Climate: Studies show that it is get warmer 2.10C in Mongolia in last 40 years. It influences ecology and decreased ecology event, succession action in ecosystem. It is interesting to study how climate change damage animal’s biology and ecology. The survey on changing ecology is rare conducted in Mongolia. Year average air temperature in Govi-Altai province got warmer 1.20C in last 30 years. Monitoring agency for meteorology and environment of Govi-Altai aimag summarized air temperature 1980-2009 (4-9 months) and it is got warmer 2.00C in Tonkhil soum.Plants: According to our research, at the above sea level around 2229-2600m dry steppe, at a.s.l 2601-2800m in steppe and water-meadow steppe at a.s.l 2801m high mountain steppe, zone plants grow. At the report of research for motion and episodic in epicenter of the marmot plague (1987-1991) aspect of plants figure by J.Batbold warm weather influence plants grow at around 100m.Animal spreading: In 1987-1991 M.sibirica spread almost part, S.erythrogenus above sea level 2300m in Ugalz mountains. Places where marmots live don’t have any marmots such as Alagiin hooloi, number of marmot is dramatically decreasing last years. It is related to climate change and hunting. Plants are changed due to influence climate animals in desert, dry steppe spread in Ugalz mountains and above sea level 2550m S.erythrogenus are according to the research, E.luteuse are spreading in front area of the Ugalz mountains, S.erythrogenus are spreading back of the Ugalz mountains.

Background: Stroke is a leading cause of death and disability, especially in low-income and middle-income countries and it impacts a tremendous medical, emotional and fiscal burden on society. Due to advances in Western healthcare, the prevalence of stroke since 1970 has decreased by 42%, whereas it has more than doubled in low-income to middle-income countries.
Stroke is a heterogeneous, multifactorial disease regulated by modifiable and nonmodifiable risk factors. Approximately 80% of stroke events could be prevented by making simple lifestyle modifications. In fact, nationwide characterization of well-known stroke factors in all social backgrounds is essential, however; populations can differ significantly not only in their socio-behavioral, legal, and geographical conditions, but also from other, historically understudied. Therefore, it is crucial to determine characterization of risk factors for ischemic stroke among Mongolian population. Objective: To determine etiology and risk factors for ischemic stroke among Mongolian population Material and methods: Our study was conducted by case-control study design. Cases were patients with acute first stroke; controls were matched with cases, recruited in a 1.2:1 ratio, for age and sex. The case series study was conducted in Stroke center of Third State Central hospital from January 2017 to December 2017. Structured questionnaires were administered and physical examinations were done in the same manner in cases and controls. Self-reported history of hypertension and diabetes mellitus or blood pressure of 140/90 mm Hg and blood sugar 6.4 mmol/L or higher was used to hypertension and diabetes mellitus, respectively. Smoking status was defined as never, former, or current smoker. Alcohol use was categorized into never or former, low intake, moderate intake, and high or episodic heavy intake. Atrial fibrillation was based on previous history, review of baseline electrocardiograph results (for cases and controls). Odds ratios (OR) and logistic regression were calculated, with 95% confidence intervals. Results: In total, 173 patients with ischemic stroke and 146 controls were included. The patients’ age ranged from 17 to 92, the mean age was 61.2. Ischemic stroke more frequent in man than women by 27.4%. Previous history of hypertension or blood pressure of 140/90 mm Hg or higher (OR 2.40, 95% CI 1.48-3.88), diabetes mellitus (OR 3.08, 95% CI 1.44-6.57), hyperlipidemia (OR 5.09, 95% CI 2.64-9.82) atrial fibrillation (OR 8.70, 95% CI 2.01-37.64 ), current smoking (OR 2.07, 95% CI 1.26-3.40), alcohol consumption (OR 4.75, 95% CI 2.58-8.73) were all significantly associated with ischemic stroke. The mean age was lower in patients with stroke of other determined etiology. The frequency of hypertension was higher in patients with lacunar infarct than other subtypes. Smoking was high frequent in patients with large artery atherosclerosis. Conclusion 6 potentially modifiable risk factors were collectively associated with ischemic stroke and were different among ischemic stroke subtypes. The odds ratios of these risk factors are higher than other countries’ study.

Research of function of vitamin D on immune system has been studying since the study revealed that vitamin D receptor is expressed on the surface of the immune cells. 1,2-dihydroxyvitamin D3 [1,25(OH)2D], physiologically active form, can be generated through hydroxylation of 25-hydroxyvitamin D3 [25(OH)D], inactive form of vitamin D, in a liver, connecting with specific VDR make biological action. Vitamin D make different biological actions depends on connecting with different immunological cells. Some studies indicated that Vitamin D plays pivotal role in antibacterial innate immune responses through regulating reaction of the main cells as macrophages and dendritic cells. Moreover, calcitriol, the active form of vitamin D, is connected with VDRE, modulates the innate immune response through directly inducing expression of catelicithin and β-defensin as antimicrobial peptides, reducing secretion of IL-1b, IL-6, TNF-a, RANKL, COX-2 as proinflammatory cytokines and increasing production of IL-10, an anti-inflammatory cytokine. Vitamin D plays in proliferation and differentiation of T and B cells and regulates the activities of over 500 genes. Vitamin D differently impacts on per se stages of T cells’ proliferation. Vitamin D indirectly mitigates the differentiation from immature B cells to plasma B cells while it directly impacts on regulation of overloaded production of antibodies in plasma B cells. In conclusion, vitamin D modulates the innate- and adaptive immune response through regulation on activation of APCells, proliferation and differentiation of immune cells, secretion of some antibacterial peptides.

