Biomedical subjects
Publications and source records attributed to A Sharma.
Molariform supernumerary teeth in the maxillary central incisor area are uncommon. This article reports the presence of a molariform mesiodens in daughter and a conical mesiodens in father. Detailed investigation into family history of patients with mesiodens is needed. Though the etiology of this dental anomaly remains unclear, genetics as a key factor in the development of supernumerary teeth is highlighted.
OBJECTIVES: To study thrombophilia states in Indian patients with acute spontaneous superior mesenteric vein thrombosis (SMVT). METHODS: Two men with this condition, a 56 year old and a 31 year old presenting with acute SMVT, demonstrated on CT scan, were subjected to a thrombophilia screen consisting of Protein C, S, antithrombin levels, lupus anticoagulant, anticardiolipin antibodies, fibrinogen levels, factor VIII levels, factor V 'Leiden' gene mutation, and paroxysmal nocturnal hematuria screen. RESULTS: A thrombophilia screen showed factor V 'Leiden' gene mutation (heterozygous) in both cases. Additionally, the first patient had high fibrinogen levels and the second high factor VIII levels. Both patients are currently on long-term anticoagulation. CONCLUSION: Factor V 'Leiden' gene mutation in association with other thrombophilic factors may predispose to spontaneous superior mesenteric vein thrombosis.
The effect of a carbohydrate supplement, offered as a diet option, on feeding behaviour, body weight gain, and endurance exercise was studied in rats exposed to hypobaric hypoxia. Male albino rats (n = 35) were randomly divided into 5 groups; hypoxic supplemented and control groups; normoxic supplemented and control groups, and an untreated control group. After treadmill training for 5 days, the hypoxic groups were exposed to simulated high altitude equivalent to 6960 m for 18 days continuously. Food and water intakes, body weight and endurance exercise were recorded before and during the exposure period. Blood glucose, insulin, muscle and liver glycogen were assayed at the end of the exposure period. Hypobaric hypoxia resulted in a significant decrease in food and water intake, and body weight, and reduced endurance exercise capacity compared to the basal and normoxic group values. The carbohydrate supplement did not ameliorate the hypoxia-induced loss in body weight, but however, significantly delayed the onset of fatigue during exercise in the supplemented rats compared to the hypoxic control group.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A total of 120 Haemophilus influenzae isolates from blood, cerebrospinal fluid, sputum and throat swabs of patients and carriers in North India was characterised by biotyping, ribotyping and random amplification of polymorphic DNA (RAPD)-PCR. Of these, 77 isolates (64%) were serotype b; the other 43 (36%) were non-typable. Biotype I was the most predominant among the typable strains and biotype II among the non-typable strains. Ribotyping with restriction endonucleases HaeIII and EcoRI differentiated the isolates into three and six ribotypes, respectively. However, RAPD fingerprints generated by the application of arbitrary primers AP1 and AP2 provided a higher level of discrimination. RAPD typing revealed distinct polymorphism among the serologically typable isolates. This study is the first report that stratifies the subtypes of H. influenzae strains from India by molecular techniques.
A 56-year-old male with chronic renal failure presented with a 6 month history of progressive dyspnoea. High resolution CT of the chest showed multiple, peripheral, centrilobular nodules in the upper and mid zones, consistent with metastatic pulmonary calcification. Some of these pulmonary nodules showed ring calcification, a pattern that to our knowledge has not been described before. Calcification was also seen in the segmental pulmonary arteries, bronchi, trachea and subcutaneous vessels of the chest wall.
OBJECTIVE: To investigate whether pre-eclampsia is associated with an exaggeration of the insulin resistance in normotensive pregnancy. DESIGN: Minimal model analysis of a frequently sampled intravenous glucose tolerance test to assess insulin sensitivity. SETTING: SMS Medical College, Jaipur (Raj.) PARTICIPANTS: Eleven women with pre-eclampsia and eleven matched normotensive pregnant women. RESULTS: Insulin sensitivity (S1) was increased in the group with pre-eclampsia compared with the normotensive women (Mean +/- SEM): 2.6 (0.4) vs 1.6 (0.2) 10(-4) min(-1) per mU/L; P = 0.028). This was accompanied by a decrease in glucose effectiveness (SG) (1-1 +/- 0.1 vs 1.7 +/- 0.1 10(-2) min(-1), P = 0.006) in the pre-eclamptic women. In the normotensive group there was a significant inverse correlation between S1 and mean arterial blood pressure (r = -0.65; P = 0.03), but no such relation existed in the group with pre-eclampsia. CONCLUSIONS: As with other forms of secondary hypertension, and unlike essential hypertension, the pathophysiology of pre-eclampsia is not associated with insulin resistance.
