Objective:To systematically evaluate the association between the hepatic lipase ( LIPC) gene rs10468017 polymorphism and susceptibility to age-related macular degeneration (AMD). Methods:A systematic search was performed in both English databases (PubMed, Embase, EBSCO, Web of Knowledge and Cochrane library) and Chinese databases (CNKI, WanFang, VIP and CBM) from database establishment to December 31, 2019.Literature about LIPC rs10468017 polymorphism and AMD was searched.Odds ratios ( OR) and 95% confidence intervals ( CI) of allele mode (T and C), heterozygous model (TC and CC) and homozygous model (TT and CC) as well as the correlation between types of AMD and races were calculated using Stata 12.0 software. Results:Twenty-one studies were included in the Meta-analysis.There were 25 649 AMD patients and 26 294 normal controls.There was a significant correlation between LIPC rs10468017 polymorphism and risk of AMD in different genetic models (T vs. C: OR=0.83, 95% CI: 0.80-0.87; TC vs. CC: OR=0.82, 95% CI: 0.75-0.90; TT vs. CC: OR=0.65, 95% CI: 0.56-0.76). The subgroup analysis showed that the LIPC rs10468017 polymorphism was significantly associated with the risk of early AMD ( OR=0.87, 95% CI: 0.78-0.96), advanced AMD ( OR=0.83, 95% CI: 0.77-0.88), geographic atrophy ( OR=0.79, 95% CI: 0.72-0.87) and choroidal neovascularization ( OR=0.83, 95% CI: 0.78-0.89). Stratified analysis by ethnicity showed that there was a significant association between T allele and the decreased risk of AMD in the Caucasian population (early AMD: OR=0.77, 95% CI: 0.67-0.89; advanced AMD: OR=0.80, 95% CI: 0.75-0.87), but not in the Asian population (early AMD: OR=0.98, 95% CI: 0.85-1.13; advanced AMD: OR=0.93, 95% CI: 0.81-1.06). Conclusions:There is a significant association between T allele of LIPC rs10468017 polymorphism and the reduced risk of AMD, which exists in different subtypes of AMD with certain racial differences.

Objective To investigate the clinical application value of anti-Mullerian hormone in the evaluation of ovarian reserve function in the child-bearing female patients with RA. Methods A total of 90 child-bearing patients with RA aged from 20 to 50 years of age who were hospitalized from December 5, 2015 to April 30, 2017 were enrolled and healthy females with matched ages were enrolled as the control group. Electrochemiluminescence assay was used to determine the anti-Mullerian hormone (AMH) and the clinical data of all patients were retrospectively analyzed. SPSS software was applied to draw the ROC curve and calculate the area under the AMH curve. Risk factors were statistically analyzed using Logistic regression method. Results (1)A total of 90 patients with RA were included in the analysis[mean age (32. 2±6. 87) years, duration of disease (3. 03±2. 03) years]. AMH levels in RA patients [(2. 74±0. 16) ng/mL] were significantly lower than those in the control group [(3. 75±0. 17) ng/mL]. (2)Pearson correlation analysis showed that the increase of age (r=0. 965, P＜0. 001) and bFSH (r=0. 664, P＜0. 001) were associated with low AMH levels. The ROC curve analysis showed that the predictive sensitivity to the ovarian reserve reduction (DOR) was 0. 828 and the specifici ty was 0. 727 when AMH was 2. 27 ng/mL. (3)AMH levels in the patients with RA exposed to Tripterygium wilfordii preparation[(1. 86±0. 16) ng/mL] were significantly lower than those in unexposed patients [(3. 27±0. 14) ng/mL]. There was no statistically significant difference in AMH levels among the patients receiving other immunosuppressive agents(including methotrexate, leflunomide, hydroxychloroquine). (4)Logistic regression analysis indicated that the use of Tripterygium wilfordii preparation was the risk factor for DOR (OR=7. 31, P=0. 019, 95％ CI 1. 39 to 38. 54). Conclusion AMH levels can be used to evaluate ovarian function in child-bearing female patients with RA. Ovarian toxicity of Tripterygium wilfordii preparations should be alerted in the its clinical application in the treatment of RA.

Background Benzo[a]pyrene (BaP) has neurotoxicity, which can induce the loss of hippocampal neurons in humans and animals and lead to spatial learning and memory dysfunction, but its mechanism is still unclear. Objective To observe the ferroptosis of mouse hippocampal neuron HT22 cells induced by 7,8-dihydroxy-9,10-epoxybenzo[a]pyrene (BPDE), an active metabolite of BaP, and to explore its potential mechanism, so as to provide a basis for the study of BaP neurotoxicity mechanism. Method Mouse hippocampal neuron HT22 cells were selected and divided into four groups: solvent control group and low, medium, and high concentration BPDE exposure groups (0.25, 0.50, and 0.75 μmol·L⁻¹). Cell survival was detected by CCK8 method. Cell morphology and ultrastructure were observed under light and electron microscopes. The levels of reactive oxygen species (ROS) and Fe²⁺ were detected by fluorescence probe method. Iron, 4-hydroxynonenoic acid (4-HNE), malondialdehyde (MDA), glutathione (GSH), and glutathione peroxidase (GSH-PX) levels were detected with commercial kits. The expression levels of acyl-CoA synthase long chain family member 4 (ACSL4), cyclooxygenase 2 (COX2), solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4) were detected by Western blotting. After interventions with ferroptosis inhibitors 20 μmol·L⁻¹ deferoxamine (DFO) and 10 μmol·L⁻¹ ethyl 3-amino-4-cyclohexylaminobenzoate (Fer-1), the cell survival rate of each BPDE exposure group and the changes of the ferroptosis characteristic indicators and protein expression levels were observed. Results With the increase of BPDE concentration, the survival rate of HT22 cells decreased gradually, and the survival rate of each BPDE group was significantly lower than that of the solvent control group (P<0.01). Under light microscope, the number of cells in the high concentration BPDE group was significantly reduced, and atrophic cells and reduced synapses were recorded. Under electron microscope, the HT22 cells in the high concentration BPDE group showed mitochondrial shrinkage, decreased crista, and increased mitochondrial membrane density. Compared with the solvent control group, the levels of intracellular lipid ROS, Fe²⁺, 4-HNE, and MDA significantly increased in the high concentration group (P<0.01), the GSH and GSH-PX levels were significantly decreased (P<0.01), the protein expression levels of ASCL4 and COX2 were significantly increased (P<0.01), and the protein expression levels of SCL7A11 and GPX4 were significantly decreased (P<0.01). The ferroptosis inhibitors DFO and Fer-1 significantly reversed the cell survival rate (P<0.01), the ferroptosis characteristic indicators (ROS, Fe²⁺, 4-HNE, MDA, GSH, and GSH-PX levels) (P<0.01), and the expression levels of ferroptosis-related proteins (ACSL4, COX2, SLC7A11, and GPX4) (P<0.01) in the high concentration BPDE group. Conclusion BPDE can induce ferroptosis in mouse hippocampal neuron HT22 cells, which may be related to the inhibition of SLC7A11/GSH/GPX4 axis and the induction of iron metabolism disorder.