Search PubMed⌕ Search

Biomedical subjects

M Gupta

Publications and source records attributed to M Gupta.

At least 235 records · Page 13Linked to original sources
PubMed1996

Observer variation in AgNOR counts in neoplastic breast lesions.

OBJECTIVE: To determine interobserver and intraobserver variability of AgNOR quantitation in neoplastic lesions of the breast. STUDY DESIGN: Forty-five cases, 20 benign and 25 malignant lesions, were included in the study. Counts were performed on one slide from each case within a pre-marked area of about 1 cm2 in a standardized manner by two observers blind to the histopathologic diagnosis and independent of each other and repeated after two weeks. Interobserver and intraobserver agreement was assessed using the Bland-Altman method. RESULTS: Our results showed small mean interobserver and intraobserver differences but wide limits of agreement. CONCLUSION: Observer variation in AgNOR counts is too high for the method to be of any diagnostic or prognostic relevance.

Breast Neoplasms↗
PubMed1996

Acquired camptothecin resistance of human breast cancer MCF-7/C4 cells with normal topoisomerase I and elevated DNA repair.

A camptothecin (CPT)-resistant cell line (MCF-7/C4) was established from MCF-7 cells by mutagenic treatment with methylmethanesulfonate and selection with CPT. MCF-7/C4 is 30-fold resistant to CPT and is cross-resistant to UV and cis-dichlorodiammineplatinum(II) but not to VP-16 or ionizing radiation. Topoisomerase I (top1)-mediated cleavable complexes in the presence of CPT, measured by oligonucleotide assay and by alkaline elution, were similar in both cell lines. Other top1 parameters such as top1 protein, RNA levels, and DNA relaxation were also similar in both cell lines. Thus, CPT resistance is not due to alterations in top1 activity but is caused by changes in the downstream pathways from the top1-induced damage. Both cell lines had similar doubling time (22 hr), but MCF-7/C4 cells showed reduced S-phase fraction in the absence of CPT and reduced G2 delay after CPT treatment. p53, GADD45, and p21WAF1/CIP1 were induced similarly by CPT in both cell lines. The overall repair capacity estimated by the ability of cells to reactivate UV-damaged pSV-CAT plasmid was increased in MCF-7/C4 cells. These observations suggest that enhanced DNA repair is one of the factors involved in CPT resistance.

Breast Neoplasms↗
PubMed1996

Influence of Ca2+ on kinetics and thermodynamics of the NADPH-dependent microsomal lipid peroxidation.

The effect of Ca2+ on kinetics and thermodynamics of lipid peroxidation in microsomes prepared from liver of male Swiss albino mice (7-8 weeks old) was studied. Ca2+ was found to increase the Vmax in temperature dependent manner. Michaelis-Menten constant (Km) also increased with temperature. However, the linearity and extent of change in Km remained unaffected in presence of Ca2+, and was suggestive of non-competitive and mixed type of activation. The activation constant (Ka) obtained by the replotting of slopes of the Lineweaver-Burk plots against the reciprocal of Ca2+ concentration showed linear variation with temperature. The linear pattern of Arrhenius plots indicated non-involvement of parallel reactions of other intermediate species in the lipid peroxidation. Thermodynamic parameters delta H degree, delta S degree and delta G degree, associated with lipid peroxidation process were studied. The positive value of delta H degree is suggestive of the endothermic nature of the process. It appears that the NADPH induced lipid peroxidation is an entropy driven process.

Animals↗
PubMed1996

Paradoxical influence of Ca(2+) on lipid peroxidation.

Lipid peroxidation and Ca2+ are suggested to be linked as a mediator of cell damage and death. Lipid peroxidation is a free radical phenomenon. It is highly destructive process and induces plethora of alterations in structure and function of cellular membranes which could lead to cell injury. Ca2+, a regulator of variety of physiological and biochemical functions, was shown to enhance as well as inhibit lipid peroxidation. The explanations provided for the protection as well as the potentiation of lipid peroxidation by Ca2+ were, to some extent, speculative in nature and some of the basic facts seem to be overlooked. Moreover, Ca2+ has a closed-shell electronic state and lacks electronic transitions and hence it may not participate directly in a free radical reaction to modulate lipid peroxidation process. Perhaps this could be the reason for conflicting reports on this aspect. In the present review, the interactions between Ca2+ and lipid peroxidation are critically examined.

Animals↗
PubMed1996

Effect of petroleum ether extract from Hygrophila spinosa on hematological parameters and hepatorenal functions in mice.

