The evolution of a school behavioral health model in the US Army.

The US Army has developed an innovative School Behavioral Health (SBH) program, part of the Child and Family Behavioral Health System, a collaborative, consultative behavioral health care model that includes SBH, standardized training of primary care providers in treatment of common behavioral health problems, use of tele-consultation/tele-behavioral health, optimizing community outreach services, and integration with other related behavioral health services. In this article, the needs of military children, adolescents, and families are reviewed, a history of this initiative is presented, key themes are discussed, and next steps in advancing this evolving, innovative system of health care featuring SBH are described.

Implementing an evidence-based practices training curriculum to U.S. Army child and family behavioral health providers.

Military Children who have experienced multiple deployments of one or both parents are more likely to have emotional and behavioral difficulties compared with their civilian peers (e.g., Chandra et al., 2010 ). The U.S. Army Medical Command has tasked the Child, Adolescent and Family Behavioral Health Office (CAF-BHO) to develop programs to address the behavioral health (BH) needs of Army Children and Families. This article will describe the efforts of the CAF-BHO Training Section to disseminate and implement an evidence based practice training curriculum for Army Child and Family Behavioral Health Providers. Specifically, this article will detail: (a) the decision making strategy used to identify the training protocol for dissemination, (b) adaptations to the training program and treatment protocol to fit a Military context, and (c) efforts to implement, maximize and sustain utilization of evidence-based practices by Military BH providers over a large geographical area with limited resources.

Calcium and zinc dyshomeostasis during isoproterenol-induced acute stressor state.

Acute hyperadrenergic stressor states are accompanied by cation dyshomeostasis, together with the release of cardiac troponins predictive of necrosis. The signal-transducer-effector pathway accounting for this pathophysiological scenario remains unclear. We hypothesized that a dyshomeostasis of extra- and intracellular Ca2+ and Zn2+ occurs in rats in response to isoproterenol (Isop) including excessive intracellular Ca2+ accumulation (EICA) and mitochondrial [Ca2+]m-induced oxidative stress. Contemporaneously, the selective translocation of Ca2+ and Zn2+ to tissues contributes to their fallen plasma levels. Rats received a single subcutaneous injection of Isop (1 mg/kg body wt). Other groups of rats received pretreatment for 10 days with either carvedilol (C), a ß-adrenergic receptor antagonist with mitochondrial Ca2+ uniporter-inhibiting properties, or quercetin (Q), a flavonoid with mitochondrial-targeted antioxidant properties, before Isop. We monitored temporal responses in the following: [Ca2+] and [Zn2+] in plasma, left ventricular (LV) apex, equator and base, skeletal muscle, liver, spleen, and peripheral blood mononuclear cells (PBMC), indices of oxidative stress and antioxidant defenses, mitochondrial permeability transition pore (mPTP) opening, and myocardial fibrosis. We found ionized hypocalcemia and hypozincemia attributable to their tissue translocation and also a heterogeneous distribution of these cations among tissues with a preferential Ca2+ accumulation in the LV apex, muscle, and PBMC, whereas Zn2+ declined except in liver, where it increased corresponding with upregulation of metallothionein, a Zn2+-binding protein. EICA was associated with a simultaneous increase in tissue 8-isoprostane and increased [Ca2+]m accompanied by a rise in H2O2 generation, mPTP opening, and scarring, each of which were prevented by either C or Q. Thus excessive [Ca2+]m, coupled with the induction of oxidative stress and increased mPTP opening, suggests that this signal-transducer-effector pathway is responsible for Isop-induced cardiomyocyte necrosis at the LV apex.

Mitochondria-targeted cardioprotection in aldosteronism.

