[Scleritis, clinical features, etiologies and treatment: a case series of 32 patients]. / Sclérites, aspects cliniques, étiologiques et thérapeutiques : à propos d'une série de 32 observations.

PURPOSE: To report on the various clinical presentations, etiological diagnosis, prognosis and treatment of patients with scleritis evaluated at a tertiary care eye center. METHODS: Retrospective, monocentric study on a series of 32 patients in a tertiary center. RESULTS: The mean age of included patients with scleritis was 46.8 years (range, 22 to 77 years). Nineteen patients were women and 13 were men. Twenty-six patients (81%) had anterior scleritis (15 nodular, 8 diffuse and 3 necrotizing), six (19%) had posterior scleritis. Unilateral inflammation was present in 24 patients (75%). Twelve out of the 32 patients (37.5%) had an underlying systemic disease: granulomatosis with polyangiitis (n=3), Behçet's disease (n=2), unspecified inflammatory arthritis (n=2), psoriatic arthritis (n=1), ankylosing spondylitis (n=1), sarcoidosis (n=1), Cogan's syndrome (n=1) and ulcerative colitis (n=1). Six patients (18.8%) were suspected of having infectious disease with herpes virus: clinical context and positive treatment response with oral valacyclovir. Systemic agents and topical agents were required in 28 patients (87.5%). The first line therapy was mainly oral non-steroidal anti-inflammatory drugs in 15 patients (47%) and oral corticosteroids in 8 (25%). Immunosuppressive drugs were required in 6 patients. The mean follow-up was 16.3 months. Six patients (19%) had a decrease in visual acuity. CONCLUSION: The number of systemic disease in our series is similar to the main series in the literature. Treatment with valaciclovir might be effective in patients with suspected herpes simplex scleritis.

Inverse relationship between the ratio of ICAM-1 expressing lymphocytes and serum TGF-beta 1 concentrations in acute rheumatic fever.

Autoimmunity in acute rheumatic fever (ARF) is triggered by group-A beta hemolytic streptococci (GAS). Although most of the recent work has focused on the major impact of lymphocytes, the exact immunopathogenesis is still unresolved. Regulation of self-tolerance in response to GAS has been investigated in various animal experiments. This study aimed to associate the ratio of lymphocytes bearing adhesion/costimulatory molecules, Bcl-2/CD95 and serum TGF-beta1 concentrations with clinical stages of ARF. Thirty-five patients were assigned according to the clinical stages. Bcl-2 expression on CD19+ and CD3+ lymphocytes was similar within patient groups and controls. CD62p expression was higher in patients with carditis. The ratio of ICAM-1 bearing lymphocytes was significantly different between patient groups and controls and was increased through acute to remission stages longitudinally. In contrast, a gradual and significant decrease in TGF-beta1 concentrations was observed longitudinally from acute to chronic stages. A positive correlation has been documented between ICAM-1+ lymphocyte ratios and Fas+ cytotoxic T cell ratios supported by a prominent increase in CD95+ T cells. These data draw our attention to the role of ICAM-1, Fas and TGF-beta1 in ARF pathogenesis through the perspective of self-tolerance in a clinical setting.

Mutations affecting the indirect flight muscles of Drosophila melanogaster.

The development of the indirect flight muscles of Drosophila melanogaster was studied by analysing mutations that cause flightlessness. Twenty-five mutations on the X-chromosome and two on the third chromosome were examined. The X-chromosomal mutations form ten complementation units. The ten loci were assigned preliminary map positions by meiotic recombination and deficiencies and duplications. The two autosomal mutations represent two genes. Gynandromorph analyses suggest that many of these mutations have their primary effect in the presumptive thoracic muscle region of the embryo. The mutations cause a variety of characteristic defects, such as absence of the bulk of the thoracic muscle mass, or absence of only one of the two fibrillar muscle groups. Electronmicroscopic studies of sixteen mutants representing all twelve loci reveal abnormal myofibrillar organization in some of these mutants, e.g. aberrant or missing Z-bands, or absence of the thin filaments. Mutant protein patterns, obtained by SDS-polyacrylamide gel electrophoresis, show the following differences from wild type: ten mutants are characterized by absence of reduction of the 54 K protein, and most mutants exhibit a reduction and modification of the 80 and 90 K proteins. The absence of reduction of the 54 K protein was strongly correlated with aberrant Z-bands.