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Biomedical subjects

S Sen

Publications and source records attributed to S Sen.

At least 163 records · Page 9Linked to original sources
PubMed1998

Achalasia cardia in infancy and childhood: an Indian experience.

Seven children with achalasia cardia, six of them infants, were seen over a 10-year period. In infantile achalasia, respiratory symptoms predominate and vomiting may easily be mistaken for gastroesophageal reflux (GER). Vomiting of uncurdled milk is characteristic of achalasia. Six children underwent esophagocardiomyotomy with good results in five. The procedure was transthoracic in two and transabdominal combined with an anterior fundoplication in the others. There was one post-operative death. Achalasia and alacrima were associated in two infants. One baby with this association also had a neurogenic bladder.

Child, Preschool↗
PubMed1998

An outbreak of Salmonella enteritidis phage type 5a infection in a residential home for elderly people.

The first outbreak of Salmonella enteritidis phage type (PT) 5a infection to be reported occurred after a party in a residential home for elderly people in May 1995. The party was attended attended by 96 residents, staff and guests. S. enteritidis PT5a was isolated from 14 of the 25 clinical cases identified after the party and S. enteritidis PT4 from another clinical case. Two elderly residents with S. enteritidis PT5a infection died. Infection with S. enteritidis PT5a was associated with consumption of prawn in mayonnaise vol-au-vents, sausage rolls, corned beef sandwiches, and sausages. The investigation of this outbreak illustrated the difficulty that elderly people may have in the completion of questionnaires. It also highlighted areas for intervention; such as reminders about basic hygiene precautions to prevent secondary spread and the importance of coordinated reinforcement in the workplace of formal food hygiene training for cooks. The Food Safety Regulations 1995 came into force soon after this outbreak: their implementation would probably have prevented it.

Adolescent↗
PubMed1997

Expression of a gene encoding a tRNA synthetase-like protein is enhanced in tumorigenic human myeloid leukemia cells and is cell cycle stage- and differentiation-dependent.

We cloned a tumorigenic phenotype-associated cDNA encoding a tRNA synthetase-like protein from an acute-phase human myeloid leukemia cell line. The cDNA was isolated by reiterative subtraction of cDNAs synthesized from tumor-generating parental leukemia cells versus those from a nontumorigenic variant of the same cells. The selected cDNA encodes a protein that is a close homolog of one subunit of prokaryote and yeast phenylalanyl-tRNA synthetase (PheRS). The expressed protein reacts specificially with polyclonal antibodies raised against mammalian phenylalanyl-tRNA synthetase. Expression of the gene (designated CML33) was directly confirmed by Northern blot hybridization to be substantially enhanced in the tumorigenic cells compared with the nontumorigenic variant. In addition, expression of CML33 in myeloid leukemia cells was sensitive to the stage of the cell cycle and to induction of differentiation. Although the relationship between these observations and the tumorigenic state of the human myeloid leukemia cell line used in these studies is unknown, to our knowledge, this is the first demonstration in mammalian cells of tumor-selective and cell cycle stage- and differentiation-dependent expression of a member of the tRNA synthetase gene family.

Amino Acid Sequence↗
PubMed1997

A putative serine/threonine kinase encoding gene BTAK on chromosome 20q13 is amplified and overexpressed in human breast cancer cell lines.

DNA amplification on chromosome 20q13 is commonly detected in breast cancer and correlates with poor prognosis. Definitive critical target genes on this amplicon have however, not yet been identified. We describe in this paper isolation of a novel gene named BTAK, encoding a putative member of protein serine/threonine kinase family localized on chromosome 20q13 that is amplified and overexpressed in breast tumor cell lines. BTAK maps close to the critical region of amplification defined earlier on this amplicon. Deduced amino acid sequence shows conservation of all the subdomains predicted in protein kinase super family. Translated BTAK peptide shows significant homology with previously cloned protein serine/threonine kinase encoding genes Ip11 from S cerevisae and aurora from Drosophila, both shown to be functionally involved in normal chromosome segregation process. Our findings suggest that amplification and overexpression of BTAK may be playing a critical role in oncogenic transformation of breast tumor cells.

