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Biomedical subjects

S Tiwari

Publications and source records attributed to S Tiwari.

At least 19 recordsLinked to original sources
PubMed2006

Evaluation of ambient air pollution impact on carrot plants at a suburban site using open top chambers.

The present experiment was done to evaluate the impact of ambient air pollution on carrot (Dacus carota var. Pusa Kesar) plants using open top chambers (OTCs) ventilated with ambient (NFCs) or charcoal filtered air (FCs) at a suburban site of Varanasi, India. Various morphological, physiological and biochemical characteristics of the plants were studied at different growth stages. Air monitoring data clearly showed high concentrations of SO2, NO2 and O3 in the ambient air of study site. SO2 and NO2 concentrations were higher during early growth stages of carrot, whereas O3 concentration was highest during later growth stages. Filtration of air has caused significant reductions in all the three pollutant concentrations in FCs as compared to NFCs. Plants growing in FCs showed significantly higher photosynthetic rate, stomatal conductance, water use efficiency and variable fluorescence as compared to plants growing in NFCs. Protein content also showed a similar pattern, however, lipid peroxidation, ascorbic acid content and peroxidase activity were higher in plants growing in NFCs as compared to FCs. Shoot length, number of leaves per plant, leaf area and root and shoot weight increased significantly upon filtration of ambient air. Total nitrogen decreased significantly in root, but increased significantly in shoot of plants grown in NFCs. Total P, Mg, Ca and K contents decreased significantly in plants grown in NFCs as compared to FCs. The individual pollutant concentrations were below threshold for plant injury, but the combined effect of all the three seems to act synergistically in causing greater adverse impact on dry weight and physiology of carrot plants. The study clearly indicates that air pollutants are high enough in the ambient air to cause significant unfavorable impact on carrot plants. The work further supports the usefulness of OTCs for assessing air pollution damage under field conditions in developing countries.

Air Pollutants↗
PubMed2006

Evaluation of cerebral blood flow by single-photon emission computed tomography in young Asian Indians with hypertension.

The objective of the study was to investigate abnormalities of regional cerebral blood flow (rCBF) in young (age 33.0+/-6.3 years; range 21-45 years) non-diabetic and normolipidemic Asian Indians with hypertension. The rCBF was assessed with single-photon emission computed tomography (SPECT) in patients with hypertension (n = 33) and healthy controls (n = 20). The SPECT findings were normal in 41 subjects and showed abnormalities of cerebral perfusion in 10 subjects, all of which were hypertensive patients. These observations are extremely important for a vast number of young hypertensive patients in India. To prevent cerebrovascular accidents in future, patients with hypertension and decreased rCBF should be carefully monitored and their hypertension should be strictly controlled. These subjects may also be researched as potential candidates for preventive antiplatelet therapy.

Adult↗
PubMed2005

Sympathetic hyperactivity in patients of bronchial asthma.

The bronchoconstricting and bronchodilating divisions of the autonomic nervous system control airway caliber of lungs. Parasympathetic hyperactivity in asthmatics eventuates in broncho-constriction. Sympathetic activity increases to combat this but fails to control bronchoconstriction due to negligible innervations of the airway smooth muscles although it causes vasoconstriction of blood vessels. In this study the effects of autonomic function test for sympathetic division were seen on selected patients and controls. Our results indicate sympathetic hyperactivity or an increased alpha-adrenergic input in asthmatics.

Adult↗
PubMed2005

Cardiac stem cell therapy for myocardial regeneration. A clinical perspective.

