Effect of slow-release FSH on embryo recovery in dairy cows

AETE, Bath, UK, 8-9 September, 2017201

Workplace bullying and the risk of cardiovascular disease and depression.

Occup Environ Med Aims: To examine exposure to workplace bullying as a risk factor for cardiovascular disease and depression in employees. Methods: Logistic regression models were related to prospective data from two surveys in a cohort of 5432 hospital employees (601 men and 4831 women), aged 18-63 years. Outcomes were new reports of doctor diagnosed cardiovascular disease and depression during the two year follow up among those who were free from these diseases at baseline. Results: The prevalence of bullying was 5% in the first survey and 6% in the second survey. Two per cent reported bullying experiences in both surveys, an indication of prolonged bullying. After adjustment for sex, age, and income, the odds ratio of incident cardiovascular disease for victims of prolonged bullying compared to non-bullied employees was 2.3 (95% CI 1.2 to 4.6). A further adjustment for overweight at baseline attenuated the odds ratio to 1.6 (95% CI 0.8 to 3.5). The association between prolonged bullying and incident depression was significant, even after these adjustments (odds ratio 4.2, 95% CI 2.0 to 8.6). Conclusions: A strong association between workplace bullying and subsequent depression suggests that bullying is an aetiological factor for mental health problems. The victims of bullying also seem to be at greater risk of cardiovascular disease, but this risk may partly be attributable to overweight. N o generally accepted definition of workplace bullying exists, but most definitions refer to aspects such as the persistence of bullying and the negative or detrimental effects perceived by the victim. 1 Examples of bullying include situations in which someone is subjected to social isolation or exclusion, the subject's work and work efforts are devalued, and the subject is threatened or otherwise worn down or frustrated. Thus, victimisation to workplace bullying may represent a social stressor related to a serious deficiency in perceived organisational justice and fairness. 2 7-9 However, the question whether workplace bullying predicts the onset of illness, such as cardiovascular disease and depression, has awaited longitudinal testing. Stress can contribute to the development of disease. Chronic overactivity or underactivity in cardiovascular and metabolic systems in relation to prolonged stress has been found to be an aetiological factor for cardiovascular disease and hypertension. 13 When representing a major chronic stressor, workplace bullying can be hypothesised to increase the victims' vulnerability to these stress related diseases. Testing this hypothesis requires repeated measurements of victimisation for the establishment of continuous bullying, a measurement strategy that has not been applied in prior occupational studies. We carried out a prospective study to examine whether exposure to workplace bullying is associated with new reports of cardiovascular disease and depression among hospital personnel. The study data on prolonged exposure to bullying were based on two surveys over two years. METHODS Study population A postal questionnaire was sent to all 10 969 employees (1712 men and 9257 women) aged 18-63 years, working in Finnish hospitals in 1998. Ten per cent of the employees were doctors, 47% nurses, 12% laboratory and x ray department staff, 12% administrative staff, and 19% maintenance, cleaners, and other workers. Respondents who were still working in the hospitals two years later, were sent a follow up questionnaire in 2000. The surveys gathered information on bullying, stress related diseases, and behavioural risks on both occasions. The approval of the Ethics Committee of the Finnish Institute of Occupational Health was obtained for the study. Measures Bullying was measured by the following question: ''Workplace bullying refers to a situation where someone is subjected to social isolation or exclusion, his or her work and efforts are devalued, he or she is threatened, derogatory comments are made about him or her in his or her absence, or other negative behaviour that is aimed to torment, wear down, or frustrate the victim occur. Have you been subjected to such bullying? ''. 5 Cardiovascular disease and depression were measured using a self administered checklist of common chronic diseases. 