Epidemiology of eating disorders part III: Social epidemiology and case definitions revisited.

Accepted manuscript version. Published version at <a href=http://doi.org/10.1080/21662630.2015.1022197>http://doi.org/10.1080/21662630.2015.1022197</a>.The previous papers in this series outlined a historical panorama and presented updated knowledge about putative risk factors and how eating disorders are distributed in various populations. In this final paper, we discuss in what way comorbidity findings and transdiagnostic issues may change our conceptions about ‘an epidemiological case’ from the current definition of eating disorders based on the recent version of the Diagnostic and Statistical Manual of Mental Disorders (i.e. the DSM-5), and to what extent an alternative definition may introduce new perspectives of prevention. The paper also provides an update on issues relevant for treatment dissemination

Quantitative Phosphoproteomic Analysis of Signaling Downstream of the Prostaglandin E2/G-Protein Coupled Receptor in Human Synovial Fibroblasts: Potential Antifibrotic Networks

The Prostaglandin E2 (PGE₂) signaling mechanism within fibroblasts is of growing interest as it has been shown to prevent numerous fibrotic features of fibroblast activation with limited evidence of downstream pathways. To understand the mechanisms of fibroblasts producing tremendous amounts of PGE₂ with autocrine effects, we apply a strategy of combining a wide-screening of PGE₂-induced kinases with quantitative phosphoproteomics. Our large-scale proteomic approach identified a PKA signal transmitted through phosphorylation of its substrates harboring the R­(R/X)­X­(S*/T*) motif. We documented 115 substrates, of which 72 had 89 sites with a 2.5-fold phosphorylation difference in PGE₂-treated cells than in untreated cells, where approximately half of such sites were defined as being novel. They were compiled by networking software to focus on highlighted activities and to associate them with a functional readout of fibroblasts. The substrates were associated with a variety of cellular functions including cytoskeletal structures (migration/motility), regulators of G-protein coupled receptor function, protein kinases, and transcriptional/translational regulators. For the first time, we extended the PGE₂ pathway into an elaborate network of interconnecting phosphoproteins, providing vital information to a once restricted signalosome. These data provide new insights into eicosanoid-initiated cell signaling with regards to the regulation of fibroblast activation and the identification of new targets for evidenced-based pharmacotherapy against fibrosis

Inhibition of collagen cleavage by prostaglandin E(PGE) and transforming growth factor (TGF)-β2

<p><b>Copyright information:</b></p><p>Taken from "Prostaglandin PGEat very low concentrations suppresses collagen cleavage in cultured human osteoarthritic articular cartilage: this involves a decrease in expression of proinflammatory genes, collagenases and , a gene linked to chondrocyte hypertrophy"</p><p>http://arthritis-research.com/content/9/4/R75</p><p>Arthritis Research & Therapy 2007;9(4):R75-R75.</p><p>Published online 7 Aug 2007</p><p>PMCID:PMC2206385.</p><p></p> The effect of 5 ng/ml TGF-β2 and PGEat various concentrations (1 pg to 10 ng/ml) on collagen cleavage in human osteoarthritic (OA) explants from patients of indicated age and gender; means ± SDs for all four patients; inhibition of type II collagen cleavage by collagenase in human OA articular explants by 10 pg/ml PGE; concentration relationship between PGEin control cultures and collagen cleavage. The average medium levels of PGEin the dose-dependent studies were as follows: 6.3 ± 1.2 pg/ml for the 77-year-old female (a); 13.9 ± 4.1 pg/ml for the 50-year-old female (b); 7.8 ± 2.1 pg/ml for the 66-year-old male (c); and 61.6 ± 7.6 pg/ml for the 82-year-old female (d). (f) Thirteen OA articular cartilage explants were cultured with (10 pg/ml PGE) or without (control) for 16 days and collagen cleavage was evaluated by the accumulation of C1,2C neoepitope in the medium and chymotrypsin-derived cartilage extracts. (g) The relationship between PGEconcentration and collagen cleavage in 16 OA explants that served as controls. Significant differences from the control (< 0.05) are indicated by asterisks

PGEdownregulates the expression of genes responsible for collagen cleavage, chondrocyte hypertrophy and inflammation

<p><b>Copyright information:</b></p><p>Taken from "Prostaglandin PGEat very low concentrations suppresses collagen cleavage in cultured human osteoarthritic articular cartilage: this involves a decrease in expression of proinflammatory genes, collagenases and , a gene linked to chondrocyte hypertrophy"</p><p>http://arthritis-research.com/content/9/4/R75</p><p>Arthritis Research & Therapy 2007;9(4):R75-R75.</p><p>Published online 7 Aug 2007</p><p>PMCID:PMC2206385.</p><p></p> Relative expression with reference to glyceraldehyde-3-phosphate dehydrogenase is shown compared with controls for genes in osteoarthritic cartilages determined by real-time PCR analyses in explant cultures at 24 hours cultured in the presence or absence (control) of 10 pg/ml prostaglandin E(PGE). Control bars are shown as 1.0 as required for relative quantification with the real-time PCR protocol. Means ± SD for all five patients are shown in . Asterisks indicate significant differences from the control (< 0.05). The age and sex of each patient are indicated. The average levels of PGEin the medium in the gene expression studies were as follows: 62.3 ± 6.1 pg/ml for the 66-year-old female (a); 7.2 ± 1.9 pg/ml for the 53-year-old female (b); 0 pg/ml for the 67-year-old female (c); 65.7 ± 7.3 pg/ml for the 90-year-old female (d); and 30.4 ± 7.6 pg/ml for the 82-year-old female (e)

The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells-3

<p><b>Copyright information:</b></p><p>Taken from "The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells"</p><p>http://www.biomedical-engineering-online.com/content/6/1/33</p><p>BioMedical Engineering OnLine 2007;6():33-33.</p><p>Published online 6 Sep 2007</p><p>PMCID:PMC2018722.</p><p></p>aces. GAPDH was used as housekeeping gene and served to normalize the results. Agarose gels are representative of 5 experiments. Quantitative results are the mean ± standard error of these five experiments. * p < 0.05 vs. PS control

The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells-0

<p><b>Copyright information:</b></p><p>Taken from "The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells"</p><p>http://www.biomedical-engineering-online.com/content/6/1/33</p><p>BioMedical Engineering OnLine 2007;6():33-33.</p><p>Published online 6 Sep 2007</p><p>PMCID:PMC2018722.</p><p></p>aces. GAPDH was used as housekeeping gene and served to normalize the results. Agarose gels are representative of 5 experiments. Quantitative results are the mean ± standard error of these five experiments. * p < 0.05 vs. PS control

The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells-1

<p><b>Copyright information:</b></p><p>Taken from "The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells"</p><p>http://www.biomedical-engineering-online.com/content/6/1/33</p><p>BioMedical Engineering OnLine 2007;6():33-33.</p><p>Published online 6 Sep 2007</p><p>PMCID:PMC2018722.</p><p></p>aces. GAPDH was used as housekeeping gene and served to normalize the results. Agarose gels are 0 standard error of these five experiments. * p < 0.05 vs. PS control

The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells-2

<p><b>Copyright information:</b></p><p>Taken from "The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells"</p><p>http://www.biomedical-engineering-online.com/content/6/1/33</p><p>BioMedical Engineering OnLine 2007;6():33-33.</p><p>Published online 6 Sep 2007</p><p>PMCID:PMC2018722.</p><p></p>aces. GAPDH was used as housekeeping gene and served to normalize the results. Agarose gels are representative of 5 experiments. Quantitative results are the mean ± standard error of these five experiments. * p < 0.05 vs. PS control