SCD Lyon 1 - rapport d\u27activité 2008

Ce rapport présente un bilan de l\u27activité du SCD Lyon 1 en 2008, aussi bien sur le plan des ressources humaines, que des projets menés au sein de l\u27établissement, des acquisitions, de la politique documentaire, de l\u27informatique documentaire, de l\u27action culturelle et de la communication

SCD Lyon 1 - rapport d\u27activité 2011

Ce rapport présente un bilan de l\u27activité du SCD Lyon 1 en 2011, aussi bien sur le plan des ressources humaines, que des projets menés au sein de l\u27établissement, des acquisitions, de la politique documentaire, de l\u27informatique documentaire, de l\u27action culturelle et de la communication

SCD Lyon 1 - rapport d\u27activité 2010

Ce rapport présente un bilan de l\u27activité du SCD Lyon 1 en 2010, aussi bien sur le plan des ressources humaines, que des projets menés au sein de l\u27établissement, des acquisitions, de la politique documentaire, de l\u27informatique documentaire, de l\u27action culturelle et de la communication

SCD Lyon 1 - rapport d\u27activité 2009

Ce rapport présente un bilan de l\u27activité du SCD Lyon 1 en 2009, aussi bien sur le plan des ressources humaines, que des projets menés au sein de l\u27établissement, des acquisitions, de la politique documentaire, de l\u27informatique documentaire, de l\u27action culturelle et de la communication

Foreign acquisitions by UK limited companies: short- and long-run performance

Article; an earlier version was issued as Xfi working paper 04/01In this paper, we consider the short- and long-run performance of UK firms following foreign acquisitions. Based on a near-exhaustive sample of significant foreign acquisitions by UK companies over the period 1985–1994, we show that short-run returns are insignificantly different from zero irrespective of the location of the acquisition. Further analysis reveals that the distribution of the event period returns is determined by changes in the exchange rate, the presence of the acquiring firm in the target country and by US tax reforms. While long-run returns are not significantly different from zero on average, they show considerable variation by region. Specifically, firms under-perform following acquisition in the US, show insignificant returns following acquisitions in the EU and acquisitions elsewhere show significant positive returns. Examination of the distribution of these returns suggest that, in accordance with the ownership–location–internalisation hypothesis of foreign direct investment (FDI), long-run performance is more likely to depend on the firm-specific advantages such as R&D

Significant evidence for a heritable contribution to cancer predisposition: a review of cancer familiality by site

<p>Abstract</p> <p>Background/Aims</p> <p>Sound and rigorous well-established, and newly extended, methods for genetic epidemiological analysis were used to analyze population evidence for genetic contributions to risk for numerous common cancer sites in Utah. The Utah Population Database (UPDB) has provided important illumination of the familial contribution to cancer risk by cancer site.</p> <p>Methods</p> <p>With over 15 years of new cancer data since the previous comprehensive familial cancer analysis, we tested for excess familial clustering using an expanded Genealogical Index of Familiality (dGIF) methodology that provides for a more informative, but conservative test for the existence of a genetic contribution to familial relatedness in cancer.</p> <p>Results</p> <p>Some new cancer sites have been analyzed for the first time, having achieved sufficiently large sample size with additions to the UPDB. This new analysis has identified 6 cancer sites with significant evidence for a heritable contribution to risk, including lip, chronic lymphocytic leukemia, thyroid, lung, prostate, and melanoma.</p> <p>Conclusions</p> <p>Both environmentally and genetically-based familial clustering have clinical significance, and these results support increased surveillance for cancer of the same sites among close relatives of affected individuals for many more cancers than are typically considered.</p

Comparison of two methods based on cross-sectional data for correcting corpus uterine cancer incidence and probabilities

BACKGROUND: Two methods are presented for obtaining hysterectomy prevalence corrected estimates of invasive cancer incidence rates and probabilities of the corpus uterine. METHODS: The first method involves cross-sectional hysterectomy data from the Utah Hospital Discharge Data Base and mortality data applied to life-table methods. The second involves hysterectomy prevalence estimates obtained directly from the Utah Behavior Risk Factor Surveillance System (BRFSS) survey. RESULTS: Hysterectomy prevalence estimates based on the first method are lower than those obtained from the second method through age 74, but higher in the remaining ages. Correction for hysterectomy prevalence is greatest among women ages 75–79. In this age group, the uncorrected rate is 125 (per 100,000) and the corrected rate based on the life-table method is 223 using 1995–97 data, 243 using 1992–94 data, and 228 from the survey method. The uncorrected lifetime probability of developing corpus uterine cancer is 2.6%; the corrected probability from the life-table method using 1995–97 data is 4.2%, using 1992–94 data is 4.5%; and based on prevalence data from the survey method is 4.6%. CONCLUSIONS: Both methods provide reasonable hysterectomy prevalence estimates for correcting corpus uterine cancer rates and probabilities. Because of declining trends in hysterectomy in recent decades, corrected estimates from the life-table method are less pronounced than those based on the survey method. These methods may be useful for obtaining corrected uterine cancer rates and probabilities in areas of the world that do not have sufficient years of hysterectomy data to directly compute prevalence

Correction of a mouse model of Menkes disease by the human Menkes gene

The brindled mouse is an accurate model of the fatal human X-linked copper deficiency disorder, Menkes disease. Males carrying the mutant allele of the Menkes gene orthologue Atp7a die in the second week of life. To determine whether the genetic defect in the brindled mice could be corrected by expression of the human Menkes gene, male transgenic mice expressing ATP7A from the chicken &beta;-actin composite promoter (CAG) were mated with female carriers of the brindled mutation (Atp7aMo-br). Mutant males carrying the transgene survived and were fertile but the copper defect was not completely corrected. Unexpectedly males corrected with one transgenic line (T25#5) were mottled and resembled carrier females, this effect appeared to be caused by mosaic expression of the transgene. In contrast, males corrected with another line (T22#2) had agouti coats. Copper concentrations in tissues of the rescued mutants also resembled those of the heterozygous females, with high levels in kidney (84.6 &plusmn; 4.9 &mu;g/g in corrected males vs. 137.0 &plusmn; 44.3 &mu;g/g in heterozygotes) and small intestine (15.6 &plusmn; 2.5 &mu;g/g in corrected males vs. 15.7 &plusmn; 2.8 &mu;g/g in heterozygotes). The results show that the Menkes defect in mice is corrected by the human Menkes gene and that adequate correction is obtained even when the transgene expression does not match that of the endogenous gene.<br /