Cluster Lenses

Clusters of galaxies are the most recently assembled, massive, bound structures in the Universe. As predicted by General Relativity, given their masses, clusters strongly deform space-time in their vicinity. Clusters act as some of the most powerful gravitational lenses in the Universe. Light rays traversing through clusters from distant sources are hence deflected, and the resulting images of these distant objects therefore appear distorted and magnified. Lensing by clusters occurs in two regimes, each with unique observational signatures. The strong lensing regime is characterized by effects readily seen by eye, namely, the production of giant arcs, multiple-images, and arclets. The weak lensing regime is characterized by small deformations in the shapes of background galaxies only detectable statistically. Cluster lenses have been exploited successfully to address several important current questions in cosmology: (i) the study of the lens(es) - understanding cluster mass distributions and issues pertaining to cluster formation and evolution, as well as constraining the nature of dark matter; (ii) the study of the lensed objects - probing the properties of the background lensed galaxy population - which is statistically at higher redshifts and of lower intrinsic luminosity thus enabling the probing of galaxy formation at the earliest times right up to the Dark Ages; and (iii) the study of the geometry of the Universe - as the strength of lensing depends on the ratios of angular diameter distances between the lens, source and observer, lens deflections are sensitive to the value of cosmological parameters and offer a powerful geometric tool to probe Dark Energy. In this review, we present the basics of cluster lensing and provide a current status report of the field.Comment: About 120 pages - Published in Open Access at: http://www.springerlink.com/content/j183018170485723/ . arXiv admin note: text overlap with arXiv:astro-ph/0504478 and arXiv:1003.3674 by other author

Agreement, reliability and validity in 3 shoulder questionnaires in patients with rotator cuff disease

Background Self-report questionnaires play an important role as outcome measures in shoulder research. Having an estimate of the measurement error of these questionnaires is of importance when assessing follow-up results after treatment and when planning intervention studies. The aim of this study was to cross-culturally adapt the Norwegian version of the OSS and WORC questionnaire and examine and compare agreement, reliability and construct validity of the disease-specific shoulder questionnaire WORC with two commonly used shoulder questionnaires, SPADI and OSS, in patients with rotator cuff disease. Methods 74 patients with rotator cuff disease were recruited from the outpatient clinic of the Physical Medicine and Rehabilitation Department at Ullevaal University Hospital in Oslo, Norway. A test-retest design was used, and the questionnaires were filled out by the patients at the clinic, with a one week interval between test administrations. Agreement (repeatability coefficient), reliability (ICC) and construct validity were examined and compared for WORC, SPADI and OSS. Results Reliability analysis was restricted to the 55 patients (51 ± 10 yrs) who reported no change between test administrations according to scoring on a global scale. The agreement, reliability and construct validity was moderate for all three questionnaires with ICC ranging from 0.83 to 0.85, repeatability coefficient from 16.1 to 19.7 and Spearman rank correlations between total scores from r = 0.57 to 0.69. There was a lower degree of floor and ceiling effects in SPADI compared to WORC and OSS. Conclusion We conclude that the agreement and reliability of the three shoulder questionnaires examined, WORC index, SPADI and OSS are acceptable and that differences between scores were small. The Norwegian version of the questionnaires is acceptable for assessing Norwegian-speaking patients with rotator cuff disease. The moderate agreement and construct validity should be taken into consideration when assessing follow-up results after treatment and in the planning of prospective studies

Factor structure of the Shoulder Pain and Disability Index in patients with adhesive capsulitis

