Objective To study the pathologic characteristics of eutopic endometrium in patients with endometriosis.Methods Pathologic characteristics of eutopic endometrium were studied in 176 patients with endometriosis in Peking Union Medical College Hospital from January 2007 to December 2008 retrospectively.Results About 72.2％(127/176)of eutopic endometrium were in proliferative phase,19.9％(35/176)of were observed as endometrial polyp,including 32 cases with simple endometrial polyp and 3 cases with abnormal hyperplasia combined with endometrial polyp.And 4.0％(7/176)showed abnormal hyperplasia.The incidence of pathologic changes in eutopic endometrium was 22.2％(39/176).Among 53 endometriosis patients combined with infertility,the incidence of pathologic changes of eutopic endometrium was 35.9％(19/53),which was significantly higher than 16.3％ in non-infertile patients (x2 =8.24,P =0.004).Among 65 cases with irregular menstruation,the incidence of endometrial polypus and endometrial hyperplasia were 20.0％(13/65)and 10.8％(7/65),which were significantly higher than 17.1％(19/111)and 0 in normal menstruation patients(x2 =13.839,P =0.003).Conclusions The eutopic endometrium of endometriosis were in proliferative phase state.The pathologic changes of eutopic endometrium were more in patients combined with infertility and irregular menstruation.

OBJECTIVE: To investigate the accurate marker to detect regulatory T cells in vivo and also to evaluate the changes of CD4+ CD25+ regulatory T cells in peripheral blood from patients with papillary thyroid carcinoma and clinical significance. METHOD: Forty patients with papillary thyroid carcinoma and 34 patients with thyroid adenoma were included in this study. The proportion of CD4+ D25+ CD127(low/-) regulatory T cells population and CD4+ CD25+ FoxP3- regulatory T cells population was evaluated by flow cytometric analysis. RESULT: Compared with control group, the proportion of CD4+ CD25+ CD127(low/-) regulatory T cells and CD4+ CD25+ FoxP3+ regulatory T cells in PTC group increased significantly (P < 0.05). The proportions of CD4+ CD25+ CD127(low/-) regulatory T cells and CD4+ CD25+ FoxP3+ regulatory T cells were significantly higher between patients with and without cervical lymph node metastasis (P < 0.05), and extraordinarily different among patients with different clinical stages (P < 0.05). CONCLUSION CD4+ CD25+ CD127(low/-) can be used as an effective membrane marker in identification of CD4+ CD25+ regulatory T cells in stead of CD4+ CD25+ FoxP3+. The CD4+ CD25+ regulatory T cells in the peripheral blood of papillary thyroid carcinoma patients are significantly increased in comparison with that in thyroid adenoma patients. The proportions of Treg of patients with different stages, cervical lymph node metastasis are different. It may be responsible for the happen, development and recurrence of the papillary thyroid carcinoma.
Adolescent ; Adult ; Aged ; Carcinoma ; blood ; Carcinoma, Papillary ; Female ; Humans ; Male ; Middle Aged ; T-Lymphocytes, Regulatory ; Thyroid Cancer, Papillary ; Thyroid Neoplasms ; blood ; Young Adult

Ozone has become one of the major global environmental pollutants, and has attracted more and more attention in the field of air quality and public health. Ground-level ozone concentrations have been increasing in recent years, causing serious burden to the human respiratory system and social economy. Asthma and chronic obstructive pulmonary disease (COPD) are two common airway diseases. Ozone exposure can induce the occurrence, development and exacerbation of chronic airway diseases, short-term ozone exposure can induce non eosinophilic asthma, long-term ozone exposure can induce COPD, and ozone exposure can also induce acute attack of asthma and acute exacerbation of COPD. The effects are mainly that ozone exposure can mediate inflammatory response, oxidative stress, airway hyperresponsiveness, and DNA damage, and lead to decreased lung function, changes in microbial communities, and disruption of the air-blood barrier. This paper reviewed a series of epidemiological studies and animal experiments on asthma and COPD related to ozone exposure in recent years, and mainly generalized the effects of ozone exposure on airway diseases. Finally, this paper summarized the shortcomings of existing studies, providing a beneficial direction and ideas for further research on the hazards of ozone exposure on asthma and COPD and for exploring new intervention targets.

