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The landslide reelection of President Ronald Reagan in 1984 prompted political analysts to consider the possibility of a national realignment of the electorate toward the Republican party. The 1986 elections, however, proved any predictions of a national realignment to be premature. A major shift in voting patterns had not taken place--except in the Mountain West, where a realignment was already in place. Once second only to the southern states in Democratic attachments, these western states (Arizona, Colorado, Idaho, Montana, Nevada, New Mexico, Utah, and Wyoming) now compose the most Republican region in the nation. The contributors to this volume assert that this substantial change in electoral patterns, which has spanned nearly forty years, resulted not from a westward migration but from a widespread conversion among those who are born and remain in the region. In analyzing this realignment, these writers--some of the nation's best electoral scholars--provide historical and contemporary overviews and assess the important issues not only for voters but also for party organizations and members of Congress. Their focus in The Politics of Realignment, however, is on the Mountain West's role in contemporary American politics. The authors present a comprehensive investigation into the meaning of this regional realignment for national politics.

AbstractAttention-deficit hyperactivity disorder (ADHD) is currently recognized as a neurobiological, genetically based disorder in both children and adults. In this article we examine whether, by using a sample of middle-aged male twin veterans, the phenotypic characterization, prevalence, heritability and the longitudinal course of the illness is comparable to results observed in samples of children and adolescents. We evaluated the utility of adult reports of lifetime ADHD symptoms by examining the heritability of retrospectively reported childhood symptoms, using both symptom-based and discrete classification- based approaches, as well as examining the persistence of ADHD symptoms into adulthood for that subsample of individuals who were judged to possibly have ADHD as children. Our results showed prevalence rates that were approximately similar to those observed in other studies, demonstrable familiality, similar item endorsement patterns, a strong genetic association between hyperactive and inattentive subtypes, and a longitudinal decline in symptom severity. We concluded that while assessing ADHD in adult probands may be less accurate than with children or adolescents, since it demonstrates several characteristics in common with other assessment techniques it remains a viable diagnostic and research strategy, even with population samples.

PUBLISHED ; Export Date: 15 September 2016 ; Here we demonstrate that liquid phase exfoliation can be used to convert layered crystals of nickel hydroxide into Ni(OH)2 nanosheets in relatively large quantities and without the need for ion intercalation. While other procedures require harsh synthesis conditions and multiple reaction steps, this method involves ultrasonication of commercially available powders in aqueous surfactant solutions and so is relatively mild and potentially scalable. Such mild exfoliation is possible because the surface energy of Ni(OH)2, as measured by inverse gas chromatography, is relatively low at ?70 mJ m?2, similar to other layered materials. TEM, AFM, XPS and Raman spectroscopy show the exfoliated nanosheets to be relatively thin (mean ?10 monolayers thick) and of good quality. Size selection by liquid cascade centrifugation allowed the production of samples with mean nanosheet lengths ranging from 55 to 195 nm. Optical measurements on dispersions showed the optical absorption coefficient spectra to be relatively invariant with nanosheet size while the scattering coefficient spectra varied strongly with size. The resultant size-dependence allows the extinction spectra to be used to estimate nanosheet size as well as concentration. We used the exfoliated nanosheets to prepare thin film electrodes for use in supercapacitors and as oxygen evolution catalysts. While the resultant capacitance was reasonably high at ?1200 F cm?3 (20 mV s?1), the catalytic performance was exceptional with currents of 10 mA cm?2 observed at overpotentials as low as 297 mV, close to the state of the art. ; This work was primarily funded by Science Foundation Ireland through the PI program (11/PI/1087). The research leading to these results has also received funding from the European Union Seventh Framework Program under grant agreement no. 604391 Graphene Flagship, the European Research Council (SEMANTICS) and the Science Foundation Ireland (SFI) funded centre AMBER (SFI/12/RC/2278)

