PubMed Health⌕ Search

Biomedical subjects

R Kumari

Publications and source records attributed to R Kumari.

At least 19 recordsLinked to original sources
PubMed2001

Macrophage migration inhibitory factor of the parasitic nematode Trichinella spiralis.

cDNAs were obtained for macrophage migration-inhibitory factor (MIF)/L-dopachrome methyl ester tautomerase homologues from the parasitic nematodes Trichinella spiralis (TsMIF) and Trichuris trichiura (TtMIF). The translated sequences, which were partly confirmed by sequencing of proteolytic fragments, show 42 and 44% identity respectively with human or mouse MIF, and are shorter by one C-terminal residue. Unlike vertebrate MIF and MIF homologues of filarial nematodes, neither TsMIF nor TtMIF contain cysteine residues. Soluble recombinant TsMIF, expressed in Escherichia coli showed secondary structure (by CD spectroscopy) and quaternary structure (by light-scattering and gel filtration) similar to that of the trimeric mammalian MIFs and D-dopachrome tautomerase. The catalytic specificity of recombinant TsMIF in the ketonization of phenylpyruvate (1.4x10(6) M(-1) x s(-1)) was comparable with that of human MIF, while that of p-hydroxyphenylpyruvate (9.1x10(4) M(-1) x s(-1)) was 71-fold lower. TsMIF showed high specificity in tautomerization of the methyl ester of L-dopachrome compared with non-esterified L-dopachrome (>87000-fold) and a high kcat (approximately 4x10(4) s(-1). The crystal structure, determined to 1.65 A (1 A=0.1 nm), was generally similar to that of human MIF, but differed in the boundaries of the putative active-site pocket, which can explain the low activity towards p-hydroxyphenylpyruvate. The central pore was blocked, but was continuous, with the three putative tautomerase sites. Recombinant TsMIF (5 ng/ml-5 pg/ml) inhibited migration of human peripheral-blood mononuclear cells in a manner similar to that shown by human MIF, but had no effect from 5 to 500 ng/ml on anti-CD3-stimulated murine T-cell proliferation. TsMIF was detected in supernatants of T. spiralis larvae cultured in vitro at 6 ng/ml (55 ng/mg total secreted protein). In conclusion TsMIF has structural, catalytic and cell-migration-inhibitory properties which indicate that it is partially orthologous to mammalian MIF.

Amino Acid Sequence↗
PubMed2001

Captopril and its time of administration in myocardial ischaemic-reperfusion injury.

The present study was designed to investigate the role of captopril in an in vivo model of myocardial ischaemic-reperfusion injury with respect to its time of administration. In open-chest pentobarbitone anaesthetized cats, the left anterior descending coronary artery was occluded for 15 min followed by 60 min of reperfusion. Vehicle (saline) or captopril (4 mg kg(-1)) was administered 10 min before instituting ischaemia (pre-treatment) or 5 min before reperfusion (post-treatment). In the vehicle-treated group, ischaemic-reperfusion injury (IRI) was evidenced by enhanced plasma renin activity, depression of global haemodynamic function (mean arterial pressure, left ventricular-end-diastolic-pressure, peak positive and negative dP/dt) along with depletion of myocardial high energy phosphate (HEP) compounds. Oxidant stress in IRI was evidenced by raised levels of myocardial thiobarbituric acid reactive substances (TBARS) and depletion of endogenous myocardial antioxidants (glutathione, superoxide dismutase and catalase). Pre-treatment with captopril prevented (i) loss of myocardial haemodynamic function, (ii) rise in TBARS and (iii) depletion of myocardial HEP compounds. However, in the post-treatment group, only partial recovery of myocardial haemodynamic function, with no significant reduction in TBARS, was observed. Glutathione, superoxide dismutase and catalase were unaffected by either treatment schedules. The results of the present study suggest that captopril is more effective in attenuating ischaemic-reperfusion injury when administered before ischaemia rather than before reperfusion.

