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Biomedical subjects

R K Gupta

Publications and source records attributed to R K Gupta.

At least 433 records · Page 24Linked to original sources
PubMed1991

An efficient method for production of purified inactivated Japanese encephalitis vaccine from mouse brains.

The efficiency of production of purified Japanese encephalitis (JE) vaccine from mouse brains was increased by reprocessing the brain material after recovery of the virus and by pooling of a few extra fractions after zonal ultracentrifugation. By the routine production method, one mouse yielded approximately 2.5 doses of the vaccine while the improved method gave about five doses from each mouse. All the batches of purified JE vaccine made by improved technology passed all the quality control tests as specified by the Minimum Requirements for biological products of the Japanese Government and World Health Organization.

Animals↗
PubMed1991

Determination of circulating antibodies directed to pertussis toxin and of agglutinogens in children vaccinated with either the whole cell or component pertussis vaccine in France, Japan and Senegal.

The antibody response to pertussis toxin (PT) and agglutinogens of children vaccinated in Japan, France and Senegal with either whole cell or component pertussis vaccine was determined at various times after immunization. Agglutinin titres were almost similar in sera of Japanese children vaccinated with either whole cell or component pertussis vaccine whereas anti-PT antibody levels were found to be higher after vaccination with whole cell vaccine than with component vaccine. The geometric mean (GM) agglutinin titres in sera of Japanese children amounted to 45.0 and 45.7, respectively, and neutralization GM titres to 71.6 and 22.6, respectively, following vaccination with the whole cell and component pertussis vaccines. Sera of French children receiving three doses of whole cell vaccine exhibited a GM agglutinin titre of 17.8, whereas only 16% of sera contained neutralizing antibodies against PT. Following the booster dose the GM agglutinin titre rose to 213.5 and 68% of the sera contained neutralizing antibodies to PT (GM titre 48.0). Sera of Senegalese children receiving three doses of whole cell vaccine exhibited a GM agglutinin titre of 18.7, whereas anti-PT neutralizing antibodies were hardly detected. Agglutinins and anti-PT antibody in sera of French and Senegalese children turned out to be lower than were found 25 years ago in sera of children immunized with the French whole cell pertussis vaccine.

Adolescent↗
PubMed1991

Adverse reactions after injection of adsorbed diphtheria-pertussis-tetanus (DPT) vaccine are not due only to pertussis organisms or pertussis components in the vaccine.

Reactions to adsorbed diphtheria-pertussis-tetanus (DPT) vaccine have mostly been attributed to the pertussis organisms or pertussis components in the vaccine. Nevertheless reactions may also be due to other factors such as sensitization induced by aluminium adjuvants and impurities present in crude toxoids that cannot be removed by purification of toxoids after formalinization. Aluminium compounds such as aluminium phosphate and aluminium hydroxide are the most commonly used adjuvants with vaccines for human use. Due to the increasing concern about the toxicity of aluminium, other adjuvants like calcium phosphate may be evaluated as an alternative to aluminium adjuvants. To minimize reactions after immunization with DPT vaccine due to impurities in the toxoids, the use of toxoided purified toxins is suggested.

Adsorption↗
PubMed1991

Intracellular free magnesium and high energy phosphates in the perfused normotensive and spontaneously hypertensive rat heart. A 31P NMR study.

We have employed 31P nuclear magnetic resonance (NMR) spectroscopy to examine the relationship between cytosolic free Mg2+ ([Mg2+]in), intracellular pH, high energy phosphates, and genetic hypertension using the Wistar-Kyoto rat (WKY) as a control and the spontaneously hypertensive rat (SHR) as a model for essential hypertension. The mean systolic blood pressures (measured using the tail cuff method) of control and hypertensive rats (aged 7 to 12 weeks) were 113 +/- 4 mm Hg (mean +/- 2 SE, n = 14) and 162 +/- 5 mm Hg (mean +/- 2 SE, n = 17), respectively. Intracellular free Mg2+ levels were significantly depleted in the isolated Langendorff perfused hypertensive rat hearts (452 +/- 39 mumol/L, mean +/- 2 SE, n = 17) compared to control hearts (756 +/- 52 mumol/L, n = 14); however, intracellular pH did not differ in the SHR hearts (7.02 +/- 0.03, mean +/- 2 SE, n = 7) compared with controls (7.03 +/- 0.03, n = 7). Although we could not demonstrate a statistically significant difference in the levels of P-creatine or ATP, intracellular Pi was two-fold higher (5.71 +/- 2.28 mmol/L v 2.92 +/- 0.66 mmol/L, n = 4) and the phosphorylation potential, [MgATP]/[MgADP][Pi], was correspondingly lower (3.0 X 10(4) +/- 1.6 x 10(4) v 8.3 X 10(4) +/- 1.4 X 10(4) (mol/L)-1, n = 4) in SHR compared to WKY hearts. These data demonstrate free magnesium depletion in heart muscle and indicate an alteration in cardiac bioenergetics in essential hypertension.

