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Biomedical subjects

H Vogel

Publications and source records attributed to H Vogel.

At least 73 records · Page 4Linked to original sources

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↗

How high are the costs of eating disorders - anorexia nervosa and bulimia nervosa - for German society?

Anorexia and bulimia are relatively rare psychogenic illnesses, which nevertheless are of great concern for society since they affect a mostly very young population and are accompanied by a significantly raised mortality risk. This cost-of-illness analysis for eating disorders in Germany considers hospitalization, rehabilitation services, and indirect costs through inability to work and premature death. The cost estimates are based on projections derived from benefit data as listed by health insurance schemes and pension insurance schemes and from epidemiological studies on the prevalence of eating disorders and mortality rates. For anorexia the cost of illness amounts to approximately 195 million euros (73 direct costs and 122 mortality costs, for bulimia it comes to around 124 million euros (12 direct costs and 112 mortality costs). The annual cost per anorexia and bulimia patient is approximately 5,300 and 1,300 euros, respectively. This cost-of-illness analysis underlines the significance of indirect costs due to premature death, but also highlights the extremely cost-intensive treatment. The hospitalization cost of 12,800 euros per anorexia patient is markedly higher than the average hospitalization cost of 3,600 euros.

Journal Article↗

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↗

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↗

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↗

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↗

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↗

Mapping the antagonist binding site of the serotonin type 3 receptor by fluorescence resonance energy transfer.

We have measured fluorescence resonance energy transfer (FRET) between a fluorescent antagonist, bound to the purified detergent-solubilized serotonin type 3 receptor, and a lipophilic acceptor probe partitioned into the micelle surrounding the detergent-solubilized receptor. The experimentally observed FRET efficiency was evaluated on the basis of the characteristic dimensions of the receptor-micelle complex and the average number of acceptor molecules in such micelles. The binding site was determined to be 5.4 +/- 0.9 nm above the center of the detergent micelle. The experiments were performed below the critical micellar concentration of the detergent (C(12)E(9)) used to solubilize the receptor, under which conditions it was demonstrated that the ligand binding activity was fully preserved. This reduces considerably the fluorescence background arising from probes not associated with the receptor, allowing a precise determination of the transfer efficiency.

Animals↗

Fluorescence resonance energy transfer shows a close helix-helix distance in the transmembrane M13 procoat protein.

During the membrane insertion process the major coat protein of bacteriophage M13 assumes a conformation in which two transmembrane helices corresponding to the leader sequence and the anchor region in the mature part of the protein coming into close contact with each other. Previous studies on the molecular mechanism of membrane insertion of M13 procoat protein have shown that this interaction between the two helices might drive the actual translocation process. We investigated the intramolecular distance between the two helices of the transmembrane procoat protein by measuring fluorescence resonance energy transfer (FRET) between the donor (Tyr) placed in one helix and the acceptor (Trp) placed in the other helix. Various mutant procoat proteins with differently positioned donor-acceptor pairs were generated, purified, and reconstituted into artificial lipid bilayers. The results obtained from the FRET measurements, combined with molecular modeling, show that the transmembrane helices are in close contact on the order of 1-1.5 nm. The present approach might be of general interest for determining the topology and the folding of membrane proteins.

Amino Acid Sequence↗

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↗

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↗

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↗

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↗

In vitro and in vivo ligand binding to the 5HT(3) serotonin receptor characterised by time-resolved fluorescence spectroscopy.

The binding of the fluorescein-labelled antagonist GR-flu ([1,2,3,9-tetrahydro-3-[(5-methyl-1H-imidazol-4-yl)methyl]-9-(3-amino-(N-fluoresceinthiocarbamoyl)propyl)-4H-carbazol-4-one]) to a purified, detergent-solubilised ligand-gated ion channel, the type-3 serotonin (5-hydroxytryptamine, 5HT) receptor (5HT(3)R), was characterised by frequency-domain time-resolved fluorescence spectroscopy (TRFS). Detailed understanding of how ligands interact with the homopentameric receptor was obtained. While a 1:1 stoichiometry was observed for the GR-flu-receptor complex, the agonist quipazine bound cooperatively to the receptor, suggesting multiple binding sites for this ligand. The GR-flu-binding site of the receptor was proven to provide an acidic environment as shown by determining the fraction of bound GR-flu in the protonated state. Fluorescence anisotropy relaxation experiments indicated a hindered but still high mobility for the receptor-bound GR-flu. Hence, the binding site is expected to present a wide opening to the ligand. Finally, we succeeded in measuring the binding of GR-flu to 5HT(3) receptors in live cells. These results show that the purified and the native receptor behave identically and demonstrate that time-resolved fluorescence measurements are suited to selectively investigate biomolecular interactions in live cells.

Algorithms↗

The standard deviation in fluorescence correlation spectroscopy.

The standard deviation (SD) in fluorescence correlation spectroscopy (FCS) has been mostly neglected in applications. However, the knowledge of the correct SD is necessary for an accurate data evaluation, especially when fitting theoretical models to experimental data. In this work, an algorithm is presented that considers the essential features of FCS. It allows prediction of the performance of FCS measurements in various cases, which is important for finding optimal experimental conditions. The program calculates the SD of the experimental autocorrelation function online. This procedure leads to improved parameter estimation, compared to currently used theoretical approximations for the SD. Three methods for the calculation of the SD are presented and compared to earlier analytical solutions (D. E. Koppel. 1974. Phys. Rev. A. 10:1938-1945.), calculation directly from fluorescence intensity values, by averaging several FCS measurements, or by dividing one measurement into a set of shorter data packages. Although the averaging over several measurements yields accurate estimates for the SD, the other two methods are considerably less time consuming, can be run online, and yield comparable results.

Computer Simulation↗

Assembly of pore proteins on gold electrodes.

Protein-protein interactions at the cell surface are important in the activity of bacterial toxins such as colicins. We have developed methods to study these events using tethered lipid bilayers, which can be probed by impedance spectroscopy and surface plasmon resonance. Recently we have attached the receptor proteins directly to gold electrodes and this offers new possibilities for measuring protein-protein interactions on solid supports.

Binding Sites↗

Mitochondrial myopathies and the role of the pathologist in the molecular era.

Mitochondrial encephalomyopathies are under increasing consideration in the differential diagnosis of diverse metabolic diseases from infancy to late adulthood. This is to be expected considering the vital importance of mitochondria to cellular respiration in all eukaryotes. the vulnerability of the mitochondrial genome to injury, and the expanding appreciation of the role of mitochondria as a common denominator in cell death in ischemia/anoxia, sepsis, and neurodegenerative diseases. Primary disease of the mitochondrial respiratory chain is estimated to occur with an incidence of between 6 and 16/100,000 individuals. Virtually all tissues have been shown to be involved in diverse mitochondriopathies, but none is more appropriate for diagnosis in most cases than skeletal muscle. The conventional histological and ultrastructural diagnosis of mitochondrial disease in muscle has been increasingly supplanted by the biochemical assessment of respiratory chain enzyme deficiencies and definitive genetic diagnosis. The use of such techniques has afforded a greater understanding for the relative lack of specificity of both light and electron microscopic observations. A review of the current situation by placing muscle pathology in the context of biochemical and genetic diagnosis serves as a paradigm for the role of the pathologist in the molecular era.

Humans↗