27 research outputs found
"Man måste brinna för att bli bränd" - en studie om en grupp kvinnors upplevelse av utbrändhet
No full textABSTRACT Author: Aferdita Haxha, Anna-lena Hulander Title: ”Man måste brinna för att bli bränd” – en studie om en grupp kvinnors upplevelse av utbrändhet Supervisor: Anders Lundberg Assessor: Mats Hilte The aim with this essay was to examine seven women’s experiences regarding burn-out. Furthermore we looked at what emotions these women experienced during their burn-out period and how their recovery was perceived. When summoned our material we found that burn-out seemed to be a less valid illness, in some cases we noticed a sense of shame connected to the sickness. Burn-out is an unclear expression that causes confusion because it’s a vague word with many meanings. The term has also been criticized for the reason that it refers to something that is burnt down, never to recover. The information our analysis is based upon is gathered through qualitative semi-structured interviews. We have applied Christina Maslach theory concerning burn-out to better understand and gather further knowledge regarding burn-out. Our conclusion is that burn-out is complex phenomenon which is caused by both work-related issues as well as personal traits
Role of the allelic variation in the 5-hydroxytryptamine receptor 1A (HTR1A) and the tryptophan hydroxylase 2 (TPH2) genes in the development of PTSD
No full textRisk Factors Associated with Childhood Asthma
No full textAsthma is the main cause of morbidity and mortality in the world and there are data that asthma prevalence has been increased in last 20 years, especially in children. The Aim of study is to analyze the risk factors that can contribute to asthma prevalence. Method. In the study there were children included, that have been admitted to hospital and after that were followed in regular basis or patients that were referred from other centers. All children with persistent asthma who were followed at least 3 months were included in the study. The collection of data was performed through an interview with parent or caregiver. Results. In our study, we had 158 children with persistent asthma and 51 children with intermittent asthma(control).The mean age is 6.63.The results show that children that have the allergy can develop asthma(p .000), allergy in the family is an important predictor of asthma (p .012) and parents with allergy (p.000),mother education is an important risk factor (p .000) in persistent asthma but not fathers education (p. 604). Birth weight under 2500gr and above 2500gr was not a significant risk factor for asthma in our study exclusively breastfeeding in the first 4 months of age is not associated with persistent asthma (p. 792). Siblings in the family did not show any significance as a risk factor for asthma (p. 433). Pets in the house did not show any significance in asthma (p. 209) in our study too. Conclusion Allergy in a child or in close family presents a high risk for asthma but also maternal education presents a risk factor for asthma prevalence in children.Keywords: child asthma, allergy, maternal education
Ideal Cardiovascular Health, Cardiovascular Remodeling, and Heart Failure in Blacks: The Jackson Heart Study
No full textFull author list omitted for brevity. For the full list of authors, see article.BACKGROUND: The lifetime risk of heart failure (HF) is higher in the black population than in other racial groups in the United States. METHODS AND RESULTS: We measured the Life's Simple 7 ideal cardiovascular health metrics in 4195 blacks in the JHS (Jackson Heart Study; 2000-2004). We evaluated the association of Simple 7 metrics with incident HF and left ventricular structure and function by cardiac magnetic resonance (n=1188). Mean age at baseline was 54.4 years (65% women). Relative to 0 to 2 Simple 7 factors, blacks with 3 factors had 47% lower incident HF risk (hazard ratio [HR], 0.53; 95% confidence interval [CI], 0.39-0.73; P/=4 factors had 61% lower HF risk (HR, 0.39; 95% CI, 0.24-0.64; P=0.0002). Higher blood pressure (HR, 2.32; 95% CI, 1.28-4.20; P=0.005), physical inactivity (HR, 1.65; 95% CI, 1.07-2.55; P=0.02), smoking (HR, 2.04; 95% CI, 1.43-2.91; P<0.0001), and impaired glucose control (HR, 1.76; 95% CI, 1.34-2.29; P<0.0001) were associated with incident HF. The age-/sex-adjusted population attributable risk for these Simple 7 metrics combined was 37.1%. Achievement of ideal blood pressure, ideal body mass index, ideal glucose control, and nonsmoking was associated with less likelihood of adverse cardiac remodeling by cardiac magnetic resonance. CONCLUSIONS: Cardiovascular risk factors in midlife (specifically elevated blood pressure, physical inactivity, smoking, and poor glucose control) are associated with incident HF in blacks and represent targets for intensified HF prevention
A CANDIDATE GENE ASSOCIATION STUDY OF FKBP5 AND CRHR1 POLYMORPHISMS IN RELATION TO WAR-RELATED POSTTRAUMATIC STRESS DISORDER
No full textBackground: Posttraumatic stress disorder (PTSD) is a highly frequent and disabling psychiatric condition among war-affected populations. TheFK506-binding protein 5 (FKBP5) gene and the corticotropin releasing hormone receptor 1 (CRHR1) gene have previously been implicated in an elevated risk of peritraumatic dissociation and PTSD development. Our aim was to investigate the association between FKBP5 and CRHR1 genotypes and PTSD diagnosis and severity among individuals who were affected by the Balkan wars during the 1990s.
