Three Scales to Measure Burnout of Primary School Teachers: Empirical Evidence on their Adequacy

This study aimed at comparing the psychometric properties of three measures of burnout administered in 320 Greek primary school teachers, namely the Maslach Burnout Inventory (Maslach and Jackson 1982), the Burnout Measure (Pines and Aronson 1988) and the Copenhagen Burnout Inventory (Kristensen et al. 2005). Confirmatory factor analysis tested a three-factor solution for each inventory, consistent to the respective theory. Results yielded a reasonably good model fit for the MBI, and merely acceptable model fit for the BM and the CBI. Overall the findings suggest that the MBI is more appropriate instrument for assessing teachers' burnout compared to the MB and the CBI, which presented not so well-defined inner structure and highly correlated subscales

Health and social care in aging population: an integrated care institution for the elderly in Greece

PURPOSE: To describe the nature of the services actually offered to the elderly in Greece by an institution of integrated care, as opposed to those that should be offered according to the relevant law, and to investigate the factors influencing the supply of those services. BACKGROUND: By the year 2020 about 20 million people will be aged 80 and over in the European Union. People of third age consist 16.9% of the total Greek population. Population aging has major implications on health services, employment and society as a whole. “Open Care Centres for the Elderly” (KAPI) is a rapidly developing and expanding institution providing integrated care for the elderly. METHODS: A questionnaire to be completed by the staff was sent to all 370 KAPI. Response rate reached 66%. For the analysis of the data multiple logistic regression analysis was performed using SPSS 10.0. RESULTS: Both medical and social care is provided by the KAPI to the elderly with different magnitude all over the country. Factors such as number of members, medical, paramedical and non-medical staff and fund availability in the KAPI mainly influence the supply of services. CONCLUSIONS: Integrated care services are offered by the KAPI. However, more steps need to be taken towards the direction of other European countries' integrated care schemes, in order to improve both quality and quantity of the services provided

Integrated primary health care in Greece, a missing issue in the current health policy agenda: a systematic review

Background: Over the past years, Greece has undergone several endeavors aimed at modernizing and improving national health care services with a focus on PHC. However, the extent to which integrated primary health care has been achieved is still questioned. <br><br> Purpose: This paper explores the extent to which integrated primary health care (PHC) is an issue in the current agenda of policy makers in Greece, reporting constraints and opportunities and highlighting the need for a policy perspective in developing integrated PHC in this Southern European country. <br><br> Methods: A systematic review in PubMed/Medline and SCOPUS, along with a hand search in selected Greek biomedical journals was undertaken to identify key papers, reports, editorials or opinion letters relevant to integrated health care. <br><br> Results: Our systematic review identified 198 papers and 161 out of them were derived from electronic search. Fifty-three papers in total served the scope of this review and are shortly reported. A key finding is that the long-standing dominance of medical perspectives in Greek health policy has been paving the way towards vertical integration, pushing aside any discussions about horizontal or comprehensive integration of care. <br><br> Conclusion: Establishment of integrated PHC in Greece is still at its infancy, requiring major restructuring of the current national health system, as well as organizational culture changes. Moving towards a new policy-based model would bring this missing issue on the discussion table, facilitating further development

The ratio of SRPK1/SRPK1a regulates erythroid differentiation in K562 leukaemic cells

AbstractSRPK1, the prototype of the serine/arginine family of kinases, has been implicated in the regulation of multiple cellular processes such as pre-mRNA splicing, chromatin structure, nuclear import and germ cell development. SRPK1a is a much less studied isoform of SRPK1 that contains an extended N-terminal domain and so far has only been detected in human testis. In the present study we show that SRPK1 is the predominant isoform in K562 cells, with the ratio of the two isoforms being critical in determining cell fate. Stable overexpression of SRPK1a induces erythroid differentiation of K562 cells. The induction of globin synthesis was accompanied by a marked decrease in proliferation and a significantly reduced clonogenic potential. Small interfering RNA-mediated down-regulation of SRPK1 in K562 cells results similarly in a decrease in proliferative capacity and induction of globin synthesis. A decreased SRPK1/SRPK1a ratio is also observed upon hemin/DMSO-induced differentiation of K562 cells as well as in normal human erythroid progenitor cells. Mass spectrometric analysis of SRPK1a-associated proteins identified multiple classes of RNA-binding proteins including RNA helicases, heterogeneous nuclear ribonucleoproteins, ribosomal proteins, and mRNA-associated proteins. Several of the SRPK1a-copurifying proteins have been previously identified in ribosomal and pre-ribosomal complexes, thereby suggesting that SRPK1a may play an important role in linking ribosomal assembly and/or function to erythroid differentiation in human leukaemic cells

Serum Thioredoxin-80 is associated with age, ApoE4, and neuropathological biomarkers in Alzheimer’s disease: a potential early sign of AD

