Background: The prognosis of stroke patients admitted to intensive care units (ICU) is commonly regarded to be poor. However, only limited data regarding outcome predictors are available. Patients and Methods: Out of 4,958 consecutive patients admitted to our stroke unit with the diagnosis of acute stroke, after analysis we identified 347 patients (164 male) in need of ICU management. In-hospital and post-rehabilitation mortality as well as functional outcome at discharge and after rehabilitation were analyzed. Results: Ischemic stroke was diagnosed in 252 patients (72.6%) and intracerebral hemorrhage occurred in 95 patients (27.4%). The mean age in our cohort was considerably high (70.8 years). One hundred patients were comatose at admission. The median NIHSS score at admission in the remaining patients was 12. Apart from stroke-related disturbances of consciousness (47.1%), the most common reasons for ICU treatment were cardiac (23.4%) and respiratory (12.1%) complications or interventional procedures requiring mechanical ventilation (11%). In all, 231/347 patients (66.6%) were mechanically ventilated (mean 84 h). In-hospital mortality (143/347; 41.2%) was associated with old age, poor NIHSS score at admission, intracerebral hemorrhage and mechanical ventilation (p < 0.001 in all). Further, admission to ICU because of stroke-related impairment of consciousness increased in-hospital mortality (p < 0.001). Similarly, poor outcome after rehabilitation was associated with old age (p = 0.029) and mechanical ventilation (p < 0.001). In patients ≥80 years with either intracerebral hemorrhage or need of mechanical ventilation, outcome was unfavorable in nearly any case. However, the overall post-rehabilitation outcome did not differ between patients with intracerebral hemorrhage and ischemic stroke (p = 0.275). Conclusion: The stroke population in our study was associated with an increased early mortality; however, given the same conditions, it was old with a high percentage of patients requiring mechanical ventilation. This did not result in increased in-hospital mortality rates compared to younger and less severely affected cohorts. Thus, ICU management is a life-saving initiative even among the elderly. However, the functional outcome was poor in older patients, thus limiting the benefits of ICU care in these patients.
Synaptic vesicle proteins (SVP) play a critical role in neurotransmitter release and neural plasticity, and have been implicated in the pathophysiology of psychiatric disorders such as depression. Antidepressant drugs not only alter the level of neurotransmitters, but also modulate de novo gene transcription and synthesis of proteins involved in neural plasticity. In order to investigate the effects of antidepressant compounds on SVP-mRNA levels, the expressions of synaptophysin, synaptotagmin, VAMP, and synapsin-I were analysed by in situ hybridization in rats which had been treated with desipramine, fluoxetine, tranylcypromine, or saline. The results demonstrate that chronic treatment with fluoxetine and tranylcypromine leads to an increased expression of synaptophysin, but decreased expression of synaptotagmin and VAMP in the hippocampus and cerebral cortex. Additionally, synapsin ImRNA levels in the hippocampus and cerebral cortex are significantly reduced in tranylcypromine-treated animals. This identifies SVP genes as target genes of antidepressant treatment. Keywords: depression; psychopharmacology; psychosis; SSRI; synapsin; synaptophysin INTRODUCTION Synaptic vesicle proteins (SVP) such as synapsin I-III, synaptophysin, synaptotagmin, and synaptobrevin (VAMP -vesicle-associated membrane protein) play a critical role in synaptic plasticity, and are required for vesicle fusion and neurotransmitter release. [1][2][3][4][5][6] Hence, changes in the expression of these proteins may contribute to the molecular effects of antidepressant treatment and associated behavioral and cognitive alterations. Previous studies have shown that antidepressants modulate de novo gene transcription and synthesis of proteins involved in neural and synaptic plasticity; in a recent transcriptomic study, a decreased expression of VAMP was found with imipramine and sertraline. 7 In order to investigate the effects of antidepressant compounds on synaptic plasticity, the expression of SVP was analysed by in situ hybridization in rats which had been treated with desipramine, fluoxetine, tranylcypromine, or saline (control group) for 2 weeks.
Disturbance of synaptic transmission is currently viewed as an important pathophysiological mechanism and therapeutic target of mood disorders. Amongst other lines of evidence this theory is based on human post-mortem investigations showing differential expression of complexins. In order to discriminate between molecular correlates of the disease itself and effects of psychotropic drugs given to patients, we performed an animal trial using subchronic antidepressant treatment. Cohorts of adult male Sprague-Dawley rats were treated over a period of 14 days with intraperitoneal injections of either saline (0.9%, n=8), desipramine (15 mg/kg, n=7), fluoxetine (10 mg/kg, n=8), or tranylcypromine (10 mg/kg, n=5). Brain slices were used for in situ hybridizations with 35S labelled RNA probes of the genes complexin I, complexin II and syntaxin 1 A, the SNARE complex protein interacting with the complexins, and assessed semi-quantitatively for region-specific expression levels. Expression of complexin I was induced only in habenular nuclei after treatment with fluoxetine. In contrast, complexin II was significantly induced by desipramine and tranylcypromine, but not fluoxetine, in several brain regions. All treatment groups, but most significantly fluoxetine-treated animals, showed higher expression levels of syntaxin 1A. Antidepressants differentially affect expression levels of complexin I and more prominently complexin II and syntaxin 1A. The induction of complexin II and syntaxin 1A might strengthen the synaptic transmission at axo-dendritic or axo-axonal synapses. Previous post-mortem findings reporting on downregulation of complexins cannot be explained as mere effects of psychotropic drug treatment.
Public health challenges such as physical inactivity are multiplex and cannot be effectively addressed by single organizations or sectors. For this reason, public health policies have to involve various sectors and foster partnerships among organizations. Social network analysis (SNA) provides a methodological toolkit that enables the investigation of relationships between organizations to reveal information about the structure and cooperation within networks. This systematic review provides an overview of studies utilizing SNA to analyze the structure of networks that promote physical activity, including the structural set-up, types, and conditions of cooperation, the existence or absence of key actors, the characteristics of organizations working together, and potential barriers limiting collaboration. In total, eight eligible studies were identified. To evaluate the quality of these studies, a quality assessment tool for SNA was created. Relevant aspects from each study were systematically outlined using a data extraction template developed for network studies. The studies reported low to moderate density scores with many ties not being realized. Organizations tend to work side by side than as real partners, whereas organizations of the same type are more strongly connected. Most of the studies identified governmental health organizations as key players in their networks. Network maturity influences network outcomes. Shared goals and geographic proximity are potential facilitators for network development. For future research, more sophisticated methods and longitudinal studies are required to describe how networks, with the aim of promoting physical activity, develop and change to identify predicting factors for an effective network structure.
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