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Dental calculus is a potential material that can be used for assessing chronic exposure to trace heavy metals in oral cavity as it is a long-term reservoir. The aim of this study was to investigate the correlation between dental calculus copper levels and risk of oral submucous fibrosis (OSF) due to chewing dried areca-nut quids in Mainland China. This study included 34 OSF (grade 1) sufferers with dried areca-nut quids chewing as the patient group and 23 healthy individuals without areca-nut chewing as the control group. The dental calculus sample was obtained from all 57 participants and evaluated by inductively coupled plasma mass spectrometry (ICP-MS) for dental calculus level of copper. This work revealed that the mean copper level of dental calculus was significantly higher in OSF (grade 1) sufferers with areca-nut chewing than those in healthy individuals without areca-nut chewing (p < 0.001). This work provided an evidence to support that there may be a positive correlation between elevated levels of copper in dental calculus caused by chewing dried areca-nut quids and an increased risk of developing OSF in Mainland China., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The peak age of onset of hepatocellular carcinoma (HCC) is continually increasing worldwide. This study aims to evaluate whether there exists any significant difference in the clinicopathological features between younger- and elderly-HCC.1082 Consecutive patients with HCC who underwent liver resection at Liver Cancer Institute, Zhongshan Hospital, Fudan University from 1995 to 1998 were studied. The patients were divided into elderly-HCC (>or=65 years of age) and younger-HCC (< 65 years of age). Important clinicopathological features of the patients and postoperative survival rates were compared between these two groups. Among 1082 patients studied, 108 were elderly-HCC and 974 were younger-HCC. The resection rate of the elderly-HCC was significantly higher than that of the younger-HCC. The 1, 3 and 5-year survival rates of the elderly-HCC were not significantly different from those of the younger-HCC. Compared with the younger-HCC, the elderly-HCC had (1) less HBsAg-positive rate; (2) more frequent anti-HCV positivity ; (3) lower proportion with AFP value >or=400 microg/dl; (4) a relatively small tumor diameter; (5) higher proportion of stage I-II patients; (6) a relatively low metastasis rate. However, there were no statistically significant differences in other clinicopathological features (including gender, symptoms, tumor number, tumor venous invasion, tumor differentiation, capsular formation, type of cirrhosis) between the two groups. There is a certain extent difference in clinicopathological features between elderly and younger-HCC patients, but the postoperative survival rate is comparable between the two groups.

Congenital long QT syndrome (LQTS) is a genetic disease that predisposes affected individuals to arrhythmias, syncope, and sudden death. Mutations in several ion channel genes have been discovered in different families with LQTS: KCNQ1 (KVLQT1, LQT1), KCNH2 (HERG, LQT2), SCN5A (LQT3), KCNE1 (minK, LQT5), and KCNE2 (MiRP1, LQT6). Previously, the P448R-KVLQT1 missense mutation has been reported as an LQT1-causing mutation. In this report, we demonstrate the presence of the P448R polymorphism in two, unrelated Chinese LQTS families. Although absent from 500 reference alleles derived from 150 white and 100 African-American subjects, P448R was present in 14% of healthy Chinese volunteers. Given the inconsistencies between the genotype (LQT1) and clinical phenotype (LQT2) in our two LQTS families, together with the finding that the P448R appears to be a common, ethnic-specific polymorphism, mutational analysis was extended to the other LQTS-causing genes resulting in the identification of distinct HERG missense mutations in each of these two families. Heterologous expression of P448R-KVLQT1 yielded normal, wild-type (WT) currents. In contrast, the two unique HERG mutations resulted in dominant-negative suppression of the WT HERG channel. Our study has profound implications for those engaged in genetic research. Importantly, one child of the original proband was initially diagnosed with LQT1 based upon the presence of P448R-KVLQT1 and was treated with beta-blockers. However, he did not possess the subsequently determined LQT2-causing mutation. On the other hand, his untreated P448R-negative brother harbored the true, disease-causing HERG mutation. These findings underscore the importance of distinguishing channel polymorphisms from mutations pathogenic for LQTS and emphasize the importance of using appropriate ethnically matched controls in the genotypic analysis of LQTS.