Amino Acid Sequence↗
PubMed1997

Nuclear magnetic resonance assignment and secondary structure of an ankyrin-like repeat-bearing protein: myotrophin.

Multidimensional heteronuclear NMR has been applied to the structural analysis of myotrophin, a novel protein identified from spontaneously hypertensive rat hearts and hypertrophic human hearts. Myotrophin has been shown to stimulate protein synthesis in myocytes and likely plays an important role in the initiation of cardiac hypertrophy, a major cause of mortality in humans. Recent cDNA cloning revealed that myotrophin has 11B amino acids containing 2.5 contiguous ANK repeats, a motif known to be involved in a wide range of macromolecular recognition. A series of two- and three-dimensional heteronuclear bond correlation NMR experiments have been performed on uniformly 15N-labeled or uniformly 15N/13C-labeled protein to obtain the 1H, 15N, and 13C chemical shift assignments. The secondary structure of myotrophin has been determined by a combination of NOEs, NH exchange data, 3JHN alpha coupling constants, and chemical shifts of 1H alpha, 13C alpha, and 13 C beta. The protein has been found to consist of seven helices, all connected by turns or loops. Six of the seven helices (all but the C-terminal helix) form three separate helix-turn-helix motifs. The two full ANK repeats in myotrophin are characteristic of multiple turns followed by a helix-turn-helix motif. A hairpin-like turn involving L32-R36 in ANK repeat #1 exhibits slow conformational averaging on the NMR time scale and appears dynamically different from the corresponding region (D65-169) of ANK repeat #2.

Amino Acid Sequence↗
PubMed1997

Changes in collagen phenotypes during progression and regression of cardiac hypertrophy.

OBJECTIVE: Excessive deposition of collagen has been implied to be responsible for abnormal stiffness and altered cardiac function during hypertrophy and heart failure. In the present paper we studied the changes in collagen and their phenotypes during development of cardiac hypertrophy in spontaneously hypertensive rats (SHR) compared to age- and sex-matched Wistar Kyoto (WKY). We also studied the changes in collagen after regression of hypertrophy, with antihypertensive therapy with ACE inhibitors, captopril (C) and lisinopril (L). METHOD: Collagen was extracted from the heart tissue by cyanogen bromide (CNBr) digestion. Collagen phenotypes were separated and quantified by SDS-polyacrylamide gel electrophoresis. The transcript levels(mRNA) of collagen phenotypes were determined by Northern analysis. RESULTS: Our studies showed that the ventricular collagen and their phenotypes did not alter in SHR during the first 6 months of progression of hypertrophy when compared to WKY. After 40 weeks, however, in SHR there was an unexpected rise in collagen content and the distribution of collagen phenotype differs compared to WKY, especially during the chronic phase of hypertrophy (65 weeks of age). In WKY during the aging process there was a gradual increase in type III collagen, whereas in SHR it plateaus after 40 weeks of age. Treatment with antihypertensive drugs captopril and lisinopril showed a similar degree of reduction in blood pressure (P < 0.001), regressed hypertrophy (P < 0.001), and reduced collagen, whereas decrease in type I to III ratio was found with captopril only, but not with lisinopril. This decrease in type I to III ratio due to captopril treatment is primarily due to an increase in type III collagen (both protein and transcript level) in SHR. CONCLUSION: Our data showed, for the first time, that during the chronic phase of hypertrophy in SHR there is a gradual reduction in type I to III ratio, primarily due to a lack of increase in type III collagen during chronic phase of hypertrophy. This suggests that quality of collagen is an important factor in determining the degree of cardiac stiffness. Our data also showed that not all ACE inhibitors have similar actions on collagen phenotype production. This suggests that perhaps the mechanism of action of ACE inhibitors on collagen are independent of its effect on angiotensin II formation.