Adenosine Triphosphate↗
PubMed2001

Agrobacterium tumefaciens-mediated genetic transformation of mungbean (Vigna radiata L. Wilczek) - a recalcitrant grain legume.

Agrobacterium-mediated transformation of Vigna radiata L. Wilczek has been achieved. Hypocotyl and primary leaves excised from 2-day-old in-vitro grown seedlings produced transgenic calli on B(5) basal medium supplemented with 5x10(-6) M BAP, 2.5x10(-6) M each of 2,4-D and NAA and 50 mg l(-1) kanamycin after co-cultivation with Agrobacterium tumefaciens strains, LBA4404 (pTOK233), EHA105 (pBin9GusInt) and C58C1 (pIG121Hm) all containing beta-glucuronidase (gusA) and neomycin phosphotransferase II (nptII) marker genes. Transformed calli were found resistant to kanamycin up to 1000 mg(.)l(-1). Gene expression of kanamycin resistance (nptII) and gusA in transformed calli was demonstrated by nptII assay and GUS histochemical analysis, respectively. Stable integration of T-DNA into the genome of transformed calli of mungbean was confirmed by Southern blot analysis. Transgenic calli could not regenerate shoots on B(5) or B(5) containing different cytokinins or auxins alone or in combination. However, for the first time, transformed green shoots showing strong GUS activity were regenerated directly from cotyledonary node explants cultured after co-cultivation with LBA4404 (pTOK233) on B(5) medium containing 6-benzylaminopurine (5x10(-7) M) and 75 mg l(-1) kanamycin. The putative transformed shoots were rooted on B(5)+indole-3-butyric acid (5x10(-6) M) within 10-14 days and resulted plantlets subsequently developed flowers and pods with viable seeds in vitro after 20 days of root induction. The stamens, pollen grains and T(0) seeds showed GUS activity. Molecular analysis of putative transformed plants revealed the integration and expression of transgenes in T(0) plants and their seeds.

Journal Article↗
PubMed2001

Effect of chronic treatment with bark of Terminalia arjuna: a study on the isolated ischemic-reperfused rat heart.

Dried pulverized bark of Terminalia arjuna Linn (TA) was administered orally to Wistar albino rats (120-150 g) in two doses [500 and 750 mg/kg in 2% carboxy methyl cellulose (CMC)], 6 days per week for 12 weeks. Thereafter, rats were sacrificed either for determination of baseline changes in cardiac endogenous antioxidant compounds [superoxide dismutase (SOD), reduced glutathione (GSH) and catalase (CAT)] or the hearts were subjected to oxidative stress associated with in vitro ischemic-reperfusion injury (IRI). There was significant increase in the baseline contents of thiobarbituric acid reactive substance (TBARS) (a measure of lipid peroxidation) with both doses of TA. However, only in the 500 mg/kg treated group, this was accompanied by a simultaneous increase in SOD, GSH and CAT levels, but not in the 750 mg/kg treated group, where only CAT was raised. Significant rise in myocardial TBARS and loss of SOD, CAT and GSH (suggestive of increased oxidative stress) occurred in the vehicle-treated hearts subjected to in vitro IRI. Only hearts, harvested from the 500 mg/kg rats treated rats, were significantly protected from oxidative stress, when subjected to in vitro IRI. The results suggest that crude bark of TA augments endogenous antioxidant compounds of rat heart and also prevents oxidative stress associated with IRI of the heart.

Animals↗
PubMed2000

Prevention of renal ischemia-reperfusion-induced injury in rats by picroliv.

