Objective To investigate the different exposure and treatment methods for the chorda tympanic nerve in middle ear surgery, and discuss the surgery techniques and the feasibility of the chorda tympanic nerve protection.Methods From September 2013 to March 2016, 155 cases of middle ear surgeries at Zhujiang hospital were included in this study, including 24 cases of type I tympanoplasty, 6 cases of atticotomy and type I tympanoplasty, 22 cases of atticotomy and type II tympanoplasty, 23 cases of canal-wall-up mastoidectomy and tympanoplasty,74 cases of canal-wall-down mastoidectomy and tympanoplasty, 6 cases of stapedotomy.The conditions of exposure and protection of the chorda tympanic nerve in the operation were compared, and their taste function at 3 days to 1 months postoperatively through questionnaires were evaluated.Results The preservation rate of the chorda tympanic nerve was up to 89.03%(138/155).There were 17 cases of chorda tympanic nerve injuries, of which 15 cases suffered hypogeusia with the rate being 88.2%(15/17).In 126 cases of the complete protection of the chorda tympanic nerve, 13 of them appeared hypogeusia at 10.3% (13/126), but they recovered within 1 months postoperatively.One case of delayed facial paralysis occurred in 16 days postoperatively, and recovered completely after 2 weeks of treatment with glucocorticoids.There was a significant difference in the incidence of postoperative abnormal taste between the complete protection of the chorda tympanic nerve and fracture during operation.Conclusion According to the different position and exposure of chorda tympanic nerve, the individual measures should be taken in middle ear surgery to protect the chorda tympanic nerve.

Objective: To explore effect of AMP-activated protein kinase (AMPK) /mammalian target of rapamycin (mTOR) /ribosomal protein S6 kinase-1 (S6K1) signaling pathways and the insulin-sensitizing effect by adiponectin in endometrial cancer HEC-1B cells. Methods: The experiments were divided into 4 groups, adiponectin (Ad) group (HEC-1B cells treated with 20 μg/ml adiponectin for 30 minutes) , inhibitor group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes) , inhibitor+ Ad group (HEC-1B cells treated with 10 μmol/L compound C for 30 minutes following incubation with 20 μg/ml adiponectin for 30 minutes) , control group (only added the culture medium without serum DMEM) . (1) Real-time quantitative PCR and western blot analysis were used to detect the level of mRNA and protein of adiponectin receptor (AdipoR) 1 and AdipoR2. (2) Western blot analysis were used to detect phosphorylation of AMPK, mTOR, S6K1 or insulin receptor substrate 1 (IRS1) protein expression with stimulation in different concentrations of adiponectin (2.5, 5, 10, and 20 μg/ml) , or following incubation with insulin 50 nmol/L for 5 minutes; or treated with 20 μg/ml adiponectin for different times (15, 30, 45, and 60 minutes) , or following incubation with insulin 50 nmol/L for 5 minutes. (3) Cell counting kit-8 (CCK-8) assay was performed to investigate the cell proliferation, and transwell chamber assay was used to detect the cell migration in different groups. Results: (1) The relative expression level of AdipoR1 mRNA and protein were higher than AdipoR2 in HEC-1B cell (8.50±0.09 to 1.00±0.00, and 0.91±0.03 to 0.69±0.03; P<0.05) . (2) The phosphorylation level of p-AMPK was significantly induced, and the phosphorylation level of p-mTOR and p-S6K1 proteins, and 20 μg/ml adiponectin at 30 minutes, AMPK protein had the highest level of activation. (3) Adiponectin induces increased tyrosine phosphorylation of IRS1 in a time-and concentration-dependent manner. (4) The proliferation inhibition ratio in Ad group (0.68±0.34) % was much more than that in inhibitor+Ad group (0.24±0.04) % (t=17.88, P<0.05) . The number of cell migration in Ad group (77±8) was much more than that in inhibitor+Ad group (132±13; t=-7.34, P<0.05) . Conclusions Adiponectin maybe inhibit proliferation and migration of endometrial cancer cells through AMPK/mTOR/S6K1 signal pathway. Adiponectin insensitizes insulin signaling may by regulating by the AMPK/S6K1/IRS1 pathway.