Subjects and methods: This study included participants with current PTSD, remitted PTSD and healthy volunteers (N=719, 487 males), who were recruited between 2013 and 2015 within the framework of the South Eastern Europe (SEE) - PTSD Study. Psychometric methods comprised the Mini International Neuropsychiatric Interview (M.I.N.I.), the Clinician Administrated PTSD Scale (CAPS), and the Brief Symptom Inventory (BSI). FKBP5 rs1360780 and CRHR1 rs17689918 genotypes were determined using a KASP genotyping assay.
Results: Tests for deviation from Hardy Weinberg equilibrium showed no significant results. Logistic and linear regression was used to examine the associations between the FKBP5 SNP rs1360780 and the CRHR1 SNP rs17689918 with PTSD diagnosis and severity, as well as general psychiatric symptom severity, separately for current and remitted PTSD patients. There were nominally significant associations under a dominant model between the rs1360780 C allele and PTSD diagnosis as well as symptom severity, which however, were not significant anymore after Bonferroni adjustment (????=0.002). For CRHR1 rs17689918 no significant associations were detected.
Conclusion: We found nominally, but not Bonferroni corrected significant associations between the FKBP5 polymorphism rs1360780 and PTSD susceptibility among individuals affected by the Balkan wars. For elucidating this gene’s real resilience/ vulnerability potential, environmental influences should be taken into account
THE ASSOCIATION OF CATECHOL-O-METHYL-TRANSFERASE AND INTERLEUKIN 6 GENE POLYMORPHISMS WITH POSTTRAUMATIC STRESS DISORDER
No full textBackground: Posttraumatic stress disorder (PTSD) is a disorder that occurs in some people who have experienced a severe traumatic event. Several genetic studies suggest that gene encoding proteins of catechol O-methyl-transferase (COMT) may be relevant for the pathogenesis of PTSD. Some researchers suggested that the elevation of interleukin-6 (IL6) correlates with major depression and PTSD. The aim of this study was to investigate whether the single nucleotide polymorphisms COMT rs4680 (Val158Met) and IL6 rs1800795 are associated with PTSD and contribute to the severity of PTSD symptoms.
Subjects and methods: This study comprised 747 participants that experienced war between 1991 and 1999 in the South Eastern Europe conflicts. COMT rs4680 (Val158Met) and IL6 rs1800795 genotypes were determined in 719 participants (369 with and 350 without PTSD). The Mini International Neuropsychiatric Interview (M.I.N.I.), the Clinician Administrated PTSD Scale (CAPS) questionnaire and the Brief Symptom Inventory (BSI) were used for data collection.