Picroliv is a potent antioxidant extracted from the roots and rhizome of Picrorhiza kurrooa. It has been shown to impart significant hepatoprotective activities, partly by modulation of free radical-induced lipid peroxidation. Lipid peroxidation and reactive oxygen species are associated with tissue injury in post-ischemic acute renal failure. The efficacy of picroliv was assessed in an in vivo model of renal ischemia-reperfusion injury (IRI) in rats at a dose of 12 mg/kg orally for 7 days. The animals were killed at various times after reperfusion. Increased lipid peroxidation and apoptotic cell number reflected the oxidative damage following renal IRI. Picroliv-pretreated rats exhibited lower lipid peroxidation, improved antioxidant status, and reduced apoptosis, indicating better viability of renal cells. Immunohistochemical studies revealed that picroliv pretreatment attenuated the expression of intercellular adhesion molecule-1 in the glomerular region. These results suggested that picroliv pretreatment protects rat kidneys from IRI, perhaps by modulation of free radical damage and adhesion molecules.

Animals↗
PubMed2000

Picroliv preconditioning protects the rat liver against ischemia-reperfusion injury.

Cell death following ischemia-reperfusion injury is a major concern in clinical issues such as organ transplantation and trauma. The need to identify agents with a potential for preventing such damage has assumed great importance. We have evaluated the efficacy of picroliv, a potent antioxidant derived from the plant Picrorhiza kurrooa, in protecting against hepatic ischemia-reperfusion injury in vivo. Picroliv was fed to male Sprague Dawley rats in a dose of 12 mg/kg once daily by oral gavage for 7 days prior to hepatic ischemia. Ischemia was induced by occluding the hepatic pedicel with a microaneurysm clip for 30 min and reperfusion was allowed thereafter for varying period (15-120 min) by releasing the microaneurysm clip. Picroliv pretreatment resulted in better hepatocyte glycogen preservation and reduced apoptosis. Reduction in apoptosis was associated with decreased mRNA expression of caspase-3 and Fas. Oxidant induced cellular damage as measured by tissue malondialdehyde (MDA) levels was significantly less following picroliv pretreatment. Both a reduction in neutrophil infiltration and an increased level of intracellular antioxidant enzyme superoxide dismutase possibly contributed to the reduction in tissue lipid peroxidation. Tissue inflammatory cytokines level of interleukin-1alpha (IL-1alpha) and interleukin-1beta (IL-1beta) was also lower in picroliv group. Furthermore, picroliv pretreatment resulted in enhanced proliferating cell nuclear antigen (PCNA) immunoreactivity. These studies strongly suggest picroliv to be a promising agent for ameliorating injury following ischemia-reperfusion.

Animals↗
PubMed2000

Regulation and manipulation of the gene clusters encoding type-I PKSs.

Modular polyketide synthases are large, multifunctional enzyme complexes that are involved in the biosynthesis of important polyketides. Recent studies have revolutionized our understanding of the linear organization of polyketide-synthase-gene clusters. They have provided crucial information on the initiation, elongation and termination of polyketide chains, and thus a rational basis for the generation of novel compounds. Combinatorial libraries have helped this field to move from a random approach to a more empirical phase. The large number of diverse analogs of antibiotics that are presently produced demonstrate the enormous potential of combinatorial biosynthesis.

Combinatorial Chemistry Techniques↗
PubMed2000

Antiproliferative effect of UTP on human arterial and venous smooth muscle cells.

We have investigated the hypothesis that responses associated with proliferation are regulated by extracellular nucleotides such as ATP and UTP in cultured human vascular smooth muscle cells (VSMC) derived from internal mammary artery (IMA) and saphenous vein (SV). Platelet-derived growth factor (PDGF), ATP, and UTP each generated an increase in cytosolic free Ca(2+) concentration ([Ca(2+)](i)) in both IMA- and SV-derived cells in the absence of detectable inositol 1,4,5-trisphosphate production. ATP alone had no effect on [(3)H]thymidine incorporation into DNA, but with a submaximal concentration of PDGF it raised [(3)H]thymidine incorporation in SV- but not IMA-derived cells. UTP alone also was without effect on [(3)H]thymidine incorporation or cell number. However, in both SV- and IMA-derived cells, UTP reduced the PDGF-stimulated [(3)H]thymidine response and PDGF-stimulated cell proliferation. This cannot be explained by an inhibitory effect on the p42/p44 mitogen-activated protein kinase (MAPK) cascade, since this response to PDGF was not attenuated by UTP. We conclude that, in human VSMC of both arterial and venous origin, UTP acts as an anti-proliferative regulator.