Multiple doses of H. spinosa were administered, ip once in a week for 4 weeks (20, 40 and 80 mg/kg body weight) and daily for one month (2, 4 and 8 mg/kg body weight). No alteration in biochemical parameters at low and moderate dose level of daily and low dose level of weekly treatment of petroleum ether extract was observed. However, the extract at moderate dose level in weekly treatment changed serum aminotransferase, alkaline phosphatase and plasma cholesterol significantly. High dose level of the extract changed all the above parameters of weekly treated mice including total bilirubin, nonprotein nitrogen, blood urea and plasma protein. High dose level of daily treatment and moderate and high dose level of weekly treatment of the root extract increased only the white blood cell count significantly. The results reveal that the weekly moderate and high dose (above 40 mg/kg body weight) and daily/therapeutic high dose (8 mg/kg) of the petroleum ether extract of H. spinosa affects liver and kidney functions and metabolism and hematological parameters whereas low weekly dose (20 mg/kg) and low and moderate daily/therapeutic dose (2 and 4 mg/kg) does not exhibit any appreciable toxic action.

Alkanes↗
PubMed1995

Chemical traumatization of adult mouse olfactory epithelium in situ stimulates growth and differentiation of olfactory neurons in vitro.

This study demonstrates that ZnSO4-induced chemical trauma results in an in situ regeneration of the olfactory epithelium which, when maintained in vitro, provides an enriched population of olfactory neurons. Therefore, the ability of the olfactory epithelium to respond to chemical trauma with increased mitotic activity can be used to increase growth of neurons in culture. Tissue obtained from normal or vehicle-treated adult mice produced few olfactory neurons, when maintained in culture, compared to cultures established from tissue following an in situ ZnSO4 trauma. Maximal neuronal yields were obtained in cultures established from tissue that was removed 4-6 days following chemical trauma. The morphological appearance and the presence of cell specific intermediate filament proteins were used to classify the cell types in these olfactory epithelial cultures. Single cells and aggregates of cells which were immunopositive for keratin, but immunonegative for neurofilament protein and GFAP, were identified as epithelioid. Flattened polygonal cells immunopositive for GFAP were identified as glia. A small population of flattened cells was immunonegative for all of the antibodies used in this study. Cells that had processes were immunonegative for GFAP and keratin. Some were immunopositive for 200 kDa and 160 kDa neurofilament proteins but immunonegative for the 68 kDa neurofilament protein. A few of these cells showed positive immunoreactivity with the olfactory marker protein (OMP) antibody and most likely represented the most mature olfactory neurons in the cultures. This trauma-induced culture model using olfactory tissue from adult mice can serve as a source of CNS neurons for comparison with cultured embryonic neurons.

Animals↗
PubMed1995

A meta-analysis of randomized trials comparing coronary artery bypass grafting with percutaneous transluminal coronary angioplasty in multivessel coronary artery disease.

We performed a meta-analysis of randomized trials that compared percutaneous transluminal coronary angioplasty (PTCA) with coronary artery bypass graft (CABG) surgery in patients with multivessel coronary artery disease. The outcomes of death, combined death, and nonfatal myocardial infarction (MI), repeat revascularization, and freedom from angina were analyzed. The overall risk of death and nonfatal MI was not different over a follow-up of 1 to 3 years (CABG:PTCA odds ratio [OR] 1.03, 95% confidence interval 0.81 to 1.32, p = 0.81). Patients randomized to CABG tended to have a higher risk of death or MI in the early, periprocedural period (OR 1.33, p = 0.091), but a lower risk in subsequent follow-up (OR 0.74, p = 0.093). CABG patients were much less likely to undergo another revascularization procedure (p < 0.00001), and were more likely to be angina free (OR 1.57, p < 0.00001). Thus, CABG and PTCA patients have similar overall risks of death and nonfatal MI at 1 to 3 years of follow-up, but relative risk differences in mortality of up to 25% cannot be excluded. CABG patients have significantly less angina and less repeat revascularization than PTCA patients.

Angioplasty, Balloon, Coronary↗
PubMed1995

The LDL receptor and LRP are receptors for beta VLDL on pigeon monocyte-derived macrophages.

