Precision Measurement of the Mass of the h_c(1P1) State of Charmonium

A precision measurement of the mass of the h_c(1P1) state of charmonium has been made using a sample of 24.5 million psi(2S) events produced in e+e- annihilation at CESR. The reaction used was psi(2S) -> pi0 h_c, pi0 -> gamma gamma, h_c -> gamma eta_c, and the reaction products were detected in the CLEO-c detector. Data have been analyzed both for the inclusive reaction and for the exclusive reactions in which eta_c decays are reconstructed in fifteen hadronic decay channels. Consistent results are obtained in the two analyses. The averaged results of the present measurements are M(h_c)=3525.28+-0.19 (stat)+-0.12(syst) MeV, and B(psi(2S) -> pi0 h_c)xB(h_c -> gamma eta_c)= (4.19+-0.32+-0.45)x10^-4. Using the 3PJ centroid mass, Delta M_hf(1P)= - M(h_c) = +0.02+-0.19+-0.13 MeV.Comment: 9 pages, available through http://www.lns.cornell.edu/public/CLNS/, submitted to PR

Precision Measurement of B(D+ -> mu+ nu) and the Pseudoscalar Decay Constant fD+

We measure the branching ratio of the purely leptonic decay of the D+ meson with unprecedented precision as B(D+ -> mu+ nu) = (3.82 +/- 0.32 +/- 0.09)x10^(-4), using 818/pb of data taken on the psi(3770) resonance with the CLEO-c detector at the CESR collider. We use this determination to derive a value for the pseudoscalar decay constant fD+, combining with measurements of the D+ lifetime and assuming |Vcd| = |Vus|. We find fD+ = (205.8 +/- 8.5 +/- 2.5) MeV. The decay rate asymmetry [B(D+ -> mu+ nu)-B(D- -> mu- nu)]/[B(D+ -> mu+ nu)+B(D- -> mu- nu)] = 0.08 +/- 0.08, consistent with no CP violation. We also set 90% confidence level upper limits on B(D+ -> tau+ nu) < 1.2x10^(-3) and B(D+ -> e+ nu) < 8.8x10^(-6).Comment: 24 pages, 11 figures and 6 tables, v2 replaced some figure vertical axis scales, v3 corrections from PRD revie

Measurement of the Absolute Branching Fraction of D_s^+ --> tau^+ nu_tau Decay

Using a sample of tagged D_s decays collected near the D^*_s D_s peak production energy in e+e- collisions with the CLEO-c detector, we study the leptonic decay D^+_s to tau^+ nu_tau via the decay channel tau^+ to e^+ nu_e bar{nu}_tau. We measure B(D^+_s to tau^+ nu_tau) = (6.17 +- 0.71 +- 0.34) %, where the first error is statistical and the second systematic. Combining this result with our measurements of D^+_s to mu^+ nu_mu and D^+_s to tau^+ nu_tau (via tau^+ to pi^+ bar{nu}_tau), we determine f_{D_s} = (274 +- 10 +- 5) MeV.Comment: 9 pages, postscript also available through http://www.lns.cornell.edu/public/CLNS/2007/, revise

J/psi and psi(2S) Radiative Transitions to eta_c

Using 24.5 million psi(2S) decays collected with the CLEO-c detector at CESR we present the most precise measurements of magnetic dipole transitions in the charmonium system. We measure B(psi(2S)->gamma eta_c) = (4.32+/-0.16+/-0.60)x10^-3, B(J/psi->gamma eta_c)/B(psi(2S)->gamma eta_c) = 4.59+/-0.23+/-0.64, and B(J/psi->gamma eta_c) = (1.98+/-0.09+/-0.30)%. We observe a distortion in the eta_c line shape due to the photon-energy dependence of the magnetic dipole transition rate. We find that measurements of the eta_c mass are sensitive to the line shape, suggesting an explanation for the discrepancy between measurements of the eta_c mass in radiative transitions and other production mechanisms.Comment: 11 pages, 3 figure

Inclusive chi_bJ(nP) Decays to D0 X

Using Upsilon(2S) and Upsilon(3S) data collected with the CLEO III detector we have searched for decays of chi_bJ to final states with open charm. We fully reconstruct D0 mesons with p_D0 > 2.5 GeV/c in three decay modes (K-pi+, K-pi+pi0, and K-pi-pi+pi+) in coincidence with radiative transition photons that tag the production of one of the chi_bJ(nP) states. We obtain significant signals for the two J=1 states. Recent NRQCD calculations of chi_{bJ}(nP) --> c cbar X depend on one non-perturbative parameter per chi_bJ triplet. The extrapolation from the observed D0 X rate over a limited momentum range to a full c cbar X rate also depends on these same parameters. Using our data to fit for these parameters, we extract results which agree well with NRQCD predictions, confirming the expectation that charm production is largest for the J=1 states. In particular, for J=1, our results are consistent with c cbar g accounting for about one-quarter of all hadronic decays.Comment: Version 2 updates include corrections to important errors in Table V and VII column headers which summarize results, and additional minor edits. 17 pages, available through http://www.lns.cornell.edu/public/CLNS

Corneal Sensitivity and Dry Eye Symptoms in Patients with Keratoconus.