Myocardial infarction and other pathologic conditions of the heart result in loss of cardiomyocytes, scar formation, ventricular remodeling, and eventually heart failure. Since pharmacologic and interventional strategies fail to regenerate dead myocardium, heart failure continues to be a major health problem worldwide. Recent studies in animal models of myocardial infarction and heart failure have demonstrated that various subsets of adult primitive cells can regenerate functional cardiomyocytes and cardiac vasculature with improvement in cardiac structure and function. Small clinical trials of cell therapy in patients with myocardial infarction and ischemic cardiomyopathy have recapitulated these beneficial effects in humans with infarct size reduction and improvement in ejection fraction, myocardial perfusion, and wall motion. Several phenotypically distinct cell populations have been utilized for cardiac regeneration, and the relative merits of one cell over another remain to be determined. The recent discovery of adult cardiac stem cells has sparked intense hope for myocardial regeneration with cells that are from the heart itself and are thereby inherently programmed to reconstitute cardiac tissue. The purpose of this review is to summarize the evidence regarding the feasibility of cardiac repair in humans via adult stem/progenitor cells, and to discuss the potential utility of cardiac stem cells for therapeutic myocardial regeneration.

Adult↗
PubMed2004

Simultaneous exposure of excess fluoride and calcium deficiency alters VDR, CaR, and calbindin D 9 k mRNA levels in rat duodenal mucosa.

Fluoride ingestion reduces intestinal calcium absorption; its molecular basis has not been studied. We studied the mRNA expression of calcium-sensing receptor (CaR), vitamin D receptor (VDR) and calbindin D 9 k (D 9 k) by northern blot analysis in the duodenal mucosa of rats. Weanling pups fed with chow diet containing adequate calcium (0.5% w/w) and drinking water (NaF < 1 ppm) served as controls (Group I) and were studied at 9 and 15 weeks. The pups, born to rats fed with a calcium-deficient diet (0.03%) and excess fluoride water (NaF 50 ppm), were continued on the same diet and water (Group II) until 9 weeks of age. Subsequently, Group II rats were divided into 4 subgroups; 3 subgroups with fluoride free water [II-A adequate calcium, II-B excess calcium (Ca 2%) and II-D calcium deficient], whereas II-C received fluorinated water and adequate calcium diet until 15 weeks. At 9 weeks, as compared to group-I, group-II had decreased VDR (P < 0.001) and D 9 k mRNA (P < 0.001), whereas CaR mRNA levels increased (P < 0.05). At 15 weeks, as compared to group-I, VDR mRNA further reduced in group II-D (P < 0.001) and II-C (P < 0.001), whereas it increased in group II-A. Removal of fluoride ingestion and calcium replenishment increased D 9 k mRNA expression, maximally in adequate calcium group (P < 0.001), while it was further reduced in group II-C (P < 0.001). CaR expression decreased significantly in all the groups. We conclude that excess fluoride reduces the mRNA levels of VDR and D 9 k in the duodenal mucosa of rats, thereby possibly reducing calcium absorption. Calcium supplementation with simultaneous fluoride removal improves their expression.

Animals↗
PubMed2003

Effect of oophorectomy on expression of calcium sensing receptor mRNA in rat duodenal mucosa.

Calcium sensing receptor (CaR) in duodenal mucosa may be involved in active calcium absorption. Estrogen deficiency results in decreased intestinal calcium absorption. Effects of bilateral oophorectomy (OVX) have been studied on calcium homeostasis, bone mineral density (BMD) and CaR mRNA levels in duodenal mucosa at 4 weeks in adult female Sprague Dawley rats and compared with those in sham-operated and control group. There was no significant change in serum corrected calcium, inorganic phosphorous, calcidiol and intact parathyroid hormone in all the three groups. OVX rats had a significant decline in serum estrogen (E2) levels and alkaline phosphatase. They also had a significant decrease in BMD (DXA) at lumbar spine in vivo, and proximal and distal tibia in vitro while there was no significant change in serum E2 and BMD parameters in sham-operated and control rats. Northern blot analysis revealed no significant change in the CaR mRNA expression in duodenal mucosa in all three groups. The results suggests that CaR mRNA expression in duodenal mucosa is not affected by physiological circulating concentrations of estradiol in rats.

Animals↗
PubMed2002

Short-term androgen deprivation does not alter CaR and VDR mRNA expression in duodenal mucosa in male rats.