Background: The effect of lipopolysaccharide (LPS) on valproic acid (VPA)-induced cell death was examined by using mouse RAW 264.7 macrophage cells. Materials and methods, results: LPS inhibited the activation of caspase 3 and poly (ADP-ribose) polymerase (PARP) and prevented VPA-induced apoptosis. LPS inhibited VPA-induced p53 activation and pifithrin-α as a p53 inhibitor as well as LPS prevented VPA-induced apoptosis. LPS abolished the increase of Bax/Bcl-2 ratio, which is a critical indicator of p53-mediated mitochondrial damage, in response to VPA. The nuclear factor (NF)-κB inhibitors, Bay 11-7082 and parthenolide, abolished the preventive action of LPS on VPA-induced apoptosis. A series of toll-like receptor (TLR) ligands, Pam3CSK4, poly I:C, and CpG DNA as well as LPS prevented VPA-induced apoptosis. Conclusion Taken together, LPS was suggested to prevent VPA-induced apoptosis via activation of anti-apoptotic NF-κB and inhibition of pro-apoptotic p53 activation.

Introduction: Coronavirus infection 2019 (Ковид-19) is an infection caused by a novel virus and induces severe ARDS. КОВИД-19 pandemic has rapidly spreaded in 221 countries, 245,373,039 cases and 4,979,421 mortalities have been reported. Pulmonary and renal thrombotic angiopathy occur in patients with complications of ARDS, sepsis, and multi-organ failure. Elevated D-dimer in КОВИД-19 patients has been reported firstly by doctors in Wuhan, China. In addition, many studies have revealed that elevated D-dimer has been associated with the severity of the diseases, an increased rate of poor prognosis. Objective: We aim to determine D-dimer in КОВИД-19 patients, and patient condition a decrease of D-dimer level after administration of anticoagulant therapy. Case report: We introduce a rare case of КОВИД-19. Laboratory test results and the effect of anticoagulant therapy have been evaluated during the infection. 85 aged women were admitted with a diagnosis other than КОВИД-19. PCR for SARS-Cov-2 was negative on the previous day of admission, and Sars-Cov-2 Ag rapid test was also negative on the admission day. However, the D-dimer test result was much higher with 7120 ng/мл and X-ray and CT revealed a similar pattern to the КОВИД-19 patient. Then anti-Sars-Cov-2 test was positive with 4,08 COI. Based on laboratory test results of D-dimer, LDH, CRP, and CT pattern the patient was diagnosed with post-КОВИД-19 pneumonia, and anticoagulant therapy was initiated additionally to prevent hypercoagulation induced by КОВИД-19. D-dimer test taken before administration of anticoagulant therapy increased more to 10910 ng/мл. 3 days later D-dimer level decreased to 8180ng/мл and the patient’s condition was improved. Conclusion The evaluation of D-dimer of the patients with КОВИД-19 is highly significant. Anticoagulant therapy might be necessary for КОВИД-19 patients with high D-dimer level in serum. Further studies are needed to assess the long-term outcome of the illness and mortality.

Background and Aims: Hepatocellular carcinoma (HCC) is a common cause of cancer related death in Mongolia. Early diagnosis is the very important management to increase successful treatment and survival rate. Glypican-3 (GPC3) protein is highly expressed in hepatocellular carcinoma (HCC) tissue and in serum of HCC patients. Recent studies have been conducted and suggested as a diagnostic biomarker for detecting HCC in the early stage. Therefore, we investigated the diagnostic value of the serum GPC3 level and compared it to the alpha-fetoprotein (AFP) level as a diagnostic biomarker of HCC. Methods: We enrolled a total of 90 participants and divided into 3 groups with HCC (30), with liver cirrhosis (LC/30) and healthy (30) as the control group (30). GPC3 and AFP serum (sGPC-3, sAFP) levels were measured using commercially available enzyme-linked immunosorbent assay kits. The diagnostic accuracy was analyzed using the receiver operating characteristics (ROC) curve and estimated sensitivity and specificity of each biomarker. Results: sGPC3 was significantly elevated in the HCC group as compared to liver cirrhosis and healthy subjects (658±138.2 pg/ml, 378±25.5 pg/ml, 356.3±29 pg/ml) respectively. sGPC-3 sensitivity was 96.6% and specificity was 100%. The area under the ROC curve (AUC) for GPC3 was 0.999 (0.996- 1.0).
In comparison, the mean of AFP was significantly higher in HCC (16.9±11.7 ng/ml) than in LC (6.7±7.6 ng/ml) and in healthy subject (3.3±2.1 ng/ml) and AFP sensitivity was 43,3 %, specificity was 95 % with an AUC of 0.808 (0.696- 0.921).
The combination of GPC-3 with AFP achieved the highest sensitivity (97.1%) and specificity (97%). Conclusion Serum GPC3 has a higher sensitivity than AFP for the early diagnosis of HCC. Combination of two markers showed greatest diagnostic accuracy.

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.

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: 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.