Prevalence of Sexual Strangulation/Choking Among Australian 18-35 Year-Olds.

In Australia, strangulation has been explicitly criminalized in all states and territories. However, it continues to be a "normalized" sexual practice despite its potentially fatal consequences and associated short and long-term sequelae. This research aimed to establish the prevalence of strangulation during sex and examine predictors of positive perceptions toward sexual strangulation in Australia. Confidential, cross-sectional online surveys were conducted with 4702 Australians aged 18-35 years. Participants were 47% cis-men, 48% cis-women, and 4% trans or gender diverse. A total of 57% reported ever being sexually strangled (61% women, 43% men, 79% trans or gender diverse) and 51% reported ever strangling a partner (40% women, 59% men, 74% trans or gender diverse). Differences were found across genders on all variables of sexual strangulation, including frequency of engagement, level of pressure on the neck, consequences, wanting and enjoyment, and how consent was given/received. However, when split by gender, sexual orientation of men and women revealed further differences in behaviors, consequences, and wanting, particularly among straight and bisexual women. After accounting for exposure to strangulation in pornography and previous experience of sexual strangulation, positive perceptions of being strangled (R2 = .51) and strangling a partner (R2 = .53) were predicted by ratings that it could be done safely and social normative factors. These findings suggest strangulation is common during sex among young Australians. Non-stigmatizing education strategies are needed to engage with young people so they have a better understanding of the risks involved and how to negotiate consent and safety regarding sexual strangulation.

Medical evidence assisting non-fatal strangulation prosecution: a scoping review.

OBJECTIVES: Non-fatal strangulation (NFS) is a serious form of gendered violence that is fast becoming an offence in many jurisdictions worldwide. However, it often leaves little or no externally visible injuries making prosecution challenging. This review aimed to provide an overview of how health professionals can support the prosecution of criminal charges of NFS as part of regular practice, particularly when externally visible injuries are absent. METHOD: Eleven databases were searched with terms related to NFS and medical evidence in health sciences and legal databases. Eligible articles were English language and peer reviewed, published before 30 June 2021; sample over 18 years that had primarily survived a strangulation attempt and included medical investigations of NFS injuries, clinical documentation of NFS or medical evidence related to NFS prosecution. RESULTS: Searches found 25 articles that were included for review. Alternate light sources appeared to be the most effective tool for finding evidence of intradermal injury among NFS survivors that were not otherwise visible. However, there was only one article that examined the utility of this tool. Other common diagnostic imaging was less effective at detection, but were sought after by prosecutors, particularly MRIs of the head and neck. Recording injuries and other aspects of the assault using standardised tools specific for NFS were suggested for documenting evidence. Other documentation included writing verbatim quotes of the experience of the assault and taking good quality photographs that could assist with corroborating a survivor's story and proving intent, if relevant for the jurisdiction. CONCLUSION: Clinical responses to NFS should include investigation and standardised documentation of internal and external injuries, subjective complaints and the experience of the assault. These records can assist in providing corroborating evidence of the assault, reducing the need for survivor testimony in court proceedings and increasing the likelihood of a guilty plea.

Sentencing, Domestic Violence, and the Overrepresentation of Indigenous Australians: Does Court Location Matter?

The significant overrepresentation of Indigenous people in Australian prisons has been the subject of numerous studies. In this article, we build on recent research suggesting that sentencing in domestic violence cases might be an important contributor to this overrepresentation of Indigenous people. We broaden the existing research by examining differences for Indigenous and non-Indigenous defendants in domestic violence cases across a range of sentencing outcomes including imprisonment, probation, fines, and good behavior orders. We also consider whether the degree of geographic remoteness of the court influences these sentencing outcomes. To accomplish this, we use administrative court data from Queensland, Australia, and employ a multinomial hierarchical modeling strategy appropriate for nested court-level multilevel data. The findings further support recent Australian research suggesting that there are sentencing disparities for Indigenous and non-Indigenous people in relation to domestic violence, and in particular, that harsher sentences such as imprisonment are disproportionately reserved for Indigenous defendants. Our research demonstrates that these disparities in the likelihood of imprisonment occur irrespective of defendants' domestic violence protection order (DVO) breach histories and the location of the sentencing court. Based on the findings, we conclude with a discussion of possible ways forward. Although there is no question that Indigenous women should be safe and free from violence, supporting a harsher sentencing regime for those who breach DVOs is not effective. Instead, we argue that flexible strategies that work within and for Indigenous communities in Australia are required.

Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells.

To characterize the function of the sodium/inositol symporter SMIT2 in skeletal muscle, human SMIT2 cDNA was transfected into L6 myoblasts using pcDNA3.1 expression vector. Compared with the pcDNA3.1 vector only transfection, this overexpression increased the uptake of [(3)H]D-chiro-inositol (DCI) by 159-fold. [(3)H]myo-Inositol uptake increased by 37-fold. In contrast, [(14)C]D-glucose, [(14)C]2-deoxy-D-glucose, or [(14)C]3-O-methyl-D-glucose uptake remained unchanged in the presence of either 0, 5.5, or 25 mM unlabeled glucose. The K(m) of DCI and myo-inositol for DCI uptake was 111.0 and 158.0 microM, respectively, whereas glucose competed for DCI uptake with a K(i) of 6.1 mM. Insulin treatment of non-transfected L6 cells (2 microM for 24 h) increased [(3)H]DCI specific uptake 18-fold. DCI transport is up regulated by insulin and competitively inhibited by millimolar levels of glucose. Therefore, expression and/or function of SMIT2, a high affinity transporter specific for DCI and myo-inositol, may be reduced in diabetes mellitus, insulin resistance and polycystic ovary syndrome causing the abnormal DCI metabolism observed in these conditions.

Finding and Keeping a Job: The Value and Meaning of Employment for Parolees.

Finding stable employment has been identified as one of the best predictors of post-release success among prisoners. However, offenders face a number of challenges in securing employment when released from prison. This article examines processes that shape the abilities and motivations of parolees to secure gainful employment by examining interview data collected from parolees in Queensland, Australia (n = 50). We explore the role of social networks and commercial employment providers in helping parolees find work, the perceived value of institutional work and training, and the meanings, challenges, and impact of managing the disclosure of one's criminal past to employers. Findings highlight that the role and influence of employment on a parolee's reintegration is conditional on his or her supportive social networks, ability to manage stigma, and personal changes in identity, which elevate the importance of work in a parolee's life. Our findings also show how employment provides opportunities for offenders to self-construct and articulate new identities.

Amino terminal 38.9% of apolipoprotein B-100 is sufficient to support cholesterol-rich lipoprotein production and atherosclerosis.

OBJECTIVE: Carboxyl terminal truncation of apolipoprotein (apo)B-100 and apoB-48 impairs their capacity for triglyceride transport, but the ability of the resultant truncated apoB to transport cholesterol and to support atherosclerosis has not been adequately studied. The atherogenicity of apoB-38.9 was determined in this study by using our apoB-38.9-only (Apob38.9/38.9) mice. METHODS AND RESULTS: ApoB-38.9-lipoproteins (Lp-B38.9) circulate at very low levels in Apob38.9/38.9 mice as small LDLs or HDLs. Disruption of apoE gene in these mice caused accumulation of large amounts of betaVLDL-like LpB-38.9 in plasma. These betaVLDL particles were more enriched with cholesteryl esters but poor in triglycerides compared with the apoB-48-betaVLDL of the apoB-wild-type/apoE-null (Apob+/+/Apoe-/-) mice. Likewise, apoB-38.9-VLDL secreted by cultured Apob38.9/38.9 mouse hepatocytes also had higher ratios of total cholesterol to triglycerides than apoB-48-VLDL secreted by the apoB-48-only hepatocytes. Thus, despite its impaired triglyceride-transporting capacity, apoB-38.9 has a relatively intact capacity for cholesterol transport. Spontaneous aortic atherosclerotic lesions were examined in apoB-38.9-only/apoE-null (Apob38.9/38.9/Apoe-/-) mice at ages 9 and 13 months. Extensive lesions were found in the Apob38.9/38.9/Apoe-/- mice as well as in their Apob+/38.9/Apoe-/- and Apob+/+/Apoe-/- littermates. CONCLUSIONS: Deleting the C-terminal 20% from apoB-48 does not impair its ability to transport cholesterol and to support atherosclerosis, thus narrowing the "atherogenic region" of apoB.

