Biomedical subjects
Publications and source records attributed to J C Wang.
Using 13.8 fb(-1) of data collected at or just below the Upsilon(4S) with the CLEO detector, we report the result of a search for the flavor changing neutral current process D0-->gammagamma. We observe no significant signal for this decay mode and determine 90% confidence level upper limits on the branching fractions B(D0-->gammagamma)/B(D0-->pi(0)pi(0))<0.033 and B(D0-->gammagamma)<2.9 x 10(-5).
Using the combined CLEO II and CLEO II.V data sets of 9.1 fb(-1) at the Upsilon(4S), we measure properties of psi mesons produced directly from decays of the B meson, where "B" denotes an admixture of B+, B-, B0, and B;(0), and "psi" denotes either J/psi(1S) or psi(2S). We report first measurements of psi polarization in B-->psi(direct)X: alpha(psi(1S))=-0.30(+0.07)(-0.06)+/-0.04 and alpha(psi(2S))=-0.45(+0.22)(-0.19)+/-0.04. We also report improved measurements of the momentum distributions of psi produced directly from B decays, correcting for measurement smearing. Finally, we report measurements of the inclusive branching fraction for B-->psiX and B-->chi(c1)X.
In e(+)e(-) collisions using the CLEO detector, we have studied the decay of the D0 to the final state K(0)(S)pi(+)pi(-) with the initial flavor of the D0 tagged by the decay D(*+)-->D0pi(+). We use the Dalitz technique to measure the resonant substructure in this final state and clearly observe ten different contributions by fitting for their amplitudes and relative phases. We observe a K(*)(892)(+)pi(-) component which arises from doubly Cabibbo suppressed decays or D0-D0; mixing.
We report on a search for charmless hadronic B decays to the three-body final states K(0)(S)h(+)pi(-), K(+)h(-)pi(0), K(0)(S)h(+)pi(0) (h(+/-) denotes a charged pion or kaon), and their charge conjugates, using 13.5 fb(-1) of integrated luminosity produced near sqrt[s]=10.6 GeV, and collected with the CLEO detector. We observe the decay B-->K0pi(+)pi(-) with a branching fraction (50(+10)(-9)(stat.)+/-7(syst.))x10(-6) and the decay B-->K(*+)(892)pi(-) with a branching fraction (16(+6)(-5)(stat.)+/-2(syst.))x10(-6).
Using 13.53 fb(-1) of CLEO data, we have measured the ratios of the branching fractions R(+)(e),R(+)(mu) and the combined branching fraction ratio R(+)(l), defined by R(+)(l)=[B(D+-->K(*0)l(+)nu(l))]/[B(D+-->K-pi(+)pi(+))]. We find R(+)(e)=0.74+/-0.04+/-0.05, R(+)(mu)=0.72+/-0.10+/-0.05, and R(+)(l)=0.74+/-0.04+/-0.05, where the first and second errors are statistical and systematic, respectively. The known branching fraction B(D+-->K-pi(+)pi(+)) leads to B(D+-->K(*0)e(+)nu(e))=(6.7+/-0.4+/-0.5+/-0.4)%, B(D+-->K(*0)mu(+)nu(mu))=(6.5+/-0.9+/-0.5+/-0.4)%, and B(D+-->K(*0)l(+)nu(l))=(6.7+/-0.4+/-0.5+/-0.4)%, where the third error is due to the uncertainty in B(D+-->K-pi(+)pi(+)).
Using the CLEO detector at the Cornell Electron Storage Ring we have observed the Omega(0)(c) (css ground state) in the decay Omega(0)(c)-->Omega(-)e(+)nu(e). We find a signal of 11.4+/-3.8(stat) events. The probability that we have observed a background fluctuation is 7.6x10(-5). We measure B(Omega(0)(c)-->Omega(-)e(+)nu(e)).sigma(e(+)e(-)-->Omega(0)(c)X)=(42.2+/-14.1(stat)+/-5.7(syst)) fb and R=[Gamma(Omega(0)(c)-->Omega(-)pi(+))]/[Gamma(Omega(0)(c)-->Omega(-)enu(e))]=00.41+/-0.19(stat)+/-0.04(syst). This is the first statistically significant observation of an individual decay mode of the Omega(0)(c) in e(+)e(-) annihilation and the first example of a baryon decaying via beta emission, where no quarks from the first generation participate in the reaction.
