Background. Cerebral palsy (CP), which is the most commonly encountered neuromuscular disorder of childhood, causes permanent physical deficits and sometimes intellectual deficits. Despite advances in the diagnosis and treatment of CP, the incidence of that disorder has not declined; it parallels the increased survival rates of premature infants. The children with CP may not have trunk control because they have spasticity and weakness in their trunk control. Goal. This study aimed to investigate the efficiency of functional electrical stimulation (FES) application on the abdomen-posterior back muscles in children with Cerebral palsy (CP). Materials and Methods. However 40 children with spastic CP, being treated in physical therapy, were selected by the way of random-sampling in the study, some of children were excluded by exclusion criteria and then 30 children have completed the study. The participants were randomly divided into two groups FES (n=15) and control groups (n=15). The control group received physical therapy 3 days a week in 45 minute for 6 weeks. The children in the FES group received physical therapy in addition to function electrical stimulation. FES was applied 5 days a week for 6 weeks to abdomen-posterior back muscles in 30 minute-long sessions. To evaluate the score of gross motor function measurement (GMFM) and to evaluate the trunk asymmetry in sitting, radiographic measurements were used. Result. The comparisons of the measurements of the two groups before and after the treatment showed that the GMFM standing score were statistical significantly (p<0.001) increased, and Cobb angles were decreased both groups, but the decrease in the control group was not statistically significant (p=0.128), and FES group was statistically significant (p=0.033). The comparison between groups GMFM standing score increased higher in the FES group than in the control group. Cobb angles after the treatment were statistically significant higher in the FES group than in the control group. Conclusion: To improve gross motor developing for children with CP, FES applied on abdomenposterior back muscles along with physical therapy is more effective than physical therapy alone.

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.

Introduction: Air pollution has become one of the major problems in socio-economic and health issues in Mongolia. Among the various hazards of particulate matter (PM) pollutants, microorganisms in PM2.5 and PM10 are thought to be responsible for various allergies and for the spread of respiratory diseases. Recent studies have shown that PM2.5 particles can cause chronic heart failure, heart arrhythmias, and strokes, as well as lung damage, cirrhosis, inflammation, cancer, cardiovascular disease, and metabolic disorders. Furthermore, some studies have concluded that PM2.5 particles in the environment are a risk factor for gastrointestinal, liver, colon, and lung cancer as well as it affects the growth and metastasis of various cancer cells caused by other factors. In our country, the health effects of air pollution and the relationship between the pathogenesis of cancer research are scarce. Therefore, the study of the effects of PM2.5 particles on cancer cell proliferation, migration (metastasis) can provide a significant role for cancer treatment, diagnosis, and prevention. Purpose: Determining the effects of PM2.5 particles on cancer cell proliferation, migration (metastasis) in in-vitro Material and Methods: A human liver cancer cell line (HepG2), human gastric cancer cell line (AGS) were obtained from the central scientific research laboratory in the Institute of medical sciences. HepG2, AGS cells were seeded at a concentration of 1*105 cells/mL in a culture flask and cultured in RPMI-1640 medium supplemented with 10% FBS, 1% antibiotic mix (penicillin, streptomycin) in a humidified atmosphere of 5% CO2 at 37 °C. The cytotoxic effect of PM 2.5 in AGS, HepG2 cells were evaluated by MTT, CCK8 assays. AGS, HepG2 cells were incubated in 96 well plates for 24h then treated with different concentrations (0, 5, 10, 25, 50 and 100 μg ) of Bayankhoshuu, Buhiin urguu, and Zaisan samples for 24h, respectively. Results: Concentrations of 10, 25, and 50 μg/ml of samples collected from the Bukhiin urguu and Zaisan in March increased HepG2 cell growth, while doses of 25, 50 μg/ml of samples collected from Bayankhoshuu in March and December increased HepG2 cell growth. Therefore, concentrations of 25 and 50 μg/ml of samples collected from Bayankhoshuu in March increased AGS cell growth, while concentrations of 25, 100 and μg/ml of samples collected in December increased AGS cell growth. However, no cytotoxic effect was observed in the sample collected from Zaisan in March, whereas the PM2.5 sample enhanced AGS cell growth in dose dependent manner in December.(p <0.05) Conclusion High levels of heavy metals were detected in samples collected in December from Bayankhoshuu, Bukhiin urguu and Zaisan of Ulaanbaatar. Concentration of 25 μg/ml of samples collected from the Bukhiin urguu and Zaisan in March increased HepG2 cell growth. Concentrations of 25 μg/ml of PM2.5 collected from three regions around Ulaanbaatar increased HepG2 and AGS cell migration.

Background: The incidence of gastric cancer has been declining worldwide in recent years; on the contrary, it has increased in the last decade in Mongolia. In Mongolia, over 80% of gastric cancer cases are diagnosed in the late stage. We performed a gastroduodenoscopy for screening and histological evaluation to diagnose gastric cancer. These methods are an effective diagnostic modality for gastric diseases; however, invasive and cause discomfort, making it an undesirable procedure for patients. Aims: To determine serum PGs and H.pylori IgG in atrophic gastritis and gastric cancer patients and evaluate the risk by ABC(D) classification. Materials and Methods: We selected 40 atrophic gastritis and 36 newly diagnosed gastric cancer patients from National Cancer Center of Mongolia, before surgery and other therapies. Besides, we enrolled population-based 38 healthy controls. Subjects of three groups were matched by age (±1) and sex. Written informed consents were obtained from all subjects. The fasting blood samples were collected and tested PGI, PGII, and H.Pylori IgG levels by enzyme-linked immunosorbent assay. Also, PGI to PGII ratio (PGI/II ratio) was calculated. We classified subjects into four groups based on ABC(D) classification. All statistical analyses were performed by SPSS (version 26.0, Chicago, IL, USA) software. Results: Median age of the subjects was 62, 52.6% (n=60) were male. Proportions of family history of gastric cancer and previous history of gastric disease were significantly higher in the gastric cancer group compared with atrophic gastritis and healthy control groups (p<0.05, p<0.05). H.pylori was positive in 67 (58.8%) subjects according to H.pylori IgG assay and there was no difference between study groups. The serum PGI level and was significantly decreased in gastric cancer and atrophic gastritis groups as compared to the healthy control (p<0.05, p<0.05). The PGI/II ratio was significantly lower in the gastric cancer group compared with the healthy control (p<0.01). The optimal cut off value of PGI was ≤35.25 ng/ml (AUC 64.3, 95% CI 51.3-77.2, p<0.05) for gastric cancer and PGI was ≤75.07 ng/ml (AUC 65.2, 95% CI 53.0-77.3, p<0.05) for atrophic gastritis. Also, the optimal cut off value of PGI/II ratio was ≤5.27 (AUC 71.6, 95% CI 69.6-82.8, p<0.01) for gastric cancer and PGI/II ratio was ≤6.25 (AUC 62.7, 95% CI 50.1-75.3, p<0.05) for atrophic gastritis. According to classification of atrophic gastritis patients and healthy control, group D had higher proportion of atrophic gastritis cases than group A, B and C (OR 5.04, 95% CI 1.13-22.50, p<0.05). According to classification of gastric cancer patients and healthy control, groups C had higher proportion of gastric cancer cases than group A, B and D (OR 6.19, 95% CI 1.04-36.78, p<0.05). Conclusion Our findings suggest that PGs level and H.pylori IgG may predict development of gastric cancer and could identifying individuals at high risk of gastric cancer and precancerous lesions who may need endoscopy.

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.

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.