Aging↗
PubMed1997

Advances in triterpenoid research, 1990-1994.

Triterpenoids isolated and characterized from various sources are reviewed. The newer spectroscopic techniques used in their structure elucidation, the new skeleta characterized, their total chemical synthesis, and their biosynthesis are discussed. A compilation of the triterpenoids isolated during the period 1990-1994 along with their occurrence, physical data, spectroscopy and X-ray analysis used for their characterization, is included. The biological activities of the triterpenoids are also discussed.

Molecular Structure↗
PubMed1997

23Na chemical shifts and local structure in crystalline, glassy, and molten sodium borates and germanates.

A simple correlation between average Na-O bond length and 23Na isotropic chemical shift in crystalline germanates and borates has been established, similar to existing correlations for sodium in silicates and carbonates. This empirical trend is discussed in terms of a decreasing paramagnetic contribution to the chemical shift with increasing average bond length. The correlation is then applied to data for sodium borate and germanate glasses and melts from room temperature to 1200 degrees C, where both structural and compositional effects on the chemical shift are apparent.

Borates↗
PubMed1997

Effect of chronic colchicine administration on the myocardium of the aging spontaneously hypertensive rat.

Colchicine has been demonstrated to suppress the release of fibroblast growth factors, retard collagen formation and augment collagenase activity. Trials with colchicine in patients with hepatic fibrosis have suggested clinical benefit. The development of impaired myocardial function in the spontaneously hypertensive rat (SHR) is associated with a marked increase in myocardial fibrosis. The present study was carried out to test the hypothesis that chronic colchicine administration to the SHR would prevent the development of fibrosis and impaired myocardial performance. Colchicine (1 mg/l drinking water) was administered to male SHR and WKY rats from at age 13 months until 24 months or until evidence of heart failure was observed. Age-matched untreated SHR and colchicine treated and untreated WKY served as controls. At study, active and passive properties of isolated left ventricular muscle preparations were determined. Myocardial fibrosis was assessed by measuring hydroxyproline and histologic determination of interstitial cross-sectional area. Increases in LV hydroxyproline and interstitial area were found in untreated SHR relative to WKY; passive myocardial stiffness was increased and active muscle properties were depressed. In comparing colchicine treated vs untreated SHR, no differences in hydroxyproline, interstitial area or intrinsic myocardial function were found. In the WKY, colchicine increased myocardial interstitium and passive stiffness without changing hydroxyproline. Active myocardial function was not depressed. Thus, chronic colchicine administration neither attenuated the development of interstitial fibrosis nor prevented impaired myocardial function in the SHR. Colchicine treatment was associated with increased interstitium in WKY with increased passive myocardial stiffness.

Aging↗
PubMed1997

Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction.

Specific binding of Hg2+ to ouabain-sensitive Na(+)-K(+)-ATPase of rat liver plasma membrane was demonstrated with a Ka of 2.64 x 10(9) and Bmax of 1.6 nmole mg-1 protein. The binding of mercury to the enzyme also causes significant inhibition of the enzyme, which is greater than its ouabain sensitivity. In the cytosol Hg2+ binding to reduced glutathione (GSH) is stimulated by GSH-S-transferase (GST), the activity of which was found to be significantly enhanced by 15 mM Na+ and 10 mM Hg2+. It is proposed that the transport of Hg2+ inside the cell takes place by increased dissociation of Hg2+ from the membrane due to greater avidity of Hg2+ towards cytosolar GSH binding. The GSH-Hg complex enters the nucleus where it dissociates to bind the metal response element (MRE) of the metallothionein (MT) gene to induce MT transcription.

Animals↗
PubMed1997

Sexually-transmitted disease (STD) markers in multitransfused children in relation to human immunodeficiency virus type-1 (HIV-1) infection: impact of STD markers in blood donors.

