129 research outputs found

    Examining Sex and Gender Differences in Anxiety Disorders

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    Several studies have examined sex differences in different anxiety disorders. Females are repeatedly found to be more likely than males to suffer from anxiety in general and to be diagnosed with most anxiety disorders, including agoraphobia (AG), panic disorder (PD), separation anxiety (SA), specific phobia (SP), social anxiety disorder (SAD), generalised anxiety disorder (GAD), obsessive-compulsive disorder (OCD), and acute and posttraumatic stress disorder (ASD and PTSD), although the latter three are technically no longer categorised as anxiety disorders according to DSM-5. This chapter provides an overview of research on sex and gender differences in anxiety disorders ranging from the well-established female preponderance in prevalence and severity to possible sex differences in the risk and protective factors associated with anxiety, sex differences in the clinical presentation of anxiety disorders, and potential sex differences in the effectiveness of different treatments. The chapter contains suggestions for future research, including important questions that remain to be answered

    Sex Differences in PTSD

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    Predictive factors for somatization in a trauma sample

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    which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Unexplained somatic symptoms are common among trauma survivors. The relationship between trauma and somatization appears to be mediated by posttraumatic stress disorder (PTSD). However, only few studies have focused on what other psychological risk factors may predispose a trauma victim towards developing somatoform symptoms. Methods: The present paper examines the predictive value of PTSD severity, dissociation, negative affectivity, depression, anxiety, and feeling incompetent on somatization in a Danish sample of 169 adult men and women who were affected by a series of explosions in a firework factory settled in a residential area. Results: Negative affectivity and feelings of incompetence significantly predicted somatization, explaining 42 % of the variance. PTSD was significant until negative affectivity was controlled for. Conclusion: Negative affectivity and feelings of incompetence significantly predicted somatization in the trauma sample whereas dissociation, depression, and anxiety were not associated with degree of somatization. PTSD as a risk factor was mediated by negative affectivity

    Forskellige prÊdiktorer for posttraumatisk vÊkst pÄ mikro-, meso- og makroniveau

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    Forskning i posttraumatisk vÊkst (PTG) har nÊsten udelukkende fokuseret pÄ vÊkst pÄ mikroniveau hos voksne og universitetsstuderende pÄ trods af, at vÊkst kan tÊnkes at komme anderledes til udtryk hos bÞrn og unge, og prÊdiktorer for vÊkst kan vÊre forbundet forskelligt med PTG pÄ mikro- (personlig vÊkst), meso- (relationel vÊkst) og makroniveau (institutionel vÊkst). NÊrvÊrende studie undersÞger effekten af kÞn, alder, tilknytning, kontrolfokus, coping, social stÞtte og posttraumatisk stress pÄ PTG pÄ forskellige vÊkstniveauer. UndersÞgelsesdeltagerne var gymnasiestuderende (N = 320), som havde deltaget i en skolefest, hvor en kvindelig gymnasieelev blev knivdrÊbt. Et manglende overlap mellem de tre vÊkstniveauer antydede en differentiering mellem PTG pÄ mikro-, meso- og makroniveau. Alder, problemfokuseret coping, perception af social stÞtte og PTSD-symptomer var signifikante prÊdiktorer for PTG pÄ forskellige vÊkstniveauer. Der var positive trends angÄende relationer mellem problemfokuseret coping, positivt billede af andre, oplevet social stÞtte og tilfredshed med social stÞtte og PTG pÄ forskellige vÊkstniveauer. KÞn og kontrolfokus var ikke relateret til PTG. PrÊdiktorer for vÊkst kan have forskellige effekter pÄ PTG pÄ mikro-, meso- og makroniveau, idet en positiv prÊdiktor for vÊkst pÄ et niveau kan vÊre en negativ prÊdiktor for vÊkst pÄ et andet niveau. NÊrvÊrende studie kan sÄledes vÊre med til at forklare forskningsfeltets hidtil inkonsistente resultater. Fremtidig forskning i PTG bÞr derfor indeholde dimensionelle vÊkstmÄl med uafhÊngige subskalaer for de tre vÊkstniveauer

    Posttraumatisk vÊkst: Et kritisk review over problemer med de nuvÊrende mÄlinger af begrebet

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    Forskning inden for posttraumatisk vÊkst (PTG) er i dag karakteriseret ved divergerende forskningsresultater, som har gjort det vanskeligt at drage en kohÊrent lÊre om fÊnomenet. NÊrvÊrende artikel er et kritisk review over publicerede artikler fra 2004 til 2010, som omhandler validiteten af de nuvÊrende mÄlinger af PTG, med sÊrligt fokus pÄ de kvantitative skalaer, der oftest anvendes til at mÄle PTG: Post Traumatic Growth Inventory (PTGI) og Stress Related Growth Scale (SRGS). Begge skalaer har vist acceptabel reliabilitet, men der er en rÊkke bekymringer vedrÞrende deres validitet. NÊrvÊrende review identificerer seks validitetsproblemer med de nuvÊrende mÄlinger af PTG og lÊgger op til en kritisk diskussion om validitetsforbedrende tiltag i forhold til fremtidig forskning i PTG

