Posttraumatic Stress Disorder, Depression, and HIV Risk Behavior Among Ohio Army National Guard Soldiers.

Posttraumatic Stress Disorder, Depression, and HIV Risk Behavior Among Ohio Army National Guard Soldiers.

Filed under: Depression Treatment

J Trauma Stress. 2013 Feb; 26(1): 64-70
Marshall BD, Prescott MR, Liberzon I, Tamburrino MB, Calabrese JR, Galea S

We examined the relationship between posttraumatic stress disorder (PTSD), major depressive disorder (MDD), and human immunodeficiency virus (HIV) risk behavior among the Ohio Army National Guard (OHARNG). We analyzed data collected from a sample of OHARNG enlisted between June 2008 and February 2009. Participants completed interviews assessing HIV risk activities defined by the Behavioral Risk Factor Surveillance System, and were screened for PTSD and MDD based on DSM-IV criteria according to the Diagnostic and Statistical Manual of Mental Disorders (4th ed., DSM-IV; American Psychiatric Association, 1994). Logistic regression was used to examine the independent and combined effects of PTSD and MDD on past-year HIV risk behavior. Of 2,259 participants, 142 (6.3%) reported at least 1 past-year HIV risk behavior. In adjusted models, relative to soldiers with neither disorder, screening positive for MDD only was associated with HIV risk behavior (adjusted odds ratio [AOR] = 2.33, 95% CI = [1.15, 4.71]), whereas PTSD was not significant (AOR = 1.60, 95% CI = [0.80, 3.20]). Participants with both PTSD and depression were most likely to report HIV risk behavior (AOR = 2.75, 95% CI = [1.06, 7.11]). Soldiers with PTSD and MDD may be at greater risk for HIV infection due to increased engagement in HIV risk behavior. Integrated interventions to address mental health problems and reduce HIV risk behavior are in need of development and evaluation.
HubMed – depression

 

Psychometric Properties of the UCLA PTSD Reaction Index. Part II: Investigating Factor Structure Findings in a National Clinic-Referred Youth Sample.

Filed under: Depression Treatment

J Trauma Stress. 2013 Feb; 26(1): 10-8
Elhai JD, Layne CM, Steinberg AM, Brymer MJ, Briggs EC, Ostrowski SA, Pynoos RS

We examined the underlying factor structure of the UCLA PTSD Reaction Index (PTSD-RI) using data from 6,591 children/adolescents exposed to trauma, presenting for treatment at any of 54 National Child Traumatic Stress Network (NCTSN) centers. Using confirmatory factor analysis, we tested the 3-factor DSM-IV PTSD model, 2 separate 4-factor models (Dysphoria vs. Emotional Numbing) and a recently conceptualized 5-factor Dysphoric Arousal model. We found a slight, but significant advantage for the Dysphoria model over the Emotional Numbing model on the PTSD-RI, with a difference in Bayesian information criterion (BIC) values of 81 points. As with several recent studies of adult trauma victims, we found a slight advantage for the Dysphoric Arousal model over the other models on the PTSD-RI, with BIC differences exceeding 300 points. Retaining the Dysphoric Arousal model, we tested the convergent validity of the PTSD-RI factors against subscales of the Trauma Symptom Checklist for Children. Supporting the convergent validity of the PTSD-RI, in the Dysphoric Arousal model, the dysphoric arousal factor related most strongly to anger, whereas the emotional numbing factor related most strongly to depression, and anxious arousal factor related most strongly to anxiety. Results support the use of the PTSD-RI for evaluating PTSD among youth.
HubMed – depression

 

Reduction of cardiomyocyte S-nitrosylation by S-nitrosoglutathione reductase protects against sepsis-induced myocardial depression.

Filed under: Depression Treatment

Am J Physiol Heart Circ Physiol. 2013 Feb 15;
Sips PY, Irie T, Zou L, Shinozaki S, Sakai M, Shimizu N, Nguyen R, Stamler JS, Chao W, Kaneki M, Ichinose F

Myocardial depression is an important contributor to morbidity and mortality in septic patients. Nitric oxide (NO) plays an important role in the development of septic cardiomyopathy, but also has protective effects. Recent evidence has indicated that NO exerts many of its downstream effects on the cardiovascular system via protein S-nitrosylation, which is negatively regulated by S-nitrosoglutathione reductase (GSNOR), an enzyme promoting denitrosylation. We tested the hypothesis that reducing cardiomyocyte S-nitrosylation by increasing GSNOR activity can improve myocardial dysfunction during sepsis. Therefore, we generated mice with a cardiomyocyte-specific overexpression of GSNOR (GSNOR-CMTg mice) and subjected them to endotoxic shock. Measurements of cardiac function in vivo and ex vivo showed that GSNOR-CMTg mice had a significantly improved cardiac function after lipopolysaccharide challenge (LPS, 50 mg/kg) compared to wild-type (WT) mice. Cardiomyocytes isolated from septic GSNOR-CMTg mice showed a corresponding improvement in contractility compared to WT cells. However, systolic Ca(2+) release was similarly depressed in both genotypes after LPS, indicating that GSNOR-CMTg cardiomyocytes have increased Ca(2+) sensitivity during sepsis. Parameters of inflammation were equally increased in LPS-treated hearts of both genotypes, and no compensatory changes in NO synthase expression levels were found in GSNOR overexpressing hearts before or after LPS challenge. GSNOR overexpression however significantly reduced total cardiac protein S-nitrosylation during sepsis. Taken together, our results indicate that increasing the denitrosylation capacity of cardiomyocytes protects against sepsis-induced myocardial depression. Our findings suggest that specifically reducing protein S-nitrosylation during sepsis improves cardiac function by increasing cardiac myofilament sensitivity to Ca(2+).
HubMed – depression

 

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