Violence Against Women: Classic Papers
Description This anthology highlights the original, classic works and critical writings in the field of violence against women. Each reading is an excerpt from a classic book or article that made a significant contribution to the field of violence against women. The anthology also highlights importance of each piece of literature to this field of study and is organized to cover three areas: sexual violence against women, physical violence against women, and interventions with perpetrators of violence against women. (Description from Amazon.com)
Social Anxiety as a Predictor of Dating Aggression
By far, most research on the behavior of socially anxious individuals has focused on the “flight” rather than the “fight” response described in the traditional conceptualization of anxiety. More recently, however, there has been some speculation and emerging evidence suggesting that social anxiety and aggression may be related. The present study examined social anxiety as a predictor of dating aggression within a late adolescent sample. Two forms of dating aggression were assessed: physical aggression, such as slapping, use of a weapon, or forced sexual activity, and psychological aggression, such as slamming doors, insulting, or refusing to talk to one’s partner. One aspect of social anxiety, Fear of Negative Evaluation (FNE), emerged as a significant predictor of male dating aggression, even after controlling for relationship quality. Notably, FNE was most predictive of increased aggression of both types when men also perceived their romantic relationship to be more antagonistic. Despite its demonstrated importance as a contextual variable, however, relationship quality did not mediate the association between FNE and psychological or physical aggression. Implications for prevailing conceptualizations of social anxiety and dating aggression are discussed.
Hyperaccumulation of FAD-linked presenilin 1 variants in vivo
Mutations in the presenilin 1 (PS1) and presenilin 2 (PS2) genes can cause Alzheimer's disease in affected members of the majority of early-onset familial Alzheimer's disease (FAD) pedigrees1–7. PS1 encodes an ubiquitously expressed, eight transmembrane protein1,8–11. PS1 is endoproteolytically processed to an amino-terminal derivative (∼27–28 kDa) and a carboxy-terminal derivative (∼17–18 kDa). These polypeptides accumulate to saturable levels in the brains of transgenic mice, independent of the expression of PS1 holoprotein12. We now document that, in the brains of transgenic mice, the absolute amounts of accumulated N- and C-terminal derivatives generated from the FAD-linked PS1 variants in which Glu replaces Ala at codon 246 (A246E) or Leu replaces Met at codon 146 (M146L) accumulate to a significantly higher degree (∼40–50%) than the fragments derived from wild-type PS1. Moreover, the FAD-linked ΔE9 PS1 variant, a polypeptide that is not subject to endoproteolytic cleavage in vivo, also accumulates in greater amounts than the fragments generated from wild-type human PS1. Thus, the metabolism of PS1 variants linked to FAD is fundamentally different from that of wild-type PS1 in vivo.