Objective To explore the efficacy of tepronone and folic acid in the treatment of chronic atrophic gastritis (CAG) evaluated by the marking targeting biopsy (MTB).Methods A total of 224 H.pylori negative CAG patients were selected and divided into group A (n 96,tepronone 50 mg/time,folic acid 10 mg/time,three times/day),group B (n=23,tepronone 50 mg/time,three times/day),group C (n=74,unspecific treatment) and group D (n=31,no treatment).The treatment course lasted for one year.The clinical symptoms improvement of each group was observed before and after treatment.The pathological improvement of gastric mucosa by MTB was inspected before and after treatment.The chi square test was performed for the comparison between groups.Results The total efficacy rates of group A,B,C and D were 43.8％ (42/96),39.1％ (9/23),33.8％(25/74) and 32.3％ (10/31) respectively,there was no significant difference between groups (x2 =2.328,P =0.507).For the significant efficacy rate of gastric mucosa pathological improvement,group A was compared with group D,group A was compared with group C and group B was comparedwith group D,the differences were significant (x2 =14.520,14.628 and 8.995,all P＜0.01).In the total efficacy rate of gastric mucosa pathological improvement,group A (49.8％,131/263) was compared with group D (24.2％,16/66),group A was compared with group C (35.9％,66/184)and group B (44.7％,21/47) was compared with group D,the differences were significant (x2 =13.953,8.535 and 5.207,all P＜0.05).Conclusion Teprenone alone or teprenone and folic acid combination can obviously improve pathological changes of CAG patients.

Background:Hydrotalcite has been used in the treatment of gastric ulcer,but its mechanism is not clear. Aims:To investigate the efficacy and mechanism of hydrotalcite on experimental gastric ulcer in rats. Methods:Experimental acetic acid-induced gastric ulcer model was established in rats. Model rats were randomly assigned into control group,low and high dose hydrotalcite groups,and 0. 9% NaCl solution,880 mg·kg - 1 ·d - 1 ,1 230 mg·kg - 1 ·d - 1 hydrotalcite were intragastrically administrated,respectively. After 14 days,macroscopic examination was performed;and HE staining, CD31 staining and VG staining were used to evaluate the histological maturity,AB-PAS staining,level of hexosamine, immunohistochemical staining,serum levels of epidermal growth factor( EGF),prostaglandin E2( PGE2 )were used to evaluate the functional maturity. Results:Compared with control group,ulcer index(UI)was significantly decreased in high dose hydrotalcite group(P < 0. 05). Thickness of restored mucosa was significantly increased(P < 0. 05),number of cystically dilated gland was significantly decreased(P < 0. 01),microvessel density(MVD),collagen fiber,secretion of mucus,level of hexosamine,expressions of EGF,EGR receptor(EGFR)and PGE2 ,serum levels of EGF and PGE2 were significantly increased in low and high hydrotalcite groups( P < 0. 05,P < 0. 01). Conclusions:Hydrotalcite could obviously improve the histological and functional maturity of regenerative mucosa,as well as the quality of ulcer healing. The mechanism might be related to the neutralization of gastric acid,enhancement of mucus-HCO3 - barrier and up-regulation of expressions of EGF and PGE2 .

Objectives:To cross-sectionally analyze the clinical characteristics of primary antiphospholipid syndrome (PAPS) patients with thrombocytopenia, risk factors associated with thrombocytopenia, and risk of symptom recurrence in these patients.Methods:The inpatients with PAPS were retrospectively analyzed in Peking Union Medical College Hospital from 2009 to 2019. Using the collected clinical and laboratory data, the clinical characteristics and risk of symptom recurrence in the PAPS patients with thrombocytopenia were compared with those in the PAPS patients with normal platelet counts. Univariate and multivariate logistic regression analyses were performed to screen the risk factors for thrombocytopenia.Results:In this study, 127 patients with PAPS were enrolled, of which 36 (28.3% ) had thrombocytopenia, with a median age of 38 years, and 63.9% were female. In the thrombocytopenia group, the average platelet count was (58.9±27.0) ×10 9/L, and the prevalence of thrombosis and morbid pregnancy was not significantly different from that in the normal platelet group. However, the thrombocytopenia group had higher incidence rate of autoimmune hemolytic anemia (19.4% vs 3.3% ) , livedo reticularis (16.7% vs 3.3% ) , chronic kidney disease (25% vs 8.8% ) and antiphospholipid antibodies triple positiveness (61.1% vs 37.4% ) , lower complement levels (C3 of 0.87 g/L vs 1.07 g/L, C4 of 0.12 g/L vs 0.18 g/L, P<0.05) , and higher adjusted Global APS Score (median score of 13 vs 9, P=0.037) than the normal platelet group. In multivariate logistic regression analysis, hypocomplementemia ( OR value 5.032, 95% CI 3.118-22.095) is an independent risk factor for thrombocytopenia. Conclusions:In patients with PAPS, thrombocytopenia is mostly mild to moderate. Hypocomplementemia may be the independent risk factor for thrombocytopenia in PAPS patients. The PAPS patients with thrombocytopenia may have a higher risk of symptom recurrence.

