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Biomedical subjects

A Chakravorty

Publications and source records attributed to A Chakravorty.

At least 19 recordsLinked to original sources
PubMed2006

Measurement of the asymmetry in the decay Omega+-->LamdaKappa+-->rhopi+Kappa+.

The asymmetry in the rho angular distribution in the sequential decay Omega+-->LamdaKappa+-->rhopi+Kappa+. has been measured to be alphaOmegaalphaLamda=[+1.16+/-0.18(stat)+/-0.17(syst)]x10(-2) using 1.89x10(6) unpolarized Omega+ decays recorded by the HyperCP (E871) experiment at Fermilab. Using the known value of alphaLamda, and assuming that alphaLamda=-alphaLamda, alphaOmega=[-1.81+/-0.28(stat)+/-0.26(syst)]x10(-2). A comparison between this measurement of alphaOmegaalphaLamda and recent measurements of alphaOmegaalphaLamda made by HyperCP shows no evidence of a violation of CP symmetry.

Journal Article↗
PubMed2005

Search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-).

A sensitive search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-) has been performed using a sample of approximately 10(9) Xi(-) hyperons produced in 800 GeV/c p-Cu collisions. We obtain B(Xi(-)-->pmu(-)mu(-))<4.0x10(-8) at 90% confidence, improving on the best previous limit by 4 orders of magnitude.

Journal Article↗
PubMed2005

Search for DeltaS = 2 nonleptonic hyperon decays.

A sensitive search for the rare decays Omega(-)--> Lambdapi(-) and Xi(0)--> ppi(-) has been performed using data from the 1997 run of the HyperCP (Fermilab E871) experiment. Limits on other such processes do not exclude the possibility of observable rates for |DeltaS| = 2 nonleptonic hyperon decays, provided the decays occur through parity-odd operators. We obtain the branching-fraction limits B(Omega(-)-->Lambdapi(-)) < 2.9 x 10(-6) and B(Xi(0)--> ppi(-)) < 8.2 x 10(-6), both at 90% confidence level.

Journal Article↗
PubMed2005

Evidence for the decay sigma+ --> pmu+ mu-.

We report the first evidence for the decay Sigma(+)-->pmu(+)mu(-) from data taken by the HyperCP (E871) experiment at Fermilab. Based on three observed events, the branching ratio is B(Sigma(+)-->pmu(+)mu(-))=[8.6(+6.6)(-5.4)(stat)+/-5.5(syst)]x10(-8). The narrow range of dimuon masses may indicate that the decay proceeds via a neutral intermediate state, Sigma(+)-->pP(0),P0-->mu(+)mu(-) with a P0 mass of 214.3+/-0.5 MeV/c(2) and branching ratio B(Sigma(+)-->pP(0),P0-->mu(+)mu(-))=[3.1(+2.4)(-1.9)(stat)+/-1.5(syst)]x10(-8).

Journal Article↗
PubMed2004

Search for CP violation in charged-Xi and Lambda hyperon decays.

We have compared the p and p angular distributions in 117 x 10(6) Xi- -->Lambdapi- -->ppi-pi- and 41 x 10(6) Xi+ -->Lambda pi+ -->p pi+pi+ decays using a subset of the data from the HyperCP experiment (E871) at Fermilab. We find no evidence of CP violation, with the direct-CP-violating parameter AXiLambda identical with (alphaXialphaLambda-alpha Xialpha Lambda)/(alphaXialphaLambda+alphaXialphaLambda)=[0.0+/-5.1(stat)+/-4.4(syst)] x 10(-4).

Journal Article↗
PubMed2003

Measurement of decay parameters for Xi- --> Lambda pi- decay.

Based on 1.35 x 10(6) polarized Xi(-) events, we measure the parameter phi(Xi) to be -1.61 degrees +/-2.66 degrees +/-0.37 degrees for the Xi(-)-->Lambda pi(-) decay. New results for the parameters beta(Xi) and gamma(Xi) are also presented. Assuming that the CP-violating phase difference is negligible, we deduce the strong phase difference between the P-wave and S-wave amplitudes of the Lambda pi final state to be 3.17 degrees +/-5.28 degrees +/-0.73 degrees, reducing the uncertainty in estimating the level of CP violation in Xi-hyperon decay.

Journal Article↗
PubMed2002

Observation of the decay K- --> pi(-)mu(+)mu(-) and measurements of the branching ratios for K+/- --> pi(+/-)mu(+)mu(-).