Adenosine Triphosphate↗
PubMed1991

Platelet function during antihypertensive treatment with quinapril, a novel angiotensin converting enzyme inhibitor.

The effect of various antihypertensive medications on platelet function is of increasing interest. Conflicting effects of captopril on platelet function are reported and the impact of angiotensin converting enzyme (ACE) inhibitors not containing a sulfhydryl group such as enalapril, lisinopril, and quinapril on platelet function remains unstudied. Therefore, the aim of the present study was to examine the effect of antihypertensive treatment with quinapril, a novel ACE inhibitor not containing a sulfhydryl group, on platelet function. Ten white men (age range of 32-61 years) with untreated mild-to-moderate essential hypertension (supine diastolic blood pressure greater than 95 mm Hg) were treated with 4 weeks each of placebo and quinapril in a double-blind, randomized, crossover design. Quinapril (20 mg twice a day) significantly lowered systolic (p less than 0.01) and diastolic blood pressure (p less than 0.01) without any significant effect on heart rate or plasma catecholamines. No significant change was noted for in vitro platelet aggregation induced by epinephrine, ADP, or collagen. Plasma concentrations of the platelet release factors beta-thromboglobulin and platelet factor 4 did not change, nor did the platelet content of norepinephrine, platelet weight (mg/10 ml of blood), circulating platelet count, or platelet size. Thus, as assessed by a broad spectrum of platelet parameters, we found that antihypertensive treatment with quinapril has no significant effect on platelet function in patients with mild-to-moderate essential hypertension. These "platelet-neutral" properties of quinapril suggest that quinapril, both from a thromboembolic and a hemostatic point of view, may be a rather safe agent for treatment of hypertension.

Adenosine Diphosphate↗
PubMed1991

Fine needle aspiration of Sister Mary Joseph's nodule.

A case of Sister Mary Joseph's nodule (umbilical metastasis) is described from a primary adenocarcinoma of the transverse colon. Needle aspiration cytology made the diagnosis which was confirmed by immunocytochemical localization of CEA, B72.3, EMA, and cytokeratin in the tumour cells. Extensive mucus production in the tumour cells was demonstrated by alcian blue and mucicarmine stains.

Abdominal Neoplasms↗
PubMed1991

31P-NMR studies of isolated adult heart cells: effect of myoglobin inactivation.

31P nuclear magnetic resonance (NMR) studies of isolated adult rat heart cells revealed that the cells maintained high-energy phosphates for up to 6 h in polyamide hollow fibers perfused with well-oxygenated nutrient medium. Glucose plus pyruvate superfused heart cells maintained [phosphocreatine]/[ATP] at 1.4 +/- 0.1, internal pH at 7.09 +/- 0.04 (external pH = 7.25), and intracellular free Mg2+ at 0.51 +/- 0.04 mM. In glucose-containing media, hypoxia was accompanied by a reversible decrease in intracellular ATP and phosphocreatine of approximately 50% and 80%, respectively, while the intracellular free Mg2+ was reversibly increased by 40%. However, inhibition of glycolysis by iodoacetate in aerobic pyruvate-containing medium did not significantly alter high-energy phosphate content. Inactivation of intracellular myoglobin with 1-2 mM sodium nitrite, which reduces the steady-state respiratory oxygen consumption rate by 30%, caused a significant (30%) decrease in intracellular phosphocreatine peak, which was reversed upon removal of sodium nitrite. The nitrite-induced decrease in phosphocreatine was also observed in iodoacetate-treated myocytes but not in oligomycin-treated cells. These results indicate that functional myoglobin enhances high-energy phosphate synthesis in well-oxygenated myocytes.

Animals↗
PubMed1991

Changes in NMR-visible kidney cell phosphate with age and diet: relationship to phosphate transport.

To test the hypothesis that growth and dietary Pi affect the intracellular concentration of Pi ([Pi]i) as well as its renal reabsorption, we measured nuclear magnetic resonance (NMR)-visible [Pi]i in isolated perfused kidneys of less than 1- and greater than 4-wk-old guinea pigs fed various amounts of Pi. Changes in [Pi]i were correlated with those in fractional Pi reabsorption (FRPi) in vivo and in capacity (Vmax) for Na(+)-Pi cotransport in microvilli derived from animals of similar age and fed the same diets. In animals fed normal (0.76% Pi) diet, [Pi]i was lower (0.91 +/- 0.14 vs. 1.85 +/- 0.23 mM, P less than 0.05), whereas FRPi was higher (0.90 +/- 0.02 vs. 0.70 +/- 0.03, P less than 0.01) in less than 1- than in greater than 4-wk-old guinea pigs. Pi deprivation decreased [Pi]i in mature animals to 0.74 +/- 0.29 mM, P less than 0.05, and increased FRPi to 0.99 +/- 0.01. Excess dietary Pi increased [Pi]i in immature animals to 1.67 +/- 0.56 mM, P less than 0.05, and decreased FRPi to 0.55 +/- 0.03. Diet-induced changes in [Pi]i were associated with reciprocal changes in Vmax of similar absolute magnitude in immature and mature animals. However, diets that resulted in comparable [Pi]i at the two ages were associated with higher (P less than 0.05) Vmax in less than 1- than in greater than 4-wk-old animals. The reciprocal nature of the relationship between [Pi]i and renal Pi transport indicates that [Pi]i is primarily determined by Pi efflux from the cells or Pi organification rather than Pi influx through Na(+)-Pi cotransport. Findings indicate that changes in [Pi]i with growth or diet may be a cause but cannot be the consequence of changes in abundance or maximal mobility of Na(+)-Pi cotransporters. Data also indicate that factors in addition to low [Pi]i contribute to the high Na(+)-Pi cotransport capacity observed in renal microvilli of growing animals.

