BACKGROUND To explore the characteristics and compare clinical outcomes of non-Australian born (migrant) and Australian-born users of an Australian national digital mental health service. METHODS The characteristics and treatment outcomes of patients who completed online treatment at the MindSpot Clinic between January 2014 and December 2016 and reported a country of birth other than Australia were compared to Australian-born users. Data about the main language spoken at home were used to create distinct groups. Changes in symptoms of depression and anxiety were measured using the Patient Health Questionnaire-9 Item (PHQ-9), and Generalized Anxiety Disorder Scale - 7 Item (GAD-7), respectively. RESULTS Of 52,020 people who started assessment at MindSpot between 1st January 2014 and 22nd December 2016, 45,082 reported a country of birth, of whom 78.6% (n = 35,240) were Australian-born, and 21.4% (n = 9842) were born overseas. Of 6782 people who completed the online treatment and reported country of birth and main language spoken at home, 1631 (24%) were migrants, 960 (59%) were from English-speaking countries, and 671 (41%) were from non-English speaking countries. Treatment-seeking migrant users reported higher rates of tertiary education than Australian-born users. The baseline symptom severity, and rates of symptom reduction and remission following online treatment were similar across groups. CONCLUSIONS Online treatment was associated with significant reductions in anxiety and depression in migrants of both English speaking and non-English speaking backgrounds, with outcomes similar to those obtained by Australian-born patients. DMHS have considerable potential to help reduce barriers to mental health care for migrants.BACKGROUND Reliable quality of life assessment is important for identification of health problems, evaluation of health interventions and planning of optimal health policies and care packages. Due to lack of a psychometrically robust measurement tool for quality of life appraisal among the Iranian older population, this study was aimed to investigate psychometric properties of the Persian version of the World Health Organization quality of life-old module (WHOQOL-OLD-P) for use on the Iranian and other Persian-speaking aged populations. METHODS The standard translate/back-translate procedure was applied to convert the English version of the WHOQOL-OLD into Persian. The face and content validities were assessed by a panel of experts including 15 specialists in geriatrics and allied fields. The Cronbach's alpha and intra-class correlation (ICC) coefficients were estimated to assess internal validity and reliability of the translated version. Factorial structure of the WHOQOL-OLD-P was also tested using confirmatory factor analyses in a sample of 400 Persian-speaking older adults (aged 60 years of old and above) residing in the city of Yazd, the capital city of Yazd province, center of Iran. RESULTS The internal consistency and reliability indices of the WHOQOL-OLD-P were in the vicinity of acceptable range (Cronbach's alpha 0.65-0.82 and ICC 0.90-0.98). The confirmatory factor analysis outputs confirmed the six-factor solution of the WHOQOL-OLD-P (RMSEA = 0.04, CFI = 0.94, TLI = 0.93, SRMR = 0.06). CONCLUSION The study findings support validity and reliability of the WHOQOL-OLD-P for use on Iranian and possibly other Persian-speaking older populations. Further cross-cultural and comparative multinational studies are recommended to provide more vigorous evidence about feasibility and acceptability of the translated tool in diverse and multicultural Persian-speaking communities.BACKGROUND How intestinal epithelial cells interact with the microbiota and how this is regulated at the gene expression level are critical questions. Smarcad1 is a conserved chromatin remodeling factor with a poorly understood tissue function. As this factor is highly expressed in the stem and proliferative zones of the intestinal epithelium, we explore its role in this tissue. RESULTS Specific deletion of Smarcad1 in the mouse intestinal epithelium leads to colitis resistance and substantial changes in gene expression, including a striking increase of expression of several genes linked to innate immunity. Absence of Smarcad1 leads to changes in chromatin accessibility and significant changes in histone H3K9me3 over many sites, including genes that are differentially regulated upon Smarcad1 deletion. We identify candidate members of the gut microbiome that elicit a Smarcad1-dependent colitis response, including members of the poorly understood TM7 phylum. CONCLUSIONS Our study sheds light onto the role of the chromatin remodeling machinery in intestinal epithelial cells in the colitis response and shows how a highly conserved chromatin remodeling factor has a distinct role in anti-microbial defense. This work highlights the importance of the intestinal epithelium in the colitis response and the potential of microbial species as pharmacological and probiotic targets in the context of inflammatory diseases.BACKGROUND Despite the utility of neuroimaging in the diagnostic and therapeutic management of patients with acute ischemic stroke (AIS), imaging characteristics in patients with preceding direct oral anticoagulants (DOAC) compared to vitamin K antagonists (VKA) have hardly been described. We aimed to determine presence of large vessel occlusion (LVO), thrombus length, infarction diameter, and occurrence of hemorrhagic transformation in AIS patients with preceding DOAC as compared to VKA therapy. METHODS Using a prospectively collected cohort of AIS patients, we performed univariate and multivariable regression analyses regarding imaging outcomes. https://www.selleckchem.com/products/kynurenic-acid.html Additionally, we provide a sensitivity analysis for the subgroup of patients with confirmed therapeutic anticoagulation. RESULTS We included AIS in patients with preceding DOAC (N = 75) and VKA (N = 61) therapy, median age 79 (IQR 70-83), 39% female. Presence of any LVO between DOAC and VKA patients (29.3% versus 37.7%, P = 0.361), and target LVO for endovascular therapy (26.