[EN] Background: Thioredoxin-80 (Trx80) is a cleavage product from the redox-active protein Thioredoxin-1 and has been previously described as a pro-inflammatory cytokine secreted by immune cells. Previous studies in our group reported that Trx80 levels are depleted in Alzheimer's disease (AD) brains. However, no studies so far have investigated peripheral Trx80 levels in the context of AD pathology and whether could be associated with the main known AD risk factors and biomarkers. Methods: Trx80 was measured in serum samples from participants from two different cohorts: the observational memory clinic biobank (GEDOC) (N = 99) with AD CSF biomarker data was available and the population-based lifestyle multidomain intervention trial Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) (N = 47), with neuroimaging data and blood markers of inflammation available. The GEDOC cohort consists of participants diagnosed with subjective cognitive impairment (SCI), mild cognitive impairment (MCI), and AD, whereas the FINGER participants are older adults at-risk of dementia, but without substantial cognitive impairment. One-way ANOVA and multiple comparison tests were used to assess the levels of Trx80 between groups. Linear regression models were used to explore associations of Trx80 with cognition, AD CSF biomarkers (A beta 42, t-tau, p-tau and p-tau/t-tau ratio), inflammatory cytokines, and neuroimaging markers. Results: In the GEDOC cohort, Trx80 was associated to p-tau/t-tau ratio in the MCI group. In the FINGER cohort, serum Trx80 levels correlated with lower hippocampal volume and higher pro-inflammatory cytokine levels. In both GEDOC and FINGER cohorts, ApoE4 carriers had significantly higher serum Trx80 levels compared to non-ApoE4 carriers. However, Trx80 levels in the brain were further decreased in AD patients with ApoE4 genotype. Conclusion: We report that serum Trx80 levels are associated to AD disease stage as well as to several risk factors for AD such as age and ApoE4 genotype, which suggests that Trx80 could have potential as serum AD biomarker. Increased serum Trx80 and decreased brain Trx80 levels was particularly seen in ApoE4 carriers. Whether this could contribute to the mechanism by which ApoE4 show increased vulnerability to develop AD would need to be further investigated.Open access funding provided by Karolinska Institute. This research was supported by the Margaretha af Ugglas Foundation, the Karolinska institutet KID funding, Gun och Bertil Stohnes Stiftelse, Stiftelsen Syskonen Svenssons, the Karolinska Institutet fund for geriatric research Stiftelsen Gamla Tjanarinnor, and the regional agreement on medical training and clinical research (ALF) between Stockholm County Council and Karolinska Institutet

Determinants of Self-Rated Health in a Representative Sample of a Rural Population: A Cross-Sectional Study in Greece

Self-rated health (SRH) is a health measure related to future health, mortality, healthcare services utilization and quality of life. Various sociodemographic, health and lifestyle determinants of SRH have been identified in different populations. The aim of this study is to extend SRH literature in the Greek population. This is a cross-sectional study conducted in rural communities between 2001 and 2003. Interviews eliciting basic demographic, health-related and lifestyle information (smoking, physical activity, diet, quality of sleep and religiosity) were conducted. The sample consisted of 1,519 participants, representative of the rural population of Tripoli. Multinomial regression analysis was conducted to identify putative SRH determinants. Among the 1,519 participants, 489 (32.2%), 790 (52%) and 237 (15.6%) rated their health as “very good”, “good” and “poor” respectively. Female gender, older age, lower level of education and impaired health were all associated with worse SRH, accounting for 16.6% of SRH variance. Regular exercise, healthier diet, better sleep quality and better adherence to religious habits were related with better health ratings, after adjusting for sociodemographic and health-related factors. BMI and smoking did not reach significance while exercise and physical activity exhibited significant correlations but not consistently across SRH categories. Our results support previous findings indicating that people following a more proactive lifestyle pattern tend to rate their health better. The role of stress-related neuroendocrinologic mechanisms on SRH and health in general is also discussed

Genetic predisposition to increased blood cholesterol and triglyceride lipid levels and risk of Alzheimer disease: a Mendelian randomization analysis.

