Objective To compare the effectiveness of the three operation mode in treatment of ovarian cyst. Methods According to the digital table,138 patients with ovarian cyst were divided into three groups,the group A (n=46 cases)were operated through open operation,group B (n =46 cases)were operated through transvaginal operation,group C(n=46 cases)were operated through laparoscopic operation.The three groups were observed the situation of operation (operation time,bleeding volume,the first exhaust time,hospitalizationtime ),complications (infection,hemorrhage,perimenopausal changes ),postoperative follow -up for 1 years.The recurrence rate was observed.Results Group A of 46 patients were successfully completed surgery,B,C groups of 1 patients was con-versed to laparotomy due to severe adhesion.B,C groups in the operation time,amount of bleeding during the opera-tion,the time of hospitalization were significantly less than that of group A (t=4.306,5.172,3.012,3.926,3.776, 2.168,P<0.05,P<0.01).B group was significantly less than those of A,C group in the first exhaust time (t=3.014,2.446,all P<0.05).In the operation time of group B was obviously less than that of group C (t=2.748,P<0.05).A,B,C three groups of postoperative complication rates were 39.1%,11.1%,15.6% respectively;the incidence of complications of B,C groups was lower than that in A group (χ2 =9.82,8.64,all P<0.01 ).After 1years follow-up,the recurrence rate in group B was significantly higher than that of A and C groups (χ2 =6.72, 6.72,all P<0.01).Conclusion Treatment of ovarian cyst vaginal surgery and laparoscopic surgery wound is small, but the person that weigh should be performed open adhesion treatment,individualized treatment.

Retinal ischemia is the common pathologic process in many ophthalmic diseases, including ischemic optic neuropathy, retinal artery and vein occlusion, carotid artery obstructive disease, retinopathy of prematurity, chronic diabetic retinopathy and glaucoma. It is very important to establish animal models to investigate pathology mechanism and explore the treatment of retinal ischemia disease. At present, the commonly used methods for establishing retinal ischemia animal models include increasing intraocular pressure, ligating of blood vessels, suture method, photochemical method, and drug injection etc. This article summarizes the methods to establish the animal models and analyzes the indication for each animal model. It is expected that the method of establishing a retinal ischemic animal model will be helpful to the experimental design of follow-up retinal ischemia studies.

AIM:To investigate the expression of poly (ADP-ribose) polymerase-1 (PARP-1) in the epithelial ovarian cancer ( EOC) and its relationship with epithelial-mesenchymal transition ( EMT) .METHODS:The expression of PARP-1, E-cadherin, vimentin and Snail was detected in the EOC and benign ovarian tumor tissues by immunohistochemi -cal method and real-time PCR.The expression of PARP-1, E-cadherin, vimentin and Snail proteins in the SKOV3 cells treated with efficient PARP-1 inhibitor PJ34 was determined by Western blotting .RESULTS:The positive expression rates of PARP-1, vimentin and Snail were significantly higher in the EOC than that in the benign ovarian tumor tissues , whereas the positive expression rate of E-cadherin was the opposite (P<0.05).The expression of PARP-1, E-cadherin, vimentin and Snail in the EOC was associated with the histological grade , clinical stage and lymphatic metastasis (P<0.05), but no relationship with age and pathological types was observed .The expression of E-cadherin in the EOC was negatively co-related to that of PARP-1.In contrast, the expression of vimentin and Snail in the EOC was positively co-related to that of PARP-1.The relative mRNA expression of PARP-1, vimentin and Snail in the EOC was significantly higher than that in the benign ovarian tumor tissues ( P<0.05) , while the mRNA expression of E-cadherin in the EOC was remarkably lower than that in the benign ovarian tumor tissues (P<0.05).The protein expression of PARP-1, vimentin and Snail in the SKOV3 cells was significantly decreased (P<0.05), while E-cadherin protein was increased after treated with PJ 34(P<0.05). CONCLUSION:PARP-1 may contribute to the onset of EMT in the EOC by regulating the expression of E -cadherin, vim-entin and Snail.The role of PARP-1, which is relevant to EMT, might be important in the development of ovarian cancer .

