The impact of traumatic exposure on psychological distress and posttraumatic stress was investigated at 14 months through self-report in 1,505 Swedish tourists who survived the 2004 Indian Ocean Tsunami. Exposure, differentiated in single and multiple types, was associated with different levels of impaired mental health measured by General Health Questionnaire (GHQ) and Impact of Event Scale-Revised (IES-R). Additionally, having sole exposure to subjective life threat brought about specific psychological effects. Some demographic factors are associated with outcome on either the GHQ or the IES-R. Identifying specific types of exposure of disaster survivors may be a way to identify individuals who could be screened for psychological ill health at a later point in time.

Our findings indicate that components in one CPG might require diverse implementation strategies because they are linked to different contextual factors.

Statin use was associated with a modest decreased risk of HCC but did not influence the risk of colon cancer. Future randomized placebo-controlled trials in HCC high-risk patients are warranted to further investigate the possible prophylactic effect of statins in HCC.

Autoimmune polyendocrine syndrome type I (APS I) is an inherited recessive disorder with a progressive immunological destruction of many tissues including the adrenal cortex, the parathyroid glands, and the gonads. APS I is caused by mutations in the AIRE gene (autoimmune regulator), expressed in cells of the thymus and spleen, suggesting a role in central and peripheral tolerance. Aire ؊/؊ mice replicate the autoimmune features of APS I patients with the presence of multiple autoantibodies and lymphocytic infiltrates in various tissues, but young mice appear clinically healthy. We here report the investigation of 15-to 24-monthold Aire ؊/؊ mice. We did not observe any endocrinological abnormalities, nor did sera from these mice recognize known APS I autoantigens. Interestingly, however, there was a high frequency of marginal zone B-cell lymphoma in Aire ؊/؊ mice and liver infiltrates of B cells, suggesting chronic antigen exposure and exaggerated activation. Furthermore, increased numbers of monocytes in blood were identified as well as augmented numbers of metallophilic macrophages in the spleen. We propose that Aire, in addition to its function in the thymus, also has a peripheral regulatory role by controlling the development of antigen-presenting cells ( IntroductionIn autoimmune polyendocrine syndrome type I 1 (APS I, or autoimmune-polyendocrinopathy-candidiasis-ectodermal dystrophy [APECED]; Online Mendelian Inheritance in Man [OMIM] no. 240300), an inherited autoimmune disorder without major histocompatibility complex (MHC) linkage, 2,3 patients progressively lose tolerance to various tissue-specific antigens, with ensuing endocrine and nonendocrine disorders. APS I patients suffer from multiple organ failures due to immunologic destruction of the adrenal cortex, the parathyroid glands, the liver, ␤-cells of the islets of Langerhans, and enterochromaffin cells of the small intestine. In addition, probably as a sign of immune dysfunction, the patients suffer from a chronic mucocutaneous candidiasis. 1 The prevalence of APS I is increased in Finland, Sardinia, and among Iranian Jews. [4][5][6] The disease-causing gene was localized to the long arm of chromosome 21 7 and has later been identified and named the autoimmune regulator (AIRE). 8,9 AIRE has been proposed to function as a transcription factor. [10][11][12][13][14] Aire is expressed in thymic medullary epithelial cells, in dendritic cells, [15][16][17][18] and in blood monocytes, 19 suggesting a role of Aire in both central and peripheral tolerance. To define the role of Aire in immunologic tolerance, we previously reported an Aire Ϫ/Ϫ mouse line engineered to reproduce the most common Finnish APS I mutation. 20 In analogy with APS I, Aire Ϫ/Ϫ mice display multiple organ-specific autoantibodies and lymphocytic infiltrates. 20,21 Since Aire is expressed in medullary epithelial cells of the thymus (mTEC), studies have so far focused on central tolerance and have addressed the role of Aire in negative selection. 21,22 Aire has been proposed to ac...

Background and purpose More evidence is needed to forward our understanding of the key determinants of poor outcome after mild traumatic brain injury (MTBI). A large, prospective, national cohort of patients was studied to analyse the effect of head CT scan pathology on the outcome. Methods One‐thousand two‐hundred and sixty‐two patients with MTBI (Glasgow Coma Scale score 15) at 39 emergency departments completed a study protocol including acute head CT scan examination and follow‐up by the Rivermead Post Concussion Symptoms Questionnaire and the Glasgow Outcome Scale Extended (GOSE) at 3 months after MTBI. Binary logistic regression was used for the assessment of prediction ability. Results In 751 men (60%) and 511 women (40%), with a mean age of 30 years (median 21, range 6–94), we observed relevant or suspect relevant pathologic findings on acute CT scan in 52 patients (4%). Patients aged below 30 years reported better outcome both with respect to symptoms and GOSE as compared to patients in older age groups. Men reported better outcome than women as regards symptoms (OR 0.64, CI 0.49–0.85 for ≥3 symptoms) and global function (OR 0.60, CI 0.39–0.92 for GOSE 1–6). Conclusions Pathology on acute CT scan examination had no effect on self‐reported symptoms or global function at 3 months after MTBI. Female gender and older age predicted a less favourable outcome. The findings support the view that other factors than brain injury deserve attention to minimize long‐term complaints after MTBI.