Background-Several theories have posited a common internalizing factor to help account for the relationship between mood and anxiety disorders. These disorders are often comorbid and strongly covary. Other theories and data suggest that personality traits may account, at least in part, for comorbidity between depression and anxiety. The present study examines the relationship between neuroticism and an internalizing dimension common to mood and anxiety disorders.

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Neuroticism has been hypothesized to be a nonspecific risk factor for both anxiety and unipolar mood disorders whereas some cognitive and personality-cognitive vulnerabilities have been hypothesized to be more specific to depression. Using a retrospective design with a sample of 575 high school juniors, we tested three competing models of the associations among these variables. Both neuroticism and the cognitive and personality-cognitive vulnerabilities had significant zero-order associations with rates of past diagnoses of both anxiety and unipolar mood disorders. Neuroticism had significant unique associations with past anxiety disorders and comorbid anxiety and unipolar mood disorders whereas the other vulnerabilities did not. In addition, gender interacted with neuroticism but not with the other vulnerabilities in associating with past diagnoses of mood disorders, showing that neuroticism is more highly associated with past unipolar mood diagnoses in males than in females. Finally, the cognitive and personality-cognitive vulnerabilities overlapped with substantial portions of the variance that neuroticism shared with diagnoses. These results suggest that, at least for retrospective associations with past anxiety and unipolar mood disorders, the cognitive and other personality-cognitive vulnerabilities are non-specific facets of neuroticism. Keywords neuroticism; cognitive vulnerability; anxiety disorders; mood disordersCorrespondence concerning this article should be addressed to either Richard Zinbarg, Department of Psychology, Northwestern University, 2029 Sheridan Rd., Evanston, Illinois 60208; rzinbarg@northwestern.edu, or Susan Mineka, Department of Psychology, Northwestern University, 2029 Sheridan Rd., Evanston, Illinois 60208; mineka@northwestern.edu. James Griffith is now at the Department of Medical Social Sciences, Northwestern University, Feinberg School of Medicine, Department of Medical Social Sciences, Chicago, Illinois. Allison Waters is now at the School of Psychology, Griffith University, Australia. Nilly Mor is now at the Hebrew University of Jerusalem.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptBehav Res Ther. Author manuscript; available in PMC 2011 May 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptSeveral personality and cognitive vulnerability models for anxiety and unipolar mood disorders have been proposed in the past few decades. Some variables such as neuroticism (N) have been proposed as a common vulnerability for all, or nearly all, of these emotional disorders, ...

The opportunistic pathogen Acinetobacter baumannii is able to persist in the environment and is often multidrug resistant (MDR), causing difficulties in the treatment of infections. Here, we show that the two-component system AdeRS, which regulates the production of the AdeABC multidrug resistance efflux pump, is required for the formation of a protective biofilm in an ex vivo porcine mucosal model, which mimics a natural infection of the human epithelium. Interestingly, deletion of adeB impacted only on the ability of strain AYE to form a biofilm on plastic and only on the virulence of strain Singapore 1 for Galleria mellonella. RNA-Seq revealed that loss of AdeRS or AdeB significantly altered the transcriptional landscape, resulting in the changed expression of many genes, notably those associated with antimicrobial resistance and virulence interactions. For example, A. baumannii lacking AdeRS displayed decreased expression of adeABC, pil genes, com genes, and a pgaC-like gene, whereas loss of AdeB resulted in increased expression of pil and com genes and decreased expression of ferric acinetobactin transport system genes. These data define the scope of AdeRS-mediated regulation, show that changes in the production of AdeABC mediate important phenotypes controlled by AdeRS, and suggest that AdeABC is a viable target for antimicrobial drug and antibiofilm discovery.

The current study compared two competing theories of the stress generation model of depression (stress causation vs. stress continuation) using interview-based measures of episodic life stress, as well as interpersonal and noninterpersonal chronic life stress. We also expanded on past research by examining anxiety disorders as well as depressive disorders. In addition, we examined the role of neuroticism and extraversion in these relationships. Participants were 627 adolescents enrolled in a two-site, longitudinal study of risk factors for depressive and anxiety disorders. Baseline and follow-up assessments were approximately one year apart. Results supported the stress causation theory for episodic stress generation for anxiety disorders, with neuroticism partially accounting for this relationship. The stress causation theory was also supported for depression, but only for more moderate to severe stressors; neuroticism partially accounted for this relationship as well. Finally, we found evidence for interpersonal and noninterpersonal chronic life stress continuation in both depressive and anxiety disorders. The present findings have implications regarding the specificity of the stress generation model to depressive disorders, as well as variables involved in the stress generation process.