OBJECTIVE: To determine whether the effects of APOE promoter polymorphisms on AD are independent of the APOE-epsilon4 allele. BACKGROUND: Recently, the -491 A-->T and -219 G-->T polymorphisms located in the APOE promoter have been suggested to be risk factors for AD. However, the effects of these polymorphisms have not always been reproduced in case-control studies, possibly because of the strong linkage disequilibrium existing at this locus or the characteristics of the populations studied. METHODS: Data collection was performed from six independent samples (1,732 patients with AD and 1,926 control subjects) genotyped for APOE exon 4 and the two APOE promoter polymorphisms. The risks associated with the APOE polymorphisms for developing AD were estimated using logistic regression procedures and calculation of odds ratios with 95% CI adjusted by age, sex, and collection center. Independence of the APOE promoter polymorphisms was tested by stratification for APOE-epsilon4 and tertile design was used for age stratification. RESULTS: The independence of the -491 AA genotype was observed in the whole sample whereas the independence of the -219 TT genotype was observed only in the oldest population. CONCLUSION: The -491 and -219 APOE promoter polymorphisms incur risk for AD in addition to risk associated with the APOE-epsilon4 allele, with age accentuating the effect of the -219 TT genotype. Because these polymorphisms appear to influence apoE levels, these results suggest that APOE expression is an important determinant of AD pathogenesis.
BACKGROUND: PD is largely a sporadic condition of unknown etiology, but specific inherited mutations are a cause of PD. OBJECTIVE: To describe a large, multi-incident Amish pedigree with PD. METHODS: Case ascertainment, calculation of population prevalence, and calculation of kinship coefficients (a measure of relatedness between two individuals) for affecteds and subjects in a large kindred with PD were conducted. Sequencing of genes with known mutations sufficient to cause PD and marker-by-marker haplotype analysis in chromosomal regions flanking previously described genes with known mutations were performed. RESULTS: The authors have examined 113 members of this pedigree and classified 67 as normal (no evidence of PD), 17 as clinically definite PD, 6 as clinically probable PD, and 23 as clinically possible PD. The mean age at onset of the clinically definite subjects was 56.7 years. The phenotype in this family is typical of idiopathic PD, including rest tremor, rigidity, bradykinesia, postural instability, and response to levodopa. In addition, dementia occurred in six of the clinically definite subjects, and many subjects experienced levodopa-related motor complications including wearing off and dopa-induced dyskinesias. In the index Amish community, a minimum prevalence of PD in the population 40 years and older of 552/100,000 was calculated. The mean kinship coefficient in the subjects with PD and those with PD by history (0.036) was higher (p = 0.007) than in a group of age-matched normal Amish control subjects (0.016), providing evidence that PD is inherited in this family. Sequence analysis did not detect any mutations in known PD genes. No single haplotype cosegregates with the disease in any of the chromosomal regions previously found to be linked to PD, and no marker in these regions exhibits increased homozygosity among definite PD cases. CONCLUSIONS: PD in this community is more common than in the general population, and this increased prevalence may be due in part to a novel gene(s).
We have studied the color-suppressed hadronic decays of neutral B mesons into the final states D*0pi(0). Using 9.67 x 10(6) BB pairs collected with the CLEO detector, we observe the decays B( 0) --> D0pi(0) and B( 0) -->D(*0)pi(0) with the branching fractions BB( 0) -->D0pi(0)) = (2.74(+0.36)(-0.32) +/- 0.55)x10(-4) and BB( 0) -->D(*0)pi(0)) = (2.20(+0.59)(-0.52) +/- 0.79)x10(-4). The first error is statistical and the second systematic. The statistical significance of the D0pi(0) signal is 12.1sigma ( 5.9sigma for D(*0)pi(0)). Utilizing the B( 0) -->D*0)pi(0) branching fractions we determine the strong phases delta(I,D(*)) between isospin 1/2 and 3/2 amplitudes in the Dpi and D*pi final states to be cosdelta(I,D) = 0.89 +/-0.08 and cosdelta(I,D*) = 0.89 +/- 0.08, respectively.
