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The gear backlash is in the process of gear and rack transmission,the gear backlash needed to be eliminated to ensure the bidirectional transmission precision of the transmission mechanism. In the designed mechanical mechanism,two racks meshing gears is driven through the axial relative displacement of the mechanism of sliding lead screw nut,and an axial relative displacement between the two racks（ gear rack staggered teeth） appeared,and the equivalent tooth thickness increased,and one mechanism is designed to eliminate gears backlash automatically. The mechanism is used in rotary table of NC machine driving by gear- rack successfully,it can obtain simple structure and high transmission precision.

Long noncoding RNAs (lncRNAs) have emerged as important regulators of cancer progression. Abnormal sialylation leads to renal cell carcinoma (RCC) malignancy. However, the mechanism by which the lncRNA maternally expressed gene 3 ( MEG3 ) mediates RCC progression by regulating ST3Gal1 transcription and EGFR sialylation is still unrevealed. Here, we found that the expression of MEG3 was higher in adjacent tissues than in RCC tissues, as well as downregulated in RCC cell lines compared to expression in normal renal cells. The proliferation, migration and invasion of RCC cells transfected with MEG3 was decreased, whereas knockdown of MEG3 had the opposite effect. The proliferative and metastatic abilities of RCC cells in vivo were concordant with their behavior in vitro ST3Gal1 expression was dysregulated in RCC and was positively correlated with MEG3 By applying bioinformatics, c-Jun (also known as JUN) was identified as a transcription factor predicted to bind the promoter of ST3Gal1 , and altered MEG3 levels resulted in changes to c-Jun expression. Furthermore, ST3Gal1 modulated EGFR sialylation to inhibit EGFR phosphorylation, which affected activation of the phosphoinositide 3-kinase (PI3K)-AKT pathway. Taken together, our findings provide a novel mechanism to elucidate the role of the MEG3 -ST3Gal1-EGFR axis in RCC progression., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)

Objective: To explore beryllium oxide induced oxidative lung injury and the protective effects of LBP., Methods: Intoxication of animals were induced by once intratracheal injection and LBP intervention by intragastric administration. The content of HIF-1, VEGF and HO-1 of lung tissues were measured by kits. The pathological changes of lung tissue were showed by pathological section. The changes of lung ultrastructure were observed by electron microscope., Results: Pathological changes of the lung tissue in beryllium oxide exposure group rats were in line with the characteristics of beryllium disease in human. Compared with the control group, HO-1 was increased in beryllium oxide exposure 40 d group and low doses of LBP group, compared with the control group, HO-1 was increased in beryllium oxide exposure 80d group and LBP treatment groups (P < 0.05 or P < 0.01). Compared with the control group, HIF-1 was increased in beryllium oxide exposure 40 d group, LBP treatment groups, beryllium oxide exposure 60 d and 80 d groups (P < 0.05 or P < 0.01). Compared with the control group, VEGF was increased of all phases, especially in beryllium oxide exposure 40d and 80 groups, LBP treatment groups and beryllium oxide exposure 60 d (P < 0.05 or P < 0.01). The content of HO-1 of beryllium oxide exposure group was higher than the LBP treatment for 40d group but below LBP treatment for 80 d group (P < 0.05). The content of HIF1 of beryllium oxide exposure group was higher than high dose of LBP treatment for 60d group and LBP treatment for 80 d group (P < 0.01). The content of VEGF of beryllium oxide exposure group was higher than LBP treatment for 40 d group and high dose of LBP treatment for 60 d (P < 0.05 or P < 0.01)., Conclusions: BeO can cause abnormal expression of related genes of lung tissue in rats, LBP has protective effects on BeO caused lung injury.