Aging↗
PubMed1991

Intracellular ions in salt-sensitive essential hypertension: possible role of calcium-regulating hormones.

To study the blood pressure, ionic, and hormonal responses to chronic dietary salt loading, we measured RBC pHi, Mgi, Nai, and Cai, and compared these with serum levels of Ca-io, 1,25-D, and free levels of PHF in salt-sensitive and salt-insensitive essential hypertension subjects on low and high (200 mEq/day less than UNaV less than 50 mEq/day) dietary salt intakes. As a group, salt loading significantly increased diastolic blood pressure (7.6 +/- /3%), Nai (25.5 +/- /8%) and Cai (27.0 +/- /11%), while Mgi (-14.2 +/- 7%) and pHi (-0.03 +/- /0.01 pH units) fell. Significant changes in pHi, Cai, and Mgi occurred only in SS individuals, who also exhibited elevated levels of 1,25-D and of PHF in association with suppression of Ca-io. Altogether, the pressor response to salt was inversely related to the basal pHi (p less than 0.001), and to the degree of salt-induced suppression of Ca-io (p less than 0.001) and Mgi (p less than 0.001), while being directly related to the basal PHF (p less than 0.001) and to the salt-induced stimulation of 1,25-D (p less than 0.005). We hypothesize that elevated levels of 1,25-D and PHF coordinately shift intracellular cation levels and stimulate cellular calcium uptake from the extracellular space. As such, these calcium-regulating hormones may be responsible, at least in part, for salt-sensitive hypertension.

Biological Factors↗
PubMed1991

Cellular ions in hypertension, diabetes, and obesity. A nuclear magnetic resonance spectroscopic study.

To investigate the cellular basis linking hypertension, non-insulin-dependent diabetes mellitus (NIDDM), and obesity, we used 31P and 19F nuclear magnetic resonance spectroscopy to measure intracellular pH (pHi), free magnesium (Mgi), and cytosolic free calcium (Cai) in erythrocytes of obese and NIDDM subjects with and without hypertension. Compared with normotensive, nondiabetic controls (Cai, 25.2 +/- 1.4 nM; Mgi, 232 +/- 8 microM), Cai was elevated in both normotensive (36.8 +/- 2.7 nM, sig = 0.005) and hypertensive (43.4 +/- 2.9 nM, sig = 0.001) NIDDM subjects, and Mgi was concomitantly suppressed (normotensive: 206 +/- 11 microM, sig = 0.05; hypertensive: 196 +/- 8 microM, sig = 0.001). Similar but less striking changes were noted in obese subjects. Values of pHi were significantly lower (sig = 0.05) in all hypertensive groups compared with their normotensive controls. Continuous relations were observed for all subjects between Cai and diastolic blood pressure (r = 0.649, p less than 0.001) and body mass index (r = 0.565, p less than 0.001), between Mgi and diastolic blood pressure (r = -0.563, p less than 0.001) and fasting blood glucose (r = -0.580, p less than 0.001), and in diabetics, between pHi and diastolic blood pressure (r = -0.680, p less than 0.001). Thus, the constellation of elevated Cai and suppressed Mgi and pHi levels is characteristic of the hypertensive state. These abnormalities of cellular ion handling in whole or in part common to hypertension, diabetes, and obesity may contribute to the pathophysiology of these syndromes and may help to explain their frequent clinical coexistence.

Calcium↗
PubMed1991

Oliguric acute renal failure due to glue-sniffing. Case report.

A 38-year-old male developed acute oliguric renal failure following repeated glue sniffing for about 8 hours. In addition, he had severe liver cell injury, mild myonecrosis and bone marrow depression indicating generalized tissue toxicity. The high urinary spot sodium during the oliguric phase and the total renal functional recovery after a period of oliguria followed by polyuria favoured a diagnosis of acute toxic tubular necrosis causing acute renal failure. Toluene which is used as the solvent is presumably the toxic agent involved in glue sniffing. It is advised that toluene inhalation be considered in the differential diagnosis of acute renal failure especially in the young. Literature on the renal toxicity of toluene is briefly reviewed.

Acute Kidney Injury↗