Chronic aldosterone/salt treatment (ALDOST) is accompanied by an adverse structural remodeling of myocardium that includes multiple foci of microscopic scarring representing morphologic footprints of cardiomyocyte necrosis. Our previous studies suggested that signal-transducer-effector pathway leading to necrotic cell death during ALDOST includes intramitochondrial Ca overloading, together with an induction of oxidative stress and opening of the mitochondrial permeability transition pore (mPTP). To further validate this concept, we hypothesized that mitochondria-targeted interventions will prove to be cardioprotective. Accordingly, 8-week-old male Sprague-Dawley rats receiving 4 weeks ALDOST were cotreated with either quercetin, a flavonoid with mitochondrial antioxidant properties, or cyclosporine A (CsA), an mPTP inhibitor, and compared with ALDOST alone or untreated, age/sex-matched controls. We monitored mitochondrial free Ca and biomarkers of oxidative stress, including 8-isoprostane and H2O2 production; mPTP opening; total Ca in cardiac tissue; and collagen volume fraction to quantify replacement fibrosis, a biomarker of cardiomyocyte necrosis, and employed terminal deoxynucleotidyl transferase dUTP nick end labeling assay to address apoptosis in coronal sections of ventricular myocardium. Compared with controls, at 4 weeks ALDOST we found a marked increase in mitochondrial H2O2 production and 8-isoprostane levels, an increased propensity for mPTP opening, and greater concentrations of mitochondrial free [Ca]m and total tissue Ca, coupled with a 5-fold rise in collagen volume fraction without any terminal deoxynucleotidyl transferase dUTP nick end labeling-based evidence of cardiomyocyte apoptosis. Each of these pathophysiologic responses to ALDOST was prevented by quercetin or cyclosporine A cotreatment. Thus, mitochondria play a central role in initiating the cellular-subcellular mechanisms that lead to necrotic cell death and myocardial scarring. This destructive cycle can be interrupted and myocardium salvaged with its structure preserved by mitochondria-targeted cardioprotective strategies.

Uncoupling the coupled calcium and zinc dyshomeostasis in cardiac myocytes and mitochondria seen in aldosteronism.

Intracellular [Ca2+]i overloading in cardiomyocytes is a fundamental pathogenic event associated with chronic aldosterone/salt treatment (ALDOST) and accounts for an induction of oxidative stress that leads to necrotic cell death and consequent myocardial scarring. This prooxidant response to Ca2+ overloading in cardiac myocytes and mitochondria is intrinsically coupled to simultaneous increased Zn2+ entry serving as an antioxidant. Herein, we investigated whether Ca2+ and Zn2+ dyshomeostasis and prooxidant to antioxidant dysequilibrium seen at 4 weeks, the pathologic stage of ALDOST, could be uncoupled in favor of antioxidants, using cotreatment with a ZnSO4 supplement; pyrrolidine dithiocarbamate (PDTC), a Zn2+ ionophore; or ZnSO4 in combination with amlodipine (Amlod), a Ca2+ channel blocker. We monitored and compared responses in cardiomyocyte free [Ca2+]i and [Zn2+]i together with biomarkers of oxidative stress in cardiac myocytes and mitochondria. At week 4 of ALDOST and compared with controls, we found (1) an elevation in [Ca2+]i coupled with [Zn2+]i and (2) increased mitochondrial H2O2 production and increased mitochondrial and cardiac 8-isoprostane levels. Cotreatment with the ZnSO4 supplement alone, PDTC, or ZnSO4+Amlod augmented the rise in cardiomyocyte [Zn2+]i beyond that seen with ALDOST alone, whereas attenuating the rise in [Ca2+]i, which together served to reduce oxidative stress. Thus, a coupled dyshomeostasis of intracellular Ca2+ and Zn2+ was demonstrated in cardiac myocytes and mitochondria during 4-week ALDOST, where prooxidants overwhelm antioxidant defenses. This intrinsically coupled Ca2+ and Zn2+ dyshomeostasis could be uncoupled in favor of antioxidant defenses by selectively increasing free [Zn2+]i and/or reducing [Ca2+]i using cotreatment with ZnSO4 or PDTC alone or ZnSO4+Amlod in combination.

The psychosocial effects of deployment on military children.