Adenosine Triphosphate↗
PubMed1999

Importance of timing of magnesium administration: a study on the isolated ischemic-reperfused rat heart.

The present study attempted to explore the antioxidant potential of magnesium (2 and 10 mM) in the postischemic isolated rat heart. Magnesium demonstrated a significant antioxidant effect, as deduced by thiobarbituric acid reactive material and glutathione levels. However, this effect was evident only when magnesium was administered prior to ischemia but not when administered during reperfusion. On the other hand, attenuation of calcium accumulation following reperfusion was noted in both treatment schedules and showed dose dependency when administered during reperfusion. Thus, the results of this study strongly suggests an antioxidant effect of magnesium which is distinct from its calcium antagonising effects and it also stresses the critical role played by the time of administration of magnesium.

Animals↗
PubMed1999

Effect of flavone in a canine model of myocardial stunning.

Putative cardioprotective action of flavone (10, 20 and 30 mg/kg) was investigated in a canine model of regional ischemia (20 min) followed by 60 min of reperfusion. In animals pretreated with vehicle, myocardial stunning was evidenced by significant changes in hemodynamic parameters (depressed mean arterial pressure, LV peak (+) dP/dt, LV peak (-) dP/dt and elevated LV end-diastolic pressure) and biochemical parameters (decreased myocardial ATP and rise in plasma malondialdehyde or MDA; a marker of free radical-induced injury). A reduction in plasma MDA was noted with 20 and 30 mg/kg flavone, although attenuation of myocardial dysfunction was evident with all the three doses. The results suggest that besides a significant dose-dependent antioxidant effect, flavone may also have some cardioprotective actions per se, which needs to be further investigated.

Adenosine Triphosphate↗
PubMed1998

Protein kinase C in platelets of depressed patients.

BACKGROUND: We studied the role of protein kinase C (PKC), a major regulatory enzyme and an important component of the phosphoinositide signaling system, in depression. METHODS: PKC was determined using [3H]phorbol dibutyrate (PDBu) as the radioligand in the membranal and cytosolic fractions of platelets obtained from hospitalized drug-free depressed patients during a baseline period and from drug-free normal control subjects. RESULTS: We observed that the [3H]PDBu binding was significantly higher in the cytosolic fraction obtained from platelets of depressed patients compared to normal control subjects. CONCLUSIONS: Our studies indicate increased formation of PKC in platelets of depressed patients. The significance and mechanisms involved in increased PKC in the cytosolic fraction of platelets are unclear, but they suggest that increased PKC may be associated with the pathophysiology of depressive illness.

Adult↗
PubMed1998

Inhibition of platelet aggregation by a protein factor present in rat peripheral polymorphonuclear leukocyte supernatant.

In the present investigation, effect of rat peripheral polymorphonuclear leukocyte (PMNL) supernatant was investigated on platelet aggregation. Rat PMNLs suspended in Hanks balanced salt solution (HBSS, pH 7.4) were incubated at 37 degrees C for different time intervals and cell-free supernatant was obtained by centrifugation. Supernatant was found to inhibit adenosine diphosphate (ADP), arachidonic acid (AA), and calcium ionophore-induced platelet aggregation. The inhibitory effect of PMNL supernatant on platelet aggregation was not blocked by methylene blue (10 microM) or adenosine deaminase (5 U ml(-1)) pretreatment, suggesting that the inhibitory effect of the supernatant on aggregation was not mediated by nitric oxide (NO) or ecto-ADPase. The effect of PMNL supernatant on platelet aggregation was abolished by preheating the supernatant at 95 degrees C for 5 minutes. Pretreatment of the supernatant with protease inhibitors abolished the inhibitory effect of supernatant on platelet aggregation suggesting that the factor may be a protein or peptide with protease activity. Partial purification of biologically active factor by fine particle liquid chromatography (FPLC) by using Superose 6B column yielded a peak with a molecular weight of approximately 30 kDa having antiaggregatory activity. The results obtained suggest that rat peripheral PMNLs release yet another factor(s) that inhibits platelet aggregation. The factor is a heat labile protein with a molecular weight of approximately 30 kDa.

