[Social and Economic Consequences of Night-Time Aircraft Noise in the Vicinity of Frankfurt/Main Airport.]

[Social and Economic Consequences of Night-Time Aircraft Noise in the Vicinity of Frankfurt/Main Airport.]

Gesundheitswesen. 2013 Mar 1;
Greiser E, Glaeske G

A prospective calculation of disease-related social and economic costs due to night-time aircraft noise in the vicinity of Frankfurt/Main airport was performed for the calendar years 2012-2021. It was based on risk estimates for a variety of diagnostic entities (cardiovascular disease, depression, psychosis, diabetes mellitus, dementia and Alzheimer’s disease, all cancers except malignancies of the respiratory system) from a previous case-control study on more than 1 million persons enrolled in compulsory sickness funds in the vicinity of the Cologne-Bonn airport, on disease-related cost estimates performed by the German Federal Statistical Office for the calender years 2002-2008, and calculations of the population exposed to night-time aircraft noise in the vicinity of Frankfurt/Main airport (2005 aircraft routes and flight frequencies). Total estimated costs came to more than 1.5 billion € with an excess of 23 400 cases of diseases treated in hospitals and of 3 400 subsequent deaths. HubMed – depression


Chronic degeneration of dorsal raphe serotonergic neurons modulates cortical spreading depression: A possible pathophysiology of migraine.

J Neurosci Res. 2013 Mar 4;
Cui Y, Li QH, Yamada H, Watanabe Y, Kataoka Y

The vascular serotonergic system in the brain has been implicated in the pathophysiology of migraine, however, involvement of the serotonergic nervous system of the brain parenchyma in the pathophysiology remains unclear. To investigate whether the brain parenchymal serotonergic nervous system is involved in the etiology of migraine, we prepared an experimental model of migraine by generation of cortical spreading depression (SD), characterized by spreading of neuronal/glial membrane depolarization accompanied by temporal elevation of the cerebral blood flow (CBF) throughout the cerebral cortical hemisphere in rats, which underwent pharmacological treatment for degeneration of serotonergic neurons in the dorsal raphe nucleus. We show here that 1) significant degeneration of serotonergic neurons in the dorsal raphe nucleus and serotonergic fibers in the cerebral cortex was observed in treated rats, 2) spreading velocity of the CBF changes was significantly increased in these rats, and 3) calculated width of the depolarization wave was significantly extended in these rats. These results indicate that the dorsal raphe serotonergic neurons modulate cortical spreading depression and might be involved in migraine pathology via a similar mechanism. © 2013 Wiley Periodicals, Inc. HubMed – depression


Evaluating Effects of EPO in Rodent Behavioral Assays Related to Depression.

Methods Mol Biol. 2013; 982: 127-40
Duman CH, Newton SS

The cytokine erythropoietin (EPO) is an important regulator of hematopoesis and has well-known tissue protective properties. Neurotrophic action is implicated as mechanistically important in the treatment of depression, and neurotrophic actions of EPO suggest potential therapeutic utility of an EPO-like mechanism in depressive disorder. Rodent behavioral models that are responsive to clinically used antidepressants as well as to neurotrophic compounds can be used to assess potential antidepressant properties of EPO and EPO-like compounds. Rodent models described here are the forced-swim test (FST), a hyponeophagia test and the novel object recognition test. Each of these models provides different information and relevance to depression and each can be tested with EPO and similar compounds. HubMed – depression


Augmentation with atypical antipsychotics for depression: a review of evidence-based support from the medical literature.

Pharmacotherapy. 2013 Mar; 33(3): 344-59
Wright BM, Eiland EH, Lorenz R

Major depressive disorder (MDD) is a chronic mental illness that affects an estimated 5-26% of adults at some time in their lives. Treatment is often started as pharmacotherapy using a single drug such as a selective serotonin reuptake inhibitor. If a patient fails to respond adequately to the initial antidepressant, typically three pharmacotherapy options are available to the practitioner. The dose of the current therapy can be maximized, a change can be made to a different drug, or the current regimen can be augmented with another drug. Atypical antipsychotics have recently become a major focus for augmentation of traditional antidepressant therapy. This review summarizes the evidence for efficacy and safety of augmenting treatment-refractory or treatment-resistant depression with atypical antipsychotics. The National Library of Medicine’s MEDLINE database was searched for all English-language articles published from January 1966-December 2011 describing the use of atypical antipsychotics in treatment-resistant depression. The literature retrieved was limited to case series, open-label trials, and randomized controlled trials (RCT). Studies of bipolar depression, psychotic depression, or studies conducted in children and adolescents were excluded. Thirty-five studies using atypical antipsychotics for augmentation treatment of depression were included in this analysis. Trials were identified for aripiprazole (six open-label; three RCT), clozapine (one case series), olanzapine (three open-label, including two case series; four RCT), quetiapine (four open-label; five RCT), risperidone (two open-label; five RCT), and ziprasidone (two open-label). The atypical antipsychotics may be effective as adjunctive therapy in MDD; however, their adverse effect profile may be unfavorable to some patients. Trying at least one alternative treatment strategy after an initial antidepressant is indicated before augmentation is implemented with these agents. If atypical antipsychotics are used, safety and efficacy should be frequently reassessed and dosage should be individualized. HubMed – depression