PubMed Health⌕ Search

Biomedical subjects

T Ferguson

Publications and source records attributed to T Ferguson.

At least 55 records · Page 3Linked to original sources
PubMed2002

Observation of B(0) --> D0pi(0) and B(0) -->D(*0)pi(0).

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.

Journal Article↗
PubMed2002

Matrix metalloproteinase mediated degradation of basement membrane proteins in Trembler J neuropathy nerves.

A single point mutation in peripheral myelin protein 22 (pmp22) of the Trembler-J (TrJ) mouse models the human peripheral neuropathy, Charcot-Marie-Tooth disease type 1 A (CMT1A). An unexplored aspect of this disease is the gradual remodeling of the extracellular matrix in affected nerves. To elucidate the mechanism responsible for these changes, the levels of the extracellular matrix molecules laminin, collagen IV, and fibronectin were determined. In TrJ nerves, laminin is modestly increased while full-length forms of collagen IV and fibronectin are decreased. Matrix metalloproteinases (MMPs) are known to degrade multiple matrix molecules; therefore, nerves were assayed for MMP-2 and MMP-9 proteins. In neuropathy nerves, elevated levels of MMP-2 and MMP-9 were detected on western blots, and gelatin zymography confirmed the up-regulation of gelatinalytic activity in affected samples. Immunostaining studies revealed an increase in the numbers of MMP-2- and MMP-9-expressing cells in TrJ nerves. Cell type-specific immunolabeling showed that infiltrating macrophages are a significant source of both MMP-2 and MMP-9. Finally, the degradation of exogenous collagen IV by TrJ nerve lysates was prevented with a specific MMP inhibitor. Together these observations suggest that infiltration by MMP-expressing macrophages contributes to the remodeling of the TrJ nerve matrix.

Animals↗
PubMed2001

Search for charmless B --> VV decays.

We have studied two-body charmless decays of the B meson into the final states rho(0)rho(0), K(*0)rho(0), K(*0)K(*0), K(*0)K(*0), K(*+)rho(0), K(*+)K(*0), and K(*+)K(*-) using only decay modes with charged daughter particles. Using 9.7x10(6) BB pairs collected with the CLEO detector, we place 90% confidence level upper limits on the branching fractions (1.4-14.1)x10(-5), depending on final state and polarization.

Journal Article↗
PubMed2001

Search for the familon via B(+/-) --> pi+/-X(0), B(+/-) --> K(+/-)X(0), and B(0) --> K(0)(S)X(0) decays.

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.

Journal Article↗
PubMed2001

Branching fraction and photon energy spectrum for b --> s gamma.

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.

Journal Article↗
PubMed2001

Hadronic mass moments in inclusive semileptonic B meson decays.

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.

Journal Article↗
PubMed2001

First measurement of gamma(D*(+)).

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).

Journal Article↗
PubMed2001

Search for the decay upsilon(1S) --> gammaeta(').

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.

Journal Article↗
PubMed2001

Bounds on the CP asymmetry in like-sign dileptons from B(0)B*(0) meson decays.

We have measured the charge asymmetry in like-sign dilepton yields from B(0)B*(0) meson decays using the CLEO detector at the Cornell Electron Storage Ring. We find a(0)(ll) identical with[N(l(+)l(+))-N(l(-)l(-))]/[N(l(+)l(+))+N(l(-)l(-))] = +0.013+/-0.050+/-0.005. We combine this result with a previous, independent measurement and obtain Re(epsilon(B))/(1+ the absolute value of epsilon(B)(2)) = +0.0035+/-0.0103+/-0.0015 (uncertainties are statistical and systematic, respectively) for the CP impurity parameter, epsilon(B).

Journal Article↗
PubMed2001

Evidence of New States Decaying into Xi(*)(c)pi.

Using 13.7 fb(-1) of data recorded by the CLEO detector at Cornell Electron Storage Ring, we report evidence of two new charmed baryons: one decaying into Xi(0')(c)pi(+) with the subsequent decay Xi(0')(c)-->Xi(0)(c)gamma, and its isospin partner decaying into Xi(+')(c)pi(-) followed by Xi(+')(c)-->Xi(+)(c)gamma. We measure the following mass differences for the two states: M(Xi(0)(c)gammapi(+))-M(Xi(0)(c)) = 318.2+/-1.3+/-2.9 MeV and M(Xi(+)(c)gammapi(-))-M(Xi(+)(c)) = 324.0+/-1.3+/-3.0 MeV. We interpret these new states as the J(P) = 1 / 2(-) Xi(c1) particles, the charmed-strange analogs of the Lambda(+)(c1)(2593).

