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Biomedical subjects

E J White

Publications and source records attributed to E J White.

At least 19 recordsLinked to original sources
PubMed2006

Observation of Psi(3770)-->gammachi(c1)-->gammagammaJ/Psi.

From e(+)e(-) collision data acquired with the CLEO detector at the Cornell Electron Storage Ring, we observe the non-DD(_) decay Psi(3770))-->gammachi(c1) with a statistical significance of 6.6 standard deviations, using the two-photon cascades to J/Psi and J/Psi-->l(+)l(-). We determine sigma(e(=)e(-)-->Psi(3770))xBeta(Psi(3770)-->gammachi(c1))=(18.0 +/- 3.3 +/- 2.5) pb and branching fraction Beta(Psi(3770)-->gammachi(c1)=(2.8 +/- 0.5+/-0.4) x 10(-3). We set 90% C.L. upper limits for the transition to chi(c2) (chi(c0)): sigma x Beta<5.7 pb (<282 pb) and Beta<0.9 x 10(-3) (<44 x 10(-3)). We also determine Gamma(Psi(3770)gammachi(c1))/Gamma(Psi(3770)-->pi(+)pi(-)J/Psi)=1.5 +/- 0.3 +/- 0.3 (>1.0 at 90% C.L.), which bears upon the interpretation of X(3872).

Journal Article↗
PubMed2006

Charmonium Decays of Y(4260), psi(4160), and psi(4040).

Using data collected with the CLEO detector operating at the CESR e+e- collider at sqrt[s]=3.97-4.26 GeV, we investigate 15 charmonium decay modes of the psi(4040), psi(4160), and Y(4260) resonances. We confirm, at 11 sigma significance, the BABAR Y(4260)-->pi+pi- J/psi discovery, make the first observation of Y(4260)--> pi(0)pi(0) J/psi (5.1 sigma), and find the first evidence for Y(4260)-->K+K- J/psi(3.7 sigma). We measure e+e- cross sections at sqrt[s]=4.26 GeV as sigma(pi+pi- J/psi)=58(+12)(-10)+/-4 pb, sigma(pi(0)pi(0) J/psi)=23(+12)(-8)+/-1 pb, and sigma(K+K- J/psi)=9(+9)(-5)+/-1 pb, in which the uncertainties are statistical and systematic, respectively. Upper limits are placed on other decay rates from all three resonances.

Journal Article↗
PubMed2006

Experimental limits on weak annihilation contributions to decays.

We present the first experimental limits on high-q2 contributions to charmless semileptonic decays of the form expected from the weak annihilation (WA) decay mechanism. Such contributions could bias determinations of /Vub/ from inclusive measurements of B-->Xulupsilon. Using a wide range of models based on available theoretical input we set a limit of GammaWA/Gammab-->u<7.4% (90% confidence level) on the WA fraction, and assess the impact on previous inclusive determinations of /Vub/.

Journal Article↗
PubMed2006

Dielectron widths of the Gamma(1S,2S,3S) resonances.

We determine the dielectron widths of the Gamma(1S), Gamma(2S), and Gamma(3S) resonances with better than 2% precision by integrating the cross section of e+e- -->Gamma over the e+e- center-of-mass energy. Using e+e- energy scans of the Gamma resonances at the Cornell Electron Storage Ring and measuring Gamma production with the CLEO detector, we find dielectron widths of 1.252+/-0.004(sigma(stat))+/-0.019(sigma(syst)) keV, 0.581+/-0.004+/-0.009 keV, and 0.413+/-0.004+/-0.006 keV for the Gamma(1S), Gamma(2S), and Gamma(3S), respectively.

Journal Article↗
PubMed2006

Observation of psi(3770) --> pi pi J/psi and measurement of Gamma ee[psi(2S)].

We observe signals for the decays psi(3770) --> XJ/psi from data acquired with the CLEO detector operating at the CESR e+ e- collider with square root of s = 3773 MeV. We measure the following branching fractions Beta(psi(3770) --> XJ/psi and significances: (189 +/- 20 +/- 20) x 10(-5) (11.6sigma) for X = pi+ pi-, (80 +/- 25 +/- 16) x 10(-5) (3.4sigma) for X = pi0 pi0, and (87 +/- 33 +/- 22) x 10(-5) (3.5sigma) for X = eta, where the errors are statistical and systematic, respectively. The radiative return process e+ e- --> gamma psi(2S) populates the same event sample and is used to measure Gamma ee[psi(2S)] = (2.54 +/- 0.03 +/- 0.11) keV.