Objective To investigate the prevalence of genital Chlamydia trachomatis (GCT) infection and associated risk factors in male clients attending sexually transmitted disease (STD) clinics in Guangdong and provide integrated intervention strategy for this group.Methods Convenient sampling was used to recruit participants from April to June in 2015 in Guangdong province.The information about their socio-demographic characteristics and sexual behaviors were collected by using a questionnaire,and blood samples were taken from them to test the antibodies against HIV,syphilis and HCV.First pass urine was taken to test GCT and gonorrhea.Results A total of 1 749 participants with the average age of 39.53 years were recruited.The majority of them were married (73.87％,1 292/1 749),residents of Guangdong (92.28％,1 614/1 749) and in Han ethnic group (99.49％,1 740/1 749).The positive rates for GCT,HIV,syphilis,HCV,Neisseria gonorrhea,and WBC in urinalysis were 6.06％ (106/1 749),0.46％ (8/1 749),3.43％ (60/1 749),0.45％ (7/1 550),2.74％ (48/1 749),7.89％ (138/1 749) respectively.Multivariate analysis showed that risk factors for GCT infection include IDUs (OR=13.98,95％CI:3.35-58.38),anal sex with men (OR=3.11,95％ CI:1.45-6.71),Neisseria gonorrhea positive (OR =9.64,95％ CI:5.09-18.24),and WBC positive (OR =1.96,95％ CI:1.08-3.55).Conclusions This study demonstrated the high prevalence of GCT infection in male clients attending STD clinics in Guangdong.Therefore precision intervention should target this population at high-risk.

Objective To investigate the mechanism by which Tougu Xiaotong Capsule(TGXTC)alleviates chondrocyte degeneration in knee osteoarthritis(KOA).Methods Thirty 2-month-old C57BL/6 mouse models of KOA established using the Hulth method were randomized into model group,TGXTC group,and diclofenac sodium group and received treatment with saline,TGXTC(368 mg/kg),and diclofenac sodium(10 mg/kg)by gavage,respectively,with another 10 untreated mice as the blank control group.All interventions were administered 6 times a week for 4 weeks.After the treatments,structural changes in the cartilage tissue were observed with morphological staining,and Nav1.7 mRNA expression and the protein expression levels of Nav1.7,MMP-3,ADAMTS-5,and COX-2 were detected using RT-qPCR and Western blotting.Fluorescence in situ hybridization(FISH)was used to detect Nav1.7 expression in the chondrocytes.In cultured KOA chondrocytes,the effect of TGXTC and lentivirus-mediated Nav1.7 knockdown on MMP-3,MMP-13,ADAMTS-4,ADAMTS-5,and COX-2 protein expressions were assessed with Western blotting.Results In KOA mice treatments with TGXTC and diclofenac sodium both significantly alleviated structural damage of the cartilage layer,reduced Nav1.7 protein and mRNA expressions and lowered the expressions of MMP-3,ADAMTS-5,and COX-2 proteins in the cartilage tissues.FISH results indicated that TGXTC treatment significantly reduced IL-1β-induced Nav1.7 expression in the chondrocytes.In Nav1.7 knockdown experiment,Nav1.7 levels were significantly lower in IL-1β+sh-Nav1.7 group than in IL-1β group,and also lower in IL-1β+TGXTC group than in IL-1β+sh-Nav1.7+TGXTC group.TGXTC treatment significantly inhibited IL-1β-induced elevation of MMP-3,MMP-13,ADAMTS-4,ADAMTS-5 and COX-2 protein expressions in the chondrocytes,but its effects were strongly weakened by Nav1.7 knockdown.Conclusion TGXTC alleviates extracellular matrix metabolic disorder in KOA chondrocytes by regulating Nav1.7,thereby mitigating chondrocyte degeneration in KOA mice.

Objective To investigate the mechanism by which Tougu Xiaotong Capsule(TGXTC)alleviates chondrocyte degeneration in knee osteoarthritis(KOA).Methods Thirty 2-month-old C57BL/6 mouse models of KOA established using the Hulth method were randomized into model group,TGXTC group,and diclofenac sodium group and received treatment with saline,TGXTC(368 mg/kg),and diclofenac sodium(10 mg/kg)by gavage,respectively,with another 10 untreated mice as the blank control group.All interventions were administered 6 times a week for 4 weeks.After the treatments,structural changes in the cartilage tissue were observed with morphological staining,and Nav1.7 mRNA expression and the protein expression levels of Nav1.7,MMP-3,ADAMTS-5,and COX-2 were detected using RT-qPCR and Western blotting.Fluorescence in situ hybridization(FISH)was used to detect Nav1.7 expression in the chondrocytes.In cultured KOA chondrocytes,the effect of TGXTC and lentivirus-mediated Nav1.7 knockdown on MMP-3,MMP-13,ADAMTS-4,ADAMTS-5,and COX-2 protein expressions were assessed with Western blotting.Results In KOA mice treatments with TGXTC and diclofenac sodium both significantly alleviated structural damage of the cartilage layer,reduced Nav1.7 protein and mRNA expressions and lowered the expressions of MMP-3,ADAMTS-5,and COX-2 proteins in the cartilage tissues.FISH results indicated that TGXTC treatment significantly reduced IL-1β-induced Nav1.7 expression in the chondrocytes.In Nav1.7 knockdown experiment,Nav1.7 levels were significantly lower in IL-1β+sh-Nav1.7 group than in IL-1β group,and also lower in IL-1β+TGXTC group than in IL-1β+sh-Nav1.7+TGXTC group.TGXTC treatment significantly inhibited IL-1β-induced elevation of MMP-3,MMP-13,ADAMTS-4,ADAMTS-5 and COX-2 protein expressions in the chondrocytes,but its effects were strongly weakened by Nav1.7 knockdown.Conclusion TGXTC alleviates extracellular matrix metabolic disorder in KOA chondrocytes by regulating Nav1.7,thereby mitigating chondrocyte degeneration in KOA mice.