Receptors for the lipoprotein, beta very low density lipoprotein (beta VLDL), have been identified through the binding of beta VLDL-gold conjugates on two ligand-induced regions of pigeon monocyte-derived macrophages. These regions were microvilli/retraction fibers and membrane ruffles. The present study investigated the location and identity of beta VLDL receptors using an antiserum directed against the epidermal growth factor (EGF) precursor region of the human low density lipoprotein (LDL) receptor. The anti-receptor serum recognized two membrane proteins from pigeon monocyte-derived macrophages, a 116 kDa (LDL receptor) protein and a 600 kDa (low density lipoprotein receptor-related protein; LRP) protein. Ligand blot analysis demonstrated that pigeon beta VLDL bound to both the LDL receptor and LRP. Immuno-gold electron microscopy using the anti-receptor serum resulted in immunoglobulin localization on the same two ligand-induced regions, microvilli/retraction fibers and membrane ruffles, to which the ligand had bound. Furthermore, simultaneous immunogold localization of the lipoprotein receptor antigens and beta VLDL-gold (ligand) binding substantiated co-localization of the receptor antigens and beta VLDL on the ligand-induced regions. Cross-competition studies with the anti-receptor serum and beta VLDL-gold conjugate documented that increasing concentration of the anti-receptor serum resulted in 70% inhibition of beta VLDL-gold conjugate binding. These data suggest that pigeon monocyte-derived macrophages utilize both the LDL receptor and LRP as receptors for pigeon beta VLDL.

Amino Acid Sequence↗
PubMed1995

Effects of deprenyl on monoamine oxidase and neurotransmitters in the brains of MPTP-treated aging mice.

Deprenyl is a selective monoamine oxidase B (MAO-B) inhibitor and has been used in the treatment of Parkinson's disease. However, it is not known whether deprenyl effects are symptomatic or pharmacological. Aging mice were partially lesioned with MPTP. Control and MPTP-treated mice were given deprenyl in drinking water for 14 days. Brain tissue (including the striatum, olfactory tubercle and cerebral cortex) was assayed for MAO-B and neurotransmitter levels. The results show that deprenyl treatment, given alone or after MPTP, reduced MAO-B activity in all the three regions. No change was seen in dopamine (DA), 3,4-dihydroxyphenyl acetic acid (DOPAC), and homovanillic acid (HVA) content in any of the three areas. Cortical norepinephrine (NE) levels were also unaltered. However, striatal serotonin (5-HT) levels were decreased while its metabolite, 5-HIAA levels were significantly increased in the olfactory tubercle in animals receiving deprenyl alone. These data suggest that deprenyl treatment reduces MAO-B activity in regions in addition to the striatum without affecting norepinephrine, dopamine (DA) and its metabolites.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

An unusual case of acute renal failure in burns.

Nowadays acute renal failure in burns is not a common occurrence, at least not when most of the wounds have already healed. We report a case of a 6-year-old child with 45 per cent flame burns, who suffered acute renal shutdown 43 days after burns when all except 1 per cent of the raw areas had already been grafted with autologous skin. There was no identifiable focus of infection and no evidence of septicemia. The patient was not receiving any nephrotoxic drugs. The child responded well to peritoneal dialysis and recovered fully.

Acute Kidney Injury↗
PubMed1995

Inhibition of human immunodeficiency virus type 1 integrase by a hydrophobic cation: the phenanthroline-cuprous complex.

The human immunodeficiency virus type 1 integrase (HIV-1 integrase) is required for integration of a double-stranded DNA copy of the viral RNA genome into a host chromosome and for HIV replication. We have examined the effects of 2:1 1,10-phenanthroline-cuprous complexes on purified HIV-1 integrase. Although the uncomplexed phenanthrolines are not active below 100 microM, four of the cuprous complexes (neocuproine, 4-phenyl neocuproine, 2,3,4,7,8,9-hexamethyl phenanthroline, and 2,3,4,7,8-pentamethyl phenanthroline) have a 50% inhibitory concentration (IC50) for integration ranging between 1 and 10 microM. Disintegration is also inhibited by these phenanthroline-cuprous complexes at slightly higher concentrations (between 10 and 40 microM). Dialysis experiments showed that the inhibition is reversible and kinetic analyses revealed that the mode of inhibition by these cuprous complexes appears to be noncompetitive with respect to the substrate DNA. Consistent with these findings, binding assays demonstrate that, although these complexes can inhibit binding to DNA at high concentrations, they do not inhibit binding of integrase to the DNA substrate at their IC50 values. Because these complexes do not bind to B-DNA below 50 microM, inhibition via binding to a specific region on the enzyme was examined. Using deletion mutants of integrase, it was determined that neither the amino-terminal (zinc finger) nor the carboxy-terminal (DNA-binding) integrase domain is required for inhibition by the phenanthroline-cuprous complexes. Therefore, inhibition via binding to the enzyme catalytic core or to the interface between the enzyme and a noncanonical DNA structure generated during the enzymatic reaction is the probable mechanism. These results suggest the utility of neocuproine-cuprous complexes in developing inhibitors of HIV-1 integrase as well as probes for drug-binding sites and enzymatic reaction mechanism.

Base Sequence↗