Abstract Objective Early HIV diagnosis reduces transmission and improves health outcomes; screening in non-traditional settings is increasingly advocated. We compared test venues by the number of new diagnoses successfully linked to the regional HIV treatment center and disease stage at diagnosis. Methods We conducted a retrospective cohort study using structured chart review of newly diagnosed HIV patients successfully referred to the region's only HIV treatment center from 1998 to 2003. Demographics, testing indication, risk profile, and initial CD4 count were recorded. Results There were 277 newly diagnosed patients meeting study criteria. Mean age was 33 years, 77% were male, and 46% were African-American. Median CD4 at diagnosis was 324. Diagnoses were earlier via partner testing at the HIV treatment center (N = 8, median CD4 648, p = 0.008) and with universal screening by the blood bank, military, and insurance companies (N = 13, median CD4 483, p = 0.05) than at other venues. Targeted testing by health care and public health entities based on patient request, risk profile, or patient condition lead to later diagnosis. Conclusion Test venues varied by the number of new diagnoses made and the stage of illness at diagnosis. To improve the rate of early diagnosis, scarce resources should be allocated to maximize the number of new diagnoses at screening venues where diagnoses are more likely to be early or alter testing strategies at test venues where diagnoses are traditionally made late. Efforts to improve early diagnosis should be coordinated longitudinally on a regional basis according to this conceptual paradigm.

AbstractMany studies that found associations between depression and nicotine dependence have ignored possible shared genetic influences associated with antisocial traits. The present study examined the contribution of genetic and environmental effects associated with conduct disorder (CD) and antisocial personality disorder (ASPD) to the comorbidity of major depression (MD) and nicotine dependence (ND). A telephone diagnostic interview, the Diagnostic Interview Schedule-III-R, was administered to eligible twins from the Vietnam Era Twin (VET) Registry in 1992. Multivariate genetic models were fitted to 3360 middle-aged and predominantly white twin pairs (1868 monozygotic, 1492 dizygotic pairs) of which both members completed the pertinent diagnostic interview sections. Genetic influences on CD accounted for 100%, 68%, and 50% of the total genetic variance in risk for ASPD, MD and ND, respectively. After controlling for genetic influences on CD, the partial genetic correlation between MD and ND was no longer statistically significant. Nonshared environmental contributions to the comorbidity among these disorders were not significant. This study not only demonstrates that the comorbidity between ND and MD is influenced by common genetic risk factors, but also further suggests that the common genetic risk factors overlapped with those for antisocial traits such as CD and ASPD in men.

AbstractThere have been long questions about the relationship of schizophrenia to other mental disorders. Lifetime DSM-III-R diagnoses of mood and anxiety disorders in twins with clinically diagnosed schizophrenia (n = 24) and their non-affected co-twins (n = 24) were compared with twins from pairs without schizophrenia (n = 3327) using a sample from the Vietnam Era Twin Registry. Schizophrenic probands had significantly elevated rates of all included disorders (bipolar disorder, major depression, dysthymia, generalized anxiety disorder, panic disorder, and PTSD) compared with controls (P < 0.01). The odd ratios comparing co-twins of schizophrenic probands with controls was greater than three for every disorder, but did not attain statistical significance. A similar pattern was observed when analyses were restricted to only monozygotic twins (n = 12). Consistent with other studies, schizophrenics appeared to have higher rates of a range of mental disorders. Our results suggest that schizophrenia per se represents a risk factor for other psychiatric disorders, but the absence of significantly elevated risk among non-schizophrenic co-twins suggested that family environmental and/or genetic factors that contribute to risk of schizophrenia do not increase the risk of mood and anxiety disorders to the same extent that the risk of these other disorders is increased by the presence of schizophrenia. Twin Research (2000) 3, 28–32.

Molecular genetic research has provided some evidence for the association between depression and metabolic disorders. We sought to determine if molecular findings are reflected in twin analyses testing if common genetic and environmental risk factors contribute to the co-occurrence of diabetes and depression. Data to derive depression and diabetes were collected from 1,237 male-male twins who participated in the 2005 Vietnam Era Twin Study of Aging (VETSA). The 1,237 twins were comprised of 347 MZ pairs, 3 MZ singletons, 267 DZ pairs and 6 unpaired twins. Depression was defined as a score below 46 on the Short Form-36 mental component summary score. Diabetes was defined by self report, use of anti-diabetic medications and insulin. Twin models were fit to estimate the correlation of genetic and environmental contributions to depression and diabetes. Consistent with other studies these data support the association between depression and diabetes (OR = 1.7; 95%CI: 1.1–2.7). Genetic vulnerability accounted for 50% (95%CI: 32%–65%) of the variance in risk for depression and 69% (95%CI: 52%–81%) of the variance in risk for diabetes. The genetic correlation between depression and diabetes was r = 0.19 (95%CI: 0–0.46) and the non-shared environmental correlation was r = 0.09 (95% CI: 0–0.45). Overall there is little evidence that common genetic and environmental factors account for the co-occurrence of depression and diabetes in middle aged men. Further research in female twins and larger cohorts is warranted.

