51 research outputs found

    Explaining regional variations in health care utilization between Swiss cantons using panel econometric models

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    <p>Abstract</p> <p>Background</p> <p>In spite of a detailed and nation-wide legislation frame, there exist large cantonal disparities in consumed quantities of health care services in Switzerland. In this study, the most important factors of influence causing these regional disparities are determined. The findings can also be productive for discussing the containment of health care consumption in other countries.</p> <p>Methods</p> <p>Based on the literature, relevant factors that cause geographic disparities of quantities and costs in western health care systems are identified. Using a selected set of these factors, individual panel econometric models are calculated to explain the variation of the utilization in each of the six largest health care service groups (general practitioners, specialist doctors, hospital inpatient, hospital outpatient, medication, and nursing homes) in Swiss mandatory health insurance (MHI). The main data source is 'Datenpool santésuisse', a database of Swiss health insurers.</p> <p>Results</p> <p>For all six health care service groups, significant factors influencing the utilization frequency over time and across cantons are found. A greater supply of service providers tends to have strong interrelations with per capita consumption of MHI services. On the demand side, older populations and higher population densities represent the clearest driving factors.</p> <p>Conclusions</p> <p>Strategies to contain consumption and costs in health care should include several elements. In the federalist Swiss system, the structure of regional health care supply seems to generate significant effects. However, the extent of driving factors on the demand side (e.g., social deprivation) or financing instruments (e.g., high deductibles) should also be considered.</p

    Environmental chemicals impact dog semen quality in vitro and may be associated with a temporal decline in sperm motility and increased cryptorchidism

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    Adverse temporal trends in human semen quality and cryptorchidism in infants have been associated with exposure to environmental chemicals (ECs) during development. Here we report that a population of breeding dogs exhibit a 26 year (1988–2014) decline in sperm quality and a concurrent increased incidence of cryptorchidism in male offspring (1995–2014). A decline in the number of males born relative to the number of females was also observed. ECs, including diethylhexyl phthalate (DEHP) and polychlorinated biphenyl 153 (PCB153), were detected in adult dog testes and commercial dog foods at concentrations reported to perturb reproductive function in other species. Testicular concentrations of DEHP and PCB153 perturbed sperm viability, motility and DNA integrity in vitro but did not affect LH stimulated testosterone secretion from adult testis explants. The direct effects of chemicals on sperm may therefore contribute to the decline in canine semen quality that parallels that reported in the human

    Removal of the endocrine disrupter butyl benzyl phthalate from the environment

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    Butyl benzyl phthalate (BBP), an aryl alkyl ester of 1,2-benzene dicarboxylic acid, is extensively used in vinyl tiles and as a plasticizer in PVC in many commonly used products. BBP, which readily leaches from these products, is one of the most important environmental contaminants, and the increased awareness of its adverse effects on human health has led to a dramatic increase in research aimed at removing BBP from the environment via bioremediation. This review highlights recent progress in the degradation of BBP by pure and mixed bacterial cultures, fungi, and in sludge, sediment, and wastewater. Sonochemical degradation, a unique abiotic remediation technique, and photocatalytic degradation are also discussed. The degradation pathways for BBP are described, and future research directions are considered

    Pan-cancer analysis of whole genomes

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    Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

    Latex allergy and filaggrin null mutations

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    Association Between IL16

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