Androgen deprivation is associated with decline in intestinal calcium absorption. The effect of androgen on CaR and VDR intestinal mucosa has not yet been studied. Calcium homeostasis, a real bone mineral density (aBMD, dual energy X-ray absorptiometry) and expression of CaR and VDR mRNA in duodenal mucosa of orchidectomized (ORX) and sham operated (Sham) adult Sprague Dawley rats at 4 week have been studied. There was no significant difference in serum calcium, alkaline phosphatase, calcidiol and calcitriol levels between both the groups. Serum testosterone (T) (ng/dl) and inorganic phosphorous (iP) (mg/dl) levels were significantly lower in ORX rats. As compared to sham rats, ORX rats had significant decline in in-vitro aBMD at proximal, middle and distal tibia, proximal, mid and distal femur and femoral neck (P < 0.05). Northern blot analysis revealed no significant alteration in the CaR and VDR mRNA expression in duodenal mucosa in ORX rats. CaR and VDR mRNA expression in duodenal mucosa is therefore, not affected by physiological concentrations of testosterone in rats.

Androgens↗
PubMed2001

The tumor autocrine motility factor receptor, gp78, is a ubiquitin protein ligase implicated in degradation from the endoplasmic reticulum.

gp78, also known as the tumor autocrine motility factor receptor, is a transmembrane protein whose expression is correlated with tumor metastasis. We establish that gp78 is a RING finger-dependent ubiquitin protein ligase (E3) of the endoplasmic reticulum (ER). Consistent with this, gp78 specifically recruits MmUBC7, a ubiquitin-conjugating enzyme (E2) implicated in ER-associated degradation (ERAD), through a region distinct from the RING finger. gp78 can target itself for proteasomal degradation in a RING finger- and MmUBC7-dependent manner. Importantly, gp78 can also mediate degradation of CD3-delta, a well-characterized ERAD substrate. In contrast, gp78 lacking an intact RING finger or its multiple membrane-spanning domains stabilizes CD3-delta. gp78 has thus been found to be an example of a mammalian cellular E3 intrinsic to the ER, suggesting a potential link between ubiquitylation, ERAD, and metastasis.

Animals↗
PubMed2001

A lineage-restricted and divergent beta-tubulin isoform is essential for the biogenesis, structure and function of blood platelets.

BACKGROUND: Mammalian megakaryocytes release blood platelets through a remarkable process of cytoplasmic fragmentation and de novo assembly of a marginal microtubule band. Cell-specific components of this process include the divergent beta-tubulin isoform beta1 that is expressed exclusively, and is the predominant isoform, in platelets and megakaryocytes. The functional significance of this restricted expression, and indeed of the surprisingly large repertoire of metazoan tubulin genes, is unclear. Fungal tubulin isoforms appear to be functionally redundant, and all mammalian beta-tubulins can assemble in a variety of microtubules, whereas selected fly and worm beta-tubulins are essential in spermatogenesis and neurogenesis. To address the essential role of beta1-tubulin in its natural context, we generated mice with targeted gene disruption. RESULTS: beta1-tubulin(-/-) mice have thrombocytopenia resulting from a defect in generating proplatelets, the immediate precursors of blood platelets. Circulating platelets lack the characteristic discoid shape and have defective marginal bands with reduced microtubule coilings. beta1-tubulin(-/-) mice also have a prolonged bleeding time, and their platelets show an attenuated response to thrombin. Two alternative tubulin isoforms, beta2 and beta5, are overexpressed, and the total beta-tubulin content of beta1-tubulin(-/-) megakaryocytes is normal. However, these isoforms assemble much less efficiently into platelet microtubules and are thus unable to compensate completely for the absence of beta1-tubulin. CONCLUSIONS: This is the first genetic study to address the essential functions of a mammalian tubulin isoform in vivo. The results establish a specialized role for beta1-tubulin in platelet synthesis, structure, and function.

Animals↗
PubMed2001

Endoplasmic reticulum (ER)-associated degradation of T cell receptor subunits. Involvement of ER-associated ubiquitin-conjugating enzymes (E2s).