AIM: To determine the effect of enalapril, angiotensin-converting-enzyme inhibitor (ACE-I) on progression of renal insufficiency in primary membranoproliferative glomerulonephritis with mild to moderate renal insufficiency. METHOD: Thirty patients with histopathologically proved MPGN having hypertension (grade I and II of JNC-VI criteria of hypertension) and mild to moderate impairment of renal function (creatinine clearance varying from 30-80 ml/min, significant albuminuria and serum creatinine 1.2-3.0 mg/dl) were initially treated with diuretics and 3-blockers to bring down BP < 140/90 mm Hg. These patients were then randomly divided into three groups of 10 each, group I--Control; group II--Nifedipine and group III--Enalapril. In group II and III Nifidepine 30 mg/day and in group III Enalapril 10 mg/day respectively were added in addition and treatment was continued for nine months. These patients were followed up monthly for drug efficacy, side effects and any adverse drug reaction. RESULTS: Out of 30, 28 patients completed the study. At the end of nine months of treatment the patients of control group revealed significant increase in serum creatinine (1.65 +/- 0.38 to 2.17 +/- 0.31 mg/dl), blood urea (34.0 +/- 3.9 to 40.0 +/- 3.1 mg/dl), and 24 hours albuminuria (3.6 +/- 0.6 to 4.2 +/- 0.6 gm) and decrease in creatinine clearance (60.3 +/- 13.3 to 37.5 +/- 11.8 m/min); however, in enalapril group there was decrease in serum creatinine (1.72 +/- 0.45 to 1.24 +/- 0.58 mg/dl), blood urea (34.6 +/- 4.7 to 28.1 +/- 6.7 mg/dl) and 24 hours albuminuria (3.3 +/- 1.0 to 1.6 +/- 1.1 gm) and increase in creatinine clearance (56A +/- 15.8 to 77.1 +/- 23.5 ml/min). The patients on nifedipine showed statistically nonsignificant changes in creatinine clearance, blood urea and serum creatinine; while albuminuria increased from 3.0 +/- 1.3 to 3.9 +/- 0.4 gm/24 hours (p < 0.01). The blood pressure was well controlled in all patients. None of the patient had side effects leading to withdrawal of drugs. No adverse drug reaction was noted. CONCLUSION: ACE-I (enalapril) provided protection against the progression of renal insufficiency in patients of MPGN having hypertension with mild to moderate renal impairment. The renoprotective effects of ACE inhibitor (enalapril) is associated with substantial decrease in albuminuria.
Five viruses are usually associated with hepatitis in humans: A-E. In addition to these viruses as aetiological agents of hepatitis, there remain a number of patients with hepatitis in whom no virus could be identified. It was therefore postulated that there may be other agents which may be causing hepatitis. Recently, two viruses have been associated with hepatitis: hepatitis G virus (HGV), and transfusion transmissible virus (TTV). Hepatitis G virus (HGV) is a single stranded RNA virus which represents a newly discovered virus belonging to the flavivirus family. HGV is distinct from hepatitis C virus (HCV) and the newly discovered GBV-A and GBV-B agents, while GBV-C represents an isolate of HGV. The structure of the HGV genome resembles that of HCV. HGV replicates in peripheral blood cells, while replication in liver cells has not been observed till date. Diagnosis of HGV infection is mainly by use of polymerase chain reaction (PCR), as serological techniques are still being developed. Epidemiological data indicate that the virus is prevalent throughout the world, including India and is transmitted via blood/blood products, sexually and vertically from infected mothers to children. The relationship between infection with the virus and presence of liver pathology is controversial and has not been proven beyond doubt, as majority of patients with HGV have no detectable evidence of disease.
The present investigation was designed to study the spermicidal activity of lidocaine, a membrane stabilizer, and its combination with 2',4'-dichlorobenzamil hydrochloride, a Na+-Ca2+ exchange inhibitor, on human semen and spermatozoa separated from semen. Both drugs per se produced dose- and time-dependent reduction in motility of ejaculated human sperm. Lidocaine was found to potentiate the spermicidal activity of benzamil resulting in significant decrease in time for producing complete loss of ejaculated sperm motility. Sperm revival test revealed irreversible loss of sperm viability indicating a spermicidal rather than spermiostatic action by both the drugs. Furthermore, both benzamil (10-40 mM) per se and benzamil-lidocaine combination (0.5 and 16 mM) produced contraception in rabbit model.