Using data collected with the HyperCP (E871) spectrometer during the 1997 fixed-target run at Fermilab, we report the first observation of the decay K--->pi(-)mu(+)mu(-) and new measurements of the branching ratios for K+/--->pi(+/-)mu(+)mu(-). By combining the branching ratios for the decays K+-->pi(+)mu(+)mu(-) and K--->pi(-)mu(+)mu(-), we measure Gamma(K+/--->pi(+/-)mu(+)mu(-))/Gamma(K+/--->all) = (9.8+/-1.0+/-0.5)x10(-8). The CP asymmetry between the rates of the two decay modes is [Gamma(K+-->pi(+)mu(+)mu(-))-Gamma(K--->pi(-)mu(+)mu(-))]/[Gamma(K+-->pi(+)mu(+)mu(-))+Gamma(K--->pi(-)mu(+)mu(-))] = -0.02+/-0.11+/-0.04.

Journal Article↗
PubMed2001

Oxygen atom transfer from nitrogenous ReVO reagents to diphosphines and subsequent transformations. Rhenium(III) products and reaction models.

The concerned diphosphines are Ph2P(CH2)nPPh2 (1), abbreviated PnP, and the ReVO reagents are ReOCl3L (2) and ReOCl3L' (3), where L and L' are the azopyridine and pyridine-imine ligands p-ClC6H4N=NC5H4N and p-MeC6H4N=CHC5H4N, respectively. One atom transfer from 2 to 1 has afforded Re(OPnP)Cl3L (4a, n = 1; 4b, n = 2; 4c, n = 3). Of these 4b and 4c are stable, but 4a undergoes spontaneous isomerization to Re(PlPO)Cl3L (5) in solution. Two-atom transfer studied with both 2 and 3 has afforded binuclear LCl3Re(OPnPO)ReCl3L (8a, n = 2; 8b, n = 3) and L'Cl3Re(OPnPO)ReCl3L' (9a, n = 2; 9b, n = 3) for n = 2, 3 and mononuclear Re(OP1PO)Cl3L (11) and Re(OP1PO)Cl3L' (12) for n = 1. The mixed system L'Cl3Re(OP2PO)ReCl3L (10) has been prepared from 3 and 4b. The complex Re(PPh3)Cl3L (7a) is furnished by the reaction of Re(OPPh3)Cl3L (6a) or 4b or 11 with PPh3. The species have been characterized with the help of spectral, electrochemical, and X-ray structural data. All the complexes have mer geometry except 5 and 7a, which have fac geometry. The latter is best suited for concurrent Re-N and Re-P back-bonding. Variable-temperature rate data of the reaction 4a-->5 are consistent with an intramolecular strongly associative transition state (delta S++, -22.6 eu) in which the dangling phosphine function lies close to the metal. Two-atom transfer to P1P is believed to proceed via a transient binuclear intermediate which undergoes cleavage at one end due to steric crowding, affording 11 and 12. Crystal data for the complexes are as follows: 5.1.5 C6H6, empirical formula C45H39Cl4N3OP2Re, crystal system triclinic, space group P1, a = 10.034(2) A, b = 10.737(2) A, c = 20.357(4) A, alpha = 89.38(3) degrees, beta = 87.79(3) degrees, gamma = 80.22(3) degrees, V = 2159.7(7) A3, Z = 2; 7a.CH2Cl2, empirical formula C30H25Cl6N3PRe, crystal system monoclinic, space group P2(1)/n, a = 11.695(6) A, b = 17.745(7) A, c = 15.459(9) A, beta = 100.94(5) degrees, V = 3150(3) A3, Z = 4; 9a, empirical formula C52H48Cl6N4O2P2Re2, crystal system monoclinic, space group C2/c, a = 19.769(12) A, b = 12.864(6) A, c = 22.20(2) A, beta = 101.76(6) degrees, V = 5530(6) A3, Z = 4; 11, empirical formula C36H30Cl4N3O2P2Re, crystal system monoclinic, space group I2/a, a = 16.866(6) A, b = 12.583(6) A, c = 34.78(2) A, beta = 99.22(4) degrees, V = 7285(7) A3, Z = 8.

Journal Article↗
PubMed2000

Chemistry of metal-bound anion radicals. A family of mono- and bis(azopyridine) chelates of bivalent ruthenium.