Journal Article↗
PubMed2006

New measurements of Cabibbo-suppressed decays of mesons with the CLEO-c detector.

Using of data collected with the CLEO-c detector, we report on first observations and measurements of Cabibbo-suppressed decays of D mesons in the following six decay modes: pi+ pi- pi0 pi0, pi+ pi+ pi- pi- pi0, pi+ pi0 pi0, pi+ pi+ pi- pi0, eta pi0, and omega pi+ pi-. Improved branching fraction measurements in eight other multipion decay modes are also presented. The measured D --> pi pi rates allow us to extract the ratio of isospin amplitudes A(DeltaI = (3/2) / A(DeltaI = (1/2)) = 0.420 +/- 0.014(stat) +/- 0.016(syst) and the strong phase shift of delta1 = (86.4 +/- 2.8 +/- 3.3) degrees, which is quite large and now more precisely determined.

Journal Article↗
PubMed2006

Observation of Bs production at the Y(5S) resonance.

Using the CLEO detector at the Cornell Electron Storage Ring, we have observed the Bs meson in e+e- annihilation at the Y(5S) resonance. We find 14 candidates consistent with Bs decays into final states with a J/psi or a Ds(*)- . The probability that we have observed a background fluctuation is less than 8 x 10(-10) . We have established that at the energy of the Y(5S) resonance Bs production proceeds predominantly through the creation of Bs*Bs* pairs. We find sigma(e+e- --> Bs*Bs*) = [0.11(-0.03))(+0.04)(stat) +/- 0.02(syst)]nb , and set the following limits: sigma(e+e- --> BsBs)/ sigma(e+ e- --> Bs*Bs*) <0.16 and [sigma(e+e- --> BsBs*) + sigma(e+e- --> Bs*Bs)]/sigma(e+e- -->Bs*Bs*) < 0.16 (90% C.L.). The mass of the Bs* meson is measured to be M(Bs*) = [5.414+/- 0.001(stat) +/- 0.003(syst)] GeV/c2 .

Journal Article↗
PubMed2006

Low doses of ionizing radiation can prevent radiation-induced colonic epithelial hyporesponsiveness to muscarinic agonists.

PURPOSE: Colonic epithelium hyporesponsiveness to different secretagogues occurs after exposure to ionizing radiation, increasing susceptibility to bacterial translocation and intraluminal toxins. Growing evidence suggests that the biological effects of radiation might be hormetic in nature. We investigated if exposure to low doses of ionizing radiation (LDR) can prevent colon hyposecretion due to subsequent larger doses. METHODS: Rats were exposed to LDR (0.05 Gy) 24 h prior to 6 Gy, high dose radiation (HDR). The cyclic adenosine monophosphate (cAMP)-mediated pathway was explored using forskolin (FSK) and the intracellular Ca2+-mediated pathway through cholinergic stimulation. Changes in the colonic epithelium at the ultrastructural level were also explored. RESULTS: Maximal short circuit current (Isc) response to carbachol was significantly reduced in the group exposed to 6 Gy HDR and this was completely prevented by prior exposure to LDR. Responses to both FSK and electrical field stimulation (EFS) were significantly reduced after HDR but they were not prevented by prior adaption of LDR. Hyposecretion was not prevented by the inducible nitric oxide synthase (iNOS) inhibitor L-N6-(l-iminoethyl)lysine (L-NIL) ruling out a role for iNOS-derived nitric oxide (NO) in the colonic hyposecretion associated with whole body radiation. Prior exposure to LDR diminished the deleterious effect of full HDR on the ultrastructure of colonic epithelium as colonocytes vacuolization, microvilli lost and separation between neighboring cells were less evident. CONCLUSIONS: Previous exposure to LDR can prevent intracellular Ca2+-mediated colonic hyposecretion associated with exposure to HDR but fails to modify cAMP-mediated hyposecretion. Morphological damage at the ultrastructural level is less evident after prior LDR.

Animals↗
PubMed2006

Induction of LFA-1-dependent neutrophil rolling on ICAM-1 by engagement of E-selectin.

