Measurement of hadron and lepton-pair production at 130 GeV<root s<140 GeV at LEP

Contains fulltext : 26240.pdf (publisher's version ) (Open Access

Risk factors for discontinuing drug therapy among children with ADHD

Compliance with drug therapy is of major concern to clinicians as well as policy makers since uncontrolled symptoms due to noncompliance present health risks for patients and may lead to social costs. Noncompliance comes in the form of skipped dosages as well as discontinuation well before a clinician deems it appropriate. The problem is especially severe in behavioral disorders among children where the symptoms can last well beyond adolescence. We use pharmacy dispensing and clinical diagnosis data on children diagnosed with attention-deficit hyperactivity disorder (ADHD) and who are on ADHD-related medications. The paper shows how the pharmacy refill data fit naturally into a discrete time hazard rate framework, and then compares estimates from alternative definitions of discontinuation. We use a long follow-up period (up to 6 years), allow for a flexible duration dependence and account for unobserved heterogeneity. The expected duration is about 18 months with significant differences across race, gender, copays, medication switching, and seasonality. We find that African-American, Hispanic and, Asian children are about 39% more likely, on average, to quit therapy in a given month than white children. Similarly, compared to a child that initiates drug therapy at age 9, a child that starts therapy at age 10 is 26.4% more likely to discontinue at any given time. Earlier literature using the hazard approach reports smaller associations between these covariates and durations. We show that this could be because of ignored unobserved heterogeneity, use of a relatively short follow-up study design and monotonic duration dependence. Finally, our results are of particular relevance to clinicians as well as to policy makers given recent changes in federal and state policies that may make early detection and diagnosis of ADHD among children less likely

Search for the Decays B-D(0)-]Gamma-Gamma and B-S(0)-]Gamma-Gamma

Contains fulltext : 26235.pdf (publisher's version ) (Open Access

Measurement of the Weak Charged Current Structure in Semileptonic B-Hadron Decays at the Z-Peak

Contains fulltext : 26230.pdf (publisher's version ) (Open Access

Biological substantiation of antipsychotic-associated pneumonia: Systematic literature review and computational analyses

INTRODUCTION: Antipsychotic (AP) safety has been widely investigated. However, mechanisms underlying AP-associated pneumonia are not well-defined. AIM: The aim of this study was to investigate the known mechanisms of AP-associated pneumonia through a systematic literature review, confirm these mechanisms using an independent data source on drug targets and attempt to identify novel AP drug targets potentially linked to pneumonia. METHODS: A search was conducted in Medline and Web of Science to identify studies exploring the association between pneumonia and antipsychotic use, from which information on hypothesized mechanism of action was extracted. All studies had to be in English and had to concern AP use as an intervention in persons of any age and for any indication, provided that the outcome was pneumonia. Information on the study design, population, exposure, outcome, risk estimate and mechanism of action was tabulated. Public repositories of pharmacology and drug safety data were used to identify the receptor binding profile and AP safety events. Cytoscape was then used to map biological pathways that could link AP targets and off-targets to pneumonia. RESULTS: The literature search yielded 200 articles; 41 were included in the review. Thirty studies reported a hypothesized mechanism of action, most commonly activation/inhibition of cholinergic, histaminergic and dopaminergic receptors. In vitro pharmacology data confirmed receptor affinities identified in the literature review. Two targets, thromboxane A2 receptor (TBXA2R) and platelet activating factor receptor (PTAFR) were found to be novel AP target receptors potentially associated with pneumonia. Biological pathways constructed using Cytoscape identified plausible biological links potentially leading to pneumonia downstream of TBXA2R and PTAFR. CONCLUSION: Innovative approaches for biological substantiation of drug-adverse event associations may strengthen evidence on drug safety profiles and help to tailor pharmacological therapies to patient risk factors