11 research outputs found

    Sexuality, partner relations and contraceptive practice after termination of pregnancy

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    The aim of this study was to determine the impact of termination of pregnancy (TOP) on women's sexual well-being, the couple and contraceptive practice. In a prospective qualitative and quantitative study, 103 women undergoing induced abortion by vacuum aspiration were interviewed before the abortion and 6 months later. The interview was performed by means of a questionnaire including open and closed questions, and two psychological tests (Locke-Wallace and Horowitz). After TOP, the majority of women did not report changes in their sexual behavior and satisfaction. Eighteen per cent of women reported a decrease in sexual desire and 17% reported orgasmic disorders. About one-third of women described psychosomatic symptoms, but a minority were traumatized by the event. Ninety-eight per cent of the women were informed about, and had practiced, contraception in the past; 69% had actually used some kind of contraception during the menstrual cycle that had resulted in pregnancy (31% had had unprotected intercourse). Six months later, 83% practiced contraception, and only 17% did not. Fourteen out of 84 couples separated after TOP (one in six). Six months after TOP, the large majority of women interviewed seemed able to cope with TOP. A minority presented some persisting sexual dysfunction and/or some psychosomatic symptoms. [Authors]]]> Abortion, Induced ; Contraception Behavior ; Sexual Dysfunction, Physiological ; Sexual Partners ; Sexuality ; Stress, Psychological oai:serval.unil.ch:BIB_37502 2022-05-07T01:15:20Z <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_37502 Accès aux soins pour tous en Suisse: une réalité? Duc, J.-L. info:eu-repo/semantics/article article 2003 AJP/PJA, pp. 539-544 oai:serval.unil.ch:BIB_37503 2022-05-07T01:15:20Z <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_37503 Après le rejet de la deuxième révision de la LAMal par le Conseil national et le changement intervenu à la tête du Département fédéral de l'intérieur. Duc, J.-L. info:eu-repo/semantics/article article 2003 AJP/PJA, pp. 631-640 oai:serval.unil.ch:BIB_37504 2022-05-07T01:15:20Z <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_37504 Prévoyance professionnelle - Examen de deux situations particulières. Duc, J.-L. info:eu-repo/semantics/article article 2003 SZS, pp. 339 ss oai:serval.unil.ch:BIB_375046944AC9 2022-05-07T01:15:20Z openaire documents urnserval <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_375046944AC9 Do sensation seeking and aggression traits moderate the association between peer influence and alcohol outcomes among young Swiss men? info:doi:10.1080/16066359.2017.1310847 info:eu-repo/semantics/altIdentifier/doi/10.1080/16066359.2017.1310847 Grazioli, Véronique S. Gmel, Gerhard Mohler-Kuo, Meichun Daeppen, Jean-Bernard Bertholet, Nicolas Studer, Joseph info:eu-repo/semantics/article article 2018-01-02 Addiction Research &amp; Theory, vol. 26, no. 1, pp. 52-62 info:eu-repo/semantics/altIdentifier/pissn/1606-6359 info:eu-repo/semantics/altIdentifier/pissn/1476-7392 <![CDATA[Peer influence is a strong predictor of drinking behaviors, yet not all young adults respond to its influence in the same way. This study aimed to identify young adults who are more vulnerable to peer influence by prospectively examining whether sensation seeking and aggression traits moderate the associations between peer influence and alcohol use and related consequences among young male drinkers. Participants (N=4,624 participants) were young Swiss men from the Cohort Study on Substance Use Risk Factors. Measures of peer influence (i.e. descriptive norms and peer pressure to engage in misconduct), sensation seeking, aggression and alcohol use and related consequences were used from the baseline and 15-month follow-up assessments. Findings indicated that neither sensation seeking nor aggression significantly moderated the associations between peer influence and alcohol-related consequences. However, they revealed that sensation seeking and aggression had a moderating effect on the association between peer influence and total drinks per year, such that this association was overall stronger among participants scoring lower on personality traits. These findings suggest that young male drinkers with low scores on sensation seeking and aggression may benefit from stand-alone selective interventions targeting peer influence, whereas those scoring higher on these personality traits may rather benefit from programs that include interventions targeting both peer influence and personality risk factors of drinking behaviors

    Mutational spectrum in a worldwide study of 29,700 families with BRCA1 or BRCA2 mutations.

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    The prevalence and spectrum of germline mutations in BRCA1 and BRCA2 have been reported in single populations, with the majority of reports focused on White in Europe and North America. The Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA) has assembled data on 18,435 families with BRCA1 mutations and 11,351 families with BRCA2 mutations ascertained from 69 centers in 49 countries on six continents. This study comprehensively describes the characteristics of the 1,650 unique BRCA1 and 1,731 unique BRCA2 deleterious (disease-associated) mutations identified in the CIMBA database. We observed substantial variation in mutation type and frequency by geographical region and race/ethnicity. In addition to known founder mutations, mutations of relatively high frequency were identified in specific racial/ethnic or geographic groups that may reflect founder mutations and which could be used in targeted (panel) first pass genotyping for specific populations. Knowledge of the population-specific mutational spectrum in BRCA1 and BRCA2 could inform efficient strategies for genetic testing and may justify a more broad-based oncogenetic testing in some populations

    An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers

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    Introduction: Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods: We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results: We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions: This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects.Peer reviewe

    Identification of 12 new susceptibility loci for different histotypes of epithelial ovarian cancer.

