Social reactions to rape victims: healing and hurtful effects on psychological and physical health outcomes.

In this study, 102 rape survivors were interviewed about the social reactions they received from family and friends post-rape. Results supported Ullman's (1996b) conclusion that the overall contribution of positive social reaction (e.g., providing support, listening, believing) on victims' recovery is negligible, but that negative social reactions (e.g., blaming) hinder recovery. In contrast to Ullman's (1996b) work, this research also examined whether rape victims have similar perceptions as to what constitutes a "positive" and "negative" social reaction. Results indicated that victims often agree as to what reactions are healing (positive), but that they do not agree as to what is hurtful (negative). By taking victims' perceptions into account, this study was able to compare the relative contributions of social reactions that were considered healing, social reactions that were considered hurtful, and the absence of social reactions. Results indicated that survivors who had someone believe their account of what happened or were allowed to talk about the assault--and considered these reactions to be healing-had fewer emotional and physical health problems than victims who considered these reactions hurtful, or victims who did not experience these reactions at all. Implications for future research on social reactions are discussed.

Community services for rape survivors: enhancing psychological well-being or increasing trauma?

This research examined how contact with the legal, medical, and mental health systems affects rape survivors' psychological well-being. Although community services may be beneficial for some victims, there is increasing evidence that they can add trauma, rather than alleviate distress (termed secondary victimization). This study examined how secondary victimization affects rape survivors' posttraumatic stress (PTS) symptoms. Adaptive and snowball sampling were used to recruit a sample of 102 rape survivors. Victims of nonstranger rape who received minimal assistance from either the legal or medical system, and encountered victim-blaming behaviors from system personnel, had significantly elevated levels of PTS. This high-risk group of rape survivors had PTS levels significantly higher than all other victims in this study, including those who did not seek community assistance postrape. However, for these high-risk rape survivors, receiving sustained mental health services after these negative experiences was associated with a significant decrease in PTS.

Loss of responsiveness to transforming growth factor beta induces malignant transformation of nontumorigenic rat prostate epithelial cells.

Transforming growth factor (TGF)-betas are multifunctional growth factors, the properties of which include the potent inhibition of epithelial cell growth. Expression patterns of TGF-betas and TGF-beta receptors in the normal prostate indicate that these growth regulators play key roles in prostatic development and proliferative homeostasis. Importantly, TGF-beta receptor levels are frequently diminished in malignant human prostate tissue. To test the hypothesis that loss of TGF-beta responsiveness is causally involved in the tumorigenic process, we have used retroviral transduction to introduce a dominant-negative mutant type II TGF-beta receptor (DNR) into the premalignant rat prostatic epithelial cell line, NRP-152. High-level expression of the DNR abolished the ability of TGF-beta to inhibit cell growth, to promote cell differentiation, and to induce apoptosis, and it partially blocked the induction of extracellular matrix gene expression. When injected into nude mice, NRP-152-DNR cells formed carcinomas at 13 of 34 sites, compared with 0 of 30 sites for parental and control cells (P = 0.0001). We conclude that the type II TGF-beta receptor is an important tumor suppressor in the prostate, and furthermore, that loss of TGF-beta responsiveness can contribute early in the tumorigenic process by causing the malignant transformation of preneoplastic cells.