Traumatic brain injury (TBI) is a quite common health problem. A lot of delayed complications are related to inflammatory responses that occurred within the brain itself. Atorvastatin is related to lipid lowering drugs carrying some anti-inflammatory properties and upon this fact this study hypothesis was built.

Methods

Twenty adult patients with TBI, Glasgow coma scale (GCS) 9–11. Patients were equally and randomly allocated into two groups (group C as control group and group S received atorvastatin 40 mg once daily for 48 h). After 48 h, participants have undergone magnetic resonance imaging brain spectroscopy examination (MRS). The spectral peaks of N-Acetyl aspartate (NAA), Choline, and Creatinine (Cr) were assessed in brain tissue. The primary outcome was presented as ratios of NAA/Cr), Cho/Cr, and NAA/Cho. Other outcomes included GCS and ICU stay

Introduction: ARID1A (AT-rich interacting domain 1A) gene, a subunit of the SWI/SNF (switch/sucrose non-fermentable) complex, is a tumor suppressor gene. Mutations of this gene with loss of the corresponding protein were detected in different types of cancer. Here, we investigated ARID1A protein expression in endometrioid endometrial carcinoma (EEC), and assessed the correlation between its expression values and the pathological features of EEC.

Materials and methods: The study included 26 cases of EEC and five cases of proliferative endometrium (PE, control group). Immunostaining was done using streptavidin staining methods and ARID1A rabbit monoclonal antibody. Slides were examined and scored for ARID1A nuclear positivity.

Results: Nuclear ARID1A protein expression was observed in all cases of PE, and in 54% of EEC cases. We found significant down-regulation of ARID1A protein expression in EEC (Immunoreactivity score [IRS] = 2.69 ± 2.42) as compared to PE (IRS = 7.4 ± 2.3). Also, there was a significant inverse correlation between ARID1A protein expression value and pathological stage of EEC (r = -0.43, p = 0.040).

Conclusions: Alterations of ARID1A protein expression seem to play a role in the pathogenesis of EEC. The diagnostic and prognostic ramifications of these alterations are open for future studies.