School-Based Interventions for Depression and Anxiety in Children and Adolescents.

School-based interventions for depression and anxiety in children and adolescents.

Evid Based Ment Health. 2013 Apr 11;
Stallard P

HubMed – depression

 

Cost-effectiveness of depression case management in small practices.

Br J Psychiatry. 2013 Apr 11;
Gensichen J, Petersen JJ, Von Korff M, Heider D, Baron S, König J, Freytag A, Krauth C, Gerlach FM, König HH

BACKGROUND: Case management undertaken by healthcare assistants in small primary care practices is effective in improving depression symptoms and adherence in patients with major depression. AIMS: To evaluate the cost-effectiveness of depression case management by healthcare assistants in small primary care practices. METHOD: Cost-effectiveness analysis on the basis of a pragmatic randomised controlled trial (2005-2008): practice-based healthcare assistants in 74 practices provided case management to 562 patients with major depression over 1 year. Our primary outcome was the incremental cost-effectiveness ratio (ICER) calculated as the ratio of differences in mean costs and mean number of quality-adjusted life-years (QALYs). Our secondary outcome was the mean depression-free days (DFDs) between the intervention and control group at 24-month follow-up. The study was registered at the International Standard Randomised Controlled Trial Number Registry: ISRCTN66386086. RESULTS: Intervention v. control group: no significant difference in QALYs; significantly more DFDs (mean: 373 v. 311, P<0.01); no significant difference in mean direct healthcare costs (€4495 v. €3506, P = 0.16); considerably lower mean indirect costs (€5228 v. €7539, P = 0.06), resulting in lower total costs (€9723 v. €11 045, P = 0.41). The point estimate for the cost-utility ratio was €38 429 per QALY gained if only direct costs were considered, and 'dominance' of the intervention if total costs were considered. Yet, regardless of decision makers' willingness to pay per QALY, the probability of the intervention being cost-effective was never above 90%. CONCLUSIONS: In small primary care practices, 1 year of case management did not increase the number of QALYs but it did increase the number of DFDs. The intervention was likely to be cost-effective. HubMed – depression

 

Norepinephrine transporter A457P knock-in mice display key features of human postural orthostatic tachycardia syndrome.

Dis Model Mech. 2013 Apr 4;
Shirey-Rice JK, Klar R, Fentress HM, Redmon SN, Sabb TR, Krueger JJ, Wallace NM, Appalsamy M, Finney C, Lonce S, Diedrich A, Hahn MK

Postural orthostatic tachycardia syndrome (POTS) is a common autonomic disorder of largely unknown etiology that presents with sustained tachycardia on standing, syncope, and elevated norepinephrine spillover. Some POTS patients experience anxiety, depression and cognitive dysfunction. Previously, we identified a mutation, A457P, in the norepinephrine (NE) transporter (NET, SLC6A2) in POTS patients. NET is expressed at presynaptic sites in NE neurons and plays a critical role in regulating NE signaling and homeostasis through NE reuptake into noradrenergic nerve terminals. Our in vitro studies demonstrate that A457P reduces both NET surface trafficking and NE transport and exerts a dominant-negative impact on wild-type NET proteins. Here we report the generation and characterization of NET A457P mice, demonstrating the ability of A457P to drive the POTS phenotype and behaviors consistent with reported comorbidities. Mice carrying one A457P allele (NET(+/P)) exhibited reduced brain and sympathetic NE transport levels compared to wild-type (NET(+/+)) mice, whereas transport activity in mice carrying two A457P alleles (NET(P/P)) was nearly abolished. NET(+/P) and NET(P/P) mice exhibited elevations in plasma and urine NE levels, reduced DHPG, and reduced DHPG/NE ratios, consistent with a decrease in sympathetic nerve terminal NE reuptake. Radiotelemetry in unanesthetized mice revealed tachycardia in NET(+/P) mice without a change in blood pressure or baroreceptor sensitivity, consistent with studies of human NET A457P carriers. NET(+/P) mice also demonstrated behavioral changes consistent with CNS NET dysfunction. Our findings support that NET dysfunction is sufficient to produce a POTS phenotype and introduces the first genetic model suitable for more detailed mechanistic studies of the disorder and its comorbidities. HubMed – depression

 


 

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