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Biomedical subjects

M Ganguli

Publications and source records attributed to M Ganguli.

At least 73 records · Page 4Linked to original sources
PubMed1991

Effects of age, gender, and education on cognitive tests in a rural elderly community sample: norms from the Monongahela Valley Independent Elders Survey.

A random sample of 1,350 persons aged 65 years and older in a rural community underwent cognitive screening as part of a survey to establish a population-based registry of dementing disorders. The screening battery included the neuropsychological tests of the assessment protocol used in the National Institute on Aging multicenter Consortium to Establish a Registry for Alzheimer's Disease (CERAD). This paper reports a large body of normative neuropsychological data from this sample with members of relatively low socioeconomic status. Age, sex, and educational level were found to have statistically significant effects on test scores. The implications of these findings for the establishment of screening cutoff scores are discussed.

Aged↗
PubMed1991

Possible human health hazards from outbreak of epizootic ulcerative syndrome (EUS) in fish in the Asia-Pacific region.

Acid fast rods, constituting chemoautotrophic nocardioform bacteria, could be repeatedly cultivated and isolated and propagated indefinitely in vitro from fish actinomycotic macrophage granuloma from the massive epizootics of ulcerative disease syndrome of fish in eastern India during 1988-90. The possible human hazards of zoonotic actinomycotic infections as a result of handling and consumption of such fish are assessed.

Actinomycetales↗
PubMed1991

In SHR rats, dietary potassium determines NaCl sensitivity in NaCl-induced rises of blood pressure.

The current study tested whether the spontaneously hypertensive rats (SHR) from Charles River Laboratories are resistant or not to NaCl-induced rises of blood pressure and deaths. These rats are fairly NaCl-resistant on a 2.1% high K diet, whereas they are quite susceptible to NaCl-induced hypertension and deaths on a 0.5% normal K diet. Thus, a high K diet strongly protects against a NaCl-induced rise of blood pressure as well as deaths in these SHR rats. Hence the level of dietary K determines the degree of NaCl sensitivity in these SHR rats.

Animals↗
PubMed1990

Dietary K determines NaCl sensitivity in NaCl-induced rises of blood pressure in spontaneously hypertensive rats.

The current study tested whether the spontaneously hypertensive rats (SHR) from Charles River Laboratories are resistant or not to NaCl-induced rises of blood pressure and stroke deaths. These rats are fairly NaCl-resistant on a 2.1% high K diet, whereas they are quite susceptible to NaCl-induced hypertension and stroke deaths on a 0.5% normal K diet. Thus, a high K diet strongly protects against an NaCl-induced rise of blood pressure as well as stroke deaths in these SHR rats. Hence the level of dietary K determines the degree of NaCl sensitivity in these SHR rats.

Animals↗
PubMed1990

Deleterious effects of high magnesium diets and beneficial effects of high potassium diets in hypertensive stroke-prone rats.

The effect of varying amounts of dietary magnesium (Mg) in conjunction with potassium (K) on hypertension and stroke mortality in hypertensive stroke-prone (SHRsp) rats was studied. These results show that high K (2.1%) diets strongly protect against stroke mortality and rises of blood pressure, while high Mg (0.26%) diets appeared to increase stroke mortality and accelerate the rise of blood pressure in SHRsp rats. Similarly, medium high (1.3%) levels of K in the diet significantly reduced blood pressure and stroke mortality but not nearly as much as the 2.1% K in the high K diet.

Animals↗
PubMed1990

Physical demonstration of a high molecular weight bacteriocin plasmid in Vibrio cholerae by genetic transformation process.

Bacteriocinogeny was transferred at high frequencies from bacteriocinogenic (Bac+) V. cholerae strains to non-bacteriocinogenic (Bac-) recipients in the in situ genetic transformation system on agar surface. DNA extracted from samples of growth of bacteria transformed to Bac+ were obtained at 2 h intervals following contact with the sterile agar surface where the donor had grown previously. This showed acquisition of a high molecular weight plasmid which could be physically demonstrated best in the 6 h sample of the Bac+ transformants; their 4 h samples failed to show this specific plasmid, while it was demonstrable only as a faint band in the 8 h samples.

Bacteriocins↗
PubMed1990

'DNA' as contaminants in antibiotics and its capacity to transform bacteria to drug resistance.

DNA/and deoxyribose sugars were detected in streptomycin (Sm), kanamycin, polymyxin, penicillin G, ampicillin, methicillin, cloxacillin and mitomycin C in small amounts/traces. Stained DNA could be feebly visualized directly in Sm run in agarose gel, which improved after its separation and concentration. These DNA materials were DNase sensitive, RNase and pronase resistant, and appeared to consist of fragments, c. less than or equal to 6 Mdal; this could repeatedly transform to SmR several recipient enterobacteria and vibrios; E. coli C600 and S. typhi 57, after such transformation revealed similar plasmid DNA bands that were absent in their wild-types. G + C mole% of plasmid and chromosomal DNA of recipient (57) along with that of Streptomyces griseus reference strain, suggested an extraneous origin for the plasmid DNA.