OBJECTIVE: The impact of the Global War on Terror on two million U.S. military children remains unknown. The purpose of this study was to describe the psychosocial profile of school age children during parental deployment utilizing standardized psychosocial health and stress measures, and to identify predictors of children at "high risk" for psychosocial morbidity during wartime deployment. METHODS: Army spouses with a deployed service member and a child aged 5-12 years completed a deployment packet consisting of demographic and psychosocial questions. The psychosocial health measures included the Pediatric Symptom Checklist (PSC), the Parenting Stress Index-Short Form and the Perceived Stress Scale-4. RESULTS: Overall, 32% of respondents exceeded the PSC cut off score for their child, indicating "high risk" for psychosocial morbidity and 42% reported "high risk" stress on the Parenting Stress Index-Short Form. Parenting stress significantly predicted an increase in child psychosocial morbidity (odds ratio 7.41, confidence interval 2.9-19.0, p < 0.01). Parents utilizing military support reported less child psychosocial morbidity (odds ratio 0.32, confidence interval 0.13-0.77, p < 0.01) and parental college education was related to a decrease in child psychosocial morbidity (odds ratio 0.33, confidence interval 0.13-0.81, p < 0.02). The effects of military rank, child gender, child age, and race or ethnic background did not reach statistical significance. CONCLUSION: Families in this study experiencing deployment identified one-third of military children at "high risk" for psychosocial morbidity. The most significant predictor of child psychosocial functioning during wartime deployment was parenting stress. Military, family and community supports help mitigate family stress during periods of deployment.

Coupled calcium and zinc dyshomeostasis and oxidative stress in cardiac myocytes and mitochondria of rats with chronic aldosteronism.

A dyshomeostasis of extra- and intracellular Ca(2+) and Zn(2+) occurs in rats receiving chronic aldosterone/salt treatment (ALDOST). Herein, we hypothesized that the dyshomeostasis of intracellular Ca(2+) and Zn(2+) is intrinsically coupled that alters the redox state of cardiac myocytes and mitochondria, with Ca(2+) serving as a pro-oxidant and Zn(2+) as an antioxidant. Toward this end, we harvested hearts from rats receiving 4 weeks of ALDOST alone or cotreatment with either spironolactone (Spiro), an aldosterone receptor antagonist, or amlodipine (Amlod), an L-type Ca(2+) channel blocker, and from age/sex-matched untreated controls. In each group, we monitored cardiomyocyte [Ca(2+)]i and [Zn(2+)]i and mitochondrial [Ca(2+)]m and [Zn(2+)]m; biomarkers of oxidative stress and antioxidant defenses; expression of Zn transporters, Zip1 and ZnT-1; metallothionein-1, a Zn(2+)-binding protein; and metal response element transcription factor-1, a [Zn(2+)]i sensor and regulator of antioxidant defenses. Compared with controls, at 4-week ALDOST, we found the following: (a) increased [Ca(2+)]i and [Zn(2+)]i, together with increased [Ca(2+)]m and [Zn(2+)]m, each of which could be prevented by Spiro and attenuated with Amlod; (b) increased levels of 3-nitrotyrosine and 4-hydroxy-2-nonenal in cardiomyocytes, together with increased H(2)O(2) production, malondialdehyde, and oxidized glutathione in mitochondria that were coincident with increased activities of Cu/Zn superoxide dismutase and glutathione peroxidase; and (c) increased expression of metallothionein-1, Zip1 and ZnT-1, and metal response element transcription factor-1, attenuated by Spiro. Thus, an intrinsically coupled dyshomeostasis of intracellular Ca(2+) and Zn(2+) occurs in cardiac myocytes and mitochondria in rats receiving ALDOST, where it serves to alter their redox state through a respective induction of oxidative stress and generation of antioxidant defenses. The importance of therapeutic strategies that can uncouple these two divalent cations and modulate their ratio in favor of sustained antioxidant defenses is therefore suggested.

