Predeployment, deployment, and postdeployment risk factors for posttraumatic stress symptomatology in female and male OEF/OIF veterans.

[Correction Notice: An erratum for this article was reported in Vol 120(4) of Journal of Abnormal Psychology (see record 2011-19996-001). In the article there was an error in the affiliation bylines for Rani Elwy and Susan Eisen. Their affiliations should have been listed as Edith Nourse Rogers Memorial Veterans Hospital and Department of Health Policy and Management, Boston University School of Public Health.] Prior research on risk factors for posttraumatic stress symptomatology (PTSS) in war-exposed Veterans has revealed both direct and indirect mechanisms of risk that span predeployment, deployment, and postdeployment timeframes. The aims of the present study were to identify the mechanisms through which previously documented risk factors contribute to PTSS in a national sample of 579 female and male Veterans deployed to Afghanistan for Operation Enduring Freedom (OEF) or to Iraq for Operation Iraqi Freedom (OIF), as well as to examine the extent to which results mirror associations observed among Vietnam Veterans (King, King, Foy, Keane, & Fairbank, 1999). Consistent with conservation of resources (COR) theory (Hobfoll, 1989, 2001), findings indicated that PTSS is accounted for by multiple chains of risk, many originating in predeployment experiences that place Veterans at risk for additional stress exposure, and foretell difficulty accessing resources in the face of subsequent stressors. Importantly, the majority of previously documented mechanisms were replicated in this study, suggesting key pathways through which risk factors may contribute to PTSS across different Veteran populations. Results also revealed a number of novel risk mechanisms for OEF/OIF female Veterans, particularly with respect to the role of deployment family relationships in risk for PTSS. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Posttraumatic stress disorder and late-onset smoking in the Vietnam era twin registry.

Epidemiological and clinical studies have consistently reported associations between smoking and posttraumatic stress disorder (PTSD). This study analyzed diagnostic interview data on 6,744 members of the Vietnam Era Twin Registry to clarify the PTSD-smoking relation and to examine whether genetic liability for smoking moderated this relation. Preexisting active (unremitted) PTSD increased risk of late-onset daily smoking. Remitted PTSD decreased risk. Active PTSD increased risk of smoking at all levels of genetic liability; the effect was strongest for those with least genetic liability. This suggests PTSD represents a nongenetic pathway to late-onset smoking among individuals who were nonsmokers prior to developing PTSD. If replicated, these results identify PTSD as a risk factor for smoking that should lead to early tobacco control treatment in this population. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A Study of the Error in a Neutron Probability of Survival Formula

The error associated with a widely used transistor neutron probability of survival formula has been assesed. The probability of survival prediction for three transistor types was compared with the actual fraction of transistors whose gain remained above a selected limit at each of several fluence levels. The agreement was very good, suggesting that the formulation used does not introduce excessive conservatism into the calculation.     

Molecularly engineered poly(ortho ester) microspheres for enhanced delivery of DNA vaccines

Genetic vaccination using plasmid DNA presents a unique opportunity for achieving potent immune responses without the potential limitations of many conventional vaccines. Here we report the design of synthetic biodegradable polymers specifically for enhancing DNA vaccine efficacy in vivo. We molecularly engineered poly(ortho ester) microspheres that are non-toxic to cells, protect DNA from degradation, enable uptake by antigen-presenting cells, and release DNA rapidly in response to phagosomal pH. One type of microsphere of poly(ortho esters) that releases DNA vaccines in synchrony with the natural development of adaptive immunity, elicited distinct primary and secondary humoral and cellular immune responses in mice, and suppressed the growth of tumour cells bearing a model antigen. This polymer microparticulate system could, with further study, have implications for advancing the clinical utility of DNA vaccines as well as other nucleic-acid-based therapeutics against viral infections and cancer.     

Butterfly proboscis: combining a drinking straw with a nanosponge facilitated diversification of feeding habits

The ability of Lepidoptera, or butterflies and moths, to drink liquids from rotting fruit and wet soil, as well as nectar from floral tubes, raises the question of whether the conventional view of the proboscis as a drinking straw can account for the withdrawal of fluids from porous substrates or of films and droplets from floral tubes. We discovered that the proboscis promotes capillary pull of liquids from diverse sources owing to a hierarchical pore structure spanning nano- and microscales. X-ray phase-contrast imaging reveals that Plateau instability causes liquid bridges to form in the food canal, which are transported to the gut by the muscular sucking pump in the head. The dual functionality of the proboscis represents a key innovation for exploiting a vast range of nutritional sources. We suggest that future studies of the adaptive radiation of the Lepidoptera take into account the role played by the structural organization of the proboscis. A transformative two-step model of capillary intake and suctioning can be applied not only to butterflies and moths but also potentially to vast numbers of other insects such as bees and flies.     