Hypobetalipoproteinemic mice with a targeted apolipoprotein (Apo) B-27.6-specifying mutation: in vivo evidence for an important role of amino acids 1254-1744 of ApoB in lipid transport and metabolism of the apoB-containing lipoprotein.

Carboxyl-terminal deletion of apoB-100 may impair its triglyceride (TG)-transporting capability and alter its catabolism. Here, we compare our newly generated apoB gene (Apob)-targeted apoB-27.6-bearing mice to our previously reported apoB-38.9 mice to understand further the relationship between the size of a truncated apoB variant and its function/metabolism in vivo. The apoB-27.6-specifying mutation produces a premature stop codon six amino acids (aa) downstream of the last codon of mouse Apob exon 24 (corresponding to aa 1254 of human apoB-100). ApoB-27.6 transcripts were 3- and 5-fold more abundant than apoB wild type and apoB-38.9 transcripts in the liver. Likewise, hepatic secretion rates of apoB-27.6 were 7-fold higher than those of apoB-48 and apoB-38.9. In contrast, apoB-27.6 heterozygotes (Apob(27.6/+)) had lower hepatic TG secretion rates and higher liver TG contents than both apoB-38.9 heterozygotes (Apob(38.9/+)) and apoB wild type mice (Apob(+/+)). ApoB-27.6 was secreted by Apob(27.6/+) hepatocytes as dense high density lipoprotein particles. Moreover, despite its high secretion rates, apoB-27.6 was barely detectable in plasma. Disruption of apoE gene in Apob(38.9/+) and Apob(27.6/+) dramatically increased plasma levels of apoB-38.9 as well as apoB-48 but caused no change in plasma apoB-27.6 concentrations. Finally, the birth rate of apoB-27.6 homozygotes (Apob(27.6/27.6)) from intercrosses of Apob(27.6/+) was 7-fold lower than that of Apob(38.9/38.9) from Apob(38.9/+) intercrosses (1.8% versus 12%). Crossbreeding of Apob(27.6/27.6) and Apob(38.9/38.9) produced viable Apob(27.6/38.9) offspring, but Apob(27.6/27.6) intercrosses produced no offspring. Together, these results demonstrate in vivo that the apoB-27.6-apoB-38.9 peptide segment (aa 1254-1744) plays a critical role, not only in supporting hepatic TG-secretion and in modulating catabolism of apoB-containing lipoproteins, but also in normal mouse embryonic development.

Hepatic secretion of apoB-100 is impaired in hypobetalipoproteinemic mice with an apoB-38.9-specifying allele.

Apolipoprotein B (apoB) truncation-specifying mutations cause familial hypobetalipoproteinemia (FHBL). Lipoprotein kinetics studies have shown that production rates of apoB-100 are reduced by 70-80% in heterozygous FHBL humans, instead of the expected 50%. To develop suitable mouse models to study the underlying mechanism, apoB-38.9-only (Apob(38.9/38.9)) mice were crossbred with Apobec-1 knockout (Apobec-1(-/-)) mice or apoB-100-only (Apob(100/100)) mice to produce two lines of apoB-38.9 heterozygous mice that produce only apoB-38.9 and apoB-100, namely Apobec-1(-/-)/Apob(38.9/+) and Apob(38.9/100) mice. In vivo rates of apoB-100 secretion were measured using [35S]Met/Cys to label proteins and Triton WR-1339 to block apoB-100 VLDL lipolysis/uptake. Rates of secretion were reduced by 80%, rather than the expected 50%, in both Apobec-1(-/-)/Apob(38.9/+) and Apob(38.9/100) mice compared with those of the respective Apobec-1(-/-)/Apob(+/+) and Apob(100/100) control mice. Continuous labeling and pulse-chase experiments in primary hepatocyte cultures revealed that rates of apoB-100 synthesis by Apobec-1(-/-)/Apob(38.9/+) and Apob(38.9/100) hepatocytes were reduced to the expected 50% of those of the respective controls, but the efficiency of secretion of apoB-100 was significantly lower in apoB-38.9 heterozygous hepatocytes. The greater-than-expected decreases in apoB-100 production rates of FHBL heterozygous humans appear to be attributable to a defect in secretion rather than in the synthesis of apoB-100 from the unaffected apoB allele.