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Biomedical subjects

N Singh

Publications and source records attributed to N Singh.

At least 397 records · Page 22Linked to original sources
PubMed1995

ABO blood groups among malaria cases from district Mandla, Madhya Pradesh.

A total of 2095 patients with fever were tested for malaria and classified according to ABO blood groups. Only 696 cases were malaria positive. While blood group A, B and O were equally susceptible to malaria infection, AB blood group had less number of persons with malaria parasites. A significantly lower frequency of Plasmodium falciparum was observed among individuals with blood groups A and O. In other two blood groups B and AB, no difference in P. vivax and P. falciparum proportions were observed. A two-year study showed that the frequency of repeated attacks between all blood groups was similar.

ABO Blood-Group System↗
PubMed1995

Cerebral malaria in Jabalpur, India.

A total of 1783 patients were admitted in Govt. Medical College Hospital, Jabalpur with fever in 1993. Out of these 152 (8.5%) patients had cerebral malaria, of which 39 (25.6%) patients died. Age and sex-wise break-up indicated that males suffered more (p < 0.01) from malaria and majority of patients belonged to 16-40 yrs age-group. Mortality was significantly higher in patients with hyperparasitaemia, hypoglycaemia and delayed diagnosis and treatment. Comatose condition was the main determinant of death.

Adolescent↗
PubMed1995

Apoptosis in health and disease.

Two distinct forms of cell death are known, necrosis which results from physical or chemical insult and apoptosis or programmed cell death results from programming within the cell for self destruction in response to internal and external stimuli. Apoptosis is a genetically governed process of cell death occurring in development and maintenance of multicellular organisms. It occurs to get rid of individual cells that become unwanted for various reasons or that present a threat to the organism. It is accompanied by distinct morphological changes. DNA fragmentation in most cases, and appears to be caused by the activities of specific genes. Its defective regulation may play a part in the aetiology of cancer, AIDS, autoimmune and degenerative diseases. Apoptosis offers potential for prevention and therapeutic modulation of these disorders.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Current status of silent myocardial ischemia.

A significant proportion of myocardial ischemia is 'silent' in nature. Furthermore, this asymptomatic ischemia portends an adverse prognosis for patients with known coronary artery disease. Silent myocardial ischemia can be objectively assessed and quantified by a number of noninvasive means; however, ambulatory electrocardiographic monitoring has emerged as a preferred method for both detection and analysis in hospital and during daily life conditions. Silent myocardial ischemia exhibits a circadian pattern. It represents an imbalance between myocardial oxygen supply and myocardial oxygen demand, and can be triggered by both physical and mental stress. The important role of endothelial dysfunction and autonomic nervous system influences has been recently elucidated. Up to 75% of ischemic episodes in patients are silent. Patients with asymptomatic coronary artery disease, chronic stable angina and unstable angina, and those postmyocardial infarction or postrevascularization who exhibit ST segment shift all show adverse short and long term prognosis compared with controls. Treatment modalities have included nitrates, beta-blockers, calcium antagonists, phosphodiesterase inhibitors, anxiolytics, anti-platelet agents and revascularization procedures. While the majority of these studies have demonstrated significant reduction in the frequency of silent myocardial ischemia, limited data on influencing prognosis are available; thus recommendations regarding treatment of these patients await the results of ongoing clinical trials.

Adrenergic beta-Antagonists↗
PubMed1995

Detection of silent ischemia adds to the prognostic value of coronary anatomy and left ventricular function in predicting outcome in unstable angina patients.

BACKGROUND: Patients with unstable angina are at increased risk of unfavourable outcomes such as myocardial infarction, death and urgent revascularization. Early risk stratification may improve subsequent outcome. Recently the presence and duration (at least 60 mins) of silent ischemia as measured by Holter monitoring has been shown to be of prognostic value. The incremental value of this information over that provided by coronary angiography and assessment of left ventricular function is not known. OBJECTIVE: To determine whether detection of silent ischemia is of independent and additional prognostic significance beyond that provided by the angiographic extent of coronary artery disease and left ventricular dysfunction. METHODS: One hundred and thirty-five unstable angina patients with 24 h of ST segment monitoring in addition to early cardiac catheterization (4 +/- 3 days) were assessed. Eighty-nine patients (66%) had ST segment shift for a total of 593 episodes (mean duration of 18 +/- 30 mins per episode) of which 92% were asymptomatic. Ten patients had a myocardial infarction and six patients died during the hospitalization. In addition, there were 33 urgent revascularization procedures. RESULTS: With the generalized additive logistic model, various clinical variables were assessed for predicting unfavourable outcomes. Duration of ST shift (P = 0.02) was second only to angiographic severity of coronary artery disease (P = 0.004) as a predictor. In the presence of these two variables left ventricular function did not have independent prognostic significance (P = 0.16). Event-free survival curves show that duration of ST shift of at least 60 mins was of incremental value in predicting unfavourable in-hospital outcomes compared with both the extent of coronary artery disease and left ventricular dysfunction. CONCLUSION: In patients with unstable angina, further stratification can be achieved early with Holter monitoring in addition to coronary angiography and assessment of left ventricular function.