Association of serological markers for various sexually transmitted diseases (STDs) with Human Immunodeficiency Virus type 1 (HIV-1) infection among heterosexually promiscuous blood donors is well recognized. However, possibility of similar association among children receiving transfusion from these donors has not been adequately explored. Study on the association of some STD markers with HIV-1 infection in multitransfused (MT) children showed that both HIV-1 positive and HIV-1 negative groups of children had significantly higher prevalence of hepatitis B virus (HBV) markers, i.e. HBsAg (23 and 30 per cent), anti-HBs (46 and 57 per cent), anti-HBc (18 and 23 per cent), antibodies to cytomegalovirus of IgM class (36 and 37 per cent) and IgG class (72.7 and 70 per cent), IgG antibodies to Herpes Simplex Virus type-2 (23 and 23 per cent) compared to control group. However, seropositivity for HIV-1 infection could not be attributed as a risk factor for any of these markers in the group of MT children. On the contrary, significant association of anti HBc, anti HCV, CMV IgG and antitreponemal antibody with HIV-1 infection could be recorded in the group of blood donors. It appeared that due to low prevalence of HIV-1 infection among blood donors in India, both HIV-1 positive and HIV-1 negative groups of MT children received transfusion from HIV negative donors predominantly resulting in a comparable prevalence of STD markers in both the groups of MT children due to cumulative effect of transfusion from HIV-1 negative donors.

Biomarkers↗
PubMed1997

Low energy transvenous cardioversion of short duration atrial tachyarrhythmias in humans using a single lead system.

The purpose of this study was to investigate the efficacy and safety of atrial cardioversion using an endocardial single lead system presently used for ventricular defibrillation. The study population consisted of 26 recipients of an ICD in combination with a conventional endocardial single lead system with the proximal spring electrode as anode in the SVC and the distal as cathode in the apex of the RV. Atrial tachyarrhythmias were induced by right atrial burst pacing. If the arrhythmia sustained > 1 minute, biphasic shocks synchronized with the R wave were delivered using the implanted device, beginning with an energy of 4 J. If 4 J failed to terminate the arrhythmia, energy was increased stepwise, if the first shock was successful, a step-down testing was performed after reinduction of atrial tachyarrhythmias. The mean atrial defibrillation threshold was 2.3 +/- 1.2 J (range, 0.5-5 J). A total of 154 shocks were delivered and no adverse effects were observed. The mean defibrillation threshold for atrial flutter was somewhat lower than that for AF (1.8 +/- 1 J vs 2.7 +/- 1.4 J, P = 0.08). There was no correlation between the atrial defibrillation threshold and a history of previously occurring atrial tachyarrhythmias, the kind of the underlying heart disease, a prescription of antiarrhythmic drugs, the dimension of the LA, the LVEF, or the ventricular DFT. Internal atrial cardioversion of short duration atrial tachyarrhythmias using a transvenous single lead system designed for ventricular defibrillation is feasible and safe at low energies, and may have important clinical applications.

Adult↗
PubMed1997

Angiotensin II and myocyte growth: role of fibroblasts.

