Repeated and Systematic Intimate Partner Violence in Rural Areas in Sweden

Violence against women lacks geographical boundaries, although research demonstrates higher rates of such violence in rural areas compared to urban areas. The repeated and systematic intimate partner violence (IPV) is especially problematic in isolated areas. This study aims to investigate how repeated and systematic IPV, was handled by the criminal justice system in rural areas in Sweden and how risk and victim vulnerability factors were related to recidivism in this longitudinal prospective study. The sample consisted of alleged perpetrators of repeated and systematic IPV who had been either reported, charged, or convicted of repeated and systematic IPV defined according to the Swedish Law Gross Violation of a Woman’s Integrity targeting such violence, in two rural Swedish police districts during 2011–2014 (N = 258). Results demonstrated that 30% of IPV perpetrators were charged with the Gross violation offense and 5% were charged for other IPV-related offenses. The conviction for the Gross violation offense was 11% and 24% for other IPV-related offenses. 56% were not charged or convicted of any IPV-related offenses. Perpetrators convicted of the Gross Violation offense were more likely to receive longer prison sentences than perpetrators convicted of other IPV-related offenses. Victim cooperation in the police investigation increased the likelihood for prosecution with 7.3 times and for a conviction with 6.1 times. In terms of recidivism 24% engaged in IPV towards the same victim and another 27% recidivated into general criminality. Recidivists had higher summary risk ratings and more individual risk factors than non-recidivists, such as general criminality, employment problems and mental health problems, and victim vulnerability factors including personal problems. To reduce re-victimization, risk and vulnerability factors and supporting victims to cooperate in the police investigation should be considered when forming risk management strategies to protect victims of repeated and systematic IPV in such rural areas

A Whole-Genome SNP Association Study of NCI60 Cell Line Panel Indicates a Role of Ca2+ Signaling in Selenium Resistance

Epidemiological studies have suggested an association between selenium intake and protection from a variety of cancer. Considering this clinical importance of selenium, we aimed to identify the genes associated with resistance to selenium treatment. We have applied a previous methodology developed by our group, which is based on the genetic and pharmacological data publicly available for the NCI60 cancer cell line panel. In short, we have categorized the NCI60 cell lines as selenium resistant and sensitive based on their growth inhibition (GI50) data. Then, we have utilized the Affymetrix 125K SNP chip data available and carried out a genome-wide case-control association study for the selenium sensitive and resistant NCI60 cell lines. Our results showed statistically significant association of four SNPs in 5q33–34, 10q11.2, 10q22.3 and 14q13.1 with selenium resistance. These SNPs were located in introns of the genes encoding for a kinase-scaffolding protein (AKAP6), a membrane protein (SGCD), a channel protein (KCNMA1), and a protein kinase (PRKG1). The knock-down of KCNMA1 by siRNA showed increased sensitivity to selenium in both LNCaP and PC3 cell lines. Furthermore, SNP-SNP interaction (epistasis) analysis indicated the interactions of the SNPs in AKAP6 with SGCD as well as SNPs in AKAP6 with KCNMA1 with each other, assuming additive genetic model. These genes were also all involved in the Ca2+ signaling, which has a direct role in induction of apoptosis and induction of apoptosis in tumor cells is consistent with the chemopreventive action of selenium. Once our findings are further validated, this knowledge can be translated into clinics where individuals who can benefit from the chemopreventive characteristics of the selenium supplementation will be easily identified using a simple DNA analysis

Sodium Selenide Toxicity Is Mediated by O2-Dependent DNA Breaks

Hydrogen selenide is a recurrent metabolite of selenium compounds. However, few experiments studied the direct link between this toxic agent and cell death. To address this question, we first screened a systematic collection of Saccharomyces cerevisiae haploid knockout strains for sensitivity to sodium selenide, a donor for hydrogen selenide (H2Se/HSe−/Se2−). Among the genes whose deletion caused hypresensitivity, homologous recombination and DNA damage checkpoint genes were over-represented, suggesting that DNA double-strand breaks are a dominant cause of hydrogen selenide toxicity. Consistent with this hypothesis, treatment of S. cerevisiae cells with sodium selenide triggered G2/M checkpoint activation and induced in vivo chromosome fragmentation. In vitro, sodium selenide directly induced DNA phosphodiester-bond breaks via an O2-dependent reaction. The reaction was inhibited by mannitol, a hydroxyl radical quencher, but not by superoxide dismutase or catalase, strongly suggesting the involvement of hydroxyl radicals and ruling out participations of superoxide anions or hydrogen peroxide. The •OH signature could indeed be detected by electron spin resonance upon exposure of a solution of sodium selenide to O2. Finally we showed that, in vivo, toxicity strictly depended on the presence of O2. Therefore, by combining genome-wide and biochemical approaches, we demonstrated that, in yeast cells, hydrogen selenide induces toxic DNA breaks through an O2-dependent radical-based mechanism

The potential role of thioredoxin 1 and CD30 systems as multiple pathway targets and biomarkers in tumor therapy

Our progress in understanding pathological disease mechanisms has led to the identification of biomarkers that have had a considerable impact on clinical practice. It is hoped that the move from generalized to stratified approaches, with the grouping of patients into clinical/therapeutic subgroups according to specific biomarkers, will lead to increasingly more effective clinical treatments in the near future. This success depends on the identification of biomarkers that reflect disease evolution and can be used to predict disease state and therapy response, or represent themselves a target for treatment. Biomarkers can be identified by studying relationships between serum, tissue, or tumor microenvironment parameters and clinical or therapeutic parameters at onset and during the progression of the disease, using systems biology. Given that multiple pathways, such as those responsible for redox and immune regulation, are deregulated or altered in tumors, the future of tumor therapy could lie in the simultaneous targeting of these pathways using extracellular and intracellular targets and biomarkers. With this aim in mind, we evaluated the role of thioredoxin 1, a key redox regulator, and CD30, a cell membrane receptor, in immune regulation. Our results lead us to suggest that the combined use of these biomarkers provides more detailed information concerning the multiple pathways affected in disease and hence the possibility of more effective treatment

Assessing risk for inpatient physical violence in a female forensic psychiatric sample - comparing HCR-20v2 with the female additional manual to the HCR-20v2

Purpose and aim: Out from the sparse literature on risk assessment for violence committed by women the Female Additional Manual (FAM) was developed to be a complement to the HCR-20v2. The aim of this study was to investigate and compare the psychometrics of the HCR-20v2 with and without the FAM on risk for inpatient physical violence for female forensic psychiatric patients.Methods: The participants were 100 female patients admitted to forensic psychiatric care in a high-security clinic, assessed by clinicians with the HCR-20v2 during their admission. Researchers performed the FAM, both retrospectively and prospectively. The follow-up period was 12months before being discharged.Results: Four main results were found; first, many risk factors were present although the summary risk ratings were mainly low to moderate. Secondly, the reliability was in general good, where the HCR-20v2 mainly showed higher reliability without than with the FAM, indicating that FAM risk factors did equal or did not contribute to a higher reliability. Third, the internal validity was higher for the HCR-20v2 than for the FAM. Risk factors correlated stronger with the summary risk ratings for the HCR-20v2 than for the FAM. Fourth, the validity for inpatient physical violence was high for the total score of both the HCR-20v2 and the FAM, but contradictory to previous finding the validity for summary risk ratings was not significant.Conclusions: The results support the use of HCR-20v2 when assessing risk for inpatient violence for female forensic psychiatric patients, but with only some support for adding or changing risk factors according to the FAM.</p