BACKGROUND: Bladder cancer is a cancer of significant morbidity and mortality in the worldwide. It is the second most common urological cancer in Mongolia. It is important to understand the risk factors of bladder cancer.We evaluated the association of smoking, alcohol intake, body mass index and other potential risk factors with bladder cancer incidence in Mongolians.MATERIALS AND METHODS: We analyzed data from a case-control study (116 histologically confirmed bladder cancer cases and 300 cancer-free healthy, age, gender-matched controls). All participants signed the consent form andfilled out the structured questionnaire including cigarette smoking, BMI, chronic urinary disease andalcohol drinking etc. Using logistic regression we estimated the covariate-adjusted odds ratio (OR) and95% confidence interval (CI) of the associations.RESULTS: Mean age of the patients with bladder cancer was 56±10.5 years and 79.3% male and 20.7% female.Cigarette smoking, history of urinary tract diseases and body mass index were associated with an increased risk of bladder cancer OR 6, 48 (95% CI 1, 61-1, 70), OR 80 (95% CI 1, 48-1, 93) and OR=9.8 (95% CI 2.32-2.91) respectively but not alcohol drinking OR 0, 26 (95% CI 1, 56-1, 66).CONCLUSIONS: The results suggest that cigarette smoking, history of urinary tract diseases and body mass indexincreased risk of bladder cancer in Mongolian patients.

Background: According to the First National Tuberculosis (TB) Prevalence Survey in Mongolia the prevalence of bacteriologically-confirmed pulmonary TB among adults was 559.6 (95% CI: 454.5–664.7) per 100000 population in 2014–2015. This was three times as high as previously estimated. Nationwide anti-tuberculosis (TB) drug resistance survey was conducted in 1999 and 2007 in Mongolia. Share of multidrug resistant TB (MDR-TB) cases among newly notified TB cases increased from 1.0% in 1999 to 1.4% in 2007. Accordingly, we aimed to perform drug susceptibility test on strains isolated from TB Prevalence Survey and to determine the prevalence of drug resistant TB. Material and Methods: All 242 MTB strains isolated from the survey TB cases were tested GenoTypeMTBDRplus test and conventional 1st line DST on solid medium. Result: Conventional DST and GenoTypeMTBDRplus tests done for 93.8% (227/242) of them and 6.2% (15/242) were tested by GenoTypeMTBDRplus only. A 61.6% (95%CI 55.3-67.4) of all cases were susceptible to first line anti-TB drugs, any drug resistance and MDR-TBdetected as 38.4% (95% CI 32.5-44.7)and 9.5% (95% CI 6.4-13.9), respectively. Prevalence of MDR-TB was7.8% (95% CI 4.9-12.4) among new and 17.9% (95% CI 9.0-32.7) among previously treated cases. The 64 strains were identified as a resistant to isoniazid, 32.8% (42/64) and 65.6% (21/64) were katG, and inhAmutation, respectively. One isolate (1.6%) was mutations in both the inhAand katGgenes.The predominant mutations detected in therpoB were S531L (91.3%) among rifampicin resistant isolates and the mutation in inhAwas C–15T (100%) and katG mutation was S315T1 (100%) among isoniazid-resistant isolates. Conclusion Prevalence of cases with DR-TB is high among prevalent TB cases, especially prevalence of MDR-TB among new cases. In comparison to previous studies, DR-TB cases seem to be increased. Rifampicin resistant strains have a mutation of the rpoBand resistance to isoniazid is predominantly associated with the inhA mutation.