AIM To study the anti-inflammatory effects and mechanisms of pristimerin. METHODS Several inflammatory models were established, such as ear edema induced by croton oil, hind paw swelling by carrageenan, elevation of capillary permeability by acetic acid in mice and a-cute peritonitis induced by carrageenan in rats. Protein content was measured by Coomassie brilliant blue method, nitric oxide (NO) content by Griess reaction assay, N-acetyl-?-D-glucosamini-dase (NAG) activity by colorimetry, superoxide dismutase (SOD) activity by hydroxylamine method, catalase (CAT) activity by ultraviolet spectro-photometry, and malondialdehyde (MDA) content by fluorescence method in peritoneal exudate in rats. RESULTS Pristimerin ip 0. 156 - 0. 625 mg ? kg-1 or im 1-4 mg - kg-1 inhibited ear edema, hind paw swelling, and elevation of capillary permeability in mice. In the rat peritonitis induced by carrageenan, pristimerin im 1 - 2 mg ?kg-1 reduced neutrophil counts, lessened protein and NO content, inhibited the production of MDA and decreased NAG activity, while augmented the SOD and CAT activity in exudate. CONCLUSION Pristimerin has a significant anti-inflammatory effect which may be related to the inhibition of NO production, scavenging oxygen free radicals, anti-lipoperoxidation and stabilizing lysosome membrane.

0.05),but enhanced the expression of CD80,CD86 significantly(P

Objective To study the mechanism of RING finger protein 34 ( RNF34 ) involved in innate immunity . Methods Recombinant PCR was used and transient expression of the plasmid was achieved in HEK 293T cells.The cells were stimulated with Sendai virus ( SeV) or N-RIG-Ⅰfor the indicated time while luciferase activity was observed using the dual-luciferase reporter assay kit .Results We constructed the plasmid pcDNA 3-Flag-RNF34 and its three mutations .The study found that when stimulated by SeV , RNF34 could inhibit the activity of NF-κB and IFN-βmore significantly than RNF34-ΔFYVE, RNF34-ΔCID and RNF34-ΔRING.We also found that RNF 34 and its three mutants had similar inhibitory effect when the activation of NF-κB and IFN-βwas stimulated by the N-RIG-Ⅰ.Conclusion RNF34 negatively regulates innate immunity by acting on the RIG-Ⅰ-MAVS signaling pathway .

Objective:To explore the mechanism of Huangqi Jiedu Decoction (HQJD) in the treatment of breast cancer with the syndrome of Zheng deficiency and toxic incandescence by network pharmacology and molecular docking technology.Methods:The main active ingredients and targets of HQJD were screened through the traditional Chinese medicine (TCM) systematic pharmacology database and analysis platform. The relevant targets of breast cancer with the syndrome of Zheng-deficiency, toxic-incandescence were obtained using OMIM, GeneGards and Drugbank databases, and the relevant targets of HQJD for the treatment of breast cancer with the syndrome of Zheng-deficiency and toxic incandescence were obtained by intersection; The Cytoscape 3.9.1 software was used to build the protein protein interaction (PPI) network and the " drug active component target disease" network on the basis of String 11.0 database, and the core active components and core targets of HQJD in treating breast cancer with the syndrome of Zheng-deficiency and toxic-incandescence were inferred according to the topological parameters. gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed on core targets using R language; and molecular docking verification on the main active ingredients and core targets were conducted.Results:230 effective targets of active ingredients of HQJD were screened, and 15 467 active ingredients of breast cancer with syndrome of Zheng-deficiency/toxic-incandescence were obtained; 217 intersection targets; GO function enrichment analysis showed that the treatment of HQJD for breast cancer with the syndrome of Zheng-deficiency and toxic-incandescence mainly involved oxidative stress and cytochemical stress; The enrichment analysis of KEGG pathway showed that HQJD treatment of breast cancer with the syndrome of Zheng-deficiency and toxic-incandescence was mainly related to phosphatidylinositol 3-protein kinase B (PI3K-Akt), interleukin-17 (IL-17) and other signal pathways. The molecular docking results showed that the main active ingredients such as β-sitosterol, stigmasterol, luteolin had good binding ability with core targets.Conclusions:HQJD has the characteristics of multi-component, multi target and multi pathway in the treatment of breast cancer with syndrome of Zheng-deficiency and toxic-incandescence, and its main mechanism may be related to PI3K-Akt, IL-17, P53 and other signal pathways.

Objective:Standardized sample resources and high-quality clinical big data are important resources for medical research, only through resource sharing can maximize its utilization.Which can be utilized to the max only through resource sharing.Methods:This paper attempts to explore the sharing mechanism of the resource sharing platform and proposes some aspects such as the platform construction background, management regulations, legal ethical system, data sharing principles, benefit distribution, etc.This article attempts to explore the sharing mechanism based on the resource sharing platform of the respiratory disease biobank, proposes the contents that should be included in the sharing mode.Detailed information including the platform construction background, management procedures, legal and ethical system, data sharing principles and benefit distribution should take into consideration in the operating mechanism of the platform.Results:Establishing a resource sharing platform matches the development of clinical research in China.The tailored sharing model which is suitable for the field of respiratory diseases will also guide the rapid development of clinical research.Conclusions:The construction of a respiratory disease biobank sharing platform is conducive to promoting the opening and sharing of biological samples and information resources in the context of big data.

