Shoulder adhesive capsulitis prevalence among patients with type 2 diabetes mellitus in Damascus, Syrian Arab Republic: a case-control study.

Diabetes mellitus is a known risk factor for shoulder adhesive capsulitis which causes disability and affects quality of life. This study determined the prevalence of shoulder adhesive capsulitis in 208 type 2 diabetes patients and 200 age- and sex-matched patients without diabetes, and with a case-control method investigated the clinical features of the diabetes patients with or without this complication. The sample was drawn from in- and outpatients at Al-Mouassat and Al-Assad university hospitals during November 2009-2010. The prevalence of shoulder adhesive capsulitis in diabetes patients was significantly higher than in those without diabetes (13.0% and 1.5% respectively, P < 0.01). Of the patients with the condition, those with diabetes were younger than those without diabetes. Shoulder adhesive capsulitis in the diabetes group was associated with diabetes duration and poor diabetes control (P < 0.05).

[Views of final-year medical students at Damascus University about clinical skills acquired before graduation].

Medical education in Syrian universities is facing many challenges that may affect the quality of the education and the standard of graduates. We therefore conducted a cross-sectional study using a self-administrated questionnaire with 76 items to investigate the perceptions of 290 final-year medical students regarding the confidence of performing some core clinical skills. A total of 271 responded (response rate 93.4%). Student responses differed. While confidence was highest for skills that do not require practice in the clinical skills laboratory, it was low for skills that need training in emergency and intensive care units, or when students were participating in patient care with partial responsibility. Our findings confirm the need for effective clinical laboratory training, student participation in emergency room shifts, and that students to be allowed to take some egree of responsibility.

Identification of a novel cell type-specific intronic enhancer of macrophage migration inhibitory factor (MIF) and its regulation by mithramycin.

The aim of this study was to determine the genetic regulation of macrophage migration inhibitory factor (MIF). DNase I hypersensitivity was used to identify potential hypersensitive sites (HS) across the MIF gene locus. Reporter gene assays were performed in different human cell lines with constructs containing the native or mutated HS element. Following phylogenetic and transcription factor binding profiling, electrophoretic mobility shift assay (EMSA) and RNA interference were performed and the effects of incubation with mithramycin, an antibiotic that binds GC boxes, were also studied. An HS centred on the first intron of MIF was identified. The HS acted as an enhancer in human T lymphoblasts (CEMC7A), human embryonic kidney cells (HEK293T) and human monocytic cells (THP-1), but not in a fibroblast-like synoviocyte (FLS) cell line (SW982) or cultured FLS derived from rheumatoid arthritis (RA) patients. Two cis-elements within the first intron were found to be responsible for the enhancer activity. Mutation of the consensus Sp1 GC box on each cis-element abrogated enhancer activity and EMSA indicated Sp1 binding to one of the cis-elements contained in the intron. SiRNA knock-down of Sp1 alone or Sp1 and Sp3 together was incomplete and did not alter the enhancer activity. Mithramycin inhibited expression of MIF in CEMC7A cells. This effect was specific to the intronic enhancer and was not seen on the MIF promoter. These results identify a novel, cell type-specific enhancer of MIF. The enhancer appears to be driven by Sp1 or related Sp family members and is highly sensitive to inhibition via mithramycin.

Glucocorticoids suppress macrophage migration inhibitory factor (MIF) expression in a cell-type-specific manner.

MIF is a potent proinflammatory cytokine involved in inflammatory arthritis. Glucocorticoids (GC) have been reported to induce secretion of MIF in rodent cells, and as MIF counteracts the anti-inflammatory effects of GC, this has implications for human inflammatory disease. Transient transfection studies showed that the MIF promoter was repressed by dexamethasone (Dex) (10 nM) in CEM C7A cells, with up to 50% suppression by 100 nM. However, there was no regulation of the promoter by GC in A549 cells. We also found that subnanomolar concentrations of Dex suppressed MIF secretion, measured by ELISA, by 80% in both human T lymphoblasts (CEM C7A) and human lung epithelial cells (A549). Endogenous MIF mRNA was also repressed by GC in CEM C7A cells, measured both by Northern blot and quantitative RT-PCR assays, but there was no such regulation in A549 cells. This suggests that GC affects translation rather than transcription of MIF in A549 cells. These results contradict earlier results with the rat cell line RAW 264.7. Therefore, we analysed MIF secretion from RAW 264.7 cells but found no GC effect on secretion. Understanding how GC regulates MIF in a cell-type-dependent manner may give insights into GC-refractory human inflammatory diseases.