Short or long sleep duration was an important sleep-related factor independently associated with memory impairment and may be a useful marker for increased risk of cognitive impairment in older people.

previously described BCL6/IG translocations with a breakpoint in the 5 0 UTR of BCL6, or in the distant ABR. 2,6 Thus, in our cases BCL6 deregulation can not be explained by promoter substitution. In case no. 2 the inactivation of BCL6 negative autoregulation sites by mutations can be hypothesized, but in case no.1, for which no mutation was found inside these regions, the most reliable hypothesis involves cis-acting elements provided by the partner sequences. The expression of TMEM75, the closest locus brought by the translocation was investigated. The transcript was detected, at a level which did not differ significantly from the mean level of the 11 previous controls. Thus, the activation of BCL6 by TMEM75 regulating sequences remains possible, but the effects of more distant regions can not be precluded. Indeed, it was demonstrated that enhancers, defined as position and orientation independent activators of transcription, can exert regulating effects several hundred kilobases from targets by DNA folding, thus bringing together enhancer and the target. 7 Regarding the pathophysiological role of the t(3;8), several hypotheses can be raised as: (i) BCL6 expression was significantly increased as compared to controls although the effects of mutations located in negatively regulating region could also explain the gene overexpression; (ii) we have shown previously that, in these cases MYC transcript was also overexpressed; (iii) the formation of MYC-BCL6 complexes at the protein level has been reported, 8 with an effect on MYC halflife, suppression of the synthesis of the p21 CIP cell cycle arrest gene, and inhibition of BCL6 acetylation. Therefore, the synergistic effect of MYC and BCL6 could explain the survival and clonal selection of a t(3;8) carrying cell in lymphoma progression.

Context: Silymarin is the main flavonoid extracted from milk thistle, which has been used to treat liver diseases. Objective: The in vivo effect of silymarin on HFD-induced insulin resistance and fatty liver in mice was studied. Materials and methods: Male C57BL/6 mice were fed with high-fat diet (HFD) to induce obesity and insulin resistance and treated with 30, 60 mg/kg silymarin for 18 days. Food intake, body weight and the content/histology of epididymal fat and liver tissue were examined; the content of lipids, AST, ALT and inflammatory cytokines in serum were estimated. Results: Administration of silymarin caused bodyweight loss in diet induced obesity (DIO) mice (HFD group: 47.7 g, 60 mg/kg group: 43.0 g) while the food intake remain unchanged. Silymarin (60 mg/kg) significantly reduced the epididymal fat mass (from 1.75 g to 1.12 g). Elevated plasma lipids (TC 6.1 mM, TG 1.3 mM, LDL 1.2 mM) in DIO mice were all suppressed by silymarin (TC 4.5 mM, TG 0.89 mM, LDL 0.9 mM), as well as insulin (5.1 ng/ml in HFD group to 2.0 ng/ml (60 mg/kg silymarin). Examination of cytokine levels (TNF-a, IL-1b and IL-6) in each group proved that silymarin treatment significantly decreased inflammation in DIO mice. Finally, silymarin effectively protected liver from HFD-induced injury as evidenced by decreasing histological damage and reducing ALT and AST levels, as follows: ALT; 47.4 U/L in HFD group to 28.4 U/L (60 mg/kg silymarin); AST; 150.1 U/L in HFD group to 88.1 U/L (60 mg/kg silymarin) in serum. Discussion and conclusion: Our results suggested that silymarin-induced alleviation of inflammatory response could be a mechanism responsible for its benefits against liver damage and insulin resistance. ARTICLE HISTORY

ObjectiveTo investigate the effects of Cushing’s disease (CD) and adrenal-dependent Cushing’s syndrome (ACS) on bone mineral density (BMD) and bone metabolism.MethodsData were retrospectively collected for 55 patients with hypercortisolism (CD, n = 34; ACS n = 21) from January 1997 to June 2014. BMD was examined in all patients, and bone turnover markers were tested in some patients. Healthy controls (n = 18) were also recruited.ResultsThe lumbar spine and femoral neck BMD were significantly lower in the ACS and CD groups than in the control group. Lumbar BMD was significantly lower in the ACS than CD group. The collagen breakdown product (CTX) concentrations were significantly higher while the osteocalcin and procollagen type I N-terminal propeptide (PINP) concentrations were significantly lower in the ACS and CD groups than in the control group. The PINP concentration was significantly lower while the CTX concentration was significantly higher in the ACS than CD group. In the CD group only, lumbar BMD and serum adrenocorticotropic hormone had a significant positive correlation.ConclusionsBone turnover markers indicated suppressed osteoblast and enhanced osteoclast activities. PINP and CTX changes might indicate bone mass deterioration. Adrenocorticotropic hormone might be protective for lumbar BMD in patients with CD.