Introduction: Electrolyte values are measured by two different analyzers: arterial blood gas (Point of care) and auto-analyzers. Those two has different methods to measure electrolytes and have several pros and cons. We evaluated if there was agreement between whole blood electrolytes measured by a point-of-care device and serum electrolytes measured using indirect ion-selective electrodes. Materials and methods: An observational cohort study was conducted in 50 paired venous samples from patients admitted in Gurvan gal central hospital. Those were analyzed on OPTC blood gas devise and Roche c-501 auto-analyzer. Statistical analyses were performed using paired t-test and persons’ correlation test. Results: Sodium mean range was 138.54 mmol/l (SD=3.69) by blood gas analyser, but by the automated analyser mean range was 140.75 mmol/l (SD=4.45). Mean difference of the normal sodium group was 1.77 (SD=1.65, p=0.039), and hyposodium group was 4.4 (SD=0.33, p=0.007). Pottasium mean range was 3.13 mmol/l (SD=0.53) by blood gas analyser, but by the automated analyser mean range was 4.42 mmol/l (SD=0.45). Mean difference of the normal sodium group was 0.18 (p<0.001), and hypokalemi group was 1.44 (p<0.001). Conclusion Clinicians should be aware of the difference between whole blood and serum electrolytes. A correction factor needs to be determined at each laboratory.

BACKGROUND:The mouse double minute 2 (MDM2) is a negative regulator of the p53 tumor suppressor protein.Overexpression of MDM2 is associated with poor survival and is a useful predictive factor for poor prognosisin various cancers in human. Studies revealed a genetic polymorphism located in intron 1 of the MDM2gene, MDM2-SNP309, (a change from T to G) is main functional polymorphism and important to developtumors. However, inconsistent associations between the MDM2-SNP309 and the risk or early onset ageof human different cancers have been reported worldwide. These conflicting results may have dependedon different patient subgroups and ethnicities studies. We studied the association of the MDM2-SNP309polymorphism andbladder cancer in Mongolian patients for the first time.OBJECTIVE:To investigate association between MDM2-SNP309 and the risk bladder cancer or early onset age of thecancer in Mongolian patients.MATERIALS AND METHODS:We genotyped MDM2-SNP309 in 44 patients with bladder cancer and 44 age and gender matched healthycontrols among Mongolian people.Genomic DNA was extracted from whole blood samples by the standardmethod of Qiagen mini blood DNA extraction kit (Qiagen Inc., Valencia, CA) and PCR amplification wasperformed using 100 ng genomic DNA template according to manufacturer’s protocol (Invitrogen, Carlsbad,CA). MDM2 SNP309 genotyping was carried out by restriction fragment length polymorphism assay.RESULTS: The allele frequencies of MDM2 SNP309 in the 44 bladder cancer patients were wild-type (T/T) 27.3%,homozygous (G/G) 34.1% and heterozygous (T/G) 38.6% whereas in the control cases were wild-type(T/T) 29.5%, homozygous (G/G) 20.5% and heterozygous (T/G) 50.0%. The proportion of homozygous(G/G) genotype was higher for bladder cancer cases than for healthy controls. Compared to the low-risk(wild type) genotype, an increased risk association with bladder cancer was shown for the GG genotype(OR=2.0, 95% CI=1.03-1.84). There is also a significant difference in median age onset of bladder cancerbetween GG low and high risk genotypes T/T and T/G (p=0,003)( p=0.0001), respectively (Figure2).CONCLUTION: The current sample data suggests that MDM2 SNP309 GG genotype may be associated withthe risk of bladder cancer as well as an earlier age onset in Mongolian patients with bladder cancer.