    Value Propositions of Public Adult Hearing Rehabilitation in Denmark

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    Objective: To obtain and evaluate detailed descriptions of potential value propositions as seen by adults undergoing hearing rehabilitation with hearing aids. Design: Semi-structured interviews with patients and audiologists, a literature search, and the inclusion of domain knowledge from experts and scientists were used to derive value propositions. A two-alternative forced-choice paradigm and probabilistic choice models were used to investigate hearing aid users’ preferences for the value propositions through an online platform. Study sample: Twelve hearing aid users (mean age 70, range 59–70) and eleven clinicians were interviewed. A total of 173 experienced hearing aid users evaluated the value propositions. Results: Twenty-nine value propositions as described by patients, clinicians, and hearing care experts where identified, from which twenty-one value propositions were evaluated. Results of the pair-wise evaluation method show that the value propositions judged to be the most important for the hearing aid users were: “13. To solve the hearing problem you have”, “09. Thorough diagnosis of the hearing”, and “16. The hearing aid solution is adapted to individual needs”, which are related to finding the correct hearing solution and to be considered in the process. The value propositions judged to be least important were: “04 Next of kin and others involved in the process”, “26. To be in the same room as the practitioner”, and “29. The practitioner’s human characteristics”, related to the involvement of others in the process and the proximity and personal manner of the practitioners.</p

    Granulocyte and monocyte CD11b expression during plasma separation is dependent on complement factor 5 (C5) – an ex vivo study with blood from a C5-deficient individual

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    This is the pre-peer reviewed version of the following article: Hardersen, R., Enebakk, T., Christiansen, D., Bergseth, G., Brekke, L.-O., Mollnes, T.E., ... Hovland, A.W. (2018). Granulocyte and monocyte CD11b expression during plasma separation is dependent on complement factor 5 (C5) ? an ex vivo study with blood from a C5-deficient individual. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 126(4), 342-352, which has been published in final form at https://doi.org/10.1111/apm.12821. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.The aim of the study was to investigate the role of complement factor 5 (C5) in reactions elicited by plasma separation using blood from a C5‐deficient (C5D) individual, comparing it to C5‐deficient blood reconstituted with C5 (C5DR) and blood from healthy donors. Blood was circulated through an ex vivo plasma separation model. Leukocyte CD11b expression and leukocyte–platelet conjugates were measured by flow cytometry during a 30‐min period. Other markers were assessed during a 240‐min period. Granulocyte and monocyte CD11b expression did not increase in C5D blood during plasma separation. In C5DR samples granulocytes CD11b expression, measured by mean fluorescence intensity (MFI), increased from 10481 ± 6022 (SD) to 62703 ± 4936, and monocytes CD11b expression changed from 13837 ± 7047 to 40063 ± 713. Granulocyte–platelet conjugates showed a 2.5‐fold increase in the C5DR sample compared to the C5D sample. Monocyte–platelet conjugates increased independently of C5. In the C5D samples, platelet count decreased from 210 × 109/L (201–219) (median and range) to 51 × 109/L (50–51), and C3bc increased from 14 CAU/mL (21–7) to 198 CAU/mL (127–269), whereas TCC formation was blocked during plasma separation. In conclusion, up‐regulation of granulocyte and monocyte CD11b during plasma separation was C5‐dependent. The results also indicate C5 dependency in granulocyte–platelet conjugates formation

    Complement C3b contributes to Escherichia coli-induced platelet aggregation in human whole blood

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    We found that compstatin, which inhibits the cleavage of complement component C3 to its components C3a and C3b, reduced the E. coli-induced platelet aggregation by 42%-76% (p = 0.0417). This C3-dependent aggregation was not C3a-mediated as neither inhibition of C3a using a blocking antibody or a C3a receptor antagonist, nor the addition of purified C3a had any effects. In contrast, a C3b-blocking antibody significantly reduced the E. coli-induced platelet aggregation by 67% (p = 0.0133). We could not detect opsonized C3b on platelets, indicating that the effect of C3 was not dependent on C3b-fragment deposition on platelets. Indeed, inhibition of glycoprotein IIb/IIIa (GPIIb/IIIa) and complement receptor 1 (CR1) showed that these receptors were involved in platelet aggregation. Furthermore, aggregation was more pronounced in hirudin whole blood than in hirudin platelet-rich plasma, indicating that E. coli-induced platelet aggregation involved other blood cells. In conclusion, the E. coli-induced platelet aggregation in human whole blood is partly C3b-dependent, and GPIIb/IIIa and CR1 are also involved in this process
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