Examining Ethnoracial Differences in Retention in Evidence-Based Treatments for Posttraumatic Stress Disorder Secondary to Military Sexual Trauma.

Improving and expanding mental health treatment for Veterans who have experienced military sexual trauma (MST) is currently a top priority in Veterans Healthcare Administration. Many of these Veterans develop posttraumatic stress disorder (PTSD), and there is increasing recognition that diversity is a core treatment consideration for Veterans who have experienced trauma. As such, more information is needed concerning the relationship between trauma-focused treatment attrition and ethnoracial identity in Veterans who have experienced MST.

Ethnoracial Disparities in Perinatal Outcomes Among Women Veterans.

Non-Hispanic Black women have increased rates of preterm birth and low infant birth weight. However, we do not know if these disparities replicate in women veterans, a population that may be at further risk for poor perinatal outcomes. This study sought to examine ethnoracial differences in preterm birth and low infant birth weight in veterans.

Posttraumatic cognitions about the self are associated with depression symptoms in veterans endorsing a history of assaultive military sexual trauma.

Depressive symptoms are a commonly observed yet understudied mental health sequalae of military sexual trauma (MST). Prior research supports the relationship between negative posttraumatic cognitions (NPCs) and the onset and course of trauma symptoms more broadly. We hypothesized that NPCs would be associated with depression symptoms in veterans endorsing a history of MST, specifically assaultive type MST.

Brief family involvement enhances veteran homework quality during trauma-focused psychotherapy.

Objective: Homework has been shown to improve outcomes in cognitive-behavioral therapy, though less is known about the importance of homework during trauma-focused psychotherapy. Similarly, prior research suggests family context plays a key role in posttraumatic stress disorder (PTSD)-related distress and treatment engagement. One potential way that families can facilitate better treatment outcomes is by promoting homework engagement.

Differential Associations Between Posttraumatic Cognitions, Posttraumatic Stress Disorder Symptoms, and Race Among Black and White Veterans Seeking Treatment for Assaultive Military Sexual Trauma.

Past research supports the role of negative posttraumatic cognitions (NPCs) in the development and maintenance of posttraumatic stress disorder (PTSD). The relationship between NPCs and PTSD may be uniquely impacted by racial status and experiences of military sexual trauma (MST), both of which may have a unique impact on one's understanding of self, others, and the world. We explored racial differences in the association between NPCs and PTSD symptom clusters in a sample of veterans endorsing MST ( = 139; 74.

The role of cardiovascular magnetic resonance in the evaluation of acute myocarditis and inflammatory cardiomyopathies in clinical practice - a comprehensive review.

Inflammatory cardiomyopathy (I-CMP) is defined as myocarditis in association with cardiac dysfunction and/or ventricular remodelling. It is characterized by inflammatory cell infiltration into the myocardium and has heterogeneous infectious and non-infectious aetiologies. A complex interplay of genetic, autoimmune, and environmental factors contributes to the substantial risk of deteriorating cardiac function, acute heart failure, and arrhythmia as well as chronic dilated cardiomyopathy and its sequelae.

Interferon inducible X-linked gene CXorf21 may contribute to sexual dimorphism in Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease, characterised by increased expression of type I interferon (IFN)-regulated genes and a striking sex imbalance towards females. Through combined genetic, in silico, in vitro, and ex vivo approaches, we define CXorf21, a gene of hitherto unknown function, which escapes X-chromosome inactivation, as a candidate underlying the Xp21.2 SLE association.

Unraveling multiple MHC gene associations with systemic lupus erythematosus: model choice indicates a role for HLA alleles and non-HLA genes in Europeans.

We have performed a meta-analysis of the major-histocompatibility-complex (MHC) region in systemic lupus erythematosus (SLE) to determine the association with both SNPs and classical human-leukocyte-antigen (HLA) alleles. More specifically, we combined results from six studies and well-known out-of-study control data sets, providing us with 3,701 independent SLE cases and 12,110 independent controls of European ancestry. This study used genotypes for 7,199 SNPs within the MHC region and for classical HLA alleles (typed and imputed).

Genetically determined partial complement C4 deficiency states are not independent risk factors for SLE in UK and Spanish populations.

Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disease. Complete deficiency of complement component C4 confers strong genetic risk for SLE. Partial C4 deficiency states have also shown association with SLE, but despite much effort over the last 30 years, it has not been established whether this association is primarily causal or secondary to long-range linkage disequilibrium.

Transancestral mapping of the MHC region in systemic lupus erythematosus identifies new independent and interacting loci at MSH5, HLA-DPB1 and HLA-G.

Objectives: Systemic lupus erythematosus (SLE) is a chronic multisystem genetically complex autoimmune disease characterised by the production of autoantibodies to nuclear and cellular antigens, tissue inflammation and organ damage. Genome-wide association studies have shown that variants within the major histocompatibility complex (MHC) region on chromosome 6 confer the greatest genetic risk for SLE in European and Chinese populations. However, the causal variants remain elusive due to tight linkage disequilibrium across disease-associated MHC haplotypes, the highly polymorphic nature of many MHC genes and the heterogeneity of the SLE phenotype.