BACKGROUND: Systemic ischaemia-reperfusion (IR) injury is in part an oxidant injury mediated by neutrophils. Diethylmaleate (DEM), an intracellular pro-oxidant agent, has been shown to alleviate neutrophil-mediated tissue injury. The aim of this study was to evaluate whether DEM could have a protective effect on neutrophil-mediated lung injury in an animal model of lower-torso IR. METHODS: Sprague-Dawley rats (seven per group) were randomized into three groups. The control group underwent midline laparotomy only; the IR group underwent laparotomy and clamping of the infrarenal abdominal aorta for 30 min followed by 2 h of reperfusion; and the third group was pretreated with DEM 6 mmol/kg intraperitoneally 1 h before the IR insult. RESULTS: IR resulted in a significant increase in both microvascular leakage and pulmonary neutrophil infiltration as measured by bronchoalveolar lavage protein concentration and pulmonary myeloperoxidase activity respectively. Pretreatment with DEM significantly attenuated both microvascular leakage and neutrophil infiltration. CONCLUSION: Preconditioning with DEM protected against IR-induced lung injury. This protective effect raises the possibility of using pro-oxidants to prevent inflammatory injury.
We have searched for the two-body decay of the B meson to a light pseudoscalar meson h = pi(+/-),K+/-,K(0)(S) and a massless neutral feebly interacting particle X(0) such as the familon, the Nambu-Goldstone boson associated with a spontaneously broken global family symmetry. We find no significant signal by analyzing a data sample containing 9.7x10(6) BBbar mesons collected with the CLEO detector at the Cornell Electron Storage Ring, and set 90% C.L. upper limits italicB(B(+/-) --> h(+/-)X(0)) = 4.9x10(-5) and italicB(B(0) --> K(0)(S)X(0)) = 5.3x10(-5). These limits correspond to a lower bound of approximately 10(8) GeV on the family symmetry breaking scale with vector coupling involving the third generation of quarks.
A series of robust, thermally stable open-framework cobalt nicotinate compounds, Co(2)(H(2)O)[C(6)H(4)O(2)N](4).0.5CH(3)CH(2)OH.0.5H(2)O (1), Co(2)(H(2)O)[C(6)H(4)O(2)N](4) (2), and Co(2)(H(2)O)[C(6)H(4)O(2)N](4).C(6)H(5)CH(2)OH (3), based on rigid dimetallic carboxylate clusters as the basic building unit have been prepared. Single-crystal X-ray crystallographic analyses of 1 and 3 reveal the host framework possessing an effective channel area with the dimensions of 10.8 x 4.5 A. These channels can accommodate guest molecules of various sizes and shapes such as ethanol, water, and benzyl alcohol. Thermogravimetric analysis shows a two-step weight loss corresponding to the loss of guest molecules followed by the loss of coordinated water. The host framework is thermally stable up to 295 degrees C. The cobalt nicotinate host remains intact, even upon the removal of the guest to form compound 2 as revealed by single-crystal X-ray diffraction analysis. Crystal data for 1: Co(2)(H(2)O)[C(6)H(4)O(2)N)](4).0.5CH(3)CH(2)OH.0.5H(2)O, fw = 656.33, triclinic, space group P(-)1, a = 10.5407(2) A, b = 11.8266(3) A, c = 14.1122(2) A, alpha = 106.878(4) degrees, beta = 102.411(2) degrees, gamma = 111.011(3) degrees, V = 1467.9(5) A(3), Z = 2. Crystal data for 2: Co(2)(H(2)O)[C(6)H(4)O(2)N](4), fw = 624.28, triclinic, space group P(-)1, a = 10.507(3) A, b = 11.824(2) A, c = 14.113(3) A, alpha = 107.06(2) degrees, beta = 102.39(2) degrees, gamma = 111.105(16) degrees, V = 1459.5(6) A(3), Z = 2. Crystal data for 3: Co(2)(H(2)O)[C(6)H(4)O(2)N](4).C(6)H(5)CH(2)OH, fw = 732.42, triclinic, space group P(-)1, a = 10.6671(6) A, b = 12.0063(7) A, c = 14.0658(8) A, alpha = 106.7180(10) degrees, beta = 102.2790(10) degrees, gamma = 111.1900(10) degrees, V = 1504.1(6) A(3), Z = 2. The magnetic exchange coupling between the dicobalt centers for compounds 1 and 3 are analyzed on the basis of both the Curie-Weiss expression and a binuclear magnetic model. The negative values of the magnetic exchange coupling constant indicate the antiferromagnetic nature within the cobalt dimer.