Potential aluminum exposure from parenteral nutrition in patients with acute kidney injury.

BACKGROUND: Patients' exposure to and potential toxicity from aluminum in parenteral nutrition (PN) formulations is an important concern of healthcare providers. OBJECTIVE: To determine the potential for aluminum toxicity caused by PN in hospitalized adults who have risk factors of both acute kidney injury and PN. METHODS: Adults who required PN and had a serum creatinine (SCr) level at least 1.5 times greater than the admission SCr on the first day of PN were studied in a retrospective fashion. Protein was administered based on whether hemodialysis was being used (0.6-1 g/kg/day without hemodialysis; 1.2-1.5 g/kg/day with hemodialysis). Aluminum exposure was determined for each patient by multiplying the volume of each PN component by its concentration of aluminum. Unpaired t-tests, Fisher's exact test, and analysis of variance were used for statistical analysis. Data are presented as mean +/- SD. RESULTS: Thirty-six patients (aged 50.4 +/- 20.4 y; weight 90.2 +/- 32.8 kg) were studied. Initial serum urea nitrogen and SCr were 47 +/- 23 and 3.3 +/- 1.4 mg/dL, respectively. Twelve patients received hemodialysis. The mean aluminum exposure was 3.8 +/- 2 microg/kg/day in the 36 patients. Of these, 29 had safe calculated aluminum exposure (<5 microg/kg/day) and 7 had high calculated aluminum exposure (>5 microg/kg/day). Patients with safe aluminum exposure had significantly higher SCr levels than did those with high aluminum exposure (3.5 +/- 1.5 vs 2.2 +/- 0.7 mg/dL; p < 0.04). Patients with high aluminum exposure received significantly more aluminum from calcium gluconate compared with those who had safe aluminum exposure (357 +/- 182 vs 250 +/- 56 microg/day; p < 0.02). Limitations of the study include its retrospective design, which resulted in calculated versus direct measurement of aluminum. CONCLUSIONS: Using our calculations, we believe that most patients with acute kidney injury who require PN do not receive excessive exposure to aluminum from the PN formulation, despite having 2 risk factors (acute kidney injury, PN) for aluminum toxicity.

Micronutrients in African-Americans with decompensated and compensated heart failure.

Heart failure is thought to be more common and of greater severity in African-Americans (AAs). Potential mechanisms remain uncertain. The importance of micronutrient deficiencies in the pathophysiologic expression of congestive heart failure (CHF) in AAs remains to be explored, including hypovitaminosis D, which can promote secondary hyperparathyroidism (SHPT), together with hypozincemia and hyposelenemia, the 2 most crucial trace minerals integral to diverse biologic functions. Serum parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), Zn, and Se were monitored in 30 AAs hospitalized during June through December 2005, with decompensated failure and reduced ejection fraction (EF) (<35%) of predominantly nonischemic origin treated with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB), furosemide, and spironolactone. Based on their symptomatic status before hospitalization, 15 patients were stratified as having protracted (>or=4 weeks) CHF, whereas 15 patients had short-term (1-2 weeks) CHF. These hospitalized patients were compared with 10 AA outpatients with stable, similarly treated compensated failure and comparable EF, and 9 AA normal volunteers without cardiovascular disease. Serum PTH was elevated in all patients with protracted CHF and in 60% of patients with short-term CHF, but not in compensated patients or normal volunteers. However, serum 25(OH)D was reduced in all patients with >or=4 weeks and 80% with either 1-2 weeks CHF or compensated failure compared with volunteers. Serum Zn was below normal in 11 of 15 patients with protracted CHF, in 8 of 15 patients with shorter duration CHF, and in 5 of 10 patients with compensated failure. Serum Se was reduced in all patients with >or=4 weeks, 60% with short-term CHF, and 90% of compensated patients. Concomitant to hypovitaminosis D, hypozincemia, and hyposelenemia, SHPT is a covariant of CHF in housebound AAs.