BACKGROUND. HCV-infected and obesity related liver diseases are leading to increases in the prevalence of advanced liver disease. So, studying liver disease, especially liver fibrosis is crucial issue of today. In Mongolia digestive system disease is second causation of non-communicable disease. Therefrom in last years hepatocellular carcinoma is most common malignancy, first of all cancers in Mongolia. In response to acute or chronic liver injury, hepatic fibrosis is the accumulation of extracellular matrix and ultimately leads to cirrhosis. Cirrhosis is the end-stage of fibrosis, resulting in nodule formation that may lead to altered hepatic function and blood flow. Defining the phase of liver fibrosis is crucial for therapeutic choice prognosis, important role in monitoring treatment. At the present time, use of direct and undirect biomarkers methods could be recommended for liver fibrosis stage. The aim of this study is to determine liver fibrosis stage and to compare undirect biomarkers in chronic viral hepatitis, cirrhosis. METHODS: 630 cases by chronic viral hepatitis and cirrhosis at third central hospital in Mongolia from retrospectively reviewed and analysed. The clinical data including AST, ALT, platelet count and INR were recorded. APRI, FIB-4, AAR and FibroQ were calculated. RESULT: From all, males 42.06% and females 57.94%, with mean age of 55.35±24.0, in 130 cases with chronic viral hepatitis and 500 cases with cirrhosis. In cases of cirrhosis, mean value of platelet count, ALT, AST, INR was 120.54±73.53, 104.55±500.22, 111.68±279.97, 2.19±10.45, respectively. And in cases of chronic viral hepatitis platelet count mean value was 211.18±6.42. APRI was detected <0.5 cutoff value (F0-F1) 11.7% non-fibrosis, 0.5-1.5 score (F2-F3) 27.5% fibrosis, >1.5 cutoff value (F4) 60.8% cirrhosis. FIB-4 was determined <1.45 cutoff value (F0-F1) 14.8% non-fibrosis, 1.45-3.25 score (F2-F3) 15.7% fibrosis, >3.25 cutoff value (F4) 69.5%, AAR was showed <0.4 cutoff value (F0-F1) 2.3% non-fibrosis, 0.4-1 score (F2-F3) 30.2% fibrosis, >1 cutoff value (F4) 67.5%. And FibroQ was detected <0.6 cutoff value (F0- F1) 0.5% non-fibrosis, 0.6-2.6 score (F2-F3) 6% fibrosis, cutoff value 2.6< (F4) 93.5 cirrhosis. In study liver fibrosis staging by APRI, AAR, FIB-4 and FibroQ score system, AAR was determined fibrosis in 190 cases. CONCLUSION: Recorded data ALT, AST, INR in cases of cirrhosis were detected 104.55±500.22, 111.68±279.97, 2.19±10.45, respectively. And in cases of chronic hepatitis platelet count mean value was 211.18±6.42. APRI, AAR, FIB-4, FibroQ was determined fibrosis 27.5%,30.16%,15.71% and 6.03%, respectively.

Background: Treatment of adult tibiofibular fractures, especially severely comminuted fractures, is technically challenging due to the lack of reduction markers and difficulty in restoring the alignment. Fixation of the fibula can facilitate reduction of the tibia fracture and restoration of the lower extremity alignment. Methods: Between 2018-2019 we have operated on 50 patients who have lie on the same plane of tibiafibular fractures. Measures of angulation were obtained from radiographs taken immediately after the surgery, a second time 3 months later, and at 3-month follow-up. The analysis was performed with STATA. Results: Fixating fractures of tibia and fibula at same level were not shown to have complications on the development of nonunion including fibular shortening, hindfoot alignment, slow process of nonunion and unstableness. Conclusions We recommend fibular fixation in all 50 distal fractures when both fractures lie on the same plane and the tibial fracture is relatively stabilized.

BACKGROUND: Toll like receptors (TLRs) are a class of proteins that key role in the innate immune system. TLR7 is expressed on monocytes, macrophages and dendritic cells, T cell, B cell and eosinophiles. TLR7, originally identified as recognizing imidaquinoline, loxibrine, broprimine and ssRNA, ssRNA viruses such as vesicular stomatitis virus, influenza A virus and human immunodefiency virus. It is known that virus ssRNA affects signaling molecule of IFN-y. Objective: To determine gene and protein activation of IFN-y signal transduction by TLR7 ligand in the endothelial cells. MATERIAL: In study we used mouse aortic linear endothelial cell which is cultured (END-D) in 5% heat- inactivated fetal calf serum (FCS), medium (DMEM) containing antibiotic mix(penicillin G, streptomycin, amphotericin B) at 37°C (5% CO2). Endothelial cells treated with synthetic IFN-γ and imiquimodligands, then the NO (nitric oxide) concentration in the supernatant is determined by Griess reagent. Endothelial cells are cultured in 6 well cell culture plate and in each well 2*104cells are expected to be grown for 24 hours of culture. Then, the cells are treated with synthetic IFN-γ and имиквимод ligand for 6 hours and the NO signaling gene activation iNOS mRNA expression which is induced by IFN-γ is determined by RT-qPCR. Endothelial cells are cultured in 12 well cell culture plate and in each well 2*104 cells are expected to be grown for 18 hours of culture. Then, the cells are treated with synthetic IFN-γ and imiquimodligands for 24 hours and the NO signaling protein iNOS expression which is induced by IFN-γ is determined by western blotting. The experiment was conducted as representation mean of at least three test results. The difference between statistical probabilities is determined by the “Students” t test. The p<0.01 value is assumed to be statistically different. RESULTS: TLR7 ligand imiquimodaugmented interferon gamma induced nitric oxide production TLR7 ligand imiquimodincreased interferon gamma induced iNOS mRNA gene expression. TLR7 ilgand imiquimodup-regulated interferon gamma induced iNOS protein expression. CONCLUSIONS: TLR7 ligand imiquimod augments IFN-γ signaling in the endothelial cells. This synergistic effect has revealed in the levels of gene and protein expression.