Objective To investigate the effects of Niuhuang (Bovis Calculus, BC) and Shexiang (Moschus) (BC-Moschus) on human hepatocellular carcinoma (HCC) cells SMMC-7721 and a nude mouse model of subcutaneous xenografts, and to explore its anti-HCC mechanism. Methods The BC-Moschus combination was applied to two liver cancer models in vivo and in vitro. SMMC-7721 was divided into the BC-Moschus group and the control group, and different doses (rude drug dosage 0.625, 1.25, 2.5, and 5 mg/mL) of BC-Moschus extract were used for the intervention. The proliferation ability of HCC cells was detected using the Cell Counting Kit-8 (CCK-8) assay, and the migration ability was detected by a wound healing assay. A subcutaneous xenograft model was prepared using nude mice with human HCC. Specific pathogen-free-grade BALB/c nude mice (5-week-old) were randomly divided into the following groups (n = 6 per group): control (0.9% physiological saline 0.2 mL/d), BC-Moschus [BC 45.5 mg/(kg·d)+ Moschus 13 mg/(kg·d)], and cisplatin (DDP, intraperitoneal injection 5 mg/kg per week) groups. All groups were administered for 14 d. The volume and mass of the subcutaneous xenografts in nude mice were observed. The expression levels of phosphatidylinositol-3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway, apoptosis-associated factor p70 S6 Kinase (S6K), Bax, Bcl-2, caspase-3, and caspase-9 in nude mice subcutaneous xenografts were measured by real-time quantitative PCR (RT-qPCR) and Western blot. Terminal Deoxynucleotidy Transferase-Mediated dUTP Nick-End Labeling (TUNEL) was used for quantitative analysis of apoptotic cells. Results The CCK-8 assay demonstrated that the BC-Moschus combination inhibited HCC cell proliferation in a superior manner to the use of BC and Moschus alone, and the inhibition effect was dose- and time-dependent (P < 0.01). The wound healing assay showed that the BC-Moschus combination inhibited HCC cell migration (P < 0.01). In the subcutaneous xenograft model of nude mice with human HCC, we found that the tumor volume and weight of the BC-Moschus group were lower than those of the control group (P < 0.01). The levels of the PI3K/AKT/mTOR signaling pathway and S6K protein in the BC-Moschus and DDP groups were significantly decreased (P < 0.01). The expression level of the anti-apoptotic gene Bcl-2 was downregulated (P < 0.05), and the expression of the pro-apoptotic gene Bax and apoptosis-related factors caspase-3 and caspase-9 were significantly upregulated (P < 0.01). The TUNEL assays further confirmed that the combination of the BC-Moschuas could promote HCC (P < 0.01). Conclusion The BC-Moschus combination inhibited the proliferation and migration ability of HCC cells SMMC-7721 and effectively inhibited the growth of subcutaneous xenografts in nude mice. The mechanism may be closely related to the downregulation of the PI3K/AKT/mTOR pathway, regulation of apoptosis-related protein caspase-3, caspase-9, Bcl-2, and Bax expression, and promotion of apoptosis.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease caused by inflammatory cells. Various inflammatory cells involved in RA include fibroblast-like synoviocytes, macrophages, CD4⁺T-lymphocytes, B lymphocytes, osteoclasts and chondrocytes. The close interaction between various inflammatory cells leads to imbalance of immune response and disorder of the expression of mRNA in inflammatory cells. It helps to drive production of pro-inflammatory cytokines and stimulate specific antigen-specific T- and B-lymphocytes to produce autoantibodies which is an important pathogenic factor for RA. Competing endogenous RNA (ceRNA) can regulate the expression of mRNA by competitively binding to miRNA. The related ceRNA network is a new regulatory mechanism for RNA interaction. It has been found to be involved in the regulation of abnormal biological processes such as proliferation, apoptosis, invasion and release of inflammatory factors of RA inflammatory cells. Understanding the ceRNA network in 6 kinds of RA common inflammatory cells provides a new idea for further elucidating the pathogenesis of RA, and provides a theoretical basis for the discovery of new biomarkers and effective therapeutic targets.
Humans ; Arthritis, Rheumatoid/genetics* ; MicroRNAs/metabolism* ; Synoviocytes/pathology* ; Cytokines/metabolism* ; RNA, Messenger/metabolism* ; Fibroblasts/pathology* ; Cell Proliferation