Self-definition and self-defense: Jewish racial identity in nineteenth-century France

This article examines how and why French Jews began to speak of themselves as a race. Though we often assume that Jewish racial identity was an invention of anti-Semites in the 1880s, Jewish publicists had in fact adopted this language as early as the 1820s. Far from unwittingly appropriating the language of their detractors, Jews borrowed the language of race from scholars neutral or sympathetic to their cause in ways that made sense in light of their larger strategies of self-defense. The scholars who pioneered modern race theory were not the late nineteenth-century Social Darwinists; they were romantic historians like the Thierrys and Michelet, who saw France as a nation composed of a plurality of peoples who had come together over time to form a unified nation. Race thus provided a framework for understanding difference as legitimate, useful and dignified at a moment when anti-Jewish publicists attacked Jews as anti-social and immoral people who brought only harm to France. Looking at what French Jews borrowed from these early historians allows us to see the interconnections between Jewish self-defense and Jewish self-definition. In seeking to guarantee their rights and social status, French Jews appropriated new terms of understanding who they were.     

About the Contributors

Biography

About the Contributors     

Alcohol,Fear, and Woman Abuse

Although there is ample evidence that alcoholusage is associated with greater frequency, incidenceand severity of spouse battering, there is alsoconsiderable evidence which does not support a direct linkage. This research investigates aheretofore neglected area, the role of substance use ininducing fear in victims. As part of a larger study ofthe police response to battering, 419 female victims of male offenders participated in intensiveinterviews; the sample consisted of 69.9% Black and28.9% White women. All the women had been victims of atleast one occurrence of misdemeanor-level abuse, and many were in chronically abusive relationships.The women participating in this study were moderatelyeducated and relatively young, with a mean age of 30years old. Relationship status was bimodal with roughly equal numbers of married and cohabitingcouples; there were relatively few who were divorced orseparated from their assailants, or were ex-cohabitants.The male partners of women represented in this sample were extremely heavy drinkerscompared to a national sample. The quantity andfrequency of alcohol use was less predictive ofthreatening or physically battering behavior than wasmale drunkenness. Frequent drunkenness was highly correlated withboth threats and with battering. Similarly, victims'fear of their partners was much more strongly associatedwith how frequently they were drunk than with drinking itself.     

Blockade of NR2B-Containing NMDA Receptors Prevents BDNF Enhancement of Glutamatergic Transmission in Hippocampal Neurons

Application of brain-derived neurotrophic factor (BDNF) to hippocampal neurons has profound effects on glutamatergic synaptic transmission. Both pre- and postsynaptic actions have been identified that depend on the age and type of preparation. To understand the nature of this diversity, we have begun to examine the mechanisms of BDNF action in cultured dissociated embryonic hippocampal neurons. Whole-cell patch-clamp recording during iontophoretic application of glutamate revealed that BDNF doubled the amplitude of induced inward current. Coexposure to BDNF and the NMDA receptor antagonist AP-5 markedly reduced, but did not entirely prevent, the increase in current. Coexposure to BDNF and ifenprodil, an NR2B subunit antagonist, reproduced the response observed with AP-5, suggesting BDNF primarily enhanced activity of NR2B-containing NMDA receptors with a lesser effect on non-NMDA receptors. Protein kinase involvement was confirmed with the broad spectrum inhibitor staurosporine, which prevented the response to BDNF. PKCI19-31 and H-89, selective antagonists of PKC and PKA, had no effect on the response to BDNF, whereas autocamtide-2-related inhibitory peptide, an antagonist of CaM kinase II, reduced response magnitude by 60%. These results demonstrate the predominant role of a specific NMDA receptor subtype in BDNF modulation of hippocampal synaptic transmission.