BACKGROUND: Although altered lipid metabolism has been extensively implicated in the pathogenesis of Alzheimer disease (AD) through cell biological, epidemiological, and genetic studies, the molecular mechanisms linking cholesterol and AD pathology are still not well understood and contradictory results have been reported. We have used a Mendelian randomization approach to dissect the causal nature of the association between circulating lipid levels and late onset AD (LOAD) and test the hypothesis that genetically raised lipid levels increase the risk of LOAD. METHODS AND FINDINGS: We included 3,914 patients with LOAD, 1,675 older individuals without LOAD, and 4,989 individuals from the general population from six genome wide studies drawn from a white population (total n=10,578). We constructed weighted genotype risk scores (GRSs) for four blood lipid phenotypes (high-density lipoprotein cholesterol [HDL-c], low-density lipoprotein cholesterol [LDL-c], triglycerides, and total cholesterol) using well-established SNPs in 157 loci for blood lipids reported by Willer and colleagues (2013). Both full GRSs using all SNPs associated with each trait at p<5×10-8 and trait specific scores using SNPs associated exclusively with each trait at p<5 × 10-8 were developed. We used logistic regression to investigate whether the GRSs were associated with LOAD in each study and results were combined together by meta-analysis. We found no association between any of the full GRSs and LOAD (meta-analysis results: odds ratio [OR]=1.005, 95% CI 0.82-1.24, p = 0.962 per 1 unit increase in HDL-c; OR=0.901, 95% CI 0.65-1.25, p=0.530 per 1 unit increase in LDL-c; OR=1.104, 95% CI 0.89-1.37, p=0.362 per 1 unit increase in triglycerides; and OR=0.954, 95% CI 0.76-1.21, p=0.688 per 1 unit increase in total cholesterol). Results for the trait specific scores were similar; however, the trait specific scores explained much smaller phenotypic variance. CONCLUSIONS: Genetic predisposition to increased blood cholesterol and triglyceride lipid levels is not associated with elevated LOAD risk. The observed epidemiological associations between abnormal lipid levels and LOAD risk could therefore be attributed to the result of biological pleiotropy or could be secondary to LOAD. Limitations of this study include the small proportion of lipid variance explained by the GRS, biases in case-control ascertainment, and the limitations implicit to Mendelian randomization studies. Future studies should focus on larger LOAD datasets with longitudinal sampled peripheral lipid measures and other markers of lipid metabolism, which have been shown to be altered in LOAD. Please see later in the article for the Editors' Summary

Alzheimer's disease biomarker profiling in a memory clinic cohort without common comorbidities

Alzheimer's disease is a multifactorial disorder with large heterogeneity. Comorbidities such as hypertension, hypercholesterolaemia and diabetes are known contributors to disease progression. However, less is known about their mechanistic contribution to Alzheimer's pathology and neurodegeneration. The aim of this study was to investigate the relationship of several biomarkers related to risk mechanisms in Alzheimer's disease with the well-established Alzheimer's disease markers in a memory clinic population without common comorbidities. We investigated 13 molecular markers representing key mechanisms underlying Alzheimer's disease pathogenesis in CSF from memory clinic patients without diagnosed hypertension, hypercholesterolaemia or diabetes nor other neurodegenerative disorders. An analysis of covariance was used to compare biomarker levels between clinical groups. Associations were analysed by linear regression. Two-step cluster analysis was used to determine patient clusters. Two key markers were analysed by immunofluorescence staining in the hippocampus of non-demented control and Alzheimer's disease individuals. CSF samples from a total of 90 participants were included in this study: 30 from patients with subjective cognitive decline (age 62.4 ± 4.38, female 60%), 30 with mild cognitive impairment (age 65.6 ± 7.48, female 50%) and 30 with Alzheimer's disease (age 68.2 ± 7.86, female 50%). Angiotensinogen, thioredoxin-1 and interleukin-15 had the most prominent associations with Alzheimer's disease pathology, synaptic and axonal damage markers. Synaptosomal-associated protein 25 kDa and neurofilament light chain were increased in mild cognitive impairment and Alzheimer's disease patients. Grouping biomarkers by biological function showed that inflammatory and survival components were associated with Alzheimer's disease pathology, synaptic dysfunction and axonal damage. Moreover, a vascular/metabolic component was associated with synaptic dysfunction. In the data-driven analysis, two patient clusters were identified: Cluster 1 had increased CSF markers of oxidative stress, vascular pathology and neuroinflammation and was characterized by elevated synaptic and axonal damage, compared with Cluster 2. Clinical groups were evenly distributed between the clusters. An analysis of post-mortem hippocampal tissue showed that compared with non-demented controls, angiotensinogen staining was higher in Alzheimer's disease and co-localized with phosphorylated-tau. The identification of biomarker-driven endophenotypes in cognitive disorder patients further highlights the biological heterogeneity of Alzheimer's disease and the importance of tailored prevention and treatment strategies

Association study of cholesterol-related genes in Alzheimer's disease

Alzheimer's disease (AD) is a genetically complex disorder, and several genes related to cholesterol metabolism have been reported to contribute to AD risk. To identify further AD susceptibility genes, we have screened genes that map to chromosomal regions with high logarithm of the odds scores for AD in full genome scans and are related to cholesterol metabolism. In a European screening sample of 115 sporadic AD patients and 191 healthy control subjects, we analyzed single nucleotide polymorphisms in 28 cholesterol-related genes for association with AD. The genes HMGCS2, FDPS, RAFTLIN, ACAD8, NPC2, and ABCG1 were associated with AD at a significance level of P ≤ 0.05 in this sample. Replication trials in five independent European samples detected associations of variants within HMGCS2, FDPS, NPC2, or ABCG1 with AD in some samples (P = 0.05 to P = 0.005). We did not identify a marker that was significantly associated with AD in the pooled sample (n = 2864). Stratification of this sample revealed an APOE-dependent association of HMGCS2 with AD (P = 0.004). We conclude that genetic variants investigated in this study may be associated with a moderate modification of the risk for AD in some sample