Though there is a considerable amount of research supporting the association between stressful life events and major depression, there is a paucity of research concerning a range of other life stress constructs, non-depressive disorders, the role of stable personality traits, and gender differences. This study addresses these deficits by: (a) focusing on the association between interpersonal and non-interpersonal chronic life stress (CLS) and both depressive and anxiety disorders, (b) examining the roles of neuroticism and low extraversion in these associations, and (c) assessing gender differences. Participants were 603 adolescents from a study examining risk factors for emotional disorders. Depression and social phobia were associated with interpersonal CLS, with neuroticism partially accounting for these associations. Low extraversion partially accounted for the association between social phobia and interpersonal CLS. Depression was also associated with non-interpersonal CLS, but only in females. This study provides preliminary evidence for the importance of personality variables in explaining shared associations between stress and depression. Additionally, the stress-social phobia relationship is highlighted, with no evidence supporting an association between other anxiety disorders and CLS.

The secreted nodulation-signaling protein NodO was purified from the supernatant of cultures of Rhizobium kguminosarum blovar viciae. The native protein has a Mr of 467,000, suggestng that it exists as a dimer since the DNA sequence predicts a Mr of 30,002. Pure NodO protein had no protease, pectinase, or cellulase activity, and no binding was observed to lipooligosaccharide modulation factors. Although NodO R. leguminosarum biovar viciae has a nodulation gene (nodO) that encodes a secreted protein (9) that is involved in pea and vetch nodulation. Although mutation of nodO does not block nodulation, it is evident that in the absence of the nodE gene, nodO is required for the nodulation of peas or vetch (10). The nodE gene product is a key determinant of host specificity and introduces functional specificity into the Nod factor by causing the production of the C18:4 acyl group MATERIALS AND METHODSBacterial Strains and Growth. The exopolysaccharidedeficient strains of R. leguminosarum, A168 and A165, with and without the symbiotic plasmid pRL1JI, have been described (14) as has been pIJ1815, which carries the cloned nodO gene (14). Typically, 25 ml of an overnight culture (OD6w00 0.4) in TY medium (15) containing streptomycin (20 Mg/ml) was inoculated into each of five 2-liter flasks containing 600 ml ofthe same medium containing 1 ,M hesperitin to induce nodO expression. The cultures were shaken at 280C for 60 h and harvested at an OD600 of 0.9-1.0, when the pH of the growth medium remained below pH 7.8. Normally, strain A168/pIJ1815 was used for purification of NodO, but for measurements of possible interactions between NodO and nodulation factors, NodO was purified using A165/ pIJ1815. NodO isolated from either strain induced channels with similar characteristics.Purification of NodO. All procedures were carried out at 40C. Cells were harvested by centrifugation (9000 rpm in a Sorvall GS3 rotor for 45 min), and the culture supernatant was adjusted to pH 5.0 using glacial acetic acid and loaded at 2 ml/min onto a column (16 mm diameter) containing a 10-ml bed volume of DEAE-Sepharose Fast Flow (Pharmacia) that had been equilibrated with 0.1 M sodium acetate buffer at pH 5.0. Proteins were eluted with 0.25 M NaCl in the acetate buffer and then precipitated by adding (NH4)2SO4 to 701% saturation. The precipitate was resuspended in 2.5 ml of 20 mM sodium acetate buffer at pH 5.0 and desalted on a PD-10 column (Pharmacia); the protein was eluted with 20 mM sodium acetate buffer at pH 5.0. Aliquots of 1.0 ml were then loaded onto a Pharmacia FPLC Mono Q column that had been equilibrated with 20 mM sodium acetate buffer at pH 5.0, and proteins were eluted at a flow rate of 1.0 ml/min using a linear gradient of0-1.0 M NaH2PO4 in 20 mM sodium acetate at pH 5.0. Peak samples (fractions 23-28, Fig. 1) were 9990 The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate t...

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