14 For each disease, the respondent was requested to indicate whether or not a medical doctor had diagnosed him or her as having the disease. Cardiovascular disease was identified if the respondent reported myocardial infarction, angina pectoris, cerebrovascular disease, or hypertension. Depression was identified if the respondent reported that a medical doctor had diagnosed him or her as having depression. Incident cases of cardiovascular disease and Other variables were: smoking (smoker versus nonsmoker, and the number of cigarettes smoked per day); alcohol consumption in grams of absolute alcohol per average week (cut offs for high consumption 280 and 190 g for men and women, respectively); weight and height for the calculation of body mass index (overweight indicated by BMI .29 kg/m 2 ); and demographics (sex, age, occupation, income, and job contract (permanent versus temporary) obtained from the employers' records). Statistical analysis We used logistic regression analysis to test predictive relations of bullying to cardiovascular disease and depression. The first step tested reversed causality. Baseline diseases and other baseline characteristics were set as predictors for incident caseness of bullying (bullied in the second survey) among employees who did not report being bullied at baseline. The second step examined whether prolonged bullying predicted incidence of cardiovascular disease and depression. Three exposure groups were formed: employees not reporting bullying in the first survey and in the second survey (the control group); employees who reported victimisation either in the first survey or the second survey (but not both); and victims of prolonged bullying (reporting victimisation in both surveys). Those with baseline diseases were excluded. Odds ratios and 95% confidence intervals (CI) for new cardiovascular disease and depression in the second survey were adjusted for sex, five year age categories, and income tertiles (calculated separately for men and women). The third step reported logistic models where the associations of bullying with cardiovascular disease and depression were additionally adjusted for those behavioural risk factors that showed significant differences between the levels of bullying. Finally, interactions between these behavioural risks and bullying on cardiovascular disease and depression were studied. All analyses were conducted using the SPSS 9.0 software package. RESULTS Response rates and sample attrition A total of 8104 employees (74%) responded to the first survey. The mean age of the respondents was 43.3 years, 88% were women, 77% had a permanent job contract, and the mean income was 1849 per month. The corresponding figures for the eligible population were 42.9 years, 84%, 75%, and 1884 per month, respectively. Thus, any differences between the respondents and all eligible employees were small. Of respondents to the first survey, 6674 were working in the target hospitals two years later at the time of the second survey. Of the 6674 eligible respondents of the first survey, 5432 (81%) responded to the second survey. Female, high income, non-depressive, and permanent employees were slightly overrepresented Reversed causality The prevalence of reported bullying was 5.2% in the first survey and 5.9% in the second survey. Bullying as a predictor of new disease Of the respondents, 1.7% reported bullying experiences in both surveys. As table 3 shows, prolonged bullying was associated with the onset of cardiovascular disease and depression. After adjustment for sex, age, and income, the odds ratio of incident cardiovascular disease for prolonged bullying, compared with no bullying, was 2.3. The corresponding odds ratio of new physician diagnosed depression was 4.8. For those who reported bullying only in one of the two surveys, the odds ratio of depression was 2.3. The role of behavioural risk factors Of the behavioural risk factors, overweight predicted the onset of new cardiovascular disease (OR 2.95, 95% CI 2.20 to 3.95). Smoking and high alcohol consumption at baseline were associated with an increased risk of depression (ORs 1.54 (95% CI 1.08 to 2.21) and 1.53 (95% CI 1.00 to 2.34), respectively). Examination of whether bullying contributes to behavioural risk factors shows that prolonged bullying, compared with no bullying, did not predict subsequent smoking (baseline adjusted OR 0.64, 95% CI 0.19 to 2.19), heavy alcohol consumption (OR 1.06, 95% CI 0.46 to 2.46), or overweight (OR 0.64, 95% CI 0.25 to 1.64). However, individuals who were bullied at both times were more often overweight at baseline than non-victims (OR 2.04, 95% CI 1.20 to 3.46). Adjustment for overweight in addition to demographic factors attenuated the association between bullying and new cardiovascular disease (OR 1.62, 95% CI 0.75 to 3.50 for bullying at both times versus at neither time), but did not affect the association between bullying and depression (OR 4.16, 95% CI 2.01 to 8.63). Interactions between bullying and overweight were not significant for cardiovascular disease (p = 0.902) and depression (p = 0.174). Main messages N There is a strong association between workplace bullying and subsequent depression. Exposure to bullying predicts the onset of depression in a doseresponse gradient. N There is also an association between bullying and incidence of cardiovascular disease. However, this association may partly be attributable to obesity. Policy implications N Evidence of depression implies that the problem of workplace bullying should be effectively treated in workplaces. N Early identification and prevention of workplace bullying may be a key factor in attempts to minimise its adverse effects on mental health

