BACKGROUND OF STUDY: Not only in developed countries but also in Mongolia it is vital problem to decide how to improve human life’s quality, to make clear the measurement to take, discover human body’s change, aging mechanism and predict from these diseases. The research on herders’ biological aging which is connected to the geography, nature, environment, climate, inhabitant, culture and labor’s specialty hasn’t been done yet. So it causes the basis to write this research. AIMS: Defining the nomadic herder’s biological aging MATERIAL AND METHODOLOGY: All the herders in Gobi-Altai were included in this research. They wereclassified into ages such as 30-39, 40-49, 50-59 and 60-69, and 202 female and 212 male herders were chosen accidentally. The model types of research “Cross-Sectional” method is used for this, the equipment called “Tanita” which is used for measuring body is used for collecting information and also SPSS-22programmis used for producing result. RESULT OF STUDY: 1. 49% of all research participants are male, 51% are female. 2. Herder’s biological aging is 50,4+9,4 and it shows that 6,3 older than calendar ages. 3. Herders’ aging was different for male and female herders. 81,8 percent of the male herders get older very fast whereas 69,4 of female herders get older slowly. CONCLUSION: • Male herder’s aging is 14 years older than womenThe older female and male herders get, the less their difference in their biological age becomes. • The percentage of the herders whose aging is getting fast is 21-26 % older than biological aging of the UB city’s people. • Biological age and sex’s connection (r=0,0001 p=0,00488) between biological age and weight’s index is (r=0,00488, p=0,001) is different and statistical significant.

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.