Introduction: In 2018, a total of 901 new cases of gastric cancer were recorded, of which 64.8% in males and 34.2% in females. The incidence rate of gastric cancer was 28.5 per 100 000 population, which 38.2 for males and 19.2 for females. Goal: We aimed to investigate the associations between some risk factors and gastric cancer among the Mongolian population. Materials and Methods: A case-control study was conducted between November 2017 and September 2019. We selected 120 cases from National cancer center of Mongolia who newly diagnosed gastric cancer. And 120 controls were selected by matching by sex, age and the place of residence. Informed consents were obtained from all subjects. All subjects were personally interviewed with researchers used by a structured questionnaire consisting of 86 questions. The SPSS 21 (version 16.0, SPSS Inc., Chicago, IL, USA) software was used for all analyses. Results: The mean age was 59.2±11.4 (26-85) years. Habits of having dinner after 6.00 pm (OR 1.42, 95%CI 1.11-1.83, p=0.008), having leftover meals (OR 2.22, 95%CI 1.27-3.86, p=0.008), daily consumption of tea with salt (OR 1.97, 95%CI 1.18-3.30, p=0.01), smoking on an empty stomach (OR 2.44, 95%CI 1.11-5.37, p=0.033), weekly consumption of ham and smoked meat (OR 1.5, 95%CI 1.17- 2.13, p=0.02), and consumption of fat grease (OR 2.09, 95%CI .03-4.24, p=0.038) were significantly increased gastric cancer risk. In contrast, habit of eating at regular times (OR 0.43, 95%CI 0.25-0.73, p=0.002), chewing thoroughly (OR 0.39, 95%CI 0.23-0.67, p=0.001), cooking meat thoroughly until it’s tender (OR 0.48, 95%CI 0.25-0.97, p=0.047), daily consumption of vegetables (OR 0.45, 95%CI 0.27-0.76, p=0.003), and daily consumption of fruit juice (OR 0.36, 95%CI 0.15-0.85, p=0.026) were significantly reduced gastric cancer risk. Furthermore, having first-degree relatives diagnosed with gastric cancer had 2-3 fold higher increased risk of gastric cancer (parents OR 2.88, 95%CI 1.07- 7.78, p=0.038, sibling (OR 3.09, 95%CI 1.09-8.81, p=0.036). Also, previous records of the digestive disease increased risk of gastric cancer (OR 3.65, 95%CI 2.10-6.35, p<0.0001). Conclusion Dietary habits, family history of gastric cancer and previous records of digestive disease were associated with risk of gastric cancer. Thus, prevention effort could be focused on the population with a family history of gastric cancer, changing bad dietary habit and screening precancerous disease of gastric cancer.

Introduction: In 2018, the overall colorectal cancer (CRC) incidence rate was 3.6%, according to the National Cancer Center of Mongolia (NCCM), and the incidence of colorectal cancer has increased slightly in recent years. According to cancer stages, late stage cancer has a 5-year survival rate of 51%, while early stage cancer has a 5-year survival rate of 79%. The overall survival rate of colorectal cancer in Mongolia has not been studied in precisely. In Asia, the 5-year survival rate for colorectal cancer was 60%. Therefore, this study investigated the colorectal cancer survival rate and prognostic factors at NCCM. Methods: A total of 108 patients diagnosed with CRC at NCCM’s General Surgery Department from 2013 to 2015 were used in this retrospective cohort study. The Kaplan-Meier method was used to develop the survival graphs, which were then compared using the Log-rank test. Results: The median survival time was 42 months, with a 95% CI (38.55-45.66). A 5-year period, the overall survival rate for CRC was 61.2%. Survival rates at the I, II, III, and IV stages were 100%, 75%, 65.4%, and 13.5%, respectively. There was a significant difference in CRC survival rates across all stages (p=0.0001). There was a statistically significant difference in determining the relationship between adjuvant chemotherapy and survival rate (p=0.0003). Conclusion The outcome of the surgery is determined by the CRC stage. The postoperative survival rate (61.2%) is directly related to tumor stage, peripheral glandular metastasis, distant metastasis, and chemotherapy effects.

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.

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: 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: 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.