Search PubMed⌕ Search

Biomedical subjects

R Sharma

Publications and source records attributed to R Sharma.

At least 361 records · Page 20Linked to original sources
PubMed1996

Melorheostosis of the hand.

We report a case of melorheostosis of the hand which showed a sclerotomal pattern of involvement, with swelling and pain. Surgical debulking resulted in correction of the deformity and relief of pain.

Adult↗
PubMed1996

Hepatitis B virus infection in pregnant women and its transmission to infants.

HBsAg was screened by Reverse Passive Haemagglutination Test (RPHA) and was confirmed by ELISA test in 157 pregnant females and their newborns. Anti-HBc and IgM anti-HBc was done in these cases by enzyme immuno-assay. The overall prevalence of HBsAg in mothers was 16 out of 157 (10 per cent) and in cord blood of newborns 5 per cent. The transplacental transmission was found in eight of 16 (50 per cent) HBsAg positive mothers. Anti-HBc was present in 12 out of 16 (75 per cent) HBsAg positive mothers and, of these, seven (58 per cent) neonates acquired HBsAg infection. IgM anti-HBc was present in seven out of eight (88 per cent) HBsAg positive neonates, suggesting active in utero infection. Fourteen out of 16 (88 per cent) neonates born to HBsAg positive mothers were alive and healthy, one was stillborn and one had a congenital anomaly.

Adult↗
PubMed1996

In situ stimulation of topoisomerase II-induced cleavage sites in the c-myc protooncogene by antitumor agent pMC540 is associated with gene expression.

The antitumor activity of pMC540 has been shown to be mediated via its interaction with topoisomerase (Topo) II eventually leading cells into apoptosis. This agent was also found to down regulate the expression of the c-myc oncogene in L1210 leukemia cells. To investigate the possibility that damage within select genomic regions may contribute to the antiproliferative activity of pMC540, differential damage in regions surrounding the c-myc locus as well as other select genes was determined. Southern blot hybridization experiments show that pMC540 treatment induces in situ DNA cleavage products in the 5' end of the c-myc oncogene of L1210 leukemia cells. In cells pre-treated with 50 microM ethidium bromide, an inhibitor of the Topo II-dependent DNA cleavage, a subsequent treatment with pMC540 failed to induce DNA cleavage, suggesting that the cleavage activity of pMC540 was Topo II dependent. pMC540-induced cleavage does not appear to correlate with the over-expression of the c-myc oncogene in these cells as another over-expressed gene c-myb was not affected. Thus, it is proposed that the c-myc gene may be a preferred target for pMC540 may mediated antiproliferative activity.

Animals↗
PubMed1996

Radiolabeled denatured RBC scintigraphy in autologous splenic transplantation.

An 18-year-old man underwent surgery for blunt abdominal trauma requiring a total splenectomy. Heterotopic splenic autotransplantation was done in the omentum. Immediate platelets counts, cell morphology, and serum immunoglobulin levels were suggestive of impaired splenic function. Radiolabeled denatured RBC splenic imaging showed evidence of functioning autotransplanted splenic tissue in the omentum. The blood parameters were found to be normal 4 weeks after transplant. Radionuclide denatured RBC imaging has been found to be useful in the localization of functional autotransplanted splenic tissue.

Abdominal Injuries↗
PubMed1996

Variations in the fluorescence intensity of intact DAPI-stained bacteria and their implications for rapid bacterial quantification.

As current techniques for the quantification of bacteria are laborious and often imprecise, instrumental approaches such as sedimentation field-flow fractionation (SdFFF) are attractive. In this technique, fluorogenic dyes specific for nucleic acids are used to identify bacterial cells. Bacterial biomass can be quantified directly with SdFFF if the specific fluorescence of bacterial cells is constant. The effect of different growth conditions on the specific fluorescence of one strain each of Escherichia coli, Pseudomonas aeruginosa, Proteus mirabilis and Staphylococcus epidermidis stained with 4',6-diamidino-2-phenylindole was examined. Specific fluorescence varied over a 500-fold range, from 0.22 to 103 arbitrary fluorescence units per cell. Specific fluorescence was highest when cells were in log phase, and lowest when cells were in stationary phase. Specific fluorescence decreased when cells harvested in log phase were starved for 7 d in a carbon-free minimal medium, and increased rapidly (within 2 h) after cells were relieved from carbon limitation. Such variations in specific fluorescence must be considered when using gross fluorescence as a direct indicator of bacterial numbers in the SdFFF technique for quantifying bacterial biomass. Moreover, they have serious implications for the application of fluorescence techniques in other instrumental approaches for bacterial enumeration in environmental samples.