The reaction of the dihydride [RuII(H)2(CO)(PPh3)3], 3, with excess azo-2,2'-bipyridine (abp) in boiling dry benzene has afforded the diradical bischelate [RuII(abp.-)2(CO)(PPh3)], 4, and the hydridic monochelate monoradical [RuII(abp.-)(H)(CO)(PPh3)2], 5. A similar reaction between 3 and 2-(p-chlorophenylazo)pyridine (Clpap) did not yield a bischelate, but the hydridic monoradical [RuII(Clpap.-)(H)(CO)(PPh3)2], 6, has been isolated. Upon treatment of 4-6 with NH4PF6 in a wet dichloromethane-acetonitrile medium, the one-electron-oxidized salts 4+PF6-, 5+PF6-, and 6+PF6- are isolated, H+ being the oxidizing agent. The X-ray structures of 4+PF6-.CH2Cl2, 5+PF6-.H2O, and 6+PF6- have been determined. In the monoradical 4+ the azo N-N bond lengths in the two chelate rings are 1.284(6) and 1.336(6) A, showing that the radical electron is localized in the latter ring. The half-filled extended Hückel HOMO is indeed found to be so localized, and it has a large azo character. Complexes 4-6 display radical redox couples with E1/2 in the range -0.5 to +0.10 V vs SCE. The E1/2 values qualitatively correlate with corresponding vco values (1900-2000 cm-1). The monoradicals (S = 1/2) 4+, 5, and 6 uniformly display a strong EPR signal near g = 2.00. Metal-mediated magnetic interaction makes the EPR-silent diradical 4 strongly antiferromagnetic with J = -299 cm-1. Crystal data are as follows: (4+PF6-.CH2Cl2, C40H33Cl2F6N8-OP2Ru) monoclinic, space group P2(1)/c (no. 14), a = 14.174(6) A, b = 16.451(4) A, c = 18.381(4) A, beta = 98.00(3) degrees, Z = 4; (5+PF6-.H2O, C47H41F6N4O2P3Ru) monoclinic, space group P2(1)/n (no. 14), a = 9.433(2) A, b = 38.914(17) A, c = 13.084(3) A, beta = 103.47(2) degrees, Z = 4; (6+PF6-, C48H39ClF6N3OP3Ru) monoclinic, space group P2(1)/n (no. 14), a = 10.496(5) A, b = 22.389(8) A, c = 19.720(6) A, beta = 90.53(3) degrees, Z = 4.

Journal Article↗
PubMed2000

Azo anion radical complexes of osmium and related nonradical species.

The reaction of [Os(H)(Br)(CO)(PPh3)3], 5, with 2-(phenylazo)pyridine (pap) in boiling dry heptane has afforded the azo anion radical complex [Os(pap.-)(Br)(CO)(PPh3)2], 6a, as the major product and [Os(pap)(H)(CO)(PPh3)2]Br, 7, as a minor byproduct. Upon replacing pap by the better pi-acceptor azo-2,2'-bipyridine (abp) in the above synthesis, the radical complex [Os(abp.-)(Br)(CO)(PPh3)2], 6b, becomes the sole product. It is proposed that 6 is formed via homolytic cleavage of the Os-H bond in 5; in the formation of 7, the Os-Br bond of 5 is heterolytically cleaved. The X-ray structures of 6b and 7.CH2Cl2 have been determined. In 6b, the N-N length is 1.35(2) A, consistent with the anion radical description; in 7.CH2Cl2 the length is 1.27(1) A. The spin-bearing extended Huckel HOMO in a model of 6 is found to be approximately 70% azo-pi* in character associated with a small metal contribution. An electronic band observed in the range 600-700 nm in solutions of 6 is assigned to the HOMO --> LUMO transition, the LUMO being 95% pyridine-pi* in character. One-electron paramagnetic 6 displays well-defined anisotropic EPR features near g = 2.00. The anisotropy arises from the metal character of HOMO and is magnified by the large spin-orbit coupling in osmium. In a moisture-free environment 6 is indefinitely stable in the solid state, but in CH2Cl2-MeCN solution 6a is rapidly oxidized by air, affording [Os(pap)(Br)(CO)(PPh3)2]+, 6a+, which has been isolated as the diamagnetic PF6- salt; 6b+PF6- has been similarly prepared. The voltammetric reduction potentials of the 6+/6 couple follow the order 6a+/6a < 6b+/6b, and the carbon monoxide stretching frequencies follow the order 6a < 6b and 6a+ < 6b+. These trends are consistent with the pi-acidity order pap < abp. Crystal data are as follows: (6b, C47H38BrN4OOsP2) monoclinic, space group P21/c (no. 14), a = 10.215(4) A, b = 17.634(7) A, c = 22.473(8) A, beta = 97.67(3) degrees , Z = 4; (7.CH2Cl2, C49H42BrCl2N3OOsP2) monoclinic, space group P2(1/n) (no. 14), a = 15.323(7) A, b = 15.201(6) A, c = 19.542(7) A, beta = 92.51(3) degrees, Z = 4.