Combat exposure is associated with increased risk of psychiatric and substance use disorders in veterans. However, it is not known whether combat exposure independently increases risk for these disorders or whether this association is accounted for by genetic vulnerability common to posttraumatic stress disorder (PTSD). This paper tests competing explanations for the association of combat exposure and PTSD with nicotine dependence (ND), alcohol dependence (AD), and major depression (MD). Data was obtained from 6,099 members of the Vietnam Era Twin Registry, a national registry of male-male twin pairs who served in the military during the Vietnam Era. Twin models were fit to estimate the genetic and environmental variance common and specific to DSM-III-R lifetime diagnoses of PTSD, combat trauma, and three comorbid conditions: ND and AD and MD. Variance specific to ND, AD and MD was due to genetic factors (48%, 36% and 12%, respectively), and unique environmental factors (36%, 42% and 58%, respectively). After accounting for variance common to PTSD, no residual genetic and environmental variance overlapped between combat and ND, combat and AD, and combat and MD. Combat exposure is not independently associated with lifetime MD, AD, and MD. The association of combat exposure with these three disorders is due to genetic and unique environmental contributions in common with PTSD. These findings suggest comorbid PTSD may represent a genetically mediated vulnerability to psychopathology following trauma.

We explored the comorbidity between panic attacks (PA), whose symptoms can include gastrointestinal discomfort, and gastrointestinal disorders (GD). Structural equation modeling was used to analyze data from 1,874 MZ and 1,498 DZ male–male twin pairs from the Vietnam Era Twin Registry. PA and GD were associated (relative risk for GD = 2). The percentage of liability due to genetic factors was estimated to be 37% for PA and 31% for GD. There was significant correlation between the genetic risk factors for PA and GD (estimated r = .55, 95% CI of 34% to 82%) and no evidence of correlation between the environmental causes of PA and GD. Therefore, PA and GD comorbidity can be explained by overlapping genetic factors and not overlapping environmental factors. Although these data cannot identify a biological pathway for such a shared liability, it suggests the presence of GD may be informative for genetic studies of panic.

AbstractWe examined the contributions of genetic and environmental factors to body mass index (BMI) over approximately 28 years. Participants were 693 male, predominantly middle-class, twins (355 monozygotic, 338 dizygotic) from the Vietnam Era Twin Registry. The phenotypic correlation between age 20 and age 48 BMI was 0.52; the genetic correlation was 0.60. Most of the remaining variance at both times was accounted for by nonshared environmental factors. Since genetic factors are not perfectly correlated, this indicates that other genes affect BMI at one or both time points, leaving room for further exploration of the genetics of body mass stability. Mean BMI increased significantly from 22.7 (normal) to 27.8 (overweight). Overweight BMI at age 20 predicted midlife adult onset diabetes (adjusted odds ratio = 4.62, 95% CI 1.91 to 11.18), but not hypertension. Depending on one's vantage point, the results indicate elements of both stability and change in BMI. Very similar phenotypic and genetic correlations were observed over a similar time period in a WW II twin sample, but without the substantial mean increase in BMI. It seems unlikely that different genes influence BMI in the two cohorts. Therefore, we argue that nonshared environmental factors are probably primarily responsible for the secular increase in midlife BMI. Our results also provide prospective evidence that early excess BMI may have serious long-term health consequences, and that this risk is not limited to minorities or adults of lower socioeconomic status.

In this longitudinal study we examined the stability of general cognitive ability (GCA), as well as heterogeneity and genetic and environmental influences underlying individual differences in change. We investigated GCA from young adulthood through late midlife in 1,288 Vietnam Era Twin Study of Aging participants at ages ~20, ~56, and ~62 years. The correlations among the three occasions ranged from .73 to .85, reflecting substantial stability. The heritability was significant on each of the three occasions and ranged from .59 to .66. The influence of the shared environment was not significant at any of the ages. The genetic correlations across the three occasions ranged from .95 to .99 and did not differ significantly from 1.0. The nonshared environmental correlations ranged from .21 to .47. Latent growth curve analysis was applied to characterize trajectories over the 42 year period. Slope was significantly different from 0 and indicated that there was modest change over time. There was a significant genetic influence on initial level of GCA (h2 = .67), but not change (h2 = .23). Genetic factors primarily contribute to stability, while change reflects the influence of nonshared environmental influences. There was a significant negative correlation between initial level of GCA and change (r = −.31). Latent class growth analysis identified four trajectories. In general, the four groups followed parallel trajectories and were differentiated mainly by differences in AFQT performance level at the time of military induction.