Short-term and medium-term health effects of 9/11.

The New York City terrorist attacks on Sept 11, 2001 (9/11), killed nearly 2800 people and thousands more had subsequent health problems. In this Review of health effects in the short and medium terms, strong evidence is provided for associations between experiencing or witnessing events related to 9/11 and post-traumatic stress disorder and respiratory illness, with a correlation between prolonged, intense exposure and increased overall illness and disability. Rescue and recovery workers, especially those who arrived early at the World Trade Center site or worked for longer periods, were more likely to develop respiratory illness than were other exposed groups. Risk factors for post-traumatic stress disorder included proximity to the site on 9/11, living or working in lower Manhattan, rescue or recovery work at the World Trade Center site, event-related loss of spouse, and low social support. Investigators note associations between 9/11 exposures and additional disorders, such as depression and substance use; however, for some health problems association with exposures related to 9/11 is unclear.

Co-occurring lower respiratory symptoms and posttraumatic stress disorder 5 to 6 years after the World Trade Center terrorist attack.

OBJECTIVES: We have described the epidemiology of co-occurring lower respiratory symptoms (LRS) and probable posttraumatic stress disorder (PTSD) 5 to 6 years after exposure to the 9/11 disaster. METHODS: We analyzed residents, office workers, and passersby (n = 16,363) in the World Trade Center Health Registry. Using multivariable logistic regression, we examined patterns of reported respiratory symptoms, treatment sought for symptoms, diagnosed respiratory conditions, mental health comorbidities, quality of life, and unmet health care needs in relation to comorbidity. RESULTS: Among individuals with either LRS or PTSD, 24.6% had both conditions. The odds of comorbidity was significantly higher among those with more severe 9/11 exposures. Independent of 9/11 exposures, participants with LRS had 4 times the odds of those without it of meeting criteria for PTSD, and those with PTSD had 4 times the odds of those without it of meeting criteria for LRS. Participants with comorbidity had worse quality of life and more unmet mental health care needs than did all other outcome groups. CONCLUSIONS: Respiratory and mental illness are closely linked in individuals exposed to 9/11 and should be considered jointly in public health outreach and treatment programs.

Evaluation of HIV incidence surveillance in New York City, 2006.

In 2005, the New York City (NYC) Department of Health and Mental Hygiene implemented a standardized human immunodeficiency virus (HIV) incidence surveillance protocol based on the serologic testing algorithm for recent HIV seroconversion deployed nationwide by the Centers for Disease Control and Prevention (CDC). We evaluated four key attributes of NYC's HIV incidence surveillance system-simplicity, data quality, timeliness, and acceptability--using CDC's guidelines for surveillance system evaluation. The evaluation revealed that the system could potentially provide HIV incidence estimates stratified by borough and major demographic groups at about nine months after the period of interest. The system strengths include its relative simplicity and integration with routine HIV/acquired immunodeficiency syndrome surveillance. Weaknesses include lack of completeness of testing history information, a critical component of incidence estimation. Continued improvements in data completeness and timeliness will improve the currently available information to inform personnel who develop HIV-prevention programs and policy initiatives in NYC and nationally.

Central oxytocin, vasopressin, and corticotropin-releasing factor receptor densities in the basal forebrain predict isolation potentiated startle in rats.

Individual differences in resiliency to particular stressors may be mediated by specific neuropeptide receptor patterns in the brain. Here, we explored this issue by using a multivariate approach to identify brain sites in which oxytocin (OTR), vasopressin (V1aR), and corticotropin-releasing factor type 1 (CRF1) or type 2 receptor binding covaried with a measure of isolation-induced anxiety: isolation potentiated startle (IPS). Partial least squares (PLS) analysis identified three binding sites, the shell of the nucleus accumbens (AccSh), lateral bed nucleus of the stria terminalis, and intermediate zone of the lateral septum, in which CRF1, V1aR, and OTR receptors, respectively, covaried with IPS. Multiple regression analysis demonstrated that the three binding sites accounted for more of the variation in IPS as a linear combination than when considered individually. Using the same multiple regression model, the linear combination of the same three binding sites/peptide receptors measured in a new group of animals successfully predicted their IPS values. There were no differences in binding between grouped and isolated animals, suggesting that the patterns are trait effects rather than a consequence of isolation. Based on the finding that CRF1 receptors in the AccSh were positively correlated with IPS, we infused CRF directly into the AccSh and found that it significantly potentiated startle after a short isolation period but not under grouped conditions. This result directly supported the predictions made by the combined PLS/regression approach. These results suggest that the integrated activity of neuropeptide systems mediating both social behavior and anxiety underlie IPS.

