Antibody signatures in patients with histopathologically defined multiple sclerosis patterns

Early active multiple sclerosis (MS) lesions can be classified histologically into three main immunopathological patterns of demyelination (patterns I-III), which suggest pathogenic heterogeneity and may predict therapy response. Patterns I and II show signs of immune-mediated demyelination, but only pattern II is associated with antibody/complement deposition. In pattern III lesions, which include Baló's concentric sclerosis, primary oligodendrocyte damage was proposed. Serum antibody reactivities could reflect disease pathogenesis and thus distinguish histopathologically defined MS patterns. We established a customized microarray with more than 700 peptides that represent human and viral antigens potentially relevant for inflammatory demyelinating CNS diseases, and tested sera from 66 patients (pattern I n = 12; II n = 29; III n = 25, including 8 with Baló's), healthy controls, patients with Sjögren's syndrome and stroke patients. Cell-based assays were performed for aquaporin 1 (AQP1) and AQP4 antibody detection. No single peptide showed differential binding among study cohorts. Because antibodies can react with different peptides from one protein, we also analyzed groups of peptides. Patients with pattern II showed significantly higher reactivities to Nogo-A peptides as compared to patterns I (p = 0.02) and III (p = 0.02). Pattern III patients showed higher reactivities to AQP1 (compared to pattern I p = 0.002, pattern II p = 0.001) and varicella zoster virus (VZV, compared to pattern II p = 0.05). In patients with Baló's, AQP1 reactivity was also significantly higher compared to patients without Baló's (p = 0.04), and the former revealed distinct antibody signatures. Histologically, Baló's patients showed loss of AQP1 and AQP4 in demyelinating lesions, but no antibodies binding conformational AQP1 or AQP4 were detected. In summary, higher reactivities to Nogo-A peptides in pattern II patients could be relevant for enhanced axonal repair and remyelination. Higher reactivities to AQP1 peptides in pattern III patients and its subgroup of Baló's patients possibly reflect astrocytic damage. Finally, latent VZV infection may cause peripheral immune activation

A discharge summary adapted to the frail elderly to ensure transfer of relevant information from the hospital to community settings: a model

<p>Abstract</p> <p>Background</p> <p>Elderly patients admitted to Geriatric Assessment Units (GAU) typically have complex health problems that require multi-professional care. Considering the scope of human and technological resources solicited during hospitalization, as well as the many risks and discomforts incurred by the patient, it is important to ensure the communication of pertinent information for quality follow-up care in the community setting. Conventional discharge summaries do not adequately incorporate the elements specific to an aging clientele.</p> <p>Objective</p> <p>To develop a discharge summary adapted to the frail elderly patient (D-SAFE) in order to communicate relevant information from hospital to community services.</p> <p>Methods</p> <p>The items to be included in the D-SAFE have been determined by means of a modified Delphi method through consultation with clinical experts from GAUs (11 physicians and 5 pharmacists) and the community (10 physicians and 5 pharmacists). The consensus analysis and the level of agreement among the experts were reached using a modified version of the RAND^®/University of California at Los Angeles appropriateness method.</p> <p>Results</p> <p>A consensus was reached after two rounds of consultation for all the items evaluated, where none was judged «inappropriate». Among the items proposed, four were judged to be « uncertain » and were eliminated from the final D-SAFE, which was divided into two sections: the medical discharge summary (22 main items) and the discharge prescription (14 main items).</p> <p>Conclusions</p> <p>The D-SAFE was developed as a more comprehensive tool specifically designed for GAU inpatients. Additional research to validate its acceptability and practical impact on the continuity of care is needed before it can be recommended for use on a broader scale.</p

Quality control and calibration of the ZEUS forward and rear calorimeters with 60Co\mathrm{^{60}Co} sources

We present the motivation for and the design of a mobile $^{60}Co$ source system used as part of the quality control and calibration monitoring scheme for the ZEUS calorimeters. A 2 mCi $^{60}Co$ source is pushed by a computer controlled drive mechanism through guide tubes which extend into the calorimeter. Measurements of induced photocurrents as a function of the source position allow checks on the calorimeter response. We present results obtained during the initial scan of all 916 towers of the forward and rear calorimeter modules

Differences between hospitals in attainment of parathyroid hormone treatment targets in chronic kidney disease do not reflect differences in quality of care

Contains fulltext : 110897.pdf (publisher's version ) (Open Access)ABSTRACT: BACKGROUND: Transparency in quality of care (QoC) is stimulated and hospitals are compared and judged on the basis of indicators of performance on specific treatment targets. In patients with chronic kidney disease, QoC differed significantly between hospitals. In this analysis we explored additional parameters to explain differences between centers in attainment of parathyroid hormone (PTH) treatment targets. METHODS: Using MASTERPLAN baseline data, we selected one of the worst (center A) and one of the best (center B) performing hospitals. Differences between the two centers were analyzed from the year prior to start of the MASTERPLAN study until the baseline evaluation. Determinants of PTH were assessed. RESULTS: 101 patients from center A (median PTH 9.9 pmol/l, in 67 patients exceeding recommended levels) and 100 patients from center B (median PTH 6.5 pmol/l, in 34 patients exceeding recommended levels), were included. Analysis of clinical practice did not reveal differences in PTH management between the centers. Notably, hyperparathyroidism resulted in a change in therapy in less than 25% of patients. In multivariate analysis kidney transplant status, MDRD-4, and treatment center were independent predictors of PTH. However, when MDRD-6 (which accounts for serum urea and albumin) was used instead of MDRD-4, the center effect was reduced. Moreover, after calibration of the serum creatinine assays treatment center no longer influenced PTH. CONCLUSIONS: We show that differences in PTH control between centers are not explained by differences in treatment, but depend on incomparable patient populations and laboratory techniques. Therefore, results of hospital performance comparisons should be interpreted with great caution