Angiotensin II (Ang II) has been implicated in stimulating myocyte growth in vitro, but the mechanism for such stimulation is still an open question. To understand the role of Ang II, we studied its effect on protein synthesis in rat neonatal and adult myocytes. Ang II (10(-8) mol/L) stimulated protein synthesis in neonatal myocytes by 43+/-3.5% over control. To prevent the proliferation of fibroblasts, bromodeoxyuridine was added, and protein synthesis in neonatal myocytes was reduced to 21+/-2.2% over control. In adult myocytes (cultured without bromodeoxyuridine), Ang II stimulated [3H]leucine incorporation by 24+/-2.3% over control; with bromodeoxyuridine, that stimulation was reduced significantly (13+/-0.93% over control). These data suggest that the presence of fibroblasts in the cultures may control myocyte growth. When supernatant from pure fibroblast culture was added to myocyte preparations, a significant increase (49.8+/-3.5% over control) in protein synthesis occurred. Pretreatment of these fibroblasts with Ang II (10(-3) mol/L) further stimulated protein synthesis, suggesting that Ang II directly stimulates the production of a factor from fibroblasts. The stimulatory effect of Ang II on the release of the factor can be completely blocked by pretreatment with losartan, an Ang II receptor (AT1) blocker. Our data are the first to demonstrate a paracrine effect of a fibroblast-derived factor that modulates myocyte growth. Fibroblast-derived factor loses its biological activity by (1) tryptic digestion, (2) exposure to pH below 4.0 and above 9.0, and (3) heating to 95 degrees C. The molecular weight of the factor is approximately 65 kD. The antibodies against fibroblast growth factor (both acidic and basic) could not inhibit this factor's stimulatory effect. Furthermore, this factor is heart specific and is produced at least up to the 16th passage of neonatal rat heart fibroblasts. Skin fibroblasts, aortic endothelial cells, and aortic smooth muscle cells do not produce this protein. Our data suggest that the observed myocyte growth by Ang II comes about via fibroblast-derived factor, which is increased by Ang II. Cross talk between fibroblasts and myocytes is an important factor in stimulating myocyte growth by Ang II.

Aging↗
PubMed1997

Interrelationship of dietary lipids and ascorbic acid with hepatic enzymes of cholesterol metabolic pathway.

Effect of unsaturated and saturated fats on cholesterol metabolism was studied in ascorbate sufficient and deficient guineapigs. Experimental animals were made chronic ascorbic acid deficient by allowing oral intake of 0.5 mg ascorbic acid/day/animal. Elevation in serum and liver cholesterol and triglyceride along with depression in cholesterol oxidation and 7 alpha-hydroxylation in liver was observed in unsaturated fat fed guineapigs with ascorbate deficiency. Liver microsomal cytochrome P-450 level was found to be low in ascorbate deficient animals. Polyunsaturated fat intake could not lower the serum cholesterol level in ascorbate deficiency. Today polyunsaturated fat in the diet is encouraged all over the world for its hypocholesterolemic effect. This study indicates that polyunsaturated fat intake with ascorbic acid deficiency may produce hypercholesterolemia.

Animals↗
PubMed1996

Phenethyl isothiocyanate modulates clastogenicity of mitomycin C and cyclophosphamide in vivo.

Phenethyl isothiocyanate (PEITC), a constituent of many cruciferous vegetables, is an effective chemopreventive agent against N-nitrosamine-induced carcinogenesis. We have investigated the extent to which PEITC modulates the clastogenicity of standard genotoxicants, mitomycin C and cyclophosphamide, using bone marrow cells of Swiss albino mice. PEITC, 1 mumol/kg body weight in corn oil was administered by gavage for 7 consecutive days to prime the animals. 24 h later, mice received a single dose of cyclophosphamide (10 or 20 mg/kg body weight) or mitomycin C (1 or 2 mg/kg body weight) intraperitoneally. Clastogenicity of the chemicals was compared using PEITC-primed and non-primed animals 24 h after clastogen treatment. As a single agent, PEITC is not clastogenic even after 7 days of priming. Oral priming with PEITC decreased the aberrations per cell values by 22-67% in all cases. PEITC could only alleviate the clastogenicity of 1 mg/kg body weight mitomycin C to near-control values (p < or = 0.05). Although PEITC is reported to be effective against N-nitrosamine-induced tumorigenesis by preventing metabolic activation and by blocking the reactive species formed, it is virtually ineffective against the clastogenicity of cyclophosphamide. The results of inhibition by PEITC of the clastogenicity of mitomycin C suggest that the modulation of mitomycin C bio-activation contributes to, but may not be sufficient for, PEITC chemoprevention of clastogenicity by mitomycin C.

Animals↗