Genetic evidence supports recolonisation by Mya arenaria of western Europe from North America

The softshell clam Mya arenaria (L.) is currently widespread on the east and west coasts of North America. This bivalve also occurs on western European shores, where the post-Pleistocene origin of the species, whether introduced or relict, has been debated. We collected 320 M. arenaria from 8 locations in Europe and North America. Clams (n = 84) from 7 of the locations were examined for mitochondrial DNA variation by sequencing a section of the cytochrome oxidase 1 (COX1) gene. These were analysed together with 212 sequences, sourced from GenBank, from the same gene from 12 additional locations, chiefly from eastern North America but also 1 site each from western North America and from western Europe. Ten microsatellite loci were also investigated in all 320 clams. Nuclear markers showed reduced levels of variation in certain European samples. The same common COX1 haplotypes and microsatellite alleles were present throughout the range of M. arenaria, although significant differences were identified in haplotypic and allelic composition between many samples, particularly those from the 2 continents (Europe and North America). These findings support the hypothesis of post-Pleistocene colonisation of European shores from eastern North America (and the recorded human transfer of clams from the east to the west coast of North America in the 19th century)

Work and family: associations with long-term sick-listing in Swedish women – a case-control study

<p>Abstract</p> <p>Background</p> <p>The number of Swedish women who are long-term sick-listed is high, and twice as high as for men. Also the periods of sickness absence have on average been longer for women than for men. The objective of this study was to investigate the associations between factors in work- and family life and long-term sick-listing in Swedish women.</p> <p>Methods</p> <p>This case-control study included 283 women on long-term sick-listing ≥90 days, and 250 female referents, randomly chosen, living in five counties in Sweden. Bivariate and multivariate logistic regression analyses with odds ratios were calculated to estimate the associations between long-term sick-listing and factors related to occupational work and family life.</p> <p>Results</p> <p>Long-term sick-listing in women is associated with self-reported lack of competence for work tasks (OR 2.42 1.23–11.21 log reg), workplace dissatisfaction (OR 1.89 1.14–6.62 log reg), physical workload above capacity (1.78 1.50–5.94), too high mental strain in work tasks (1.61 1.08–5.01 log reg), number of employers during work life (OR 1.39 1.35–4.03 log reg), earlier part-time work (OR 1.39 1.18–4.03 log reg), and lack of influence on working hours (OR 1.35 1.47–3.86 log reg). A younger age at first child, number of children, and main responsibility for own children was also found to be associated with long-term sick-listing. Almost all of the sick-listed women (93%) wanted to return to working life, and 54% reported they could work immediately if adjustments at work or part-time work were possible.</p> <p>Conclusion</p> <p>Factors in work and in family life could be important to consider to prevent women from being long-term sick-listed and promote their opportunities to remain in working life. Measures ought to be taken to improve their mobility in work life and control over decisions and actions regarding theirs lives.</p

Nucleophosmin Phosphorylation by v-Cyclin-CDK6 Controls KSHV Latency

Nucleophosmin (NPM) is a multifunctional nuclear phosphoprotein and a histone chaperone implicated in chromatin organization and transcription control. Oncogenic Kaposi's sarcoma herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma, primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD). In the infected host cell KSHV displays two modes of infection, the latency and productive viral replication phases, involving extensive viral DNA replication and gene expression. A sustained balance between latency and reactivation to the productive infection state is essential for viral persistence and KSHV pathogenesis. Our study demonstrates that the KSHV v-cyclin and cellular CDK6 kinase phosphorylate NPM on threonine 199 (Thr199) in de novo and naturally KSHV-infected cells and that NPM is phosphorylated to the same site in primary KS tumors. Furthermore, v-cyclin-mediated phosphorylation of NPM engages the interaction between NPM and the latency-associated nuclear antigen LANA, a KSHV-encoded repressor of viral lytic replication. Strikingly, depletion of NPM in PEL cells leads to viral reactivation, and production of new infectious virus particles. Moreover, the phosphorylation of NPM negatively correlates with the level of spontaneous viral reactivation in PEL cells. This work demonstrates that NPM is a critical regulator of KSHV latency via functional interactions with v-cyclin and LANA

Genetic basis and outcome in a nationwide study of Finnish patients with hypertrophic cardiomyopathy

Aims Nationwide large-scale genetic and outcome studies in cohorts with hypertrophic cardiomyopathy (HCM) have not been previously published.Methods and results We sequenced 59 cardiomyopathy-associated genes in 382 unrelated Finnish patients with HCM and found 24 pathogenic or likely pathogenic mutations in six genes in 38.2% of patients. Most mutations were located in sarcomere genes (MYBPC3, MYH7, TPM1, and MYL2). Previously reported mutations by our study group (MYBPC3-Gln1061Ter, MYH7-Arg1053Gln, and TPM1-Asp175Asn) and a fourth major mutation MYH7-Val606Met accounted for 28.0% of cases. Mutations in GLA and PRKAG2 were found in three patients. Furthermore, we found 49 variants of unknown significance in 31 genes in 20.4% of cases. During a 6.7 +/- 4.2 year follow-up, annual all-cause mortality in 482 index patients and their relatives with HCM was higher than that in the matched Finnish population (1.70 vs. 0.87%; P < 0.001). Sudden cardiac deaths were rare (n = 8). Systolic heart failure (hazard ratio 17.256, 95% confidence interval 3.266-91.170, P = 0.001) and maximal left ventricular wall thickness (hazard ratio 1.223, 95% confidence interval 1.098-1.363, P < 0.001) were independent predictors of HCM-related mortality and life-threatening cardiac events. The patients with a pathogenic or likely pathogenic mutation underwent an implantable cardioverter defibrillator implantation more often than patients without a pathogenic or likely pathogenic mutation (12.9 vs. 3.5%, P < 0.001), but there was no difference in all-cause or HCM-related mortality between the two groups. Mortality due to HCM during 10 year follow-up among the 5.2 million population of Finland was studied from death certificates of the National Registry, showing 269 HCM-related deaths, of which 32% were sudden.Conclusions We identified pathogenic and likely pathogenic mutations in 38% of Finnish patients with HCM. Four major sarcomere mutations accounted for 28% of HCM cases, whereas HCM-related mutations in non-sarcomeric genes were rare. Mortality in patients with HCM exceeded that of the general population. Finally, among 5.2 million Finns, there were at least 27 HCM-related deaths annually