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This article reviews recent scholarship around the issue of nonfatal strangulation in cases of domestic violence. In the mid-1990s, the San Diego City Attorney's Office began a systematic study of attempted strangulation among 300 domestic violence cases, becoming one of the first systematic research studies to specifically examine the prevalence of attempted strangulation as a form of injury associated with ongoing domestic violence. Prior to this time, most of the research into strangulation was conducted postmortem, and little was known about the injuries and signs of attempted strangulation among surviving victims. This article reviews the research that has since been conducted around strangulation in domestic violence cases, highlighting topics that are more or less developed in the areas of criminology, forensic science, law, and medicine, and makes recommendations for future research and practice.

Efforts to partner researchers and practitioners have the potential to significantly improve both research and response to non-fatal strangulation within the context of domestic violence. Non-fatal strangulation is far more common than most formal data suggest and is a highly gendered form of domestic assault often used to control or intimidate a partner; however, depending on how the assault takes place, it can leave little obvious physical evidence to an untrained investigator. The present study estimates the occurrence of strangulation cases and possible strangulation cases that may not be explicitly classified as such in official police reports due to inadequacies in law enforcement training. We offer a description of these types of cases as they compare with domestic violence police reports from non-strangulation cases. Results highlight the gendered nature of strangulation as well as the importance of practitioners and researchers critically reflecting on issues within the criminal justice system in an effort to redress inadequacies, hold offenders accountable, and save lives.

Using a sample of 1,010 women from a southeastern state university, we explore whether associations between fear of sexual assault and other crime-specific fears vary based on presumed victim-offender relationship. More specifically, we assess the extent to which fear of stranger-and acquaintance-perpetrated sexual assaults differ in the extent to which they are correlated with fear of other crime victimizations. Multivariate logistic regression analysis revealed that both fear of stranger-perpetrated sexual assault and fear of acquaintance-perpetrated sexual assault were positively associated with nearly all other crimespecific fears under examination. However, associations were particularly strong between fear of sexual assault by a stranger and fear of other stranger-perpetrated crimes. Findings have significant implications for how academic institutions should comprehensively address direct and indirect negative influences of violence against college women.

Background and Purpose The sphingosine 1‐phosphate receptor subtype 1 (S1P1R) is modulated by phosphorylated FTY720 (pFTY720), which causes S1P1R internalization preventing lymphocyte migration thus limiting autoimmune response. Studies indicate that internalized S1P1Rs continue to signal, maintaining an inhibition of cAMP, thus raising question whether the effects of pFTY720 are due to transient initial agonism, functional antagonism and/or continued signalling. To further investigate this, the current study first determined if continued S1P1R activation is pathway specific. Experimental Approach Using human and rat astrocyte cultures, the effects of S1P1R activation on cAMP, pERK and Ca2+ signalling was investigated. In addition, to examine the role of S1P1R redistribution on these events, a novel biologic (MNP301) that prevented pFTY720‐mediated S1P1R redistribution was engineered. Key Results The data showed that pFTY720 induced long‐lasting S1P1R redistribution and continued cAMP signalling in rat astrocytes. In contrast, pFTY720 induced a transient increase of Ca2+ in astrocytes and subsequent antagonism of Ca2+ signalling. Notably, while leaving pFTY720‐induced cAMP signalling intact, the novel MNP301 peptide attenuated S1P1R‐mediated Ca2+ and pERK signalling in cultured rat astrocytes. Conclusions and Implications These findings suggested that pFTY720 causes continued cAMP signalling that is not dependent on S1P1R redistribution and induces functional antagonism of Ca2+ signalling after transient stimulation. To our knowledge, this is the first report demonstrating that pFTY720 causes continued signalling in one pathway (cAMP) versus functional antagonism of another pathway (Ca2+) and which also suggests that redistributed S1P1Rs may have differing signalling properties from those expressed at the surface.