OBJECTIVE: To study rolling of mouse neutrophils on E-selectin and ICAM-1 in an ex vivo flow chamber system. METHODS: The authors developed a small autoperfused flow chamber (20 x 200-microm cross section) that allows direct visualization of cells with and without fluorescent labeling and does not require recirculation of blood. RESULTS: Neutrophils rolled on E-selectin alone, but were unable to interact with immobilized ICAM-1. When ICAM-1 was co-immobilized with E-selectin, the number of cells that rolled was doubled, but no significant firm adhesion was observed. This phenomenon was specific for E-selectin, and no enhancement of rolling was observed when P-selectin was immobilized with ICAM-1. The increased neutrophil rolling seen on E-selectin and ICAM-1 substrates required beta2 integrins. Treating mice with antibodies to the beta2 integrins LFA-1 and Mac-1 showed that LFA-1 was primarily responsible for mediating rolling on ICAM-1 in this model. Increased rolling on E-selectin and ICAM-1 was significantly reduced following administration of a specific p38 mitogen-activated protein kinase (MAPK) inhibitor. CONCLUSION: The data show that neutrophil rolling on E-selectin leads to partial activation of LFA-1, enabling LFA-1-dependent rolling on ICAM-1. This mechanism is likely to amplify and accelerate neutrophil recruitment in inflammation.

Animals↗
PubMed2005

Evidence for Bs* Bs* production at the Gamma(5S) resonance.

We use data collected by the CLEO III detector at the Cornell Electron Storage Ring to measure the inclusive yields of D(s) mesons as B(Y(5S) --> D(s)X) = (44-7 +/- 4.2 +/- 9.9)% and B(Y(4S) --> D(s)X) = (18.1 +/- 0.5 +/- 2.8)%. From these measurements, we make a model dependent estimate of the ratio of B(s)*B(s)* to the total bb quark pair production of (16.0 +/- 2.6 +/- 5.8)% at the Y(5S) energy.

Journal Article↗
PubMed2005

Improved measurement of B(D+ --> mu+nu) and the pseudoscalar decay constant fD+.

We extract a relatively precise value for the decay constant of the meson by measuring B(D+ --> mu+nu) = (4.40 +/-0.66(+0.09)(-0.12) x 10(-4) using 281 pb(-1) of data taken on phi(3770) the resonance with the CLEO-c detector. We find fD+ = (222.6 +/- 16.7(+2.8)(-3.4)) MeV, and compare with current theoretical calculations. We also set a 90% confidence upper limit on B(D+e+nu)< 2.4 x 10(-5) which constrains new physics models.

Journal Article↗
PubMed2005

Search for rare and forbidden decays D+ --> h+/- e+/- e+.

Using 0.8 x 10(6) D+ D- pairs collected with the CLEO-c detector at the psi(3770) resonance, we have searched for flavor-changing neutral current and lepton-number-violating decays of D+ mesons to final states with dielectrons. We find no indication of either, obtaining 90% confidence level upper limits of B(D+ --> pi+ e+ e-) < 7.4 x 10(-6), B(D+ --> pi- e+ d+) < 3.6 x 10(-6), B(D+ --> K+ e+ e-) < 6.2 x 10(-6), and B(D+ --> K- e+ e+) < 4.5 x 10(-6).

Journal Article↗
PubMed2005

Observation of the hc(1P1) state of charmonium.

The h(c)((1)P(1)) state of charmonium has been observed in the reaction psi(2S) --> pi(0)h(c) --> (gammagamma)(gammaeta(c)) using 3.08 x10(6) psi(2S) decays recorded in the CLEO detector. Data have been analyzed both for the inclusive reaction, where the decay products of the eta(c) are not identified, and for exclusive reactions, in which eta(c) decays are reconstructed in seven hadronic decay channels. We find M(h(c)) = 3524.4 +/- 0.6 +/- 0.4 MeV which corresponds to a hyperfine splitting DeltaM(hf)(1P) triple-bond pi(0)h(c)) x B(h(c) --> gammaeta(c)) = (4.0 +/- 0.8 +/- 0.7) x 10(-4).

Journal Article↗
PubMed2005

Observation of thirteen new exclusive multibody hadronic decays of the psi(2S).

Using data accumulated with the CLEO detector corresponding to an integrated luminosity of [symbol: see text] = 5.63 pb(-1) on the peak of the psi(2S) [3.08 x 10(6) psi(2S) decays] and 20.70 pb(-1) at square root of[s] = 3.67 GeV, we report first measurements of the branching fractions for the following 13 decay modes of the psi(2S): eta3pi, &eta'3pi, rhoK+K-, K+K-pi+pi-pi0, 2(K+K-), 2(K+K-)pi0, rhopp, pppi+pi-pi0, etapp, ppK+K-, lambdalambdapi+pi-, lambdapK+, and lambdapK+pi+pi-, and more precise measurements of 8 previously measured modes: 2(pi+pi-), rhopi+pi-, 2(pi+pi-)pi0, omegapi+pi-, K+K-pi+pi-, omegaK+K-, phiK+K-, and pppi+pi-. We also report new branching fraction measurements of phipi+pi- and omegapp and upper limits for etapi+pi-, etaK+K-, and phivpp. Results are compared, where possible, with the corresponding J/psi branching ratios to provide new tests of the 12% rule.