Results: Regarding the COMT gene polymorphism, the results of the regression analyses for BSI total score were significant in the lifetime PTSD group in the dominant (P=0.031) and the additive allelic model (P=0.047). Regarding the IL6 gene, a significant difference was found for the recessive model predicting CAPS total score in the lifetime PTSD group (P=0.048), and indicated an association between the C allele and higher CAPS scores. n the allelic, genotypic and rezessive model, the results for BSI total score were significant in the lifetime PTSD group (P=0.033, P=0.028 and P=0.009), suggesting a correlation of the C allele with higher BSI scores
Conclusion: Although our nominally significant results did not withstand correction for multiple tests they may support a relevance of the COMT (Val158Met) and IL6 rs1800795 polymorphism for aspects of PTSD in war traumatized individuals
MOLECULAR MECHANISMS OF POSTTRAUMATIC STRESS DISORDER (PTSD) AS A BASIS FOR INDIVIDUALIZED AND PERSONALIZED THERAPY: RATIONALE, DESIGN AND METHODS OF THE SOUTH EASTERN EUROPE (SEE)-PTSD STUDY
No full textPosttraumatic Stress Disorder (PTSD) is a major health problem in South Eastern Europe (SEE). Available treatment options
are not efficient enough and the course is often chronic. Little is known about molecular mediators and moderators of pathogenesis
and therapy. Genetic and epigenetic variation may be one central molecular mechanism.
We therefore established a consortium combining clinical expertise on PTSD from SEE countries Bosnia-Herzegovina (Sarajevo,
Tuzla and Mostar), Kosovo (Prishtina) and Croatia (Zagreb) with genetic and epigenetic competence from Germany (Würzburg) in
2011 within the framework of the DAAD (Deutscher Akademischer Austauschdienst)-funded Stability Pact for South Eastern Europe.
After obtaining ethical votes and performing rater trainings as well as training in DNA extraction from EDTA blood between
2011 and 2013, we recruited 747 individuals who had experienced war-related trauma in the SEE conflicts between 1991 and 1999.
236 participants had current PTSD, 161 lifetime PTSD and 350 did not have and never had PTSD.
Demographic and clinical data are currently merged together with genetic and epigenetic data in a single database to allow for
a comprehensive analysis of the role of genetic and epigenetic variation in the pathogenesis and therapy of PTSD. Analyses will be
done to a great degree by PhD students from participating SEE centers who in addition to participation in the project had an
opportunity to take part in spring and summer schools of the DFG (Deutsche Forschungsgemeinschaft) funded Research Training
Group (RTG) 1253 and thus meet PhD students from Germany and other countries
We are confident that our project will not only contribute to a better understanding of genetic and epigenetic mechanisms of PTSD
as a basis for future individualized and personalized therapies, but also to the academic development of South Eastern Europe
ASSOCIATIONS OF GENE VARIATIONS IN NEUROPEPTIDE Y AND BRAIN DERIVED NEUROTROPHIC FACTOR GENES WITH POSTTRAUMATIC STRESS DISORDER
No full textBackground: Individuals who are exposed to traumatic events are at an increased risk of developing posttraumatic stress disorder (PTSD), a condition during which an individual's ability to function is impaired by emotional responses to memories of those events. The gene coding for neuropeptide Y (NPY) and the gene coding for brain-derived neurotrophic factor (BDNF) are among the number of candidate gene variants that have been identified as potential contributors to PTSD. The aim of this study was to investigate the association between NPY and BDNF and PTSD in individuals who experienced war-related trauma in the South Eastern Europe (SEE) conflicts (1991-1999).
Subjects and methods: This study included participants with current and remitted PTSD and healthy volunteers (N=719, 232 females, 487 males), who were recruited between 2013 and 2015 within the framework of the South Eastern Europe (SEE) - PTSD Study. Psychometric methods comprised the Mini International Neuropsychiatric Interview (M.I.N.I.), the Clinician Administered PTSD Scale (CAPS), and the Brief Symptom Inventory (BSI). DNA was isolated from whole blood and genotyped for NPY rs5574 via PCR - RFLP and NPY rs16147 and BDNF rs6265 using the KASP assay.
Results: Tests for deviation from Hardy-Weinberg equilibrium showed no significant results. Analyses at the categorical level yielded no associations between the affected individuals and all three SNPs when compared to controls. Within lifetime PTSD patients, the major alleles of both NPY variants showed a nominally significant association with higher CAPS scores (p=0.007 and p=0.02, respectively). Also, the major allele of rs5574C>T was associated with higher BSI scores with a nominal significance among current PTSD patients (p=0.047). The results did not withstand a Bonferroni adjustment (????=0.002).
