Violence and crime among male inpatients with severe mental illness: attempting to explain ethnic differences

Background

Studies report that in the UK, among men with severe mental illness (SMI), those of black Caribbean ethnicity display increased risk of aggressive behaviour, criminal convictions, and schizophrenia. The study aimed to compare aggressive behaviour and criminal convictions among men with SMI of white British, black Caribbean and black African ethnicity, and to explore factors associated with differences across ethnicities.

Method

Sample 1 included 1,104 male inpatients with SMI. Sample 2 included a representative sub-sample of 165 who completed interviews, and authorized access to medical and criminal files. Ethnicity was self-ascribed.

Results

Staff-rated violence prior to admission, self-reported aggressive behaviour, and convictions for non-violent and violent crimes differed among men with SMI of different ethnicities. Relative to men with SMI of white British ethnicity, those of black African ethnicity showed decreased risk of aggressive behaviour, and those of black Caribbean ethnicity showed elevated risk of convictions for non-violent, and marginally, for violent crimes. Relative to men with SMI of black African ethnicity, those of black Caribbean ethnicity showed elevated risk of aggressive behaviour and criminal convictions. Proportionately more of the men of both black African and black Caribbean ethnicity, than those of white British ethnicity, presented schizophrenia spectrum disorders. Multivariate analyses failed to identify factors that would explain differences in aggressive behaviour, and criminal convictions across ethnic groups.

Conclusions

Differences in four different measures of aggressive and antisocial behaviour among men with SMI of different ethnicities were observed but factors associated with these differences were not found.     

Characterization of nuclear acceptor sites for mammalian progesterone receptor: comparison with the chick oviduct system

We performed binding studies with hamster uterine progesterone receptor (Rp) and various chromatin-cellulose preparations to determine whether Rp acceptor sites exist in mammalian uterus analogous to those observed in the chick oviduct. Chick and hamster Rp acceptor site assays were done according to the method of Spelsberg et al. [(1983) Recent Prog. Horm. Res. 39, 463-513]. Hamster Rp bound to hamster uterine chromatin-cellulose, NAP-cellulose (a 4 M guanidine hydrochloride-extracted fraction) and DNA-cellulose in a manner similar to that observed in the chick oviduct. Hamster Rp binding was tissue specific as evidenced by higher Rp binding to target-tissue vs non-target-tissue chromatin. The greatest degree of Rp binding occurred in the NAP fraction, and the higher level of binding seen in NAP-chromatin as compared with that in crude chromatin may be attributed to extraction of "masking proteins" which inhibit Rp-chromosomal protein interactions. When guanidine hydrochloride at greater than 4 M was used to extract crude chromatin, Rp binding decreased, indicating that the Rp acceptor sites were removed or denatured. These findings demonstrate the existence of Rp acceptor sites in the mammalian uterus which are similar to avian oviduct acceptor sites, suggesting that such sites may play a role in mediating Rp-induced gene expression.     

Innovations in osteomyelitis research: A review of animal models

Infection of bone tissue, or osteomyelitis, has become a growing concern in modern healthcare due in no small part to a rise in antibiotic resistance among bacteria, notably Staphylococcus aureus. The current standard of care involves aggressive, prolonged antibiotic therapy combined with surgical debridement of infected tissues. While this treatment may be sufficient for resolving a portion of cases, recurrences of the infection and associated risks including toxicity with long‐term antibiotic usage have been reported. Therefore, there exists a need to produce safer, more efficacious options of treatment for osteomyelitis. In order to test treatment regimens, animal models that closely mimic the clinical condition and allow for accurate evaluation of therapeutics are necessary. Establishing a model that replicates features of osteomyelitis in humans continues to be a challenge to scientists, as there are many variables involved, including choosing an appropriate species and method to establish infection. This review addresses the refinement of animal models of osteomyelitis to reflect the clinical disease and test prospective therapeutics. The aim of this review is to explore studies regarding the use of animals for osteomyelitis therapeutics research and encourage further development of such animal models for the translation of results from the animal experiment to human medicine.     

