Objective To inject PPTA into the cochlea of guinea pigs through scala tympani fenestration ,to study the protective effect of PPTA injection on the cochlear damage induced by gentamicin and mechanism of oxy-gen free radical .Methods Randomly divided were the guinea pigs with normal hearing into three groups :the con-trol group ,GM group and PPTA group .We injected the artificial perilymph 10μl /d into cochlea through scala tym-pani fenestration on control group for 3 days ,injected GM 160 mg · kg -1 · d-1 on GM group for 3 days ,injected the PPTA 10 μl /d into the cochlea through scala tympani fenestration and injected GM 160 mg · kg -1 · d-1 at the same time on PPTA group for 3 days .We tested ABR and analyzed the hearing changes .We tested the OFR level reacted by SOD and GSH of the cochlea tissue .SEM and TEM were performed to observe the change of cell mor-phology .Results For ABR ,the control group was 12 .75 ± 3 .796 ,GM group 28 .230 ± 4 .953 ,PPTA group23 .47 ±9 .211 dB SPL(P<0 .05) .For SOD ,the normal group was 50 .241 ± 9 .080 ,GM group 28 .230 ± 4 .953 ,PPTA group 43 .089 ± 4 .587 U/mgprot(P<0 .05) .For GSH ,the normal group was 3 .03 ± 0 .33 ,GM group 1 .51 ± 0 .13 ,PP-TA group 2 .50 ± 0 .16 Ggsh/L(P<0 .05) .The changes of hair cells of PPTA group were obviously less severe than that of GM group .For TEM ,the changes of spiral ganglion and stria vascularis of PPTA group were obviously less severe than that of GM group .Conclusion Injecting PPTA through scala tympani fenestration can protect cochlea by generating the excess of OFR when confronting against GM .

Objective:To evaluate the possible role of cytokines in pathophysiology and treatment of nasal polyps.Method:The expressions of Th1-typed cytokines IFN-γ、IL-2 、IL-12 and Th2-typed cytokines IL-4、IL-5、IL-8、IL-10、IL-13 were investigated with enzyme-linked immune sorbent assay(ELISA) in 25 patients with nasal polyps.Result:There was a significant upregulation of Th2-typed cytokines IL-4、IL-5、IL-8、IL-10、IL-13 in nasal polyps compared with normal nasal mucosa, especially　IL-4 and IL-5 (3.9 times and 8.8 times higher than normal mucous respectively) while the expression of Th1-typed cytokines IFN-γ、IL-2、IL-12 drcreased after treated with local glucocorticoid. The levels of Th2-typed cytokines decreased significantly and Th1-typed cytokines had no obvious change.Conclusion:The upregulation of Th2-typed cytokines such as IL-4、IL-5、IL-8、IL-10、IL-12 may play an important role in the pathophysiology of nasal polyps and Th2-typed cytokines can be viewed as a target of treatment to nasal polyps.

Cuproptosis is a new type of cell death that depends on intracellular copper accumulation to trigger the aggregation of mitochondrial lipoacylated protein and the degradation of iron-sulfur cluster protein,with a different mechanism of action from autophagy,ferroptosis,pyroptosis,and necroptosis.Cuproptosis is closely association with the development of liver cancer and resistance to antitumor drugs,as well as the progression of various liver diseases such as hereditary liver diseases,nonalcoholic fatty liver disease,viral hepatitis,and liver cirrhosis.This article summarizes the mechanism of cuproptosis and its role in liver diseases,in order to provide a reference for further research and treatment of liver diseases.

Objective: To make a quantitative evaluation on the short term effect of particulate matter with aerodynamic diameter no more than 2.5 μm (PM_2.5) on cumulative excess mortality rate (CER) and years of life lost (YLL) in residents in Changping district of Beijing. Methods: The death data in local residents, daily mortality, meteorology data and air pollution data (PM_2.5, SO₂ and NO₂ concentrations) in Changping from 2014 to 2017 were collected. Distributed lag non-linear model was used to assess the age and gender specific cumulative lag effects of PM_2.5 on cardiovascular CER and daily YLL in Changping. Results: The effects of PM_2.5 on cardiovascular CER and YLL were obvious on lag 7 days and lag 9 days, respectively, peaking on day 14, and lasting for 21 days. On lag0-21 days, for a 10 μg/m³ increase in PM_2.5, the population based CER of cardiovascular disease death was 0.021% (95%CI: 0.004%-0.038%), and the YLL was 1.47 (95%CI: 0.23-2.70) years. Greater PM_2.5 effect were observed in males and the elderly. Conclusion PM_2.5 increased the risk of cardiovascular disease death and YLL.