Bacteria↗
PubMed1996

Alteration of glomerular permeability to macromolecules induced by cross-linking of beta 1 integrin receptors.

Altered glomerular epithelial cell attachment to the glomerular basement membrane is an important pathogenetic factor in increased glomerular permeability to proteins. We have previously presented evidence that antibodies reactive with integrin matrix receptors on glomerular epithelial cells inhibit adhesion of these cells and may be involved in the production of proteinuria in vivo. Therefore, we utilized intact glomeruli in an in vitro system to directly assess the effect of anti-beta 1-integrin antibody on glomerular permeability. Permeability to albumin (Palb) was calculated from the volume response of glomeruli to a transcapillary oncotic gradient. Anti-beta 1-integrin increased Palb in a dose- and time-dependent manner. Palb was increased to 0.70 +/- 0.05 whereas normal rabbit IgG had no effect (0.10 +/- 0.04). F(ab')2 fragments of antibody increased Palb to a similar degree whereas Fab fragments had no effect (0.10 +/- 0.06). Cross-linking of Fab fragments, however, with a second antibody restored their ability to increase Palb (0.60 +/- 0.09), demonstrating the importance of integrin cross-linking in producing the observed effect. Intact, F(ab')2 and Fab fragments of anti-beta 1 antibody all inhibited adhesion of glomerular epithelial cells to fibronectin, laminin, and types I and IV collagen, although the degree of inhibition by Fab fragments was significantly less on collagens. No cytotoxic effects were observed with anti-beta 1 antibody or its fragments. These results suggest that antibodies to integrin matrix receptors on glomerular cells alter cell interactions with the glomerular basement membrane and lead to increased glomerular permeability to proteins via a process that is initiated by integrin cross-linking rather than through simple interference with cell adhesion per se.

Albumins↗
PubMed1996

Purification and kinetic characterization of chicken liver inorganic pyrophosphatase.

Soluble inorganic pyrophosphatase (EC 3.6.1.1) was isolated from chicken liver, RIR breed, to apparent homogeneity. The enzyme showed a molecular mass of 100 kDa as estimated by gel filtration and a subunit mass of 49 kDa on SDS-PAGE. The enzyme was very specific for pyrophosphate (PPi) and magnesium, and there was no measurable activity on replacing Mg2+ with Zn2+. At optimal conditions of assay, 50% of the enzyme activity was inhibited at 42 microM Ca2+, 70 microM fluoride and 0.91 mM Cd2+. There was a 50% inactivation of enzyme activity at 0.1 M guanidine hydrochloride (GuHCl). Kinetic analysis of GuHCl inactivation revealed 2 essential binding sites for this ligand. The enzyme showed allosteric behaviour with the substrate PPi and Mg2+. The apparent Hill coefficient of 1.47 and 1.48 for PPi and Mg2+, respectively indicate positive cooperatively. Hill plots also gave [S]0.5 of 0.177 mM and 2.5 microM for Mg2+ and PPi, respectively.

Animals↗
PubMed1995

Neuroprotective use-dependent blockers of Na+ and Ca2+ channels controlling presynaptic release of glutamate.