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We have measured the branching fraction and photon energy spectrum for the radiative penguin process b-->s gamma. We find Beta(b-->s gamma) = (3.21+/-0.43+/-0.27(+0.18)(-0.10))x10(-4), where the errors are statistical, systematic, and from theory corrections. We obtain first and second moments of the photon energy spectrum above 2.0 GeV, = 2.346+/-0.032+/-0.011 GeV, and - (2) = 0.0226+/-0.0066+/-0.0020 GeV(2), where the errors are statistical and systematic. From the first moment, we obtain (in the modified minimal subtraction renormalization scheme, to order 1/M(3)(B) and beta(0)alpha(2)(s)) the heavy quark effective theory parameter Lambda = 0.35+/-0.08+/-0.10 GeV.
We have measured the first and second moments of the hadronic mass-squared distribution in B-->X(c)l nu, for P(lepton)>1.5 GeV/c. We find = 0.251+/-0.066 GeV(2), <(M(2)(X)- )(2)> = 0.576+/-0.170 GeV(4), where M macro(D) is the spin-averaged D meson mass. From that first moment and the first moment of the photon energy spectrum in b-->s gamma, we find the heavy quark effective theory parameter lambda(1) (in the modified minimal subtraction renormalization scheme, to order 1/M(3)(B) and beta(0)alpha(2)(s)) to be -0.24+/-0.11 GeV(2). Using these first moments and the B semileptonic width, and assuming parton-hadron duality, we obtain absolute value of V(cb) = 0.0404+/-0.0013.
We present the first measurement of the D*(+) width using 9/fb of e(+)e(-) data collected near the Upsilon(4S) resonance by the CLEO II.V detector. Our method uses advanced tracking techniques and a reconstruction method that takes advantage of the small vertical size of the Cornell Electron-positron Storage Ring beam spot to measure the energy release distribution from the D*(+)-->D(0)pi(+) decay. We find gamma(D*(+)) = 96+/-4 (stat)+/-22 (syst) keV. We also measure the energy release in the decay and compute Delta m identical with m(D*(+))-m(D(0)) = 145.412+/-0.002 (stat)+/-0.012 (syst) MeV/c(2).
We report on a search for the radiative decay Upsilon(1S)-->gammaeta(') in 61.3 pb(-1) of data taken with the CLEO II detector at the Cornell Electron Storage Ring. Three decay chains were investigated, all involving eta(')-->pi(+)pi(-)eta, followed by eta-->gammagamma, eta-->pi(0)pi(0)pi(0), or eta-->pi(+)pi(-)pi(0). We find no candidate events in any of the three cases and set a combined upper limit of 1.6x10(-5) at 90% C.L., significantly smaller than the previous limit. We compare our result to other radiative Upsilon decays, to radiative J/psi decays, and to theoretical predictions.
The Sgs1 protein of the budding yeast Saccharomyces cerevisiae is a member of the RecQ DNA helicase family that includes the human Bloom, Werner, and Rothmund-Thompson syndrome proteins. The N-terminal region outside the central DNA helicase core of Sgs1, particularly the part containing the first 100 amino acid residues of the 1,447-residue protein, is known to be functionally important and has been implicated in Sgs1-DNA topoisomerase III (Top3) interaction. We show in this work that the functionality of a truncated Sgs1 lacking its N-terminal 106 residues can be restored by replacing the truncated region with Top3. Fusion of Top3 to a mutant Sgs1 with a Val-29 to Glu substitution, which interferes with Sgs1-Top3 interaction, similarly restores the functionality of the mutant Sgs1(V29E) protein. The Top3-Sgs1(Delta1-106) and Top3-Sgs1(V29E) fusion proteins behave like wild-type Sgs1 in complementing several aspects of the sgs1 phenotype, including the hypersensitivity of sgs1 cells to methyl methanesulfonate and hydroxyurea. Complementation by the fusion proteins required both the topoisomerase activity of Top3 and the helicase activity of the Sgs1 polypeptide. These results suggest that the sole function of the N-terminal 106 amino acid residues of Sgs1 is for Top3 binding, and that the coordinated actions of Sgs1 and Top3 are important in cellular processes such as the processing of DNA after exposure of cells to DNA-damaging agents.