Objective : To investigate whether Mitochondria-targeted antioxidant peptide SS-31 can inhibit the ozone ( O3 ) -induced mice lung airway hyperresponsiveness and mucus hypersecretion． Methods : Eight-week C57BL /6 mice were randomized into four groups，including phosphate buffer saline (PBS) + Air group，SS-31 + Air group， PBS + O3 group and SS-31 + O3 group．C57BL /6 mice were injected intraperitoneally with SS-31 ( 10 mg / kg) one hour before ozone exposure ，and then single-exposed to ozone at a concentration of 5. 01 × 10 －6 mol / m3 for 3 hours．After 24 hours，airway hyperresponsiveness(AHR) and bronchoalveolar lavage fluid (BALF) cells numbers were measured．Lung tissue schiff periodic acid shiff (PAS) staining，malondialdehyde (MDA) ，inflammatory factors ( interleukin，IL ) -1 β , IL-6 ，IL-18 and monocyte chemoattractant protein-1 ( MCP-1 ) ) and mucin factor (MUC5B) were detected，and the protein expression levels of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) ，pro-Caspase 1 / Caspase 1 (p20) ，Gasdermin D ( GSDMD) and Cleaved GSDMD were determined by Western blot. Results: O3 exposure caused both mice lung airway hyperresponsiveness and mucus hypersecretion．However，SS-31 could inhibit the O3 -induced airway hyperresponsiveness and mucus secretion，reduce the levels of oxidative stress and inflammatory factor mRNA expression ，and downregulate the protein expression level of NLRP3 and the activated forms of Caspase 1 and GSDMD． Conclusion SS-31 could suppress O3 -induced mice airway hyperresponsiveness and mucus hypersecretion by inhibiting the NLRP3 / Caspase 1 / GSDMD signaling pathway.

Objective:To summarize the clinical experiences of 9 ABO-incompatible kidney transplantation at our center and explore its clinical application value.Methods:Methods From April 2016 to December 2019, there were 9 living kidney transplants of ABO incompatible relatives, including type A to type B (n=3), type B to type O (n=3), type B to type A (n=1) and type AB to type B (n=2). Immunosuppressant plus single membrane plasmapheresis (PE) and/or double filtration plasmapheresis (DFPP) and rituximab were employed for pretreating recipients. Adverse reactions of recipients were observed during and after pretreatment. Blood group antibody titer, complications and other related parameters were recorded before and after transplantation before and after monitoring pretreatment.Results:After pretreatment, IgM, IgG and total titer of blood group antibodies were ≤1: 4 on the day of transplantation and the titer of non-blood group antibodies rebounded within 2 weeks (≤1: 8). During preconditioning, 2 patients experienced oral numbness and involuntary dithering during plasmapheresis and there was 1 case of infusion reaction after rituximab dosing. The early recovery of renal function was all excellent. Renal biopsy was performed in 4 patients with slow elevation of serum creatinine and 1 case developed acute antibody-mediated rejection. The survival rate of all recipients at the last follow-up was 100%.Conclusions:Live kidney transplantation of ABO-incompatible relatives is both safe and feasible so that it may help alleviate some shortage of donor kidney.

AIM: To investigate the mechanism of baicalin-induced apoptosis in human laryngeal cancer cells. METHODS: AMC-HN-8 cells were selected for the study, and baicalin was applied to the cells at different concentrations (0, 10, 30, 100, and 300 μmol/L), and the half-inhibitory concentration (IC50) was measured by the CCK-8 method. Bax, cleaved-caspase-3, Cyto-c, IRF4 protein expression by protein blotting (Western blot); miR-125b-5p and IRF4 expression by RT-qPCR. Dual-luciferase reporter gene validation of Targetscan prediction (binding of miR-125b-5p to IRF4-3'UTR); apoptosis and necrosis inhibitors explore the way baicalein induces death in laryngeal cancer cells. AMC-HN-8 was then divided into blank group, baicalein (IC50), miR-125b-5p inhibitor group, baicalein + inhibitor NC group, baicalein+miR-125b-5p inhibitor group, and cell invasion and clone formation assays to detect cell invasion and proliferation ability, respectively. Apoptosis was detected by flow cytometry. RESULTS: Baicalein inhibited the proliferation of AMC-HN-8 cells in a dose-dependent manner with an IC50 value of 47.31 μmol/L. Compared with the blank group, 47.31 μmol/L baicalin induced apoptosis and inhibited cell invasion, while upregulating the expression of miR-125b-5p and suppressing the mRNA and protein levels of IRF4. The luciferase results showed that the miR-125b-5p mimic was able to inhibit the activity of the IRF4-3'UTR promoter relative to the NC mimic (mimic) group. Baicalein induces laryngeal cancer cell death in an apoptotic manner. In addition, the combination of 47.31 μmol/L baicalin and miR-125b-5p inhibitor affected the behavior of AMC-HN-8 cells, showing that compared with the blank group, the baicalin group showed a decrease in the number of cell clones, weakened invasion ability, and increased apoptosis; the miR - 125b-5p inhibitor group showed an increase in the number of cell clones, enhanced invasion ability and decreased apoptosis. The baicalin+ inhibitor NC group was consistent with baicalin, with no significant effect of inhibitor NC on cell behavior. The cloning, invasion, and apoptosis of cells in the baicalin+miR-125b-5p inhibitor group were intermediate between the baicalin and miR-125b-5p inhibitor groups. CONCLUSION: Baicalin inhibits the proliferation of AMC-HN-8 cells, and the mechanism may be related to miR-125b-5p targeting to inhibit the expression of IRF4, inducing the pro-apoptotic proteins Bax, cleaved-caspase3, and Cyto-c, and inhibiting the apoptosis suppressor protein Bcl-2 thereby inducing apoptosis.