Journal Article↗
PubMed2004

Ion channels in interstitial cells of Cajal as targets for neurotransmitter action.

Interstitial cells of Cajal (ICC) are involved in generation of gut pacemaker activity, neurotransmission and stretch sensation. Pacemaker ICC exhibit spontaneous cyclic calcium oscillations that are in synchrony with its pacemaker activity. The spontaneous rhythmic inward currents in ICC that underlie gut pacemaker activity are linked to this calcium oscillation. It is probable that more than one type of channel contributes to the inward current with a high conductance chloride channel and a nonselective cation channel being the main candidates. The activation of these channels is linked to intracellular calcium cycling mechanism and involves inositol 1,4,5-trisphosphate (IP3)-mediated calcium release from the sarcoplasmic reticulum, and calcium uptake into mitochondria. This ion channel activity is modulated by signalling through neurotransmitter receptors, including the NK1 receptor. This finding and the presence of other neurotransmitter receptor mRNA transcripts indicates that ion channels in ICC are targets for neurotransmitter action. The ether-a-go-go-related (ERG) K channel is probably the most important K channel contributing to the resting membrane potential and excitability of the ICC. Many ion channels in ICC are regulated by second messenger systems which makes them highly susceptible to neurotransmitter modulation.

Animals↗
PubMed2000

Potent inhibition of werner and bloom helicases by DNA minor groove binding drugs.

Maintenance of genomic integrity is vital to all organisms. A number of human genetic disorders, including Werner Syndrome, Bloom Syndrome and Rothmund-Thomson Syndrome, exhibit genomic instability with some phenotypic characteristics of premature aging and cancer predisposition. Presumably the aberrant cellular and clinical phenotypes in these disorders arise from defects in important DNA metabolic pathways such as replication, recombination or repair. These syndromes are all characterized by defects in a member of the RecQ family of DNA helicases. To obtain a better understanding of how these enzymes function in DNA metabolic pathways that directly influence chromosomal integrity, we have examined the effects of non-covalent DNA modifications on the catalytic activities of purified Werner (WRN) and Bloom (BLM) DNA helicases. A panel of DNA-binding ligands displaying unique properties for interacting with double helical DNA was tested for their effects on the unwinding activity of WRN and BLM helicases on a partial duplex DNA substrate. The levels of inhibition by a number of these compounds were distinct from previously reported values for viral, prokaryotic and eukaryotic helicases. The results demonstrate that BLM and WRN proteins exhibit similar sensitivity profiles to these DNA-binding ligands and are most potently inhibited by the structurally related minor groove binders distamycin A and netropsin (K(i) </=1 microM). The distinct inhibition of WRN and BLM helicases by the minor groove binders suggest that these helicases unwind double-stranded DNA by a related mechanism.

Adenosine Triphosphatases↗
PubMed2000

Severe inflammatory defect and reduced viability in CD18 and E-selectin double-mutant mice.

CD18-deficient mice (CD18(-/-) mice) have a severe leukocyte recruitment defect in some organs, and no detectable defect in other models. Mice lacking E-selectin (CD62E(-/-) mice) have either no defect or a mild defect of neutrophil infiltration, depending on the model. CD18(-/-)CD62E(-/-), but not CD18(-/-)CD62P(-/-), mice generated by crossbreeding failed to thrive, reaching a maximum body weight of 10-15 grams. To explore the mechanisms underlying reduced viability, we investigated lethally irradiated CD62E(-/-) mice that were reconstituted with CD18(-/-) bone marrow. These mice, but not single-mutant controls, showed tenfold-increased rolling velocities in a TNF-alpha-induced model of inflammation. Leukocyte adhesion efficiency in CD18(-/-)CD62E(-/-) mice was reduced by 95%, and hematopoiesis was drastically altered, including severe bone marrow and blood neutrophilia and elevated G-CSF and GM-CSF levels. The greatly reduced viability of CD18(-/-)CD62E(-/-) mice appears to result from an inability to mount an adequate inflammatory response. Our data show that cooperation between E-selectin and CD18 integrins is necessary for neutrophil recruitment and that alternative adhesion pathways cannot compensate for the loss of these molecules.

Animals↗