Recovery, empowerment and rehabilitation: Do inpatient psychiatric rehabilitation services empower the individual?

Perceptions of the course and outcome from serious mental illness have changed over the last century and, more recently, the concept of recovery has gained prominence in this field. This paper reviews recent literature on recovery from serious mental illness and discusses both the meaning of the concept and the key contributing factors. Research suggests that empowerment is one of the most salient factors contributing to recovery and the relationship between recovery and empowerment is examined. Most research in the area of empowerment has, to date, focused on community settings and this paper considers the relevance of these ideas in other mental health settings. The relationship between empowerment, recovery and mental health services is discussed. Finally, conclusions are drawn and recommendations for further research are outlined

Influence of TGF-β1 on short- and long-term expansion and senescence.

<p>MSCs were stimulated for 7 days with increasing concentrations of TGF-β1 and proliferation was estimated using the MTT assay (<b>A</b>; n = 5). MSCs were cultured with or without 1 ng/mL TGF-β1 until they stopped proliferation. Cumulative population doublings (cPDs) were calculated throughout culture expansion and depicted by symbols for each passage (<b>B</b>; n = 6). The average culture period until proliferation arrest is shorter if cells are continuously cultured with TGF-β1 (<b>C</b>; n = 6). Comparison of cPDs for the first seven passages for TGF-β1 treated and un-treated MSC revealed a proliferative advantage particularly in the initial three passages (<b>D</b>; n = 6). The maximal cPDs at the time of ultimate proliferation arrest were similar with and without TGF-β1 treatment (<b>E</b>; n = 6). SA-β-gal activity was measured in MSCs cultured either with or without TGF-β1 for 7 passages by histochemical analysis with X-gal staining (<b>E</b>) or flowcytometric analysis of C₁₂FDG (<b>F</b>; n = 3; *p < 0.05; **p < 0.01).</p

Gene expression changes upon TGF-β1 treatment in early and later passages.

<p>Hierarchical clustering of global gene expression profiles (Euclidean distance) revealed inter-donor variation, a close relationship of early and late passages, and continuous changes with TGF-β1 stimulation (<b>A</b>). This was also reflected by principal component analysis (<b>B</b>; components 1 [PC1] and 2 [PC2] are depicted). TGF-β1-induced gene expression changes were compared in MSCs of early passage (P3 - P5) and later passage (P10) upon stimulation for either 1, 4, or 12 hours. Some genes are predominantly induced in early passage (depicted in blue) or in late passage (depicted in red) but the induced gene expression changes were overall very similar in MSCs of early and later passage (<b>C</b>). </p

Effect of TGF-β1 on senescence-associated DNA-methylation signature.

<p>MSCs were cultured for three passages either with or without TGF-β1. Then the state of cellular senescence was tracked using our recently described Epigenetic-Senescence-Signature which is based on DNA-methylation (DNAm) changes at six specific CpG sites in the genome [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077656#B35" target="_blank">35</a>,<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077656#B36" target="_blank">36</a>]. Predicted passage numbers and real passage numbers correlated well for controls, whereas the passage number was significantly overestimated for TGF-β1 treated cells (<b>A</b>; *p < 0.05). Comparison of predicted and real cumulative population doublings (cPDs) reflected the proliferative advantage with TGF-β1. Overall, the number of cPDs was slightly overestimated by the Epigenetic-Aging-Signature but this cannot be attributed to TGF-β1 stimulation (<b>B</b>). Symbols represent different MSC preparations that were cultured with (black color) or without TGF-β1 (grey color).</p

Additional file 5: of Clinical, biochemical and genetic spectrum of 70 patients with ACAD9 deficiency: is riboflavin supplementation effective?

Figure S1. Representative picture of Complex I assembly in fibroblasts of individual 1 (A, upper panels) Two-dimensional BN/SDS-PAGE separation and quantification of fluorescent-labelled mitochondrial complexes from 10 mg patient (left) and control fibroblasts (right) are shown. (A, lower panels) show silver stained 2 D gels. (B) Quantified Supercomplexes in 2D gels from control and patient fibroblast with and without bezafibrate treatment for 72 h. (C) Panoramaplots of 2D gels with assignment of signals used for quantification of complexes. Assignment of complexes: O, OGDC, oxoglutarate dehydrogenase complex; V, complex V or ATP synthase; III, complex III or cytochrome c reductase; IV, complex IV or cytochrome c oxidase; S, supercomplexes composed of respiratory chain complexes I, III, and IV. 2-D gels were scanned side by side for direct comparison and are shown as pseudocolors. (pdf). (PDF 1109 kb

Additional file 4: of Clinical, biochemical and genetic spectrum of 70 patients with ACAD9 deficiency: is riboflavin supplementation effective?

Table S3. Clinical characteristics of the 67 patients present in this study (DOCX 72 kb