An intriguing association between dental and mental pathology in addicted and control subjects: A cross-sectional survey

Recent clinical studies suggest that substance use may be associated with an acceleration of the ageing process, possibly related to a deficit of stem cell number or function. As this clinic had access to both medical and drug dependent patients, we tested the hypothesis that there may be an association between previously identified deficits.A cross-sectional survey was performed looking at both dental and mental dysfunction. Both a dental index (DI) and a mental index (MI) were defined as previously described and utilised as summary measures of such pathology.From 249 substance use disorder (SUD) and 134 general medical controls (N-SUD), 248 and 91 patients were selected with ages less than 57 years as the primary focus of analysis. The mean (+/- S.D.) ages (32.59 +/- 7.98 vs 35.65 +/- 15.45 years) were similar. The DI was found to correlate with the MI in a significant manner in SUD (R = 0.14, p = 0.03), N-SUD (R = 0.27, p = 0.009) and in the whole group (R = 0.17, p = 0.001). The (univariate) association of MI with DI (p = 0.019) and DI with MI (p = 0.0037) remained highly significant at multivariate regression after adjustment for psychiatric diagnoses and measures of dose-duration exposure to common addictive drugs. The qualitative appearance of the surfaces of best fit for the relationship between age, DI and MI was different in the two groups.These results suggest that the robust statistical association between dental and mental pathology may be related to common underlying pathophysiological mechanisms such as a progeroid or stem cell deficiency process in clinical addiction

Galectin-1 and Its Involvement in Hepatocellular Carcinoma Aggressiveness

Hepatocellular carcinoma is one of the most common cancers worldwide. Despite several efforts to elucidate hepatocellular carcinoma molecular pathogenesis, it is still not fully understood. To acquire further insights into the molecular mechanisms of hepatocellular carcinoma, we performed a systematic functional genomic approach on human HuH-7 and JHH-6 cells. The subsequent analysis of the differentially expressed genes in human specimens revealed a molecular signature of 11 genes from which we selected the LGALS1 gene, which was overexpressed in hepatocellular carcinoma. The expression analysis in humans of Galectin-1 (Gal-1), the protein encoded by LGALS1, showed a Gal-1 preferential accumulation in the stromal tissue around hepatocellular carcinoma tumors. Moreover, a significant association between increased expression of Gal-1 in hepatocellular carcinoma and the presence of metastasis was observed. Interestingly, Gal-1 overexpression resulted in an increase of cell migration and invasion. In conclusion, this study provides a portfolio of targets useful for future investigations into molecular marker–discovery studies on a large number of patients and functional assays. In addition, our data provide evidence that Gal-1 plays a role in hepatocellular carcinoma cell migration and invasion, and we suggest that further studies should be conducted to fully establish the role of Gal-1 in hepatocellular carcinoma pathogenesis and evaluate Gal-1 as a potential molecular therapeutic target