Objective: To investigate the mechanism of action of Prim-O-glucosylcimifugin (POG) to improve cholesterol metabolism in osteoarthritic (OA) chondrocytes based on the long noncoding RNA nuclear-enriched transcript 1 (lncRNA NEAT1)/microRNA-128-3p (miR-128-3p) pathway. Methods: For in vivo experiments, 60 mice were divided into the normal, sham operation, model, and POG groups using the random number table method, with 15 mice per group. The osteoarthritis mouse model was constructed using the modified Hulth method in the model and POG groups. Mice in the POG group were administered 30 mg/(kg·d)POG by gavage. The other groups were administered an equal amount of normal saline for 8 weeks. The cartilage tissue structure of mice in each group was observed using hematoxylin and eosin staining. Real-time PCR was used to detect changes in the lncRNA NEAT1 and miR-128-3p mRNA expression levels in the cartilage tissues of mice. Western blotting was used to detect the protein expressions of ATP-binding cassette transporter A1 (ABCA1), liver X receptor β (LXRβ), matrix metalloprotein-3 (MMP-3), and B-lymphoblastoma-2-associated X protein (Bax) in articular cartilage of mice. An enzyme-linked immunosorbent assay was used to measure the tumor necrosis factor-α (TNF-α) content in the synovial fluid of mice. A biochemical microplate assay was used to measure the total cholesterol level in the synovial fluid of mice. The in vitro experiments were divided into the negative control, interleukin-1β(IL-1β), IL-1β+ POG, IL-1β+ oe-lncRNA NEAT1, IL-1β+ oe-lncRNA NEAT1 + POG, IL-1β + miR-128-3p inhibition, and IL-1β+ miR-128-3p inhibition+ POG groups. An OA model was established by inducing chondrocytes with IL-1β for 24 h, and 90 mg/L of POG and miR-128-3p inhibitor(50 nmol/L) were administered for 48 h as an intervention. lncRNA NEAT1 expression in chondrocytes was detected using fluorescence in situ hybridization. A dual luciferase assay was used to detect the targeting relationship between lncRNA NEAT1 and miR-128-3p. Lentiviral plasmids overexpressing lncRNA NEAT1 were used to transfect mouse chondrocytes. Real-time PCR was used to detect the effect of lncRNA NEAT1 overexpression on the mRNA level of miR-128-3p in chondrocytes. Western blotting was used to detect ABCA1, LXRβ, MMP-3, and Bax protein expression in chondrocytes after lncRNA NEAT1 overexpression and miR-128-3p inhibition. Results: POG significantly reduced OA cartilage tissue damage. Compared with the model group, the lncRNA NEAT1 mRNA level decreased, whereas the miR-128-3p mRNA level increased in the cartilage tissue of the POG group (P<0.05). Compared with the model group, ABCA1 and LXRβ protein expression increased in the POG group, whereas MMP-3 and Bax protein expression decreased (P<0.05). The TNF-α levels decreased in the POG group compared to the model group (P<0.05). Compared with the model group, the total cholesterol level in the synovial fluid of the joint of mice in the POG group decreased (P<0.05). The mean fluorescence intensity of lncRNA NEAT1 in the IL-1β+ POG group decreased compared with the IL-1β group (P<0.05). The relative luciferase activity in the miR-128-3p mimics group bound to the lncRNA NEAT1-WT plasmid decreased compared with the miR-128-3p negative control group (P<0.05). The lncRNA NEAT1 mRNA levels decreased, whereas the miR-128-3p mRNA levels increased in the IL-1β+ oe-lncRNA NEAT1 + POG group compared with the IL-1β+ oe-lncRNA NEAT1 group (P<0.05). Compared with the IL-1β+ POG group, ABCA1 and LXRβ protein expression decreased, whereas MMP-3 and Bax protein expression increased (P<0.05). Conclusion POG mediates lncRNA NEAT1/miR-128-3p to improve cholesterol metabolism in OA chondrocytes.