A VR-based system using a CyberGlove and a Rutgers Master II-ND haptic glove was used to rehabilitate four post-stroke patients in the chronic phase. Each patient had to perform a variety of VR exercises to reduce impairments in their finger range of motion, speed, fractionation and strength. Patients exercised for about two hours per day, five days a week for three weeks. Results showed that three of the patients had gains in thumb range (50-140%) and finger speed (10-15%) over the three weeks trial. All four patients had significant improvement in finger fractionation (40-118%). Gains in finger strength were modest, due in part to an unexpected hardware malfunction. Two of the patients were measured against one-month post intervention and showed good retention. Evaluation using the Jebsen Test of Hand Function showed a reduction of 23-28% in time completion for two of the patients (the ones with the higher degrees of impairment). A prehension task was performed 9-40% faster for three of the patients after the intervention illustrating transfer of their improvement to a functional task.
Polymorphisms in the regulatory region of the human apolipoprotein E gene (gene, APOE; protein, apoE) have been implicated in Alzheimer's disease. Here we describe in detail the advantages of a simple method for haplotype analysis of this region (at -491 and -427 bases relative to the transcription start site of the gene). The promoter region of the APOE gene was amplified by polymerase chain reaction (PCR) and this fragment was then used as a template for PCR with "nested" primers to generate a 228-bp product incorporating both the -491 and the -427 loci. PCR products were then digested with DraI and AluI together and subjected to polyacrylamide gel electrophoresis. The distinct pattern of bands appearing on the gel was then used to ascribe [-491,-427] haplotypes to each subject, from which -491 and -427 genotypes were inferred. -491 and -427 genotypes were also confirmed by digestion with DraI alone or AluI alone. Haplotype analysis was successful in all 20 samples analyzed and was 100% consistent with genotyping. We suggest that this is a reliable, time-saving method that the will be useful in large-scale APOE promoter genotyping studies.
BACKGROUND: Naturally occurring antibodies (Nabs) that bind to terminal galactose alpha1,3-galactose carbohydrate structures (Gal) are present in humans and Old World monkeys but are negatively regulated in other mammalian species because they express Gal epitopes on their cell surfaces. A Gal knockout mouse (Gal-/-) model, generated by homologous disruption of alpha1,3-galactosyltransferase gene, is capable of producing natural anti-Gal Abs. METHODS: To study the genetic control of the anti-Gal response, we have generated anti-Gal hybridomas from Gal-/- mice and analyzed VH genes of anti-Gal Abs from naïve animals and from mice stimulated by rat heterotopic heart transplantation. RESULTS: Six immunoglobulin (Ig)M anti-Gal hybridomas derived from naïve Gal-/- mice exhibited anti-Gal binding activity with some cross-reactivity to related carbohydrate structures. These naïve anti-Gal Abs used five different VH genes in a germline configuration. Anti-Gal IgM hybridomas isolated after a rat heterotopic heart xenograft (4 days) utilized germline VH gene segments from the VH7183 family and exhibited less cross-reactivity. In contrast to mice 4 days after xenograft, we have predominantly isolated IgG anti-Gal hybridomas from mice 21 days after rat heterotopic heart xenografts, indicating an isotype switch. Nine of the IgG anti-Gal hybridomas secreted IgG3 subclass and one produced IgG1. Sequence analysis of the VH gene usage from the induced anti-Gal IgG antibodies demonstrated a restricted gene utilization (VHJ606-V14A). CONCLUSION: Our results demonstrate that the anti-Gal response in naïve Gal-/- mice is encoded by multiple germline progenitors. In response to a xenograft, the induced anti-Gal Abs exhibited a restricted gene usage and somatic mutations, indicating a positive selection.
Plants express a variety of proteins at the cell surface responsible for the transduction of regulatory information into the cell via receptors. In the present study, an attempt has been made to identify the components of the brassinosteroids (BRs) signaling transduction cascades in transgenic rice (Oryza sativa) expressing the antisense strand of OsBRI1 transcript. A 60 kDa protein, immunologically characterized as mitogen-activated protein kinase (MAPK), showed reduced phosphorylation activity in the membrane fractions of the OsBRI1 antisense rice over control, demonstrating the inhibition in the perception of BRs by the BRI1 receptor, when compared with the exogenously applied brassinolide. The phosphorylation activity of the 50 kDa Ca(2+)-dependent protein kinase was however increased in the cytosolic fractions of OsBRI1 antisense over control. The data obtained suggest that MAPK and Ca(2+)-dependent protein kinase in rice are discrete but parallel signaling cascades and might involve receptors other than BRI1 in response to BR stimulus.