PURPOSE: To investigate corneal sensitivity to selective mechanical, chemical, and thermal stimulation and to evaluate their relation to dry eye symptoms in patients with keratoconus. METHODS: Corneal sensitivity to mechanical, chemical, and thermal thresholds were determined using a gas esthesiometer in 19 patients with keratoconus (KC group) and in 20 age-matched healthy subjects (control group). Tear film dynamics was assessed by Schirmer I test and by the non-invasive tear film breakup time (NI-BUT). All eyes were examined with a rotating Scheimpflug camera to assess keratoconus severity. RESULTS: KC patients had significatly decreased tear secretion and significantly higher ocular surface disease index (OSDI) scores compared to controls (5.3+/-2.2 vs. 13.2+/-2.0 mm and 26.8+/-15.8 vs. 8.1+/-2.3; p0.05). The mean threshold for selective mechanical (KC: 139.2+/-25.8 vs. control: 109.1+/-24.0 ml/min), chemical (KC: 39.4+/-3.9 vs. control: 35.2+/-1.9%CO2), heat (KC: 0.91+/-0.32 vs. control: 0.54+/-0.26 Delta degrees C) and cold (KC: 1.28+/-0.27 vs. control: 0.98+/-0.25 Delta degrees C) stimulation in the KC patients were significantly higher than in the control subjects (p0.05), whereas in the control subjects both mechanical (r = 0.52, p = 0.02), chemical (r = 0.47, p = 0.04), heat (r = 0.26, p = 0.04) and cold threshold (r = 0.40, p = 0.03) increased with age. In the KC group, neither corneal thickness nor tear flow, NI-BUT or OSDI correlated significantly with mechanical, chemical, heat or cold thresholds (p>0.05 for all variables). CONCLUSIONS: Corneal sensitivity to different types of stimuli is decreased in patients with keratoconus independently of age and disease severity. The reduction of the sensory input from corneal nerves may contribute to the onset of unpleasant sensations in these patients and might lead to the impaired tear film dynamics

Cigarette Smoke-Related Hydroquinone Dysregulates MCP-1, VEGF and PEDF Expression in Retinal Pigment Epithelium in Vitro and in Vivo

Age-related macular degeneration (AMD) is the leading cause of legal blindness in the elderly population. Debris (termed drusen) below the retinal pigment epithelium (RPE) have been recognized as a risk factor for dry AMD and its progression to wet AMD, which is characterized by choroidal neovascularization (CNV). The underlying mechanism of how drusen might elicit CNV remains undefined. Cigarette smoking, oxidative damage to the RPE and inflammation are postulated to be involved in the pathophysiology of the disease. To better understand the cellular mechanism(s) linking oxidative stress and inflammation to AMD, we examined the expression of pro-inflammatory monocyte chemoattractant protein-1 (MCP-1), pro-angiogenic vascular endothelial growth factor (VEGF) and anti-angiogenic pigment epithelial derived factor (PEDF) in RPE from smoker patients with AMD. We also evaluated the effects of hydroquinone (HQ), a major pro-oxidant in cigarette smoke on MCP-1, VEGF and PEDF expression in cultured ARPE-19 cells and RPE/choroids from C57BL/6 mice.MCP-1, VEGF and PEDF expression was examined by real-time PCR, Western blot, and ELISA. Low levels of MCP-1 protein were detected in RPE from AMD smoker patients relative to controls. Both MCP-1 mRNA and protein were downregulated in ARPE-19 cells and RPE/choroids from C57BL/6 mice after 5 days and 3 weeks of exposure to HQ-induced oxidative injury. VEGF protein expression was increased and PEDF protein expression was decreased in RPE from smoker patients with AMD versus controls resulting in increased VEGF/PEDF ratio. Treatment with HQ for 5 days and 3 weeks increased the VEGF/PEDF ratio in vitro and in vivo.We propose that impaired RPE-derived MCP-1-mediated scavenging macrophages recruitment and phagocytosis might lead to incomplete clearance of proinflammatory debris and infiltration of proangiogenic macrophages which along with increased VEGF/PEDF ratio favoring angiogenesis might promote drusen accumulation and progression to CNV in smoker patients with dry AMD

Packages of Care for Attention-Deficit Hyperactivity Disorder in Low- and Middle-Income Countries

In the sixth in a series of six articles on packages of care for mental disorders in low- and middle-income countries, Alan Flisher and colleagues discuss the treatment of attention-deficit hyperactivity disorder

Autoantibodies to muscarinic acetylcholine receptors found in patients with primary biliary cirrhosis

<p>Abstract</p> <p>Background</p> <p>Autoantibodies to the human muscarinic acetylcholine receptor of the M3 type (hmAchR M3) have been suggested to play an etiopathogenic role in Sjögren's syndrome. Primary biliary cirrhosis (PBC) often is associated with this syndrome. Therefore, we studied the co-presence of hmAchR M3 autoantibodies in patients with PBC.</p> <p>Methods</p> <p>Frequency of hmAchR M3 autoantibodies was assessed by Western blotting analysis as well as by an ELISA using a 25-mer peptide of the 2^ndextracellular loop of hmAchR M3. Co-localization of hmAchR M3/PBC-specific autoantibodies was studied by confocal laser scanning microscopy. Finally, sera from patients with PBC as well as from healthy controls were tested.</p> <p>Results</p> <p>Western blotting analysis as well as results from ELISA testing revealed a significantly enhanced IgG reactivity in PBC patients in contrast to healthy controls. Co-localization of autoantibodies with the hmAchR M3 receptor-specific autoantibodies was observed in 10 out of 12 PBC-patients but none of the 5 healthy controls. Antibodies of the IgM type were not found to be affected.</p> <p>Conclusions</p> <p>For the first time, our data demonstrate the presence of autoantibodies to the hmAchR M3 in PBC patients. These findings might contribute to the understanding of the pathogenesis of this disease. Further studies have to focus on the functionality of hmAchR M3 autoantibodies in PBC patients.</p