The main goal is to determine main cause of hemorrhage, peculiarity of blood, blood products replacement and supply of the blood cells in practice of First Maternity Hospital during last years. The study subjects were recruited the medical data of pregnant women being delivered at the First Maternity Hospital last 10 years. WHO diagnostic criteria were used to define hemorrhage. The data with the hemorrhage were analyzed prospectively by computer programm and was writed in word. Factor analysis was performed to group of normal and pathology delivery and etc. and analyses factors hemorrhage. Conclusion: The main causes of pre and postpartum hemorrhage arc miscarriage, non-legal abortion, pathology of placenta based on the extra gcnitlll diseases and pathology of pregnancy of mothers Hemorrhage is to be on 3 place amongst the serious complications of obstetrics In First Maternity Hospital as to increased number of delivery year by year the percentage of complications of delivery also are grow. Therefore the transfusion of blood and blood products also increasing.

Background: Since its first identification of Pandemic H1N1 2009 in Oct 12, 09 in Mongolia, the cases have increased dramatically spreading in much of cities and provinces of Mongolia. We aimed to identify and compare the transmissibility of the infection in different household settings, so to add understanding of special characteristics of this infection.Methods: We selected 20 laboratory confirmed 2009 H1N1 influenza as the index cases from the National Surveillance System. We searched for Influenza like illness (ILI) cases in the households by questioning index-cases and household-contacts. Secondary case was defined as household-contact who developed one of the signs such as fever, dry cough, sore throat, runny nose and diarrhea within one week of symptom onset in index case. We calculated and compared attack rates in ger and apartment areas.Results: Transmissibility of 2009 H1N1 influenza was studied in 20 households. Each half was from ger and apartment residency of Ulaanbaatar city, Mongolia. The study involved 20 indexcases and 72 household-contacts. Secondary transmission occurred in 13 (65%) households with 22 (30.5%) household cases of probable Pandemic H1N1 influenza virus infection. The incidence in ger and apartment areas was 36.1% and 25.0% relatively. Cases in ger residency were 1.2 times more likely than in apartment residency to develop ILI (RR = 1.2, 95%CI: 0.86- 1.60).Conclusions: Overall secondary attack rate in this study was 30.5%, which is similar to that of 30% secondary attack rate for laboratory-confirmed 2009 H1N1 influenza in tourist group members in China. Though statistically not significant, the risk estimation of secondary ILI compared in ger and apartment residency indicates ger area residents have 20% higher risk for ILI development after illness in index case.

Background: High blood pressure is both a cause and a complication of chronic kidney disease. As complication, high blood pressure may develop early during course of chronic kidney disease and is associated with adverse outcomes, in particular faster loss of kidney function and development of cardiovascular disease. The purpose of this study is early detection of chronic kidney disease in patients with hypertension by defining the prevalence of microalbuminuria.Methods: The study population consisted of 169 subjects with a hypertension. Individuals were considered to have hypertension if the blood pressure measured greater than 140/90 mmHg or if they were taking blood pressure lowering medications. Microalbuminuria was defined as 20 mg/l or greater. Results: We are presenting data on 169 subjects :male 38 (22.5%) female 131 (77.5%), average age 51.6±0.89 At screening, 14.8% of all participants were smokers, 62.1 % engaged in low levels of physical activity, 72.8% - were having tea with salt (table1). Microalbuminuria and renal failure, as GFR<60 ml/ min/1.73 m2, were documented in 34.3% and 16.6% of subjects, respectively. There is positive correlation between MAU and increasing-range of blood pressure (table2). Correlation was found between albuminuria and GFR(r= -0.2 p<0.01) and serum creatinine(r=0.31 p<0.01) the regression result has shown that GFR is associated with MAU and serum creatinine (table 3).Conclusions:1. In 34.3% of patient with hypertension was found nephropathies with MAU2. Microalbuminuria is increased with decline of GFR and raise of systolic blood pressure. GFR decline is with the raise of age and serum. It is important to implement in clinical practice screening of MAU hypertensive patients.3. In 2/3 of all screened subjects was found 1 and more risk factors for CVD.

Introduction: Valproic acid (VPA) has been used in the treatment of seizures and bipolar disorders. In the present study, we examined how VPA affected PI3K-Akt pathway in response to LPS by using mouse RAW 264.7 macrophage cells. Material and methods: Mouse RAW 264.7 macrophage-like cells cultured and the cell viability checked by MTT and TUNEL assay. In addition, protein expression and protein interaction were detected by immune blotting and immune precipitation, respectively. TLR4 expression on cell surface studied by FACS analysis. Results: The MTT and TUNEL assays demonstrated no significant difference between VPA at 2 mM treated and untreated control cells. VPA attenuated LPS-induced phosphorylation of phosphatidylinositol 3-kinase (PI3K) and Akt, but not nuclear factor (NF)-κB and mitogen activated protein kinases (MAPKs). There was no significant difference in the TLR4 expression on the cell surface between cells treated with or without VPA. VPA inhibited LPS-induced PI3K/Akt signal transduction in a dose dependent manner. Conclusion VPA at 2mM exhibits nontoxic effect in the RAW 264.7 cells. VPA down regulates LPS-induced phosphorylation of Akt via inhibition of PI3K activation.

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: 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.