We investigated the instability of the moving rim in dewetting of slipping polymer films. Small fluctuations of the width of the rim get spontaneously amplified since narrower sections of the rim move faster than wider ones due to frictional forces being proportional to the width of the rim. Instability leads eventually to an autocontrol of the rim width by the continuous formation of droplets with a mean size proportional to the initial film thickness. Surprisingly, the mean dewetting velocity at late stages, averaged over the length of the rim, was found to be constant. Thus, the instability of the rim enabled a more efficient, i.e., faster, "drying" of the substrate. Nonslipping films did not show this instability.
Dopamine D4 receptors (D4 receptors) mediate dopamine-stimulated, folate-dependent phospholipid methylation. To investigate possible regulation of this multi-step D4 receptor-mediated phospholipid methylation cycle by protein kinases, specific kinase activators and inhibitors were studied in SK-N-MC human neuroblastoma cells, using [14C] formate to label folate-derived single-carbon groups. Phorbol dibutyrate (PDB), an activator of protein kinase C, stimulated basal phospholipid methylation and also shifted the dose-response curve for dopamine-stimulated phospholipid methylation to the right by more than an order of magnitude. Calphostin C, an inhibitor of protein kinase C, had little effect on basal phospholipid methylation but significantly inhibited dopamine-stimulated phospholipid methylation and also blocked the stimulatory response to PDB. Chelerythrine, which inhibits protein kinase C and other kinases, strongly inhibited both basal and dopamine-stimulated phospholipid methylation. Forskolin, an activator of protein kinase A, inhibited basal and dopamine-stimulated phospholipid methylation, but only at high concentrations while Rp-cAMP, an inhibitor of protein kinase A, did not block this effect. Inhibition of protein kinase G produced a modest decrease in dopamine-stimulated phospholipid methylation, but neither sodium nitroprusside, which increases nitric oxide (NO) production and activates protein kinase G, nor the NO synthase inhibitor N-nitro-L-arginine had any effect on basal or dopamine-stimulated phospholipid methylation. These observations indicate that protein kinase C is an important regulator of basal and D4 receptor-mediated folate-dependent phospholipid methylation, whereas protein kinase A and protein kinase G have a lesser or minimal role.
To explore the role of lipid peroxidation (LPO) products in the initial phase of stress mediated signaling, we studied the effect of mild, transient oxidative or heat stress on parameters that regulate the cellular concentration of 4-hydroxynonenal (4-HNE). When K562 cells were exposed to mild heat shock (42 degrees C, 30 min) or oxidative stress (50 microM H2O2, 20 min) and allowed to recover for 2 h, there was a severalfold induction of hGST5.8, which catalyzes the formation of glutathione-4-HNE conjugate (GS-HNE), and RLIP76, which mediates the transport of GS-HNE from cells (Awasthi, S., Cheng, J., Singhal, S. S., Saini, M. K., Pandya, U., Pikula, S., Bandorowicz-Pikula, J., Singh, S. V., Zimniak, P., and Awasthi, Y. C. (2000) Biochemistry 39, 9327-9334). Enhanced LPO was observed in stressed cells, but the major antioxidant enzymes and HSP70 remained unaffected. The stressed cells showed higher GS-HNE-conjugating activity and increased efflux of GS-HNE. Stress-pre-conditioned cells with induced hGST5.8 and RLIP76 acquired resistance to 4-HNE and H2O2-mediated apoptosis by suppressing a sustained activation of c-Jun N-terminal kinase and caspase 3. The protective effect of stress pre-conditioning against apoptosis was abrogated by coating the cells with anti-RLIP76 IgG, which inhibited the efflux of GS-HNE from cells, indicating that the cells acquired resistance to apoptosis by metabolizing and excluding 4-HNE at a higher rate. Induction of hGST5.8 and RLIP76 by mild, transient stress and the resulting resistance of stress-pre-conditioned cells to apoptosis appears to be a general phenomenon since it was not limited to K562 cells but was also evident in lung cancer cells, H-69, H-226, human leukemia cells, HL-60, and human retinal pigmented epithelial cells. These results strongly suggest a role of LPO products, particularly 4-HNE, in the initial phase of stress mediated signaling.