Anti-Bacterial Agents↗
PubMed1989

Acute prostaglandin reduction with indomethacin and chronic prostaglandin reduction with an essential fatty acid deficient diet both decrease plasma flow to the renal papilla in the rat.

Renal distribution of prostaglandin synthetase is mainly medullary, whereas the major degrading enzyme, prostaglandin dehydrogenase is primarily cortical. This suggests that prostaglandins (PG) released from the renal medulla could affect the medullary blood vessels. In two different experiments we studied the role of PG in the regulation of renal papillary plasma flow in the rat. First study: PG synthesis were stimulated in 34 adult Sprague-Dawley rats by bleeding from the femoral artery 1% of the body weight over a period of 10 minutes. Following this, indomethacin (a PG inhibitor, 10 mg/kg i.v.) was given slowly and then renal papillary plasma flow was measured 25 minutes after the end of infusion. In 17 indomethacin rats the renal papillary plasma flow averaged 18.8 ml/100 g/minute, whereas it averaged 23.0 in 17 non-indomethacin rats given diluent, an 18% reduction (p less than .025). Second study: Male Sprague-Dawley rats were made prostaglandin deficient by fasting rats for one week, followed by 10% dextrose fluid for one week and subsequent institution of an essential fatty acid (EFA) deficient diet for two weeks. With urinary PG excretion in prostaglandin deficient rats 28 ng/24 hours compared to 149 ng in control rats, they could be considered as prostaglandin deficient. When renal papillary plasma flow was measured, the 16 prostaglandin deficient rats had a 16% lower papillary plasma flow than 16 control rats, 21.6 vs 25.6 (p less than .005). These results clearly demonstrate that PG inhibition in rats decreases plasma flow to the papilla, strongly suggesting that PG are vasodilators for the vessels supplying the renal papilla.

Animals↗
PubMed1989

High magnesium diets increase blood pressure and enhance stroke mortality in hypertensive SHRsp rats.

The effect of varying amounts of dietary magnesium in conjunction with potassium (K) on hypertension and stroke mortality in hypertensive stroke prone (SHRsp) rats was studied. These results show that high K (2.1%) diets strongly protect against stroke mortality and rises of blood pressure, while high magnesium (Mg) (0.26%) diets appeared to increase stroke mortality and accelerate the rise of blood pressure in SHRsp rats. Similarly, medium-high (1.3%) levels of K in the diet significantly reduced blood pressure and stroke mortality but not nearly as much as the 2.1% K in the high K diet.

Animals↗
PubMed1985

Assessing depression in primary medical and psychiatric practices.

A two-stage assessment of newly admitted outpatients at community mental health centers and primary medical care centers found the Center for Epidemiological Studies Depression Scale to be highly sensitive but relatively nonspecific when compared with assessments of depression by the Diagnostic Interview Schedule. Considerably higher than usual screening scores are recommended with both patient populations to improve the efficiency of the Center for Epidemiological Studies Depression Scale. The reasons for our finding that primary care clinicians underdiagnose depressive disorder while psychiatric clinicians overdiagnose it relative to the Diagnostic Interview Schedule include varied presentations by each sector's patients, differing clinical acumen, and factors affecting third-party reimbursement.

Adult↗
PubMed1982

Effect of an anteroventral third ventricle lesion on NaCl hypertension in Dahl salt-sensitive rats.

An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.

Animals↗
PubMed1977

Evidence that prostaglandin synthesis inhibitors increase the concentration of sodium and chloride in rat renal medulla.

Thirty minutes after indomethacin (10 mg/kg, iv), a prostaglandin synthesis inhibitor, had been given to 10 rats, the Na concentration in renal papilla averaged 349 mEq/kg H2O, whereas it averaged only 181 in 14 "non-indomethacin" control rats (P less than 0.0001). Papillary plasma flow was closely similar in both groups. In a subsequent study, eight "indomethacin" rats had the same papillary flow as seven non-indomethacin rats but had a papillary Na concentration of 358 vs. 185 in the non-indomethacin controls (P less than 0.0001). In nine more rats, indomethacin increased Cl concentration in papillas by 66% (P less than 0.0001), while Na concentration increased 60% (P less than 0.0001). In eight other rats, micropuncture indicated that indomethacin does not greatly alter delivery of fluid out of late proximal tubule. Meclofenamate, another inhibitor, increased papillary Na just as much as indomethacin. Papillary urea is not changed with indomethacin. Thus, papillary Na concentration was almost twice as high in indomethacin rats, despite similar papillary plasma flow and late proximal flow. Apparently, inhibiting prostaglandin synthesis is associated with either a great increase in Na or Cl "pumping" or a great decrease in Na or Cl "leak" in either collecting duct or ascending limb, or in both. The collecting duct and papillary interstitial cells both synthesize prostaglandins, which seem to have a profound effect on medullary net Na transport.

Animals↗