Adenosine Deaminase↗
PubMed1998

Alterations in the vasoreactivity of hypertensive rat aortic rings: role of nitric oxide and superoxide radicals.

OBJECTIVES: Present study was undertaken to investigate involvement of nitric oxide (NO) and superoxide radicals in the modulation of vasoreactivity in a model of renal hypertension. METHOD: Hypertension was induced in the male Sprague Dawley rats by aortic banding just above the left kidney. Relaxation or contraction following cumulative addition of acetylcholine (Ach, 1 x 10(-8) to 1 x 10(-5) M) or phenylephrine (PE, 1 x 10(-8) to 1 x 10(-5) mol/l) was studied in the aortic rings obtained from sham operated normotensive, hypertensive and captopril pretreated rats. Ach and PE responses were taken in the presence or absence of NO synthase inhibitor (L-NAME; 1 x 10(-5) and 1 x 10(-4) mol/l). Spontaneous release of NO from the aortic rings was evaluated by studying the inhibition of adenosine diphosphate stimulated platelet aggregation, while superoxide radicals were estimated by cytochrome c reduction method. RESULTS: Ach induced vasorelaxation in PE precontracted rings was impaired following 8 wk after aortic banding, while spontaneous release of NO remained unaffected. Captopril pretreatment restored the aortic ring responsiveness to Ach. An increase in the superoxide radical generation and PE induced contraction following L-NAME treatment in the hypertensive rat aortic rings was observed. CONCLUSION: Attenuation in the Ach induced NO release and augmentation in the superoxide radical generation seems to play an important role in the modulation of vasoreactivity following renal hypertension in rats.

Acetylcholine↗
PubMed1998

Susceptibility status of malaria vectors to insecticides in India.

The use of chemical insecticides for control of malaria vector populations continues to be the mainstay of malaria control strategy in India. Monitoring vector susceptibility to chemical insecticides is an important activity under the National Malaria Eradication Programme to ensure judicious and effective use of chemical Insecticides. 72 entomological zones were established under NMEP in 1977 for undertaking entomological studies in the malaria problematic areas. These zones have been generating insecticide susceptibility data in respect of the various malaria vectors. In this paper the insecticide susceptibility data, in respect of major vectors of malaria as on 1997, is presented.

Animals↗
PubMed1997

Alterations in the free radical generation and nitric oxide release from rat peripheral polymorphonuclear leukocytes following thrombosis.

The present investigation was undertaken to study the alterations in free radical generation and release of nitric oxide (NO) from polymorphonuclear leukocytes (PMNLs) following thrombosis. Thrombosis was induced in rats by intravenous injection of collagen and adrenaline. PMNLs were separated from rat blood by using dextran sedimentation and Ficoll-Hypaque. Arachidonic acid (AA), formyl methionine leucine phenylalanine (FMLP) and opsonized zymosan (OZ) induced free radical generation was estimated as luminol (LCL) and Lucigenin (LUCDCL) dependent chemiluminescence. PMNLs nitric oxide synthase (NOS) activity and NO release were measured by using [14C] L-Arginine (L-Arg) and oxy-hemoglobin respectively. LCL and LUCDCL responses in rat PMNLs were significantly attenuated following thrombosis. There was no change in the release of myeloperoxidase enzyme (MPO) from PMNLs obtained following thrombosis. PMNLs NOS activity and NO release were also found to be increased after thrombosis. Pretreatment of rat PMNLs with 10 mM L-NAME (NO precursor) or 100 microM sodium nitroprusside (NO donor), resulted in significant reduction of AA induced LCL response. Results obtained indicate that NO release form PMNLs was augmented while free radical generation response was attenuated after the induction of thrombosis.

Animals↗