Introduction: When human body encounters external pathogens primary/innate immunity cells are activated by recognizing them and secondary/adaptive immunity is activated consecutively. Immune cell surface receptors, called Toll-like receptors (TLRs) recognize and bind pathogens. In our previous study, we revealed that there is a synergistic action between TLR9 and IFN-γ signaling in the endothelial cells. Purpose: To determine the role of negative and positive regulatory proteins on the IFN-γ/TLR9 synergistic signaling pathway Materials and Methods: This study was held in the Core Laboratory, Science Technology Center, Mongolian National University of Medical Sciences (MNUMS). In this study, murine endothelial cell (END-D) culture was used. The negative and positive regulator protein expression was detected by Western blotting. Result: Result of immunoblotting assay indicated that CpG DNA enhanced IFN-γ positive regulator protein p38 phosphorylation in the endothelial cells. Treatment by TLR9 ligand CpG DNA and IFN-γ increased p38 activation in 0.5 hour and 1 hour. CpG DNA inhibited IFN-γ negative regulator SOCS1 protein expression in 4 hr and 8 hr. Therefore, TLR9 ligand CpG DNA increased IFN-γ signal transduction in the endothelial cell line. Conclusion TLR9 ligand CpG DNA has decreased IFN-γ negative regulator protein SOCS1 expression. CpG DNA has increased IFN-γ positive regulator protein p38 phosphorylation.

Introduction: Toll like receptors (TLRs) are a class of proteins that key role in the innate immune system. The SOCS1 and SHP2 proteins are negative-feed loop inhibitors of signaling of JAK/STAT and TLRs pathways. Purpose: To determine negative regulator protein activation which is activated through TLR7 ligand/IFN-γ signal transduction in endothelial cells. Methods: We used mouse aortic linear endothelial cell (END-D); protein expressio was detected by western blotting Results: We analyzed a time dependent stimulation effects of negative regulator proteins stimulated by TLR7 ligand/IFN-γ in endothelial cell cultures. Imiquimod of 10 μg/ml treatment of 1 hr was followed by 100 ng/ml IFN-γ stimulation for 1-8hr to analysis of negative regulator SOCS1 and SHP2 protein expression.
In untreated cells, there was low activations of negative regulator SOCS1 and SHP2 proteins. IFN-γ stimulation alone had increased SOCS1 and SHP2 protein expressions, also imiquimod treatment highly elevated SOCS1 and SHP2 expressions. However imiquimod and IFN-γ doubled treatment have decreased activation of negative regulator SOCS1 and SHP2 proteins. These findings suggest SOCS1 and SHP2 proteins are inhibitors in the TLR7 ligand/IFN-γ signaling. Conclusion Negative regulators, SOCS1 and SHP2 strongly suppressed activations of TLR7 ligand/IFN-γ signaling

Introduction: The aim of this research project is to elucidate the crosstalk of innate and adaptive immune reactions against the DNA containing bacteria. : This study held in the Core laboratory, Science Technology Center, Mongolian National University of Medical Sciences (MNUMS). Murine aortal endothelial cells, END-D cultured and the cell viability checked by MTT assay. In addition, the NO production, protein and gene expression studied by Griess Reagent assay, R.T-PCR and immunoblotting, respectively. Results: 0.1µM, 1µM and 10µM of TLR9 ligand exhibited no cytotoxic action against the cells by MTT assay. IFN-ү alone induced NO production in END-D cells. In the other hand, TLR9 ligand at 0.1µM, 1µM and 10µM up-regulated IFN-ү induced NO production in dose dependent manner. RTPCR results exhibit that TLR9 ligand up regulates iNOS mRNA. Immunoblotting analysis showed the enhanced iNOS protein expression and phosphorylation of STAT1 in cells pre-treated with TLR9 ligand. Discussion: We have demonstrated CpG DNA, TLR9 ligand, up-regulates IFN-ү induced NO via enhanced IFN-ү signaling. The result of Western Blotting and RT-PCR support the up-regulation of NO. CpG DNA can be used as agent against virus and bacteria. Further research need to be conducted. Conclusion TLR9 ligand, CpG DNA up-regulates IFN-ү induced NO production in time and dose dependent manner. TLR9 ligand augments the expression of iNOS mRNA and STAT1 phosphorylation in response to IFN-ү.

Introduction: When human body encounters external pathogens primary/innate immunity cells are activated by recognizing them and secondary/adaptive immunity is activated consecutively. In our previous study, we revealed that there is a synergistic action between TLR9 and IFN-γ signaling in the endothelial cells. Purpose: To determine the role of negative and positive regulator proteins on the IFN-γ/TLR9 signaling pathway. Methods: In this study, murine endothelial cell (END-D) culture was used. END-D cells pre-treated with TLR9 ligand CpG DNA and then stimulated with IFN-γ. The negative (SHP-2, SOCS1, PIAS1) and positive (p38) regulator protein expression was detected by Western blotting. Results and Conclusion Treatment by TLR9 ligand CpG DNA and IFN-γ increased positive regulator p38 phosphorylation in 0.5 hour. CpG DNA inhibited IFN-γ negative regulator PIAS1 protein expression in 6 hour and SOCS1 and SHP-2 expression could not affect in 4 hour.