112 research outputs found

    Is comorbidity in adolescence a predictor for adult low back pain? A prospective study of a young population

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    BACKGROUND: It has previously been shown that low back pain (LBP) often presents already in the teenage years and that previous LBP predicts future LBP. It is also well documented that there is a large degree of comorbidity associated with LBP, both in adolescents and adults. The objective of this study is to gain a deeper insight into the etiology of low back pain and to possibly develop a tool for early identification of high-risk groups. This is done by investigating whether different types of morbidity in adolescence are associated with LBP in adulthood. METHODS: Almost 10,000 Danish twins born between 1972 and 1982 were surveyed by means of postal questionnaires in 1994 and again in 2002. The questionnaires dealt with various aspects of general health, including the prevalence of LBP, classified according to number of days affected during the previous year (0, 1–7, 8–30, >30). The predictor variables used in this study were LBP, headache, asthma and atopic disease at baseline; the outcome variable was persistent LBP (>30 days during the past year) at follow-up. Associations between morbidity in 1994 and LBP in 2002 were investigated. RESULTS: LBP, headache and asthma in adolescence were positively associated with future LBP. There was no association between atopic disease and future LBP. Individuals with persistent LBP at baseline had an odds ratio of 3.5 (2.8–4.5) for future LBP, while the odds ratio for those with persistent LBP, persistent headache and asthma was 4.5 (2.5–8.1). There was a large degree of clustering of these disorders, but atopic disease was not part of this pattern. CONCLUSION: Young people from 12 to 22 years of age with persistent LBP during the previous year have an odds ratio of 3.5 persistent LBP eight years later. Both headache and asthma are also positively associated with future LBP and there is a large clustering of LBP, headache and asthma in adolescence

    Improved Measurement of the Pseudoscalar Decay Constant fDsf_{D_{s}}

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    We present a new determination of the Ds decay constant, f_{Ds} using 5 million continuum charm events obtained with the CLEO II detector. Our value is derived from our new measured ratio of widths for Ds -> mu nu/Ds -> phi pi of 0.173+/- 0.021 +/- 0.031. Taking the branching ratio for Ds -> phi pi as (3.6 +/- 0.9)% from the PDG, we extract f_{Ds} = (280 +/- 17 +/- 25 +/- 34){MeV}. We compare this result with various model calculations.Comment: 23 page postscript file, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    First Observation of τ→3πηντ\tau\to 3\pi\eta\nu_{\tau} and τ→f1πντ\tau\to f_{1}\pi\nu_{\tau} Decays

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    We have observed new channels for τ\tau decays with an η\eta in the final state. We study 3-prong tau decays, using the η→γγ\eta\to\gamma\gamma and \eta\to 3\piz decay modes and 1-prong decays with two \piz's using the η→γγ\eta\to\gamma\gamma channel. The measured branching fractions are \B(\tau^{-}\to \pi^{-}\pi^{-}\pi^{+}\eta\nu_{\tau}) =(3.4^{+0.6}_{-0.5}\pm0.6)\times10^{-4} and \B(\tau^{-}\to \pi^{-}2\piz\eta\nu_{\tau} =(1.4\pm0.6\pm0.3)\times10^{-4}. We observe clear evidence for f1→ηππf_1\to\eta\pi\pi substructure and measure \B(\tau^{-}\to f_1\pi^{-}\nu_{\tau})=(5.8^{+1.4}_{-1.3}\pm1.8)\times10^{-4}. We have also searched for η′(958)\eta'(958) production and obtain 90% CL upper limits \B(\tau^{-}\to \pi^{-}\eta'\nu_\tau)<7.4\times10^{-5} and \B(\tau^{-}\to \pi^{-}\piz\eta'\nu_\tau)<8.0\times10^{-5}.Comment: 11 page postscript file, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    Search for the Decays B^0 -> D^{(*)+} D^{(*)-}

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    Using the CLEO-II data set we have searched for the Cabibbo-suppressed decays B^0 -> D^{(*)+} D^{(*)-}. For the decay B^0 -> D^{*+} D^{*-}, we observe one candidate signal event, with an expected background of 0.022 +/- 0.011 events. This yield corresponds to a branching fraction of Br(B^0 -> D^{*+} D^{*-}) = (5.3^{+7.1}_{-3.7}(stat) +/- 1.0(syst)) x 10^{-4} and an upper limit of Br(B^0 -> D^{*+} D^{*-}) D^{*\pm} D^\mp and B^0 -> D^+ D^-, no significant excess of signal above the expected background level is seen, and we calculate the 90% CL upper limits on the branching fractions to be Br(B^0 -> D^{*\pm} D^\mp) D^+ D^-) < 1.2 x 10^{-3}.Comment: 12 page postscript file also available through http://w4.lns.cornell.edu/public/CLNS, submitted to Physical Review Letter