Species and sex differences in brain distribution of corticotropin-releasing factor receptor subtypes 1 and 2 in monogamous and promiscuous vole species.

Corticotropin-releasing factor (CRF) receptor subtypes 1 and 2 have been implicated in rodent models of anxiety, but much less is known about the CRF system and social behavior. Both corticosterone and central CRF receptors modulate pair bonding in the monogamous prairie vole. Using receptor autoradiography, we mapped CRFR(1) and CRFR(2) in the brains of two monogamous vole species, the prairie vole and pine vole, and two promiscuous vole species, the meadow vole and montane vole. We found markedly different patterns of brain CRFR(1) and CRFR(2) binding among the four species, including species differences in the olfactory bulb, nucleus accumbens, lateral septum, hippocampus, laterodorsal thalamus, cingulate cortex, superior colliculus, and dorsal raphe. Interestingly, we also observed striking sex differences in voles: CRFR(2) binding was higher in the encapsulated bed nucleus of the stria terminalis in males than females for all four vole species. These results suggest possible sites of action for CRF-induced facilitation of pair bond formation in prairie voles, as well as potential sex differences in the CRF modulation of pair bonding. Further examination of CRF receptors in vole species may reveal a novel role for CRF in social behavior. Ultimately, our results identify several brain regions with conserved CRF receptor patterns across rodent and primate species, in contrast to several brain regions with phylogenetically plastic CRF receptor patterns, and have interesting implications for the evolution of CRF receptor patterns and behavior.

The CRF system mediates increased passive stress-coping behavior following the loss of a bonded partner in a monogamous rodent.

Social relationships significantly influence physiology and behavior, including the hypothalamo-pituitary-adrenal axis, anxiety, and mental health. Disruption of social bonds through separation or death often results in profound grieving, depression, and physical illness. As the monogamous prairie vole forms enduring, selective pair bonds with the mating partner, they provide an animal model to study the physiological consequences of pair bonding and, thus, the loss of the bonded partner. Male prairie voles were paired with a novel female or male sibling. After 5 days, half of the males of each group were separated from the partner. Elevated plus-maze, forced swim, and tail suspension tests were used to assess anxiety-like and passive stress-coping behaviors indicative of depressive-like behavior. Following 4 days of separation from the female but not the male partner, experimental males displayed increased passive stress-coping. This effect was abolished by long-term intracerebroventricular infusion of a nonselective corticotropin-releasing factor (CRF) receptor antagonist without disrupting the bond itself. Both CRF type 1 and 2 receptors were involved in the emergence of passive stress-coping behavior. Furthermore, pairing with a female was associated with elevated CRF mRNA in the bed nucleus of the stria terminalis, and partner loss elicited a pronounced increase in circulating corticosteroid and adrenal weight. We speculate that the CRF system may mediate an aversive affect following separation from the female partner, which may facilitate proximity seeking between the pair-bonded individuals. Hence, the prairie vole model may provide insights into brain mechanisms involved in the psychopathological consequences of partner loss.

Vasopressin and pair-bond formation: genes to brain to behavior.

Microtine rodents provide an excellent model for the study of the neurobiology of social bonds. In this review, we discuss how the presence of a microsatellite sequence in the prairie vole vasopressin receptor gene may determine vasopressin receptor binding patterns in the brain and how these patterns may in turn affect social behavior.

Application of adeno-associated viral vectors in behavioral research.

Viral vectors afford the capability of genetically manipulating the expression of neurotransmitters, neuropeptides, hormones, and their receptors in specific brain sites of adult animals of any species. Hence, they are a powerful tool for investigating the neurochemistry underlying complex cognitive processes and behaviors. Here we discuss how the recombinant adeno-associated virus (rAAV) can be engineered for use in neurobehavioral studies, techniques for site-specific delivery of vector into the brain, characterization of expression profiles, and biosafety issues. Finally, we discuss issues of experimental design and interpretation of behavioral results in viral vector studies.