The legend and myth of school phobia.

Many phrases are well-known for describing behavior problems in children and adolescents, but perhaps the one most overused and least understood is "school phobia." Although variously defined, school phobia has referred generally to children and adolescents avoidant of school due to overwhelming fearfulness. Given the construct's debatable discriminant validity, however, a critique of its clinical utility seems appropriate. The authors outline the historical development of school phobia, including the transition from viewing the problem as a syndrome to a symptom of general school refusal behavior. A review of the research evidence supports the contention that school phobia violates 2 contemporary criteria for a phobia, i.e., excessiveness and specificity. Given the questionable validity of the construct, recommendations are made regarding future classification, assessment, and treatment methods for youngsters with school refusal behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A role for glutamate and its receptors in the regulation of oligodendrocyte development in cerebellar tissue slices

We tested the hypothesis that the neurotransmitter glutamate would influence glial proliferation and differentiation in a cytoarchitecturally intact system. Postnatal day 6 cerebellar slices were maintained in organotypic culture and treated with glutamate receptor agonists or antagonists. After dissociation, cells were stained with antibodies for different oligodendrocyte developmentally regulated antigens. Treatment of the slices with the glutamate receptor agonists kainate or alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid significantly decreased the percentage of LB1(+), NG2(+) and O4(+) cells, and their bromodeoxyuridine labeling index. The non-N-methyl-D-aspartate glutamate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione increased the percentage and bromodeoxyuridine labeling of LB1(+), NG2(+) and O4(+) cells. In intact slices, RNA levels of the oligodendrocyte gene for 2',3'-cyclic nucleotide 3'-phosphodiesterase were decreased by kainate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, and increased by 6,7-dinitroquinoxaline-2,3-dione. The percentage of astrocytes was not modified by kainate, alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid or 6, 7-dinitroquinoxaline-2,3-dione. Treatment with the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid did not alter the percentage of O4(+) cells, nor their proliferation. Incubation with the gamma-aminobutyric acid receptor antagonist bicuculline did not modify the percentage of LB1(+), A2B5(+) and O4(+) cells. In purified cerebellar oligodendrocyte progenitor cells, glutamate receptor agonists blocked K+ currents, and inhibited cell proliferation and lineage progression. The K+ channel blocker tetraethylammonium also inhibited oligodendrocyte progenitor cell proliferation. These findings indicate that in rat cerebellar tissue slices: (i) glutamate specifically modulates oligodendrocyte but not astrocyte development through selective activation of alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, and (ii) cell depolarization and blockage of voltage-dependent K+ channels is likely to be the triggering mechanism.     

Regulation of neuronal specification in the zebrafish spinal cord by Delta function

A subset of patients with pediatric onset obsessive-compulsive disorder (OCD) and tic syndromes (e.g. Tourette's syndrome) have symptom onset or exacerbation associated with infection. Some of these patients have been demonstrated to have antineuronal antibodies reactive with nuclei of the basal ganglion. It has been hypothesized that these patients have an immune process initiated by infection that affects the basal ganglion and causes obsessive-compulsive symptoms. The term pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) has been coined to describe those patients with evidence of recent group A beta hemolytic streptococcal infection. We tested the serum from 13 adult patients with obsessive-compulsive disorder for panels of autoantibodies that serve as markers of autoimmunity in the practice of neurology and internal medicine. We investigated the frequency of neuron-specific autoantibodies [N-type and P/Q-type voltage-gated calcium channel antibodies, type 1 Purkinje cell antibodies, types 1 and 2 antineuronal nuclear antibodies, amphiphysin antibodies, and glutamic acid decarboxylase (65 kDa) antibodies], other organ-specific autoantibodies (muscle acetylcholine receptor-binding antibodies, striated muscle antibodies, thyroid microsomal and thyroglobulin antibodies), and non-organ-specific autoantibodies (antinuclear antibodies, antimitochondrial antibodies, and smooth muscle antibodies) to determine if any of these antibodies might serve as a serological marker for adult OCD or yield evidence of an autoimmune diathesis. Although most of our subjects had onset of OCD before 19 years of age (N=8) or before puberty (N=4), the study revealed no humoral evidence of autoimmunity involving the neuron-, organ-, and non-organ-specific antibodies that we assayed.