    ΛΛˉ\Lambda\bar{\Lambda} Production in Two-Photon Interactions at CLEO

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    Using the CLEO detector at the Cornell e+e−e^+e^- storage ring, CESR, we study the two-photon production of ΛΛˉ\Lambda \bar{\Lambda}, making the first observation of γγ→ΛΛˉ\gamma \gamma \to \Lambda \bar{\Lambda}. We present the cross-section for γγ→ΛΛˉ \gamma \gamma \to \Lambda \bar{\Lambda} as a function of the γγ\gamma \gamma center of mass energy and compare it to that predicted by the quark-diquark model.Comment: 10 pages, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    Observation of the Decay Ds+→ωπ+D_{s}^{+}\to \omega\pi^{+}

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    Using e+e- annihilation data collected by the CLEO~II detector at CESR, we have observed the decay Ds+ to omega pi+. This final state may be produced through the annihilation decay of the Ds+, or through final state interactions. We find a branching ratio of [Gamma(Ds+ to omega pi+)/Gamma(Ds+ to eta pi+)]=0.16+-0.04+-0.03, where the first error is statistical and the second is systematic.Comment: 9 pages, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    Changes in the incidence of occupational disability as a result of back and neck pain in the Netherlands

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    BACKGROUND: Back pain (including neck pain) is one of the most prevalent health problems for which physicians are consulted. Back pain can decrease the quality of life considerably during a great part of the lives of those who suffer from it. At the same time it has an enormous economic impact, mainly through sickness absence and long-term disability. The objective of this paper is to compare the incidence of occupational disability as a result of back and neck pain in 1980–1985 to 1999–2000 and to explain the findings. METHODS: A descriptive study was performed at population level of changes in incidence of occupational disability as a result of back and neck pain. Statistics from the National Institute of Social Insurance in the Netherlands are used to calculate age and gender specific incidence rates for back pain diagnoses based on the ICD-classification. Incidence rate ratios stratified according to gender and adjusted for age were calculated to indicate changes over time. RESULTS: The incidence of occupational disability as a result of back pain decreased significantly by 37% (95% CI 37%–38%) in men and with 21% (95% CI 20%–24%) in women, after adjustment for age. For overall occupational disability as a result of all diagnoses this was 18% (95% CI 18%–19%) and 34% (95% CI 33%–35%) respectively. Changes were not homogeneous over diagnostic subcategories and age groups. Spondylosis decreased most in men by 59% (95% CI 57%–61%). The incidence of non-specific back pain and neck pain increased most by 196% (95% CI 164%–215%). Post-laminectomy syndrome increased over all age categories both for men (85%, 95% CI 61%–113%) and women (113%, 95% CI 65%–179%). CONCLUSION: The decrease in occupational disability as a result of back pain was larger than the decrease in occupational disability over all diagnoses. However, time trends were not homogeneous over age-, nor over sex- nor back pain categories. Most of this decrease was due to general changes such as legal and economic changes. One of several additional explanations for a decrease is the changed view on management of back pain

    Selective BRAFV600E Inhibitor PLX4720, Requires TRAIL Assistance to Overcome Oncogenic PIK3CA Resistance

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    Documented sensitivity of melanoma cells to PLX4720, a selective BRAFV600E inhibitor, is based on the presence of mutant BRAFV600E alone, while wt-BRAF or mutated KRAS result in cell proliferation. In colon cancer appearance of oncogenic alterations is complex , since BRAF, like KRAS mutations, tend to co-exist with those in PIK3CA and mutated PI3K has been shown to interfere with the successful application of MEK inhibitors. When PLX4720 was used to treat colon tumours, results were not encouraging and herein we attempt to understand the cause of this recorded resistance and discover rational therapeutic combinations to resensitize oncogene driven tumours to apoptosis. Treatment of two genetically different BRAFV600E mutant colon cancer cell lines with PLX4720 conferred complete resistance to cell death. Even though p-MAPK/ ERK kinase (MEK) suppression was achieved, TRAIL, an apoptosis inducing agent, was used synergistically in order to achieve cell death by apoptosis in RKOBRAFV600E/PIK3CAH1047 cells. In contrast, for the same level of apoptosis in HT29BRAFV600E/PIK3CAP449T cells, TRAIL was combined with 17-AAG, an Hsp90 inhibitor. For cells where PLX4720 was completely ineffective, 17-AAG was alternatively used to target mutant BRAFV600E. TRAIL dependence on the constitutive activation of BRAFV600E is emphasised through the overexpression of BRAFV600E in the permissive genetic background of colon adenocarcinoma Caco-2 cells. Pharmacological suppression of the PI3K pathway further enhances the synergistic effect between TRAIL and PLX4720 in RKO cells, indicating the presence of PIK3CAMT as the inhibitory factor. Another rational combination includes 17-AAG synergism with TRAIL in a BRAFV600E mutant dependent manner to commit cells to apoptosis, through DR5 and the amplification of the apoptotic pathway. We have successfully utilised combinations of two chemically unrelated BRAFV600E inhibitors in combination with TRAIL in a BRAFV600E mutated background and provided insight for new anti-cancer strategies where the activated PI3KCA mutation oncogene should be suppressed
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