[Association between mild cognitive impairment and all-cause mortality in elderly population in China: a Meta analysis].

Objective: To quantitatively evaluate the association between mild cognitive impairment and all-cause mortality. Methods: The research papers of the association between cognitive impairment and all-cause mortality in the elderly in the databases of PubMed, EMBASE, Wang Fang data and CNKI published as of August 1, 2021 were comprehensively retrieved. Software R 4.02 was used for Meta-analysis. Results: A total of 9 research papers were included, involving 48 709 patients. The quality of included papers was high. The results of Meta-analysis showed that the association between mild cognitive impairment and the increased risk of all-cause mortality was statistically significant. Compared with the normal cognitive population, the risk of mortality in the elderly with mild cognitive impairment increased by 39% (HR=1.39, 95%CI: 1.18-1.63). Conclusions: The current research evidence showed that mild cognitive impairment assessed by MMSE screening scale can be used as an independent predictor of the increased risk of all-cause mortality in the elderly population in China. However, due to the limitation of the number of included studies and sample size, the conclusions need to be supported by more evidence studies.

[Small interference of transcription factor Snail contribute to enhanced cisplatin sensitivity on human laryngeal resistant cancer cells].

Objective:To study the relationship between transcription factor Snail and the sensitivity of cisplatin on human laryngeal resistant cancer cells.Method:siRNA interference of Snail was transfected by small RNA interference technology. The interference efficiency on mRNA level were detected by RT-qPCR assay; the expression of Snail protein level was assessed by immunofluorescence. The inhibition ratio of different cisplatin concentration (0, 1, 2, 4, 8, 16 µg/ml) was detected by CCK-8 assay; the protein level of Snail, E-cadherin, MDR1were detected by Western blot assay.Result:RT-qPCR assay show the expression of Snail on mRNA level was decreased to (67.85±9.50)% after transfection in Hep-2/CDDP cell(P<0.05). Immunofluorescence show fluorescence intensity of si-Hep-2/CDDP group was reduced both in nucleus and cytoplasm; CCK-8 assay show the inhibitory ratio of transfected group was increased compared to negative control and Hep-2/CDDP group in different cisplatin concentration (0, 1, 2, 4, 8, 16 µg/ml) (P<0.05). Western blot assay show the protein expression of Snail and MDR1 were down-regulated in transfected Hep-2/CDDP cells (allP<0.05), while epithelial marker E-cadherin was up-regulated in protein level (P<0.05).Conclusion:Small interference of transcription factor Snail could increase the expression of E-cadherin while decrease the expression of MDR1, and it was confirmed that interference Snail contribute to enhanced cisplatin sensitivity on human laryngeal resistant cancer cells.

[Investigation of epithelial-mesenchymal transition induced by cisplatin on human laryngeal resistant cancer cells].

Objective:To investigate the mechanism between epithelial-mesenchymal transition (EMT) and cisplatin induced resistant cell subline and the malignant biological characteristics, to explore EMT in human hep-2 laryngeal resistant cells. Method:Using cisplatin-resistant cells (hep-2/CDDP) and non-resistant cells (hep-2) established in our previous study; the invasion and migration biological behaviors were detected by transwell and scratch assay; the expressions of E-cadherin, Zo-1, Snail, Slug, Twist1, Vimentinon in the mRNA level were detected by RT-qPCR and the protein level by Western blot. Result:Transwell and scratch assay show the invasion and migration behaviors were increased in hep-2/CDDP cells (P<0.05), the epithelial marker E-cadherin and Zo-1 were downregulated in hep-2/CDDP cells (all P<0.05), transcription factor Snail, Slug were upregulated in mRNA and protein level (all P<0.01) while Twist1 had no significant changed in protein level (P>0.05), the expression of mesenchymal marker Vimentin was also increased in mRNA and protein levels in cisplatin resistant cells (P<0.01). It was confirmed that the hep-2/CDDP cells possessed EMT phenotypes. Conclusion:The cisplatin resistant laryngeal cancer cells perform higherinvasion and migration biological behaviors,and the mechanisms of increased ability of invasion and migration induced by cisplatin was associated to eEMT, study on signal path related to EMT may overcome cisplatin resistance and reduce invasion and migration behaviors.

A maternal hereditary deafness pedigree of the A1555G mitochondrial mutation, causing aminoglycoside ototoxicity predisposition.

OBJECTIVE: To characterise the hearing loss, and the frequency of the mitochondrial deoxyribonucleic acid 12S ribosomal ribonucleic acid A1555G mutation, in a large pedigree of aminoglycoside-induced deafness. DESIGN: Hearing loss was clinically assessed. Blood samples were collected from 27 family members (19 matrilinear and eight non-matrilinear) and leukocyte deoxyribonucleic acid was extracted. Mitochondrial deoxyribonucleic acid fragments, spanning the 1555 location, were amplified by polymerase chain reaction. Polymerase chain reaction products were analysed by restriction fragment length polymorphism and deoxyribonucleic acid sequencing. RESULTS: We detected the A1555G mutation in all 19 matrilinear relatives. Of these 19, two exhibited congenital deafness, four had no hearing deficits and the remaining 13 suffered mild to profound hearing loss. CONCLUSION: We confirmed that the A1555G mutation is a 'hot spot' associated with non-syndromic, inherited hearing loss. This mutation may play a vital role in the pathogenesis of hearing impairment, and can result in various grades of deafness.