Journal Article↗
PubMed2000

Chemistry of the rhenium-azopyridine family: an oxo parent and derivatives thereof including a novel oxo-imido dimer.

The concerned azo ligands are 2-(phenylazo)pyridine (HL) and 2-((p-chlorophenyl)azo)pyridine (ClL). The reaction of KReO4 with HL in hot concentrated HCl is attended with metal reduction and ligand chlorination affording the oxo complex ReVOCl3(ClL), 2, which furnishes ReIII(OPPh3)Cl3(ClL), 3, upon treatment with PPh3. Aromatic amines, ArNH2, convert 2 to the imido complex ReV(NAr)Cl3(ClL), 5, and the unusual oxo-imido dimer (ClL)-Cl2(O)ReVOReV(NAr)Cl2(ClL), 7. The complex ReIII(OPPh3)Cl3(HL), 4, has been generated from ReVOCl3(PPh3)2 and HL. Reaction of 4 with HL has yielded ReV(NPh)Cl3(HL), 6, via azo splitting. The complexes have been characterized with the help spectral, magnetic, and X-ray structural data (2, 3, 5c (Ar = pClC6H4) and 7.CH2Cl2 (Ar = pMeC6H4)). In 2, 3, and 5c the ReCl3 fragment is meridionally disposed, and in 7 the ReCl2 fragments have a trans configuration. The Re-O(oxo) bond, 1.663(6) A, in 2 and Re-N(imido) bond, 1.719(5) A, in 5c are triple bonds. The corresponding bonds are slightly longer in 7 wherein the (O)Re(1)-O(2)-Re(2)(NAr) bridge is angular (151.0(5) degrees) and unsymmetrical, the Re(1)-O(2) bond, 1.849(7) A, having a large double-bond character (Re(2)-O(2), 1.954(7) A). In effect, cis-ReVO2 acts as a monodentate oxygen ligand toward ReVNAr in 7. In all cases the pyridine nitrogen binds trans to the oxo, OPPh3, or NAr donor. Bond length data are consistent with the presence of substantial d(Re)-pi*(azo) back-bonding. In acetonitrile solution the complexes display electrochemical one-electron metal (ReVI/ReV or ReIV/ReIII) and azo redox. The imido ligand in 5 stabilizes the ReVI state (E1/2 approximately 1.4 V) better than the oxo ligand in 2 (approximately 1.9 V). Parallely it is more difficult to reduce the azo group in 5 (approximately -0.4 V) than in 2 (approximately 0.0 V). In 7 the metal (approximately 1.0 V) and azo (approximately -0.4 V) couples correspond to the imido and oxo halves, respectively. The significantly higher (by 0.2-0.6 V) metal reduction potentials of the azopyridine compared to pyridine-2-aldimine complexes is ascribed to the superior pi-acidity and electron-withdrawing character of the azo function relative to the aldimine function. This also makes the transfer of the ReVO oxygen function much more facile under azopyridine chelation as in 2. For the same reason, ReOCl3(PPh3)2 reacts with HL affording only 4 while it reacts with pyridine-2-aldimines furnishing oxo species. Crystal data for the complexes are as follows: 2, empirical formula C11H8Cl4N3ORe, crystal system triclinic, space group P1, a = 7.118(4) A, b = 8.537(4) A, c = 13.231(9) A, alpha = 79.16(5) degrees, beta = 78.03(5) degrees, gamma = 70.96(4) degrees, V = 737.2(7) A3, Z = 2; 3, empirical formula C29H23Cl4N3OPRe, crystal system monoclinic, space group P2(1)/n, a = 11.264(2) A, b = 15.221(3) A, c = 17.628(4) A, beta = 94.21(3) degrees, V = 3014(1) A3, Z = 4; 5c, empirical formula C17H12Cl5N4Re, crystal system triclinic, space group P1, a = 9.683(3) A, b = 10.898(3) A, c = 11.522(3) A, alpha = 63.67(2) degrees, beta = 71.24(2) degrees, gamma = 86.79(2) degrees, V = 1026(1) A3, Z = 2; 7.CH2Cl2, empirical formula C30H25Cl8N7O2Re2, crystal system triclinic, space group P1, a = 12.522(6) A, b = 12.857(8) A, c = 13.182(7) A, alpha = 67.75(4) degrees, beta = 88.30(4) degrees, gamma = 82.09(4) degrees, V = 1945(2) A3, Z = 2.