Hormone therapy and antioxidant vitamins do not improve endothelial vasodilator function in postmenopausal women with established coronary artery disease: a substudy of the Women's Angiographic Vitamin and Estrogen (WAVE) trial

We measured flow-mediated dilation (FMD) by high-resolution brachial ultrasound in 61 women who participated in the Women's Angiographic Vitamin and Estrogen (WAVE) trial, a randomized controlled trial. There were no significant differences in the baseline demographics of women receiving hormone therapy (0.625 mg/day of conjugated equine estrogen plus 2.5mg of medroxyprogesterone acetate for women who had not had a hysterectomy) or placebo; or vitamins (400 IU of Vitamin E and 500 mg of Vitamin C twice daily) or placebo. Baseline FMD was impaired in all subjects (3.3+/-7.6%). Neither hormone therapy (4.1+/-5.2% at baseline, 4.2+/-5.0% at 3 months, and 4.1+/-6.5% at 34 months) nor antioxidant vitamins (3.0+/-8.3% at baseline; 3.5+/-4.6% at 3 months; 3.1+/-7.6% at 34 months) improved FMD (all p-values=NS). Endothelium-independent vasodilation, induced by nitroglycerin (NTG) was similar at baseline and was not affected by either therapy. In univariate and multivariate analysis, neither hormone therapy nor antioxidant vitamins were associated with FMD. Women with established coronary artery disease have impaired flow-mediated vasodilation of the brachial artery that does not improve after 3 months or up to 34 months of treatment with postmenopausal hormone therapy or antioxidant vitamins.     

Multipotent adult progenitor cell‐loaded demineralized bone matrix for bone tissue engineering

Multipotent adult progenitor cells (MAPCs) from bone marrow have been shown to be capable of forming bone, cartilage and other connective tissues. In addition, MAPCs differentiate into lineages that are different from their germ layers of origin. Previous studies showed the ability of MAPCs to improve cardiac function and control allogenic‐reactive responses associated with acute graft versus host disease. In the current study, we evaluated the ability of MAPCs to produce bone matrix on demineralized bone allograft substrates. Specifically, MAPCs expressed alkaline phosphatase, produced extracellular matrix proteins and deposited calcium‐containing mineral on demineralized bone matrices. Furthermore, the addition of MAPCs on demineralized bone matrix (DBM) scaffolds enhanced osteoinductivity of the carrier in a rat ectopic pouch model. These results demonstrated the potential of MAPCs as a new approach for bone repair in tissue‐engineering applications. Copyright © 2013 John Wiley & Sons, Ltd.     

Cytotoxicity-Related Gene Expression and Chromatin Accessibility Define a Subset of CD4+ T Cells That Mark Progression to Type 1 Diabetes

Type 1 diabetes in children is heralded by a preclinical phase defined by circulating autoantibodies to pancreatic islet antigens. How islet autoimmunity is initiated and then progresses to clinical diabetes remains poorly understood. Only one study has reported gene expression in specific immune cells of children at risk associated with progression to islet autoimmunity. We analyzed gene expression with RNA sequencing in CD4⁺ and CD8⁺ T cells, natural killer (NK) cells, and B cells, and chromatin accessibility by assay for transposase-accessible chromatin sequencing (ATAC-seq) in CD4⁺ T cells, in five genetically at risk children with islet autoantibodies who progressed to diabetes over a median of 3 years (“progressors”) compared with five children matched for sex, age, and HLA-DR who had not progressed (“nonprogressors”). In progressors, differentially expressed genes (DEGs) were largely confined to CD4⁺ T cells and enriched for cytotoxicity-related genes/pathways. Several top-ranked DEGs were validated in a semi-independent cohort of 13 progressors and 11 nonprogressors. Flow cytometry confirmed that progression was associated with expansion of CD4⁺ cells with a cytotoxic phenotype. By ATAC-seq, progression was associated with reconfiguration of regulatory chromatin regions in CD4⁺ cells, some linked to differentially expressed cytotoxicity-related genes. Our findings suggest that cytotoxic CD4⁺ T cells play a role in promoting progression to type 1 diabetes.