Focal Myositis Localised in Gastrocnemius Muscle: is it Different from Isolated Gastrocnemius Myositis? A Case Report

@#Focal myositis is a rare disease defined by an isolated inflammatory pseudotumour usually restricted to one skeletal muscle. Approximately, 250 cases of focal myositis have been described in the literature, and two recent large cohorts have been used to help in the diagnosis. Isolated gastrocnemius myositis, a rare immune-mediated condition, is a diagnostic entity used by internal medicine clinician in the gastrocnemius myalgia syndrome associated with Crohn’s disease (CD). However, focal myositis and isolated gastrocnemius myositis with Crohn's disease share clinical, haematological, pathological, and radiological similarities. We present a case of unilateral focal myositis of the gastrocnemius muscle in a patient with no underlying diseases, including Crohn’s disease. At clinical evaluation, we encountered a challenge in differentiating between focal myositis and the isolated gastrocnemius myositis of Crohn’s due to similarities in clinical manifestation. We attempt to clarify focal myositis and isolated gastrocnemius myositis through our case report and a review of literature.

PPARγ induces growth inhibition and apoptosis through upregulation of insulin-like growth factor-binding protein-3 in gastric cancer cells

Peroxisome proliferator activator receptor-gamma (PPARγ) is a ligand-activated transcriptional factor involved in the carcinogenesis of various cancers. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a tumor suppressor gene that has anti-apoptotic activity. The purpose of this study was to investigate the anticancer mechanism of PPARγ with respect to IGFBP-3. PPARγ was overexpressed in SNU-668 gastric cancer cells using an adenovirus gene transfer system. The cells in which PPARγ was overexpressed exhibited growth inhibition, induction of apoptosis, and a significant increase in IGFBP-3 expression. We investigated the underlying molecular mechanisms of PPARγ in SNU-668 cells using an IGFBP-3 promoter/luciferase reporter system. Luciferase activity was increased up to 15-fold in PPARγ transfected cells, suggesting that PPARγ may directly interact with IGFBP-3 promoter to induce its expression. Deletion analysis of the IGFBP-3 promoter showed that luciferase activity was markedly reduced in cells without putative p53-binding sites (-Δ1755, -Δ1795). This suggests that the critical PPARγ-response region is located within the p53-binding region of the IGFBP-3 promoter. We further demonstrated an increase in PPARγ-induced luciferase activity even in cells treated with siRNA to silence p53 expression. Taken together, these data suggest that PPARγ exhibits its anticancer effect by increasing IGFBP-3 expression, and that IGFBP-3 is a significant tumor suppressor.