Background: Endometriosis is a condition in which cells in the endometrium, layer of tissue normally covers uterine cavity, which grows outside to ovaries and other pelvic organs [1-4]. That may happen chronic pelvic pain, adhesion and pelvic organs dysfunction which leads to infertility later life [1-4]. In worldwide, 19-45 aged women have endometriosis, which is counted for 176 million, from 44% women have ovarian endometrioma [5]. In our country, 56% women received laparoscopic surgery due to ovarian cysts, which is diagnosed endometrioma. In recent years, ovarian endometriosis treated by synthetic progestin, gonadotropin analogues, combined contraceptive pills, intra-uterine device containing with progestin, and non-steroid anti-inflammatory drugs and laparoscopic surgeries [6, 7]. Serum antimullerian hormone (AMH) is key marker to define ovarian reserve, which correlates ovarian number of antral follicle counts [6, 7]. Material and Methods: We studied 129 patients who has diagnosed with ovarian endometrioma, aged 20-46 years, using case-control study design. There are 4 groups with medication and surgeries.
Approval for the study was obtained from the review board and the ethics committee of MNUMS. All the recruited patients provided their informed written consents. Results: When treatment groups were compared, level of AMH before synthetic progestin therapy was 3.48±0.9 and after it 3.41±1.0 (p-0.456), and that was before non-steroid anti-inflammatory drugs 3.68±0.8 and after it 3.11±0.8 ng/ml (p-0.212). Before laparoscopic surgeries for severe endometrioma, average level of AMH was 2.3±1.8ng/ml for synthetic progestin therapy group and it was 1.68±0.2ng/ml (p-0.007) after surgical peeling of endometrioma. For patients of 4th group who had not taking oral synthetic progestin before laparoscopic surgeries average level of AMH was 3.11±1.88 ng/ml before surgery and it became 2.21±0.28 ng/ml (p-0.005). Level of СА-125 marker was before medical therapy for group 1 was 37,9±5,25 IU/ml and after therapy - 20,6±2,03 IU/ml. For group 2 it was 69,9±9,79IU/ml and 35.1±6.76 IU/ml respectively. Average level for group 4 before surgical treatment it was 96.6±36.6 IU/ml, and after surgery became 25.71±2.96 IU/ml, and that for group 3 was before surgery 102±29.1 IU/ml and decreased after surgery to 29.2±4.15 IU/ml.
There are significant reduction of pain in patients who received synthetic progestin (p=0.001) groups. Serum AMH were 3.48±0.9 before treatment and 3.41±1.0 after treatment respectively (p=0.456). Prior treatment of laparoscopic surgery with progestin 3 months, it decreases abdominal lower pain (p=0.001) and dysmenorrhea (p=0.001). Serum AMH level were 3.11±1.8 before surgery and 2.21±0.2 after surgery,respectively, (p=0.005). Conclusion
1. There were little decrease in level of antimullerian hormone and less risk for ovarian reserve when mild endometrioma was treated with synthetic progestin and non-steroid anti-inflammatory drugs in two groups.
When severe and middle degree of endometrioma was treated with laparoscopic surgery there were significant decrease of antimullerian hormone, but it was less in group that had synthetic progestin therapy before surgery and it was more effective that surgical therapy without preparation.
2. Comparison of Serum level of СА-125, marker of ovarian tumor, was decreased less in group of non-steroid anti-inflammatory drugs, and was decreased more or it was more effective.

Introduction: Stinging nettle (Urtica dioica L.) belongs to the family of Urticaceae. Three species of Urticaceae (Urtica cannabina, Urtica angustifolia, Urtica dioica L) was grown in Mongolia. U. dioica has recently been shown to have antibacterial, antioxidant, analgesic, anti-inflammatory, antiviral, anti-colitis, anticancer and antiAlzheimer activities. Flavonoids, tannins, scopoletin, sterols, fatty acids, polysaccharides, isolectins and sterols are phytochemicals which are reported from this plant. But effect of hair growth is unclear yet. Goal: We investigated the effect of Urtica dioica L extracts on hair growth by using in-vitro and ex-vivo study methods. Materials and Methods: Human single hair follicle and dermal papilla cells obtained from scalp skin samples of healthy volunteers. We evaluated the effect of Urtica Dioica L on hDPCs and on ex-vivo hair follicle organ culture. Hair follicle matrix cell’s proliferation marker Ki-67 identified by immunoflurescence staining. Result: Urtica Dioica L ethanol extracts promoted elongation of the hair shaft and reduced catagen transition of human hair follicles in organ culture model. E.extract of Urtica Dioica L increased Ki-67 positive matrix keratinocytes. Conclusion Urtica Dioica L ethanol extract enhanced human hair growth in ex-vivo organ culture model. Needed future study to investigate the related mechanism of hair growth.

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.

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.

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.