Degradation of proteins from the endoplasmic reticulum is fundamental to quality control within the secretory pathway, serves as a way of regulating levels of crucial proteins, and is utilized by viruses to enhance pathogenesis. In yeast two ubiquitin-conjugating enzymes (E2s), UBC6p and UBC7p are implicated in this process. We now report the characterization of murine homologs of these E2s. MmUBC6 is an integral membrane protein that is anchored via its hydrophobic C-terminal tail to the endoplasmic reticulum. MmUBC7, which is not an integral membrane protein, shows significant endoplasmic reticulum colocalization with MmUBC6. Overexpression of catalytically inactive MmUBC7 significantly delayed degradation from the endoplasmic reticulum of two T cell antigen receptor subunits, alpha and CD3-delta, and suggests a role for the ubiquitin conjugating system at the initiation of retrograde movement from the endoplasmic reticulum. These findings also implicate, for the first time, a specific E2 in degradation from the endoplasmic reticulum in mammalian cells.

Amino Acid Sequence↗
PubMed1999

PTPROt: an alternatively spliced and developmentally regulated B-lymphoid phosphatase that promotes G0/G1 arrest.

Protein tyrosine phosphatases (PTP) regulate the proliferation, differentiation, and viability of lymphocytes by modulating their signaling pathways. By using the differential display assay, we have cloned a putative receptor-type PTP, which is predominantly expressed in B-lymphoid tissues (lymph nodes and spleen). This PTP, termed PTPROt (truncated), is a tissue-specific alternatively-spliced form of a human epithelial PTP, PTPRO (PTPU2/GLEPP1). Whereas the epithelial PTPRO includes an approximately 800-amino acid extracellular domain, the major (3 kb) PTPROt cDNA predicts a unique 5' untranslated region and truncated (8 amino acids) extracellular domain with a conserved transmembrane region and single catalytic domain. PTPROt cDNAs encode functional approximately 47-kD and approximately 43-kD PTPs, which are most abundant in normal naive quiescent B cells and decreased or absent in germinal center B cells and germinal center-derived diffuse large B-cell lymphomas. Because PTPROt was predominantly expressed in naive quiescent B cells, the enzyme's effects on cell-cycle progression were examined. When multiple stable PTPROt sense, antisense, and vector only B-cell transfectants were grown in reduced serum and synchronized with nocodazole, PTPROt sense clones exhibited markedly increased G0/G1 arrest. Taken together, these data implicate PTPROt in the growth control of specific B-cell subpopulations.

Alternative Splicing↗
PubMed1999

Recurrent acute coronary events in a patient with primary antiphospholipid syndrome: successful management with intracoronary stenting.

Patients with Antiphospholipid syndrome usually present with recurrent deep vein thrombosis, pulmonary thromboembolism and thromboembolic stroke. Recurrent coronary events, though reported, are rare. We describe an unusual case of Antiphospholipid syndrome who presented with recurrent acute ischaemic events in two different coronary territories, who was managed successfully with intracoronary stenting.

Adult↗
PubMed1999

A role for dipeptidyl peptidase IV in suppressing the malignant phenotype of melanocytic cells.

Dipeptidyl peptidase IV (DPPIV) is a cell surface peptidase expressed by normal melanocytes, epithelial cells, and other cells. Malignant cells, including melanomas and carcinomas, frequently lose or alter DPPIV cell surface expression. Loss of DPPIV expression occurs during melanoma progression at a stage where transformed melanocytes become independent of exogenous growth factors for survival. Tetracycline-inducible expression vectors were constructed to express DPPIV in human melanoma cells. Reexpressing DPPIV in melanoma cells at or below levels expressed by normal melanocytes induced a profound change in phenotype that was characteristic of normal melanocytes. DPPIV expression led to a loss of tumorigenicity, anchorage-independent growth, a reversal in a block in differentiation, and an acquired dependence on exogenous growth factors for cell survival. Suppression of tumorigenicity and reversal of a block in differentiation were dependent on serine protease activity, assessed using mutant DPPIV molecules containing serine-->alanine substitutions. Surprisingly, dependence on exogenous growth factors was not dependent on serine protease activity. Reexpression of either wild-type or mutant DPPIV rescued expression of a second putative cell surface serine peptidase, fibroblast activation protein alpha, which can form a heterodimer with DPPIV. This observation suggests that rescue of fibroblast activation protein alpha may play a role in regulating growth of melanocytic cells. These results support the view that downregulation of DPPIV is an important early event in the pathogenesis of melanoma.