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    To identify common alleles associated with different histotypes of epithelial ovarian cancer (EOC), we pooled data from multiple genome-wide genotyping projects totaling 25,509 EOC cases and 40,941 controls. We identified nine new susceptibility loci for different EOC histotypes: six for serous EOC histotypes (3q28, 4q32.3, 8q21.11, 10q24.33, 18q11.2 and 22q12.1), two for mucinous EOC (3q22.3 and 9q31.1) and one for endometrioid EOC (5q12.3). We then performed meta-analysis on the results for high-grade serous ovarian cancer with the results from analysis of 31,448 BRCA1 and BRCA2 mutation carriers, including 3,887 mutation carriers with EOC. This identified three additional susceptibility loci at 2q13, 8q24.1 and 12q24.31. Integrated analyses of genes and regulatory biofeatures at each locus predicted candidate susceptibility genes, including OBFC1, a new candidate susceptibility gene for low-grade and borderline serous EOC

    Assessing Associations between the AURKA-HMMR-TPX2-TUBG1 Functional Module and Breast Cancer Risk in BRCA1/2 Mutation Carriers

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    While interplay between BRCA1 and AURKA-RHAMM-TPX2-TUBG1 regulates mammary epithelial polarization, common genetic variation in HMMR (gene product RHAMM) may be associated with risk of breast cancer in BRCA1 mutation carriers. Following on these observations, we further assessed the link between the AURKA-HMMR-TPX2-TUBG1 functional module and risk of breast cancer in BRCA1 or BRCA2 mutation carriers. Forty-one single nucleotide polymorphisms (SNPs) were genotyped in 15,252 BRCA1 and 8,211 BRCA2 mutation carriers and subsequently analyzed using a retrospective likelihood approach. The association of HMMR rs299290 with breast cancer risk in BRCA1 mutation carriers was confirmed: per-allele hazard ratio (HR) = 1.10, 95% confidence interval (CI) 1.04 - 1.15, p = 1.9 x 10(-4) (false discovery rate (FDR)-adjusted p = 0.043). Variation in CSTF1, located next to AURKA, was also found to be associated with breast cancer risk in BRCA2 mutation carriers: rs2426618 per-allele HR = 1.10, 95% CI 1.03 - 1.16, p = 0.005 (FDR-adjusted p = 0.045). Assessment of pairwise interactions provided suggestions (FDR-adjusted p(interaction) values > 0.05) for deviations from the multiplicative model for rs299290 and CSTF1 rs6064391, and rs299290 and TUBG1 rs11649877 in both BRCA1 and BRCA2 mutation carriers. Following these suggestions, the expression of HMMR and AURKA or TUBG1 in sporadic breast tumors was found to potentially interact, influencing patients' survival. Together, the results of this study support the hypothesis of a causative link between altered function of AURKA-HMMR-TPX2-TUBG1 and breast carcinogenesis in BRCA1/2 mutation carriers.Peer reviewe

    Identification of six new susceptibility loci for invasive epithelial ovarian cancer.

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    Assessing Associations between the AURKA-HMMR-TPX2-TUBG1 Functional Module and Breast Cancer Risk in BRCA1/2 Mutation Carriers

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    The <i>HMMR</i> locus and breast cancer risk in <i>BRCA1</i> mutation carriers.

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    <p>(<b>A</b>) Forest plots showing rs299290 HRs and 95% CIs (retrospective likelihood trend estimation) for participating countries (relatively small sample sets are not shown) ordered by sample size. Left and right panels show results for <i>BRCA1</i> and <i>BRCA2</i> mutation carriers, respectively. The sizes of the rectangles are proportional to the corresponding country/study precision. (<b>B</b>) The rs299290-containing region, including the genes, variation and regulatory evidence mentioned in HMECs. Exons are marked by black-filled rectangles and the direction of transcription is marked by arrows in the genomic structure. The chromosome 5 positions (base pairs (bp)) and linkage disequilibrium structure from Caucasian HapMap individuals are also shown.</p

    Gene expression interactions in breast cancer survival.

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    <p>(<b>A</b>) Kaplan–Meier survival curves based on categorization of <i>HMMR</i> (probe NM_012484) and <i>AURKA</i> (NM_003600) expression in tertiles (low, medium or high expression). For simplicity, only the tertiles for “high” <i>AURKA</i> are shown. The tumours with high expression levels for both genes were not those with the poorest prognosis. (<b>B</b>) Kaplan–Meier survival curves based on categorization of <i>HMMR</i> (NM_012484) and <i>TUBG1</i> (NM_016437) expression in tertiles (low, medium or high expression). For simplicity, only the tertiles for “high” <i>HMMR</i> are shown. The cases with high expression levels for both genes were those with the poorest prognosis.</p

    Potential GxG associated with breast cancer risk in <i>BRCA1/2</i> mutation carriers.

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    <p>*Each estimate is derived from the interaction term of a Cox regression model.</p><p>Potential GxG associated with breast cancer risk in <i>BRCA1/2</i> mutation carriers.</p
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