Reliability, construct validity and measurement potential of the ICF comprehensive core set for osteoarthritis

<p>Abstract</p> <p>Background</p> <p>This study aimed to investigate the reliability and construct validity of the International Classification of Functioning, Disability and Health (ICF) Comprehensive Core Set for osteoarthritis (OA) in order to test its possible use as a measuring tool for functioning.</p> <p>Methods</p> <p>100 patients with OA (84 F, 16 M; mean age 63 yr) completed forms including demographic and clinical information besides the Short Form (36) Health Survey (SF-36^®) and the Western Ontario and McMaster Universities Index of Osteoarthritis (WOMAC). The ICF Comprehensive Core Set for OA was filled by health professionals. The internal construct validities of "Body Functions-Body structures" (BF-BS), "Activity" (A), "Participation" (P) and "Environmental Factors" (EF) domains were tested by Rasch analysis and reliability by internal consistency and person separation index (PSI). External construct validity was evaluated by correlating the Rasch transformed scores with SF-36 and WOMAC.</p> <p>Results</p> <p>In each scale, some items showing disordered thresholds were rescored, testlets were created to overcome the problem of local dependency and items that did not fit to the Rasch model were deleted. The internal construct validity of the four scales (BF-BS 16 items, A 8 items, P 7 items, EF 13 items) were good [mean item fit (SD) 0.138 (0.921), 0.216 (1.237), 0.759 (0.986) and -0.079 (2.200); person item fit (SD) -0.147 (0.652), -0.241 (0.894), -0.310 (1.187) and -0.491 (1.173) respectively], indicating a single underlying construct for each scale. The scales were free of differential item functioning (DIF) for age, gender, years of education and duration of disease. Reliabilities of the BF-BS, A, P, and EF scales were good with Cronbach's alphas of 0.79, 0.86, 0.88, and 0.83 and PSI's of 0.76, 0.86, 0.87, and 0.71, respectively. Rasch scores of BF-BS, A, and P showed moderate correlations with SF-36 and WOMAC scores where the EF had significant but weak correlations only with SF36-Social Functioning and SF36-Mental Health.</p> <p>Conclusion</p> <p>Since the four different scales derived from BF-BS, A, P, and EF components of the ICF core set for OA were shown to be valid and reliable through a combination of Rasch analysis and classical psychometric methods, these might be used as clinical assessment tools.</p

Involvement of cell surface TG2 in the aggregation of K562 cells triggered by gluten

Gluten-induced aggregation of K562 cells represents an in vitro model reproducing the early steps occurring in the small bowel of celiac patients exposed to gliadin. Despite the clear involvement of TG2 in the activation of the antigen-presenting cells, it is not yet clear in which compartment it occurs. Herein we study the calcium-dependent aggregation of these cells, using either cell-permeable or cell-impermeable TG2 inhibitors. Gluten induces efficient aggregation when calcium is absent in the extracellular environment, while TG2 inhibitors do not restore the full aggregating potential of gluten in the presence of calcium. These findings suggest that TG2 activity is not essential in the cellular aggregation mechanism. We demonstrate that gluten contacts the cells and provokes their aggregation through a mechanism involving the A-gliadin peptide 31-43. This peptide also activates the cell surface associated extracellular TG2 in the absence of calcium. Using a bioinformatics approach, we identify the possible docking sites of this peptide on the open and closed TG2 structures. Peptide docks with the closed TG2 structure near to the GTP/GDP site, by establishing molecular interactions with the same amino acids involved in stabilization of GTP binding. We suggest that it may occur through the displacement of GTP, switching the TG2 structure from the closed to the active open conformation. Furthermore, docking analysis shows peptide binding with the β-sandwich domain of the closed TG2 structure, suggesting that this region could be responsible for the different aggregating effects of gluten shown in the presence or absence of calcium. We deduce from these data a possible mechanism of action by which gluten makes contact with the cell surface, which could have possible implications in the celiac disease onset

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Renal association clinical practice guideline in post-operative care in the kidney transplant recipient

These guidelines cover the care of patients from the period following kidney transplantation until the transplant is no longer working or the patient dies. During the early phase prevention of acute rejection and infection are the priority. After around 3-6 months, the priorities change to preservation of transplant function and avoiding the long-term complications of immunosuppressive medication (the medication used to suppress the immune system to prevent rejection). The topics discussed include organization of outpatient follow up, immunosuppressive medication, treatment of acute and chronic rejection, and prevention of complications. The potential complications discussed include heart disease, infection, cancer, bone disease and blood disorders. There is also a section on contraception and reproductive issues.Immediately after the introduction there is a statement of all the recommendations. These recommendations are written in a language that we think should be understandable by many patients, relatives, carers and other interested people. Consequently we have not reworded or restated them in this lay summary. They are graded 1 or 2 depending on the strength of the recommendation by the authors, and AD depending on the quality of the evidence that the recommendation is based on