Journal Article↗
PubMed2000

Hepatitis G virus (HGV) infection in voluntary and commercial blood donors in India.

The prevalence of hepatitis G virus (HGV) has been determined in commercial as well as voluntary blood donors from India by detecting viral RNA genome using reverse transcription polymerase chain reaction (RT-PCR) assay. 45 professional blood donors from private blood banks and 50 healthy controls who opted for voluntary blood donation were recruited for the study. Both the groups were also screened serologically for HBV and HCV infection. The prevalence of HGV in the general population in India was found to be 4% but significantly a higher frequency (46.6%; p<0.001) of HGV was observed in commercial blood donors.

Blood Donors↗
PubMed2000

The changing epidemiological pattern of hepatitis A in an urban population of India: emergence of a trend similar to the European countries.

The present study was undertaken to determine the seroprevalence of the antibody against hepatitis A virus (IgG anti-HAV) in an urban population sample from Delhi (India) and to assess any change in the epidemiological pattern of HAV infection in this part of the world. A total of 500 healthy subjects were enrolled and divided into groups on the basis of age, sex and per capita income and evaluated for the presence of IgG anti HAV antibodies using a commercially available kit. The mean age of all the subjects was 32.6 +/- 13.2 yr. and the male:female ratio was 1.5:1. The overall prevalence of IgG anti-HAV in all subjects was 71.2% (356/500). The prevalence in subjects >35 years (92.1% [186/202]) was significantly higher than that in subjects <35 years (92.1% [186/202]) was significantly higher than in subjects <35 years (57% [170/298]). No statistically significant difference was observed between male and female subjects (71.4% [217/304] vs. 70.9% [139/196]) or between subjects belonging to middle and low socioeconomic groups (68.9% [135/196] vs. 72.7% [221/304]). These findings when compared with the results that were obtained in 1982, showed a decreasing prevalence of IgG anti-HAV, most significantly in younger age groups (16-35 years). Thus, we may conclude that the seroepidemiology of hepatitis A virus infection in urban population of India seems to be changing with seroprevalence in the younger population approaching a figure similar to that of the more developed European countries.

Adolescent↗
PubMed1999

Corticotropin-releasing hormone stimulates P450 17alpha-hydroxylase/17,20-lyase in human fetal adrenal cells via protein kinase C.

CRH directly stimulates dehydroepiandrosterone sulfate (DHEAS) production in human fetal adrenal cells. In the human fetal and adult pituitary, CRH acts via protein kinase A (PKA). We determined the CRH signal transduction pathway in fetal adrenal cells, i.e. whether CRH modulates human fetal adrenal steroidogenesis via PKA and/or protein kinase C (PKC). In primary cultures, CRH increased inositol trisphosphate. After CRH treatment, inositol tris-, bis-, and monophosphates increased within 1 min, reaching maximal levels at 5 min. In contrast, PGF2alpha, known to act via PKC, induced a sustained response for up to 20 min. The response to CRH was dose dependent, maximal at 1 micromol/L at both 1 and 5 min. CRH increased DHEAS production, with a much lesser effect on cortisol. CRH did not stimulate inositol phospholipid in adult adrenal glands, suggesting that this pathway is unique to the fetal adrenal. CRH increased messenger ribonucleic acid encoding 17alpha-hydroxylase/17,20 lyase (P450c17), but not 3beta-hydroxysteroid dehydrogenase/delta(4-5) isomerase. However, 3betaHSD expression was stimulated by ACTH. PKC, but not PKA, inhibitors blocked CRH-stimulated P450c17 induction, whereas PKA inhibitors blocked ACTH-stimulated cortisol. Thus, CRH is coupled to the phospholipase C-inositol phosphate second messenger system and preferentially induces the expression of P450c17 and DHEAS, suggesting a unique role of CRH regulating human fetal adrenal function via PKC.

3-Hydroxysteroid Dehydrogenases↗