<p>Abstract</p> <p>Background</p> <p>The Shoulder Pain and Disability Index (SPADI) is a self-administered questionnaire that aims to measure pain and disability associated with shoulder disease. It consists of a pain section and a disability section with 13 items being responded to on visual analogue scales. Few researchers have investigated SPADI validity in specified diagnostic groups, although the selection of an evaluative instrument should be based on evidence of validity in the target patient group. The aim of the present study was to investigate factor structure of the SPADI in a study population of patients with adhesive capsulitis.</p> <p>Methods</p> <p>The questionnaire was administered to 191 patients with adhesive capsulitis. Descriptive statistics for items and a comparison of scores for the two subscales were produced. Internal consistency was analyzed by use of the Cronbach alpha and a principal components analysis with varimax rotation was conducted. Study design was cross-sectional.</p> <p>Results</p> <p>Two factors were extracted, but the factor structure failed to support the original division of items into separate pain and disability sections.</p> <p>Conclusion</p> <p>We found minimal evidence to justify the use of separate subscales for pain and disability. It is our impression that the SPADI should be viewed as essentially unidimensional in patients with adhesive capsulitis.</p

ANCA-associated vasculitis.

The anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAVs) are a group of disorders involving severe, systemic, small-vessel vasculitis and are characterized by the development of autoantibodies to the neutrophil proteins leukocyte proteinase 3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA). The three AAV subgroups, namely granulomatosis with polyangiitis (GPA), microscopic polyangiitis and eosinophilic GPA (EGPA), are defined according to clinical features. However, genetic and other clinical findings suggest that these clinical syndromes may be better classified as PR3-positive AAV (PR3-AAV), MPO-positive AAV (MPO-AAV) and, for EGPA, by the presence or absence of ANCA (ANCA+ or ANCA-, respectively). Although any tissue can be involved in AAV, the upper and lower respiratory tract and kidneys are most commonly and severely affected. AAVs have a complex and unique pathogenesis, with evidence for a loss of tolerance to neutrophil proteins, which leads to ANCA-mediated neutrophil activation, recruitment and injury, with effector T cells also involved. Without therapy, prognosis is poor but treatments, typically immunosuppressants, have improved survival, albeit with considerable morbidity from glucocorticoids and other immunosuppressive medications. Current challenges include improving the measures of disease activity and risk of relapse, uncertainty about optimal therapy duration and a need for targeted therapies with fewer adverse effects. Meeting these challenges requires a more detailed knowledge of the fundamental biology of AAV as well as cooperative international research and clinical trials with meaningful input from patients

Longitudinal studies of patients with ANCA vasculitis demonstrate concurrent reactivity to complementary PR3 protein segments cPR3m and cPR3C and with no reactivity to cPR3N

Antibodies recognizing the complement of the middle of PR3 (cPR3m) occur in ~30% of PR3-ANCA-vasculitis patients and immunization of animals with a peptide complementary to the middle of PR3 (cPR3m) induces not only anti-complementary PR3 antibodies, but also anti-PR3 antibodies derived through an anti-idiotypic response. PR3 epitopes recognized by patient ANCA however, are not restricted to the middle of PR3. This prompted us to test for antibodies that react with proteins complementary to the terminal regions of PR3 (cPR3C and cPR3N) in PR3-ANCA patients. Anti-cPR3C reactivity was detected in 28% of patients but anti-cPR3N reactivity in only 15%. Ranked anti-cPR3C and anti-cPR3m reactivity correlated in the cohort, whereas there was no significant relationship between cPR3C and cPR3N reactivity. Serial samples from three patients’ revealed that anti-cPR3C and anti-cPR3m reactivity followed a similar pattern over time. Serial samples from a fourth patient demonstrated an anti-cPR3N response without concurrent cPR3m or cPR3C reactivity. Epitope determination by mass spectrometry identified a thirteen amino acid sequence on cPR3C that contained a common binding site recognized by antibodies from three patients. This peptide sequence contains a “PHQ” motif which was reported to be the basis for cross-reactivity of anti-cPR3m antibodies with plasminogen. Why these antibodies are detected in only ~30% of the patients remains unclear. The data reveal it is not due to lack of inclusion of flanking regions of complementary PR3 during screening. Instead, quite unexpectedly, the data demonstrate that patients’ antibodies react with a restricted epitope that exists in both cPR3m and cPR3C