Expression of fragile histidine triad (FHIT) protein and Ki-67 in transformed epithelial cells induced by Yunnan tin mine dust / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the expression and significance of fragile histidine triad (FHIT) and Ki-67 in transformed epithelial cells induced by Yunnan tin mine dust.</p><p><b>METHODS</b>Every second generation of immortalized human bronchial epithelial cells (BEAS-2B) and human embryo lung fibroblasts (WI-38) were exposed to 100 µg/ml Yunnan tin mine dust for 72 h, until the ninth generation. The cells were subsequently co-cultured from the 11th generation. Experimental setup: B group, B (W) group, B (W 100) group, B100 group, B100 (W) group, B100 (W100) group. The expressions of FHIT and Ki-67 in epithelial cells were determined by the method of immunocytochemistry at the 16th, 26th and 36th generation. The percentage of Ki-67 positive cells was calculated as proliferation index.</p><p><b>RESULTS</b>The expression of FHIT was observed in BEAS-2B cells. The expression levels of FHIT among B group, B (W) group and B (W 100) group had not instinctive difference. At the 16th generation, the expression of FHIT in the B100 group was decreased compared with that in the B group and the expression of FHIT between B100 (W) group and B100 (W100) group was lower than that in the B100 group. At the 26th generation, the expression of FHIT was decreased compared with that at the 16th generation in the B100, B100 (W) and B100 (W100) groups. However, At the 36th generation, positive expression were observed again in the B100, B100 (W) and B100 (W100) groups and the expression levels were in incremental order. At the 16th, 26th and 36th generation, the proliferation indexes of B group, B (W) group and B (W 100) group were all < 3%. The proliferation indexes of B100, B100 (W) and B100 (W100) were increased step by step with the generation elongation.</p><p><b>CONCLUSIONS</b>FHIT could be a target at which Yunnan tin mine dust induces transformation of BEAS-2B cells. The proliferation activation of BEAS-2B cells can be improved by Yunnan tin mine dust.</p>

The histological research between the mode of invasion and cervical lymph node metastasis in squamous cell carcinoma of the oral cavity / 华西口腔医学杂志

<p><b>OBJECTIVE</b>The relationship between the mode of tumor invasion in the tumor-host borderline and the frequency of cervical lymph node metastasis was investigated in squamous cell carcinoma of the oral cavity.</p><p><b>METHODS</b>200 cases with histologically proven squamous cell carcinoma of the oral cavity were studied by histological method with HE stained. The mode of invasion in the tumor-host relationship was classified into five grades by Yamamoto's criteria.</p><p><b>RESULTS</b>With regard to the relationship between the mode of invasion and metastasis, the more invasive the tumor tissue was, the more frequent the metastasis formed (P < 0.001). The frequency of metastasis in grades 1 and 2 was low (0 and 5.9%, respectively), The frequency of metastasis in grades 3 was moderate (14.3%), and that in grades 4c and 4d was highly rapid (63.0% and 82.9%, respectively). Single node metastases were frequent in grade 3 and grade 4c (66.7% and 58.8%, respectively), while plural node metastases were frequent in grade 4d (70.6%, P < 0.05). Moreover, the distribution of metastasized lymph nodes was focused on level 1 (41.2%) or level 1 and 2 (79.4%) in grade 4c and was dispersed from level 1 to 4 in grade 4d (P < 0.05). In the present study, the degree of differentiation did not correlate well with the frequency of metastasis.</p><p><b>CONCLUSION</b>These results indicate that the more invasive the tumor cells were to the host, the more frequent the metastasis formed. The different mode of invasion would accompany with different frequency of metastasis, different number and distribution of metastasized lymph nodes.</p>

Prader-Willi syndrome and genomic imprinting / 中华儿科杂志

<p><b>OBJECTIVE</b>Prader-Willi syndrome (PWS) is an example of a human genetic disorder that involves imprinting genes on the proximal long arm of chromosome 15 and SNRPN gene as a candidate gene for this syndrome. The purpose of this study was to show the molecular genetic defects and genomic imprinting basis in Chinese PWS patients and to evaluate the clinical applications of a differential diagnostic test for PWS.</p><p><b>METHODS</b>Fluorescence in situ hybridization (FISH) and methylation-specific PCR (MSPCR) techniques were applied for 4 clinically suspected PWS patients. Using three probes, including SNRPN probe for identification of the critical locus in PWS region, D15Z1 and PML control probes for identification of the 15p arm and 15q arm, the authors detected the deletions 15q in PWS. MSPCR was based on sodium bisulfite treatment of DNA and PCR primers specific for the maternal and paternal allele.</p><p><b>RESULTS</b>When hybridized with mixed probes, it was found in 2 patients that the central specific signal was absent, but both the flanking control signals were retained, indicating SNRPN gene deletion of chromosome 15q11-13. Bisulfite-modified DNA from all PWS children amplified with methylated allele-specific primer pair showed only maternal 131bp PCR product, indicating the maternal uniparental disomy (UPD15).</p><p><b>CONCLUSION</b>Genomic imprinting plays an important role in the molecular pathogenesis of PWS that caused by paternal microdeletions of 15q11-q13 or maternal UPD of chromosome 15. The basic defect seemed to be an absence of function of PWS genes that are normally expressed only from the paternal chromosome 15. MSPCR is a rapid and simple PCR-based assay compared with other cyto-molecular tests and its results were consistent with the clinical diagnosis of PWS, so it seems to be a reliable diagnostic method for PWS patients who show abnormal methylation at SNRPN. The genetic differential tests for PWS are important in determining familial recurrence risk.</p>