3,704 research outputs found

    Repatriation from expedition ship in South America

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    This is my first hand account, being on board as part of the expedition team — in the role of a field guide / geology lecturer / zodiac driver / general naturalist — during the entire COVID-19 crisis as it unfolded on the ship.https://dc.ewu.edu/covid/1018/thumbnail.jp

    Colorectal cancer linkage on chromosomes 4q21, 8q13, 12q24, and 15q22

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    A substantial proportion of familial colorectal cancer (CRC) is not a consequence of known susceptibility loci, such as mismatch repair (MMR) genes, supporting the existence of additional loci. To identify novel CRC loci, we conducted a genome-wide linkage scan in 356 white families with no evidence of defective MMR (i.e., no loss of tumor expression of MMR proteins, no microsatellite instability (MSI)-high tumors, or no evidence of linkage to MMR genes). Families were ascertained via the Colon Cancer Family Registry multi-site NCI-supported consortium (Colon CFR), the City of Hope Comprehensive Cancer Center, and Memorial University of Newfoundland. A total of 1,612 individuals (average 5.0 per family including 2.2 affected) were genotyped using genome-wide single nucleotide polymorphism linkage arrays; parametric and non-parametric linkage analysis used MERLIN in a priori-defined family groups. Five lod scores greater than 3.0 were observed assuming heterogeneity. The greatest were among families with mean age of diagnosis less than 50 years at 4q21.1 (dominant HLOD = 4.51, α = 0.84, 145.40 cM, rs10518142) and among all families at 12q24.32 (dominant HLOD = 3.60, α = 0.48, 285.15 cM, rs952093). Among families with four or more affected individuals and among clinic-based families, a common peak was observed at 15q22.31 (101.40 cM, rs1477798; dominant HLOD = 3.07, α = 0.29; dominant HLOD = 3.03, α = 0.32, respectively). Analysis of families with only two affected individuals yielded a peak at 8q13.2 (recessive HLOD = 3.02, α = 0.51, 132.52 cM, rs1319036). These previously unreported linkage peaks demonstrate the continued utility of family-based data in complex traits and suggest that new CRC risk alleles remain to be elucidated. © 2012 Cicek et al

    The association between psychiatric diagnosis and violent re-offending in adult offenders in the community.

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    BACKGROUND: High rates of repeat offending are common across nations that are socially and culturally different. Although psychiatric disorders are believed to be risk factors for violent reoffending, the available evidence is sparse and liable to bias. METHOD: We conducted a historical cohort study in Sweden of a selected sample of 4828 offenders given community sentences who were assessed by a psychiatrist during 1988-2001, and followed up for an average of 5 years for first violent offence, death, or emigration, using information from national registers. Hazard ratios for violent offending were calculated by Cox regression models. RESULTS: Nearly a third of the sample (n = 1506 or 31.3%) offended violently during follow-up (mean duration: 4.8 years). After adjustment for socio-demographic and criminal history variables, substance use disorders (hazard ratio 1.97, 95% CI, 1.40-2.77) and personality disorders (hazard ratio 1.71, 1.20-2.44) were significantly associated with an increased risk of violent offending. No other diagnoses were related to recidivism risk. Adding information on diagnoses of substance use and personality disorders to data recorded on age, sex, and criminal history improved only minimally the prediction of violent offending. CONCLUSION: Diagnoses of substance use and personality disorders are associated with the risk of subsequent violent offending in community offenders about as strongly as are its better documented demographic and criminal history risk factors. Despite this, assessment of such disorders in addition to demographic and criminal history factors enhances only minimally the prediction of violent offending in the community.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

    An Assessment of the Impact of Hafting on Paleoindian Point Variability

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    It has long been argued that the form of North American Paleoindian points was affected by hafting. According to this hypothesis, hafting constrained point bases such that they are less variable than point blades. The results of several studies have been claimed to be consistent with this hypothesis. However, there are reasons to be skeptical of these results. None of the studies employed statistical tests, and all of them focused on points recovered from kill and camp sites, which makes it difficult to be certain that the differences in variability are the result of hafting rather than a consequence of resharpening. Here, we report a study in which we tested the predictions of the hafting hypothesis by statistically comparing the variability of different parts of Clovis points. We controlled for the potentially confounding effects of resharpening by analyzing largely unused points from caches as well as points from kill and camp sites. The results of our analyses were not consistent with the predictions of the hypothesis. We found that several blade characters and point thickness were no more variable than the base characters. Our results indicate that the hafting hypothesis does not hold for Clovis points and indicate that there is a need to test its applicability in relation to post-Clovis Paleoindian points

    Risk of colorectal cancer for carriers of mutations in MUTYH, with and without a family history of cancer

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    We studied 2332 individuals with monoallelic mutations in MUTYH among 9504 relatives of 264 colorectal cancer (CRC) cases with a MUTYH mutation. We estimated CRC risks through 70 years of age of 7.2% for male carriers of monoallelic mutations (95% confidence interval [CI], 4.6%-11.3%) and 5.6% for female carriers of monoallelic mutations (95% CI, 3.6%-8.8%), irrespective of family history. For monoallelic MUTYH mutation carriers with a first-degree relative with CRC diagnosed by 50 years of age who does not have the MUTYH mutation, risks of CRC were 12.5% for men (95% CI, 8.6%-17.7%) and 10% for women (95% CI, 6.7%-14.4%). Risks of CRC for carriers of monoallelic mutations in MUTYH with a first-degree relative with CRC are sufficiently high to warrant more intensive screening than for the general population
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