Angina, Unstable↗
PubMed1995

Elevated platelet-derived microparticle levels during unstable angina.

OBJECTIVE: To use fluorescent-activated flow cytometry coupled with activation-dependent and -independent platelet-specific monoclonal antibodies in a pilot study to assess the degree and time course of platelet activation events in patients presenting within 24 h of onset of Canadian Cardiovascular Society class 4 angina. BACKGROUND: Although activated platelets play a key role in the pathogenesis of unstable angina, the development of simple assays to quantify platelet activation events directly is lacking. METHODS: Blood samples were drawn from six unstable angina patients from the coronary care every 4 h over a 24 h period into a fixative and analyzed the following day. All patients were on acetylsalicylic acid and heparin. Comparisons were made with six healthy, medication-free volunteers. Platelets were defined by flow cytometry as positive for fluorochrome-labelled monoclonal antibody to glycoprotein Ib (AP1) and within the single intact platelet window defined by scatter characteristics. The presence of the fluorochrome-labelled activation-specific monoclonal antibody (KC4.1 for anti-P-selectin, PAC-1 for activated glycoprotein IIb/IIIa) was used to determine the percentage of activated platelets. Platelet activation-dependent microparticles were identified by gating on AP1-positive events and defining microparticles (percentage of total platelet events) as being smaller (forward size scatter) than single intact platelets. RESULTS: There was a marked, sixfold increase in microparticle generation (17 +/- 7% versus 2.8 +/- 1.4%) in the unstable angina patients (P = 0.001) compared with healthy volunteers. Further assessment of six coronary care unit patients with nonischemic cardiac disorders demonstrated a highly variable intermediate level of microparticle generation (11 +/- 7%). No differences in activated glycoprotein IIb/IIIa expression were noted for the various groups and P-selectin expression was lower in the unstable angina patients (6 +/- 2% versus 12 +/- 3%, (P = 0.007). CONCLUSIONS: This pilot study suggests that measuring circulating platelet microparticle levels is a simple yet useful parameter for the assessment of platelet activation in unstable angina compared with activation markers on intact whole platelets. Despite antiplatelet and antithrombin therapy, significant platelet activation occurred in these patients over the initial 24 h. Flow cytometry may be a useful tool in assessing the efficacy of newer therapeutic modalities.

Adult↗
PubMed1995

Prevalence of malaria among pregnant and non-pregnant women of district Jabalpur, Madhya Pradesh.

In the study period of two years 145 pregnant and 79 non-pregnant women with malarial infection were recorded. Plasmodium falciparum was the most prevalent species accounting for 72% of the total malaria infection in pregnant women while, in non-pregnant women it accounted for 58%. Results were analysed according to the species to which the parasite belonged, period of gestation and parity. While cerebral malaria, abortions, intrauterine foetal death, maternal anaemia were common in pregnant patients, only one neonatal death was recorded. Malaria parasites were not found in infants born to mothers with very heavy parasitaemia at the time of delivery. Even though pregnant women of all age groups and parity remain highly susceptible to malaria throughout pregnancy and puerperium from this area, some striking differences like malaria infection more prevalent in primigravidas than multigravidas and in second trimester than in third trimester were noticed in comparison to northern India. Results emphasize the need to target malaria control for this group of women. Failure to clear parasitaemia after chloroquine administration in P. falciparum was common in both pregnant and non-pregnant women. This is an area, where there is a great need to introduce effective malaria interventions. As chloroquine resistant parasites spread a better understanding of the problem is needed leading to a few chemotherapeutic options for pregnant women.

Adult↗
PubMed1995

C-JUN/AP-1 as possible mediators of tumor necrosis factor-alpha-induced apoptotic response in mouse JB6 tumor cells.

Sensitivity to cell killing by tumor necrosis factor (TNF)-alpha was seen in the JB6-derived transformed mouse RT101 cell variants previously described as resistant to 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced killing, while the TPA-sensitive variants were resistant to killing by TNF-alpha. Morphological and biochemical changes characteristic of apoptosis were found to precede TNF-alpha-induced cell death in TNF-alpha-sensitive (TNFs) but not TNF-alpha-resistant (TNFr) cells. In TNFr cells, TNF-alpha increased the cell cycle rate. The onset of cellular damage in TNFs cells, as indicated by propidium iodide uptake, was seen as early as 6 h after TNF-alpha treatment. 4,6-diamidino-2-phenylindole staining revealed chromosomal condensation approximately 4-6 h after TNF-alpha treatment. The DNA oligonucleosomal ladder of 180 bp and its multiples, a characteristic feature of apoptosis, was seen at 48 h. Little or no significant differences were found in the basal or induced levels of mRNA expression of several potential apoptosis mediator genes or apoptosis inhibitor genes. A dephosphorylated species of anti-c-Jun immunoprecipitated protein appeared in TNFs cells at 3 h posttreatment, accompanied by a parallel increase in AP-1 activity. Higher constitutive levels of the antioxidant enzymes superoxide dismutase and catalase were found in TNFr cells, but TNF-alpha did not significantly affect the activities of these enzymes or differentially induce their expression. The findings suggest that the preferential and transient increase in c-Jun dephosphorylation and AP-1 transcriptional activity may contribute to the preferential apoptotic response in TNFs cells; and that the greater constitutive oxidant defense in TNFr cells may contribute to their resistance.

