Objective:To observe the clinical effects of conservative sequence method in the treatment of anterior disk displacement without reduction(ADDWR).Methods:300 patients with ADDWR were included.200 patients were treated by conservative sequence method (including upper articular cavity lavage with single needle + injection of sodium hyaluronate gel + physical therapy + gimmick reset + oral exercise) (group 1);the other 100 were treated by injection of sodium hyaluronate gel(group 2).Maximum mouth opening (MM0) and pain visual analogue scale(VAS) were measured and compared before and after treatment.Results:In group 1 the effective rate was 95.5％,before treatment MMO was (22.90 ± 3.18) mm,VAS (5.81 ± 0.32);3 months after treatment MMO (37.05 ± 4.43) mm,VAS (1.29 ± 0.19);6 months after treatment MMO (36.29 ± 4.08) mm,VAS (1.37 ± 0.22);12 months after treatment MMO (35.76 ±3.87) mm,VAS (1.52 ±0.28),respectively.In group 2,the effective rate was 78％,before treatment MMO was(23.12 ±4.02) mm,VAS (6.11 ±0.67);3 months after treatment MMO (36.11 ±4.02),VAS (1.89 ±0.21);6 months after treatment MMO (35.49 ±3.78),VAS (2.21 ±0.32);12 months after treatment MMO (31.53 ±4.87) mm,VAS (3.88 ±0.51)mm,respectively.By statistics,all the measurments showed statistical significance(P ＜ 0.05) between 2 groups.Conclusion:Conservative sequence method is more effective in the treatment of ADDWR.

It has been discovered that intestinal fungi play important roles in microecological systems of human body, which affect the human health by influencing gut microbiota directly or indirectly. This article reviews the research progress about the fungi-bacteria interaction, and effects of intestinal fungi and their products on host’s health. The article also discusses the correlation of intestinal fungi with inflammatory bowel disease, colorectal cancer, HBV-related liver diseases, metabolism-associated fatty liver disease and alcoholic liver disease, indicating that intestinal fungi are widely involved in the development of human diseases.

ObjectiveTo investigate the induction of ferroptosis by polyphyllin Ⅱ （PPⅡ） in hepatocellular carcinoma HepG2 cells and its underlying mechanism. MethodThe effect of PPⅡ （0， 1.5， 3.0， 4.5， 6.0， 9.0， 18.0 mg·L^-1） on the in vitro proliferation of HepG2 cells was assessed using the methyl thiazolyl tetrazolium （MTT） assay. Colony formation ability of HepG2 cells was evaluated through a colony formation assay. Cell migration ability was assessed via a scratch assay. Lactate dehydrogenase （LDH） content in HepG2 cells was measured using a kit. Reactive oxygen species （ROS） levels in HepG2 cells were observed using a fluorescence inverted microscope. Malondialdehyde （MDA）， glutathione （GSH）， and free Fe²⁺ content in HepG2 cells were detected using respective kits. The mitochondrial ultrastructure in HepG2 cells was observed by transmission electron microscopy. The expression of ferroptosis-related proteins p53， solute carrier family 7 member 11 （SLC7A11）， glutathione peroxidase 4 （GPX4）， long-chain acyl-CoA synthetase 4 （ACSL4）， and transferrin receptor 1 （TFR1） in HepG2 cells was detected using Western blot. ResultCompared with the control group， the PPⅡ treatment groups showed significantly decreased survival rate of HepG2 cells in a dose-dependent manner （P<0.01）， significantly reduced number of cell colonies （P<0.01）， significantly shortened scratch healing distance， inverse correlation of the migration distance with drug concentration （P<0.01）， significantly increased LDH leakage in cells （P<0.01）， significantly enhanced relative fluorescence intensity of intracellular ROS， and significantly increased accumulation of lipid peroxide MDA （P<0.01）， decreased intracellular GSH content with increasing drug concentration （P<0.01）， and significantly enhanced fluorescence intensity of FeRhoNox-1 in cells （P<0.01）. Moreover， cells exhibited vacuolation， and mitochondria showed significant shrinkage with reduced or even disappeared cristae. Compared with the results in the control group， the expression of p53， ACSL4， and TFR1 proteins significantly increased， while the expression of SLC7A11 and GPX4 proteins significantly decreased in the PPⅡ treatment groups （P<0.05）. ConclusionIn summary， PPⅡ induces ferroptosis in HepG2 cells by regulating the p53/SLC7A11/GPX4 signaling axis， promoting ACSL4 expression and Fe³⁺ uptake， leading to an imbalance in the antioxidant system.