Conclusion: Nominally significant associations between NPY polymorphisms and PTSD susceptibility were found that did not withstand Bonferroni correction
GENETIC SUSCEPTIBILITY TO POSTTRAUMATIC STRESS DISORDER: ANALYSES OF THE OXYTOCIN RECEPTOR, RETINOIC ACID RECEPTOR-RELATED ORPHAN RECEPTOR A AND CANNABINOID RECEPTOR 1 GENES
No full textBackground: Exposure to life-threatening events is common and everyone will most likely experience this type of trauma during their
ifetime. Reactions to these events are highly heterogeneous and seems to be influenced by genes as well. Some individuals will develop posttraumatic stress disorder (PTSD), while others will not. In this study, our aim was to analyze the correlation between single nucleotide polymorphisms (SNPs) within the oxytocin receptor (OXTR) gene (rs53576 and rs2254298), the RAR-related orphan receptor A (RORA) gene (rs8042149) and the cannabinoid receptor 1 (CNR1) gene (rs1049353) and PTSD. All candidate genes have been previously associated with stress related disorders and the reaction to traumatic events.
Subjects and methods: Participants (N=719) have been exposed to war-related trauma during the war in South-Eastern Europe (Bosnia and Herzegovina, Croatia and Kosovo). We correlated the presence and absence of current and lifetime PTSD as well as PTSD severity (Clinician Administered PTSD scale (CAPS)) and current psychopathology (Brief Symptom Inventory (BSI) score) with the mentioned SNPs. DNA was isolated from whole blood and genotyped for OXTR rs2254298 and rs53576 following previously published protocols, for RORA rs8042149 via PCR-RFLP and CNR1 rs1049353 via KASP.
Results: Nominally significant results were found for OXTR rs53576 in connection with the CAPS and BSI scores within lifetime PTSD patients. The additive allelic model indicated that G allele carriers achieved lower CAPS (p=0.0090) and BSI (p=0.0408) scores than participants carrying one or two copies of the A allele. These results did not withstand correction for multiple tests. No significant results were observed for OXTR rs2254298, RORA rs8042149 and CNR1 rs1049353 although the results for RORA showed a slight tendency that rs8042149 may influence the level of BSI scores in current PTSD patients.
Conclusions: This study points to a role of the OXTR gene in PTSD and the related psychopathology following war related trauma
Association of polygenic risk scores, traumatic life events and coping strategies with war-related PTSD diagnosis and symptom severity in the South Eastern Europe (SEE)-PTSD cohort
No full textOBJECTIVES: Posttraumatic stress disorder (PTSD) is triggered by extremely stressful environmental events and characterized by high emotional distress, re-experiencing of trauma, avoidance and hypervigilance. The present study uses polygenic risk scores (PRS) derived from the UK Biobank (UKBB) mega-cohort analysis as part of the PGC PTSD GWAS effort to determine the heritable basis of PTSD in the South Eastern Europe (SEE)-PTSD cohort. We further analyzed the relation between PRS and additional disease-related variables, such as number and intensity of life events, coping, sex and age at war on PTSD and CAPS as outcome variables. METHODS: Association of PRS, number and intensity of life events, coping, sex and age on PTSD were calculated using logistic regression in a total of 321 subjects with current and remitted PTSD and 337 controls previously subjected to traumatic events but not having PTSD. In addition, PRS and other disease-related variables were tested for association with PTSD symptom severity, measured by the Clinician Administrated PTSD Scale (CAPS) by liner regression. To assess the relationship between the main outcomes PTSD diagnosis and symptom severity, each of the examined variables was adjusted for all other PTSD related variables. RESULTS: The categorical analysis showed significant polygenic risk in patients with remitted PTSD and the total sample, whereas no effects were found on symptom severity. Intensity of life events as well as the individual coping style were significantly associated with PTSD diagnosis in both current and remitted cases. The dimensional analyses showed as association of war-related frequency of trauma with symptom severity, whereas the intensity of trauma yielded significant results independently of trauma timing in current PTSD. CONCLUSIONS: The present PRS application in the SEE-PTSD cohort confirms modest but significant polygenic risk for PTSD diagnosis. Environmental factors, mainly the intensity of traumatic life events and negative coping strategies, yielded associations with PTSD both categorically and dimensionally with more significant p-values. This suggests that, at least in the present cohort of war-related trauma, the association of environmental factors and current individual coping strategies with PTSD psychopathology was stronger than the polygenic risk
