antibodies provides a new approach to discern the role of PKC isoforms in multidrug resistance in various tumor cells.

Animals↗
PubMed1995

Thyroid-stimulating hormone activates phospholipase D in FRTL-5 thyroid cells via stimulation of protein kinase C.

We studied whether TSH or phorbol myristate acetate (PMA) stimulates the hydrolysis of phospholipids, predominantly phosphatidylcholine, via phospholipase D (PLD) in FRTL-5 thyroid cells and whether this occurs as a consequence of protein kinase C (PKC) activation. FRTL-5 thyroid cells were labeled with [3H]myristate followed by incubation with 200 mM ethanol before the addition of agonist. PLD activity was assessed by the measurement of [3H]phosphatidylethanol from [3H]phospholipid (predominantly [3H]phosphatidylcholine). Compared to control values, bovine TSH (100 microU/ml) increased PLD activity by 480% and 600%, respectively, after 30 and 60 min of exposure. Studies with purified human and bovine TSH revealed similar results, indicating that this effect was due to TSH itself. PMA (100 nM) increased PLD activity at 10 min (630% of the control value), and this effect persisted up to 60 min (600% of the control value). To determine whether the effects of TSH on PLD occurred as a consequence of PKC activation, FRTL-5 thyroid cells were preincubated with the PKC inhibitor, chelerythrine (1 microM for 10 min), or were pretreated for 24 h with PMA (100 nM) to down-regulate PKC. PLD stimulation by TSH and PMA was largely abolished by such treatments. These studies indicate that in FRTL-5 thyroid cells, TSH and PMA are capable of stimulating PLD, and that PKC activation is responsible for this stimulation. The role of PLD activation could be to amplify and prolong the PKC signal by further production of diacylglycerol.

Animals↗
PubMed1995

P-glycoprotein expression and regulation. Age-related changes and potential effects on drug therapy.

P-Glycoprotein is a member of a superfamily of adenosine triphosphate-binding cassette transporter proteins and plays an important role in multidrug resistance in cancer cells. P-Glycoprotein is known to transport a wide variety of substances ranging from ions to peptides. P-Glycoprotein is expressed on a variety of normal cells, however its physiological function is unclear. The apical and polar distribution on secretory cells suggests a secretory role for P-glycoprotein. More recently, cells of the immune system have been shown to express P-glycoprotein. There is evidence to suggest that P-glycoprotein may play a role in the secretion of certain cytokines (especially those lacking signal sequence) and cytotoxic molecules. In this article, the basic structure, gene regulation and expression of P-glycoprotein are reviewed. Furthermore, age-related changes in the expression of P-glycoprotein and potential effects on drug therapy in the elderly are discussed.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Exacerbation of nickel induced oxidative response by vitamin E.

Vitamin E (alpha-tocopherol), a well known naturally occurring chain breaking antioxidant and a free radical scavenger was found to exacerbate nickel (Ni) toxicity in mice. Vitamin E (Vit. E) mediated enhancement of nickel toxicity was demonstrated by (i) enhanced mortality in mice treated with Ni and Vit. E (ii) increased hepatic lipid peroxidation, (iii) increased rate of benzoate hydroxylation, and (iv) liposomal membrane damage.

Animals↗
PubMed1995

Efficacy of liposome encapsulated triethylenetetraamine hexaacetic acid (TTHA) against cadmium intoxication: role of lipid composition.

Efficacy of Triethylenetetraamine hexaacetic acid (TTHA) encapsulated in liposomes having different lipid compositions was examined in animals pre-exposed to cadmium. Mice were injected with cadmium as cadmium (II) chloride 0.5 mg/kg b. wt. intraperitoneally daily for five days. Four weeks after the last injection of cadmium they were administered three injections of TTHA encapsulated in liposomes composed of either phosphatidyl choline:cholesterol (PC:Chol) or sphingomyelin:cholesterol (SM:Chol) in 1:1 molar ratio at a gap of 48 h. Urinary and fecal elimination of cadmium and its distribution in liver, kidneys and spleen were examined. Treatment with TTHA encapsulated in liposomes mobilized higher amount of cadmium from liver and spleen. The overall efficiency for cadmium mobilization was better in TTHA encapsulated in SM:Chol liposome treated group which also led to enhanced excretion of cadmium through urine and feces. The results indicate that TTHA encapsulated in SM:Chol liposomes exhibited highest efficacy in mobilizing cadmium from the body of pre-exposed mice followed by PC:Chol liposomes and the free drug.

Animals↗
PubMed1995

Migratory polyarthritis associated with Plesiomonas shigelloides infection.

Migratory polyarthritis was observed in a child with Plesiomonas shigelloides infection of the gastrointestinal tract. All symptoms and signs of arthritis resolved following successful treatment of infection with the appropriate antibiotic. Plesiomonas shigelloides should be added to the list of microbial agents associated with polyarthritis.

Anti-Bacterial Agents↗