Apoptosis↗
PubMed1998

Influence of sub valvular pathology on immediate results and follow up events of Inoue balloon mitral valvotomy.

We evaluated the influence of sub valvular pathology (SVP) on the immediate results and follow up events of Inoue Balloon Mitral Valvotomy (IBMY) in 206 patients with severe SVP (Group I) and compared their outcome with 206 age and sex matched patients selected from the rest of 619 patients having mild/moderate SVP (Group II). Pre-procedure echocardiographic recordings were reviewed and mitral valve morphology was evaluated using U.S. California Score. The severe SVP group had lower mitral valve areas (MVA) (0.7 cm2 vs. 0.8 cm2) and higher mean pulmonary artery pressure (MPAP) (46.3+/-16.9 mmHg vs. 40.7+/-16.25 mmHg) and mean pulmonary capillary wedge pressure (PCWP) (27.5+/-7.3 mmHg vs. 25.7+/-8.0 mmHg) (p<0.001). IBMV was done using standard technique. The procedure was technically successful in 192/206 patients (93.2%) in group I and 187/206 (91%) in group II (p=ns). The mean transmitral gradient decreased from 24.8+/-7.6 mmHg to 7.46+/-3.4 mmHg while mean PCWP fell from 27.5+/-7.3 mmHg to 12.2+/-5.6 mmHg and MPAP fell from 46.3+/-16.9 mmHg to 23.6+/-12.2 mmHg (p=<0.001). MVA increased from 0.7+/-0.2 cm2 to 1.7+/-0.4 cm2 (p=<0.001). Severe mitral regurgitation (MR) occurred in 2 patients out of which one patient, who had associated coronary artery disease, died post operatively, and moderate MR occurred in 8 patients. The results achieved in patients with severe SVP were not statistically different from those with mild/moderate SVP. The benefits achieved immediate post IBMV were sustained in 184 patients with severe SVP who were available for follow up at a mean duration of 15.2 months (range 3 months to 51 months). Thus IBMV is safe and effective in patients with severe SVP. This group of patients with severe SVP are more hemodynamically deranged pre-BMV and also achieve better hemodynamic benefit compared to those with mild/moderate SVP. Severe SVP does not have any adverse effect either on immediate results (success/occurrence of MR) or on intermediate term follow up.

Adult↗
PubMed1998

p130, p107, and pRb are differentially regulated in proliferating cells and during cell cycle arrest by alpha-interferon.

We have determined how the phosphorylation of the retinoblastoma family (pRb, p107, and p130) is governed in individual cell cycle phases of Daudi B-cells during cell cycle exit triggered by alpha-interferon (alpha-IFN). alpha-IFN causes dephosphorylation of pRb and loss of p130 phosphorylated Form 3. However, the change in p130 phosphorylation in response to alpha-IFN occurs before dephosphorylation of pRb is complete because loss of p130 Form 3 occurs throughout the cell cycle prior to complete arrest in G1, whereas pRb is dephosphorylated only in G1. In contrast, p107 is dephosphorylated and is then depleted from cells as they exit the cell cycle. p130, predominantly in Form 1, and hypophosphorylated pRb bind an E2F DNA binding site; p130 complexes E2F-4, whereas pRb binds both E2F-4 and E2F-1. The phosphorylated forms of E2F-4 that bind to the E2F DNA site are different from hyperphosphorylated E2F-4, which predominates in primary hemopoietic cells in G0. We conclude that although cell cycle arrest induced by alpha-IFN may be mediated in part by formation of a complex containing p130 and E2F-4, alpha-IFN does not induce hyperphosphorylation of E2F-4, which characterizes primary hemopoietic cells in G0.

B-Lymphocytes↗