We have originated a family of N,N'-disubstituted guanidines that block the voltage-activated Ca2+ and Na+ channels governing glutamate release. These compounds, CNS 1237 (N-acenaphthyl-N'-methoxynaphthyl guanidine) and its analogues, are "use dependent" in their ability to attenaute neurotransmitter release: they block glutamate release with greater efficacy under conditions of persistent or repetitive depolarization, as would be encountered under pathophysiological circumstances, relative to their ability to block glutamate release elicited by brief, transient depolarizations more characteristic of normal physiological release events in nonischemic brain. Using electrophysiological and rapid kinetic methods, we have differentiated the use-dependent block of the relevant Na+ and Ca2+ channels governing neurotransmitter release from the mechanism of channel antagonism exhibited by, respectively, the substituted guanidine Na+ channel blocker tetrodotoxin (TTX) and venom peptide Ca2+ antagonists. To characterize use-dependent Na+ channel block by CNS 1237, we have employed whole-cell voltage-clamp recordings from a Chinese hamster ovary (CHO) cell line expressing cloned mammalian type II Na+ channels. These experiments demonstrated that, in contrast to the actions of TTX under the same conditions, the potency of Na+ channel block by CNS 1237 is greatly enhanced by depolarizing stimuli in a frequency-dependent manner. Ca2+ channel-activated glutamate release from brain nerve terminal preparations was measured with approximately 300 msec time resolution over a 5-second period of high K(+)-depolarization, using a rapid superfusion technique. CNS 1237 and analogues, at 1-3 microM, accelerated the decay of glutamate release by 40-70%, reflecting depolarization-induced enhancement of block. In contrast, blockade of glutamate release by the Ca2+ channel antagonist peptide toxins omega-aga IV-A (from spider venom) and omega-conotoxin M-VII-C (from cone snail venom) exhibited "reverse-use-dependence:" at concentrations of 0.3 microM, which blocked the initial amplitude of glutamate release by 40-60%, the decay time constant for glutamate release was significantly increased, indicating depolarization-induced relief of block. These findings establish that CNS 1237 and other members of this compound series are use-dependent blockers of the voltage-activated ion channels governing glutamate release. Studies of CNS 1237 in the rat middle cerebral artery occlusion (MCAO) focal stroke model have indicated infarct size reduction comparable to that observed by the same investigators for the glutamate release blocker (BW 619C89 (Burroughs-Wellcome, now in clinical development). Maximal infarct size reduction is achieved with a 3-mg/kg bolus followed by a 4-hour infusion of 0.75 mg/kg/hr.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Structure-activity studies of RFamide analogues on central neurones of Helix aspersa.

The effects of FMRFamide were compared with those of FMRFamide analogues, FLRFamide, LFRFamide, FFRFamide, LLRFamide, D-FMRFamide, F-D-MRFamide and FM-D-RFamide, and the fragments, MRFamide and LRFamide, on identified central neurones, F1, F2, F5 and E16, of the snail Helix aspersa, using intracellular recording and two electrode voltage clamp techniques. All FMRFamide analogues showed an inhibitory effect on F1 neurones with an order of potency: FLRFamide > FMRFamide > FFRFamide > LFRFamide >> LLRFamide. FMRFamide and FLRFamide exhibited a biphasic response on F2 neurones. At lower concentrations (< 10 microM), both peptides usually only excited while at higher concentrations (> 30 microM), exhibited an excitation followed by an inhibition. FFRFamide only excited F2 while LFRFamide and LLRFamide only inhibited F2. LRFamide and MRFamide (100 microM) were inactive on both F1 and F2. FLRFamide, LFRFamide, LLRFamide, FFRFamide and D-FMRFamide showed cross-interaction on the outward current induced by FMRFamide in F5. All peptides induced an outward current and also reduced the FMRFamide-induced current reversibly. In contrast, MRFamide, LRFamide and F-D-MRFamide failed to have direct effects on these neurones nor interact with the FMRFamide-induced current. We conclude that on F2 neurones Phe is essential for the activation of the RFamide receptor mediating the excitation and Met or Leu are important to activate the RFamide receptors mediating the inhibition. Removal of the N-terminal Phe, to give LRFamide and MRFamide render the peptides inactive. Therefore a tetrapeptide sequence is essential for the biological activity of FMRFamide analogues on these Helix neurones. FLRFamide, LFRFamide, LLRFamide, FFRFamide and D-FMRFamide exhibit a cross-interaction with FMRFamide. It is possible that these peptides also act on the same class of RFamide receptors as agonists to cause cross desensitization.

Animals↗