Journal Article↗
PubMed2001

Observation of B --> phiK and B --> phiK*.

We have studied two-body charmless hadronic decays of B mesons into the final states straight phiK and phiK(*). Using 9.7 million B&Bmacr; pairs collected with the CLEO II detector, we observe the decays B- --> phiK- and B0--> phiK(*0) with the following branching fractions: B(B--->phiK-) = (5.5(+2.1)(-1.8)+/-0.6)x10(-6) and B(B0--> phiK(*0)) = (11.5(+4.5+1.8)(-3.7-1.7))x10(-6). We also see evidence for the decays B0-->phiK0 and B---> phiK(*-). However, since the statistical significance is not overwhelming for these modes, we determine upper limits of <12.3x10(-6) and <22.5x10(-6) ( 90% confidence level), respectively.

Journal Article↗
PubMed1998

Epidemiology of IgA nephropathy in central and eastern Kentucky for the period 1975 through 1994. Central Kentucky Region of the Southeastern United States IgA Nephropathy DATABANK Project.

Population-based incidence data for IgA nephropathy (IgAN) are available for some countries but not for the United States. The purpose of this study was to determine the incidence of IgAN in central and eastern Kentucky for 5- and 10-yr periods between 1975 and 1994 and to examine differences among patient groups between those periods. The incidence of IgAN was 5.4 cases per one million population per year (MPPY) for period 1A (1975 through 1979), increasing to 12.4 cases per MPPY for period 2B (1990 through 1994) (P < 0.001). Males had a 2.7 times higher incidence than females for period 1 (1975 through 1984) and 2.2 times higher for period 2 (1985 through 1994). For period 1A, the incidence for Fayette County, which includes the city of Lexington, was lower than that of the rest of the study area (P=0.26), whereas for period 2 the incidence was higher for Fayette County (P=0.052). During period 1, the highest incidence of IgAN for any age and gender group was 24.3 cases per MPPY for males ages 30 through 39. For period 2, the incidence for males was similar for each decade between ages 20 and 59 (approximately 19 cases per MPPY). No African-American was diagnosed during period 1, but in period 2 incidences for blacks and whites were similar (10.7 and 10.2 cases per MPPY, respectively). For the last 5 yr of the study (1990 through 1994), the incidence of end-stage renal disease (ESRD) due to IgAN was 5.5 cases per MPPY: 8.4 for males and 2.7 for females. The incidence of IgAN in Kentucky for period 2B was still much lower than that in European studies, but the incidence of ESRD due to IgAN may be similar. Thus, IgAN may be as important a condition with respect to ESRD in Kentucky as it is in other regions of the world.

Adolescent↗
PubMed1998

Enhanced de novo lipogenesis in the leptin-unresponsive pancreatic islets of prediabetic Zucker diabetic fatty rats: role in the pathogenesis of lipotoxic diabetes.

Overaccumulation of fat in pancreatic islets of obese ZDF fa/fa rats is believed to cause beta-cell failure and diabetes. Previously, we demonstrated that ZDF islets have an increased capacity to esterify fatty acids imported via the circulation. Here we examine the capacity of ZDF islets to synthesize fatty acids de novo. Compared with age-matched wild-type (+/+) control islets, acetyl CoA carboxylase (ACC) mRNA was fivefold and sixfold higher and fatty acid synthetase (FAS) was fourfold and sevenfold higher in prediabetic and diabetic ZDF islets, respectively. Incorporation of label from [14C]glucose into lipids was 84% higher in ZDF islets and was not suppressed normally by fatty acids. Chronic hyperleptinemia, induced by adenoviral transfer of leptin cDNA, reduced ACC and FAS mRNA in +/+ islets by 93 and 80%, respectively, but did not decrease the high ACC and FAS expression in islets of fa/fa rats. Recombinant leptin cultured with islets isolated from +/+ rats lowered ACC and FAS expression by 66 and 47%, respectively, but had no effect in fa/fa islets. We conclude that de novo lipogenesis in islets is controlled by leptin and remains low in leptin-responsive islets. It is increased in leptin-insensitive fa/fa islets, contributing to the fat overload that leads to beta-cell dysfunction and diabetes.

Acetyl-CoA Carboxylase↗