Determination of the loss of function complement C4 exon 29 CT insertion using a novel paralog-specific assay in healthy UK and Spanish populations.

Genetic variants resulting in non-expression of complement C4A and C4B genes are common in healthy European populations and have shown association with a number of diseases, most notably the autoimmune disease, systemic lupus erythematosus. The most frequent cause of a C4 "null" allele, following that of C4 gene copy number variation (CNV), is a non-sense mutation arising from a 2 bp CT insertion into codon 1232 of exon 29. Previous attempts to accurately genotype this polymorphism have not been amenable to high-throughput typing, and have been confounded by failure to account for CNV at this locus, as well as by inability to distinguish between paralogs.

Investigation of the HIN200 locus in UK SLE families identifies novel copy number variants.

We undertook a candidate locus study of the HIN200 gene cluster on 1q21-23 in UK systemic lupus erythematosus (SLE) families. To date, despite mounting evidence demonstrating the importance of these proteins in autoimmune disease, cancer, apoptosis, inflammation, and cell cycle arrest, there has been a dearth of data with respect to the genetic characterisation of the HIN200 locus in SLE or any other disease. We typed 83 single nucleotide polymorphisms (SNPs) across 317 kb of the HIN200 cluster in 428 UK SLE families and sought replication from a European-American lupus cohort.

Assessment of complement C4 gene copy number using the paralog ratio test.

The complement C4 locus is in the class III region of the MHC, and exhibits copy number variation. Complement C4 null alleles have shown association with a number of diseases including systemic lupus erythematosus (SLE). However, most studies to date have used protein immunophenotyping and not direct interrogation of the genome to determine C4 null allele status.

Mapping of multiple susceptibility variants within the MHC region for 7 immune-mediated diseases.

The human MHC represents the strongest susceptibility locus for autoimmune diseases. However, the identification of the true predisposing gene(s) has been handicapped by the strong linkage disequilibrium across the region. Furthermore, most studies to date have been limited to the examination of a subset of the HLA and non-HLA genes with a marker density and sample size insufficient for mapping all independent association signals.

Defining the role of the MHC in autoimmunity: a review and pooled analysis.

The major histocompatibility complex (MHC) is one of the most extensively studied regions in the human genome because of the association of variants at this locus with autoimmune, infectious, and inflammatory diseases. However, identification of causal variants within the MHC for the majority of these diseases has remained difficult due to the great variability and extensive linkage disequilibrium (LD) that exists among alleles throughout this locus, coupled with inadequate study design whereby only a limited subset of about 20 from a total of approximately 250 genes have been studied in small cohorts of predominantly European origin. We have performed a review and pooled analysis of the past 30 years of research on the role of the MHC in six genetically complex disease traits - multiple sclerosis (MS), type 1 diabetes (T1D), systemic lupus erythematosus (SLE), ulcerative colitis (UC), Crohn's disease (CD), and rheumatoid arthritis (RA) - in order to consolidate and evaluate the current literature regarding MHC genetics in these common autoimmune and inflammatory diseases.

Familial clustering of non-nuclear autoantibodies and C3 and C4 complement components in systemic lupus erythematosus.

Objective: To determine whether key features of systemic lupus erythematosus (SLE), namely, production of non-nuclear antibodies (anti-C1q and anticardiolipin antibodies [aCL]) and depletion of complement components C3 and C4, aggregate in families. In addition, we examined relationships between anti-C1q and C3 and C4 levels.

Methods: The study cohort comprised 1,037 predominantly white (82%) nuclear families in which at least 1 member had SLE.

Conversion of discoid lupus to antiphospholipid syndrome and SLE.

Background: A 64-year-old man was admitted to hospital with increasing seizure frequency, lethargy and confusion. He had a history of discoid lupus erythematosus, complex partial seizures, cerebral thromboses associated with antiphospholipid syndrome (APS) and hypertension. After admission to hospital, he developed autoimmune hemolytic anemia, thrombocytopenia, severe hypertension, proteinuria and a fluctuating level of consciousness.

Genome-wide association scan in women with systemic lupus erythematosus identifies susceptibility variants in ITGAM, PXK, KIAA1542 and other loci.

Systemic lupus erythematosus (SLE) is a common systemic autoimmune disease with complex etiology but strong clustering in families (lambda(S) = approximately 30). We performed a genome-wide association scan using 317,501 SNPs in 720 women of European ancestry with SLE and in 2,337 controls, and we genotyped consistently associated SNPs in two additional independent sample sets totaling 1,846 affected women and 1,825 controls. Aside from the expected strong association between SLE and the HLA region on chromosome 6p21 and the previously confirmed non-HLA locus IRF5 on chromosome 7q32, we found evidence of association with replication (1.

Identification of two independent risk factors for lupus within the MHC in United Kingdom families.

The association of the major histocompatibility complex (MHC) with SLE is well established yet the causal variants arising from this region remain to be identified, largely due to inadequate study design and the strong linkage disequilibrium demonstrated by genes across this locus. The majority of studies thus far have identified strong association with classical class II alleles, in particular HLA-DRB1*0301 and HLA-DRB1*1501. Additional associations have been reported with class III alleles; specifically, complement C4 null alleles and a tumor necrosis factor promoter SNP (TNF-308G/A).