Animals↗
PubMed1995

Use of neem oil as a mosquito repellent in tribal villages of mandla district, madhya pradesh.

A field study was carried out to evaluate the mosquito repellent action of neem (Azadirachta indica) oil in tribal forested villages of District Mandla. Various concentrations of neem oil mixed in coconut oil (1-4%) were applied to the exposed body parts of human volunteers. Results revealed 81-91% protection during 12 h period of observation from the bites of anopheline mosquitoes. Neem oil is an indigenous product and a practical solution to curtail mosquito nuisance.

Animals↗
PubMed1994

The demonstration of a glutamate dehydrogenase-NADP-L-glutamate charge-transfer complex and its location on the reaction pathway.

In previous transient state kinetic work from this laboratory, we proposed a new mechanism for the glutamate dehydrogenase-catalyzed oxidative deamination reaction involving an initial replacement of a proton from lysine 126 by a single bound water molecule, followed by closure of the active site cleft and expulsion of bulk water, providing a hydrophobic environment for the ensuing hydride transfer step. Here, we report the results of further transient state fluorescence, absorbance, and kinetic isotope effect studies, which demonstrate the occurrence of an unusual intermediate in the early steps of that reaction. This phenomenon is revealed by an initial fluorescence burst that occurs in the time period where the absorbance signal is still in its lag phase. Using an extension of the proton/product ratio approach we have described earlier, we show that this intermediate is a strongly fluorescent but weakly absorbing species whose absorption maximum is red-shifted beyond that of other known complexes of this enzyme. The transient state kinetic isotope effects of the fluorescence and absorbance signals are compatible only with a reaction scheme in which the formation of the fluorescent complex precedes the hydride transfer step. The optical properties of this enzyme-oxidized coenzyme-substrate intermediate strongly suggest that it is a charge-transfer complex, similar in nature to the complex responsible for the well known "Racker band" reported in 1952 for glyceraldehyde-3-phosphatase dehydrogenase (Racker, E., and Krimsky, I. (1952) Nature 169, 1043-1044). The crystal structure studies of the enzyme-coenzyme and enzyme-L-glutamate complexes of the closely analogous Clostridium symbosium glutamate dehydrogenase, reported by the Sheffield group (Stillman, T. J., Baker, P. J., Britton, K. L., and Rice, D. W. (1993) J. Mol. Biol. 234, 1131-1139), provide a basis for a physical explanation of the phenomenon. We conclude that the charge transfer phenomenon is caused by the near apposition of the unprotonated alpha-amino group of the substrate in a form of the enzyme in which a conformational change has caused the complete closing of the active site cleft.

Animals↗
PubMed1994

Infectious complications in liver transplant recipients on tacrolimus. Prospective analysis of 88 consecutive liver transplants.

This prospective study characterizes the incidence, etiology, timing, risk factors, and outcome of the infectious complications after 88 consecutive liver transplantations in 79 patients receiving tacrolimus (FK506) as primary immunosuppression with a median follow-up of 880 days. Infections occurred in 59% (47/79) of the patients, and 39% had major infections. Of the major infections, 55% were bacterial, 22% were viral, and 22% were fungal. Bacteremia accounted for 30% of major bacterial infections. Sixty percent of bacteremias occurring within the first 3 months were catheter related, while 75% of those occurring more than 3 months after transplant were of a biliary source. Patients with recurrent hepatitis C virus hepatitis and patients requiring dialysis after transplant had a significantly higher rate of infections as compared with other patients. Overall mortality was 18%, and 29% of all deaths were associated with infection. Only invasive aspergillosis was associated with infectious mortality. Our data suggest that the potent immunosuppressive agent FK506 is not associated with a higher incidence of infectious complications as compared with previous studies using CsA.

Adult↗
PubMed1994

A kinetic mechanism of the allosteric control of enzyme-coenzyme binding: glutamate dehydrogenase-NADPH-phosphate-acetate-hydrogen ion interactions.

We have previously characterized the thermodynamic relationships which govern the dissociation of NADPH from bovine liver glutamate dehydrogenase and the allosteric control of that mechanically and physiologically important process by a variety of effectors. We have found that the cooperative occupancy of a specific anion binding, while the occupancy of a second allosteric acetate binding site disrupts that anion binding site and opposes those effects (Singh & Fisher, 1994). We report here the results of transient-state studies on the kinetics of the various processes involved in this complex equilibrium. We find that the only intrinsically slow steps are those of NADPH binding and dissociation, that the complex kinetic behavior of the overall system is due solely to very rapid equilibrium binding processes involving phosphate, acetate, and hydrogen ions, and that these ions exert their various effects on the kinetics of the binding process by altering the equilibrium concentrations of the two kinetically significant reactive species, E and E-NADPH. The slow intrinsic rates of NADPH association and dissociation are ascribed to a ligand-induced conformational change involving a major alteration in the degree of closure of the enzyme's active-site cleft.

Acetates↗