Within the spectrum of diagnostic procedures in hepatology, the procurement of a liver specimen plays an important role. The method has been diversifi ed to encompass not only different needle types for cutting and aspiration but also different routes proceeding transvenously or transcutaneously. Over the subsequent 50 years the technique of obtaining liver biopsy samples has been modifi ed regarding the approach, the needle type, and the combination with diagnostic imaging techniques such as ultrasound, computed tomography, angiography and laparoscopy. Histological analyses are capable of establishing the etiology of a chronic or acute liver disease, are determined the inflammatory activity (Grading), degree of fi brosis/cirrhosis (Staging), are relevant for the prognosis of the patient and for indication for cost-intensive as well as potentially side are effect-prone therapies. In general, the accepted mortality rate from liver biopsy is between 0,1% and 0,01%. Among the most feared complications of liver biopsies are hemorrhage, seeding of cancer cells, infections, and injury to the viscera. The increasing number of liver transplant patients within the hepatological spectrum requires regular, safe, and high quality biopsies and their appropriate.

According to international medical organizations, the use of efferent therapy that COVID-19 convalescent plasma has shown some results.
Convalescent plasma that contains antibodies to severe acute respiratory syndrome coronavirus 2 or SARS-CoV-2. This is being studied for administration to patients with COVID-19. Use of convalescent plasma has been studied in outbreak of other respiratory infections, including the 2003 SARS-CoV-1, the 2009-2010 H1N1 influenza virus, and the 2012 MERS-CoV.
Although promising, convalescent plasma has not yet been shown to be safety and efficacy of COVID-19 convalescent plasma in clinical trials.
Plasmapheresis and membrane plasmapheresis of efferent therapy has been used in clinical toxicology since 1995, in Mongolia.

Introduction: In 2018, a total of 901 new cases of gastric cancer were recorded, of which 64.8% in males and 34.2% in females. The incidence rate of gastric cancer was 28.5 per 100 000 population, which 38.2 for males and 19.2 for females. Goal: We aimed to investigate the associations between some risk factors and gastric cancer among the Mongolian population. Materials and Methods: A case-control study was conducted between November 2017 and September 2019. We selected 120 cases from National cancer center of Mongolia who newly diagnosed gastric cancer. And 120 controls were selected by matching by sex, age and the place of residence. Informed consents were obtained from all subjects. All subjects were personally interviewed with researchers used by a structured questionnaire consisting of 86 questions. The SPSS 21 (version 16.0, SPSS Inc., Chicago, IL, USA) software was used for all analyses. Results: The mean age was 59.2±11.4 (26-85) years. Habits of having dinner after 6.00 pm (OR 1.42, 95%CI 1.11-1.83, p=0.008), having leftover meals (OR 2.22, 95%CI 1.27-3.86, p=0.008), daily consumption of tea with salt (OR 1.97, 95%CI 1.18-3.30, p=0.01), smoking on an empty stomach (OR 2.44, 95%CI 1.11-5.37, p=0.033), weekly consumption of ham and smoked meat (OR 1.5, 95%CI 1.17- 2.13, p=0.02), and consumption of fat grease (OR 2.09, 95%CI .03-4.24, p=0.038) were significantly increased gastric cancer risk. In contrast, habit of eating at regular times (OR 0.43, 95%CI 0.25-0.73, p=0.002), chewing thoroughly (OR 0.39, 95%CI 0.23-0.67, p=0.001), cooking meat thoroughly until it’s tender (OR 0.48, 95%CI 0.25-0.97, p=0.047), daily consumption of vegetables (OR 0.45, 95%CI 0.27-0.76, p=0.003), and daily consumption of fruit juice (OR 0.36, 95%CI 0.15-0.85, p=0.026) were significantly reduced gastric cancer risk. Furthermore, having first-degree relatives diagnosed with gastric cancer had 2-3 fold higher increased risk of gastric cancer (parents OR 2.88, 95%CI 1.07- 7.78, p=0.038, sibling (OR 3.09, 95%CI 1.09-8.81, p=0.036). Also, previous records of the digestive disease increased risk of gastric cancer (OR 3.65, 95%CI 2.10-6.35, p<0.0001). Conclusion Dietary habits, family history of gastric cancer and previous records of digestive disease were associated with risk of gastric cancer. Thus, prevention effort could be focused on the population with a family history of gastric cancer, changing bad dietary habit and screening precancerous disease of gastric cancer.

Introduction: Cancer is a major public health issue both in Asia and in Mongolia. The most prevalent cancer related deaths in Mongolia are registered for the stomach, esophagus and liver. Purpose: We aimed to investigate the incidence of stomach and esophageal cancer in Mongolian population. Materials and Methods: Epidemiologic data were collected from 2009 to 2018 through the oncology cabinet of all hospitals and medical centers from all provinces, soums (the smallest unit of provinces) and major districts of the capital city. The incidence of stomach and esophageal cancer was calculated by appropriate methods and it was presented by ArcGIS Pro 9.2 software. A P-value of less than 0.05 was considered to be statistically significant and based on two side hypotheses. All calculations were performed in the IBM SPSS Statistics software. The study design in concordance with ethical guidelines was approved by the Ethics Committee of Ministry of Health Mongolia. All clinical investigations were conducted according to the principles laid down in the Declaration of Helsinki. Results: The incidence of esophageal cancer in last ten years (2009-2018) was 10.09 in 100000 populations and the highest incidence were registered in Uvs (38.13), Bayan-Ulgii (24.15) and Zavkhan (18.18) provinces, respectively. The incidence of stomach cancer was 20.33 in 100000 populations and the highest incidences were registered in Uvs (53.01), Khovd (46.02) and Darkhan-Uul (40.50) provinces, respectively. Conclusion
1. Incidence rates for esophageal and stomach cancer are high among the Mongolian population. In the last decade, the incidence of esophageal cancer had not decreased significantly, but it’s constant.
In our study, the esophageal cancer incidence was 10.09 per 100’000 people, which includes one of the high incidence rate countries according to the WHO classification. More than 10 aimags incidence rate of esophageal cancer was higher than the National average. Most of them have occurred in the western region of the country. Most of the Western, some of Khangai and Eastern soums have had the highest incidence of esophageal cancer what we have shown on the mapping.
2. The incidence rates of stomach cancer were registered as 20.33 per 100’000 people in the last 10 years at the national level. It has shown that according to the WHO classification, our country is also one of the countries with the highest incidence of stomach cancer. The stomach cancer incidence trend was increased in the last 10 decades. Therefore, some of aimag’s soums has included the highest rate classification. In addition, some soums in the Western, Khangai, and Eastern aimags had have a very high incidence of stomach cancer.
According to results in the above, the nationwide targeted prevention program is needed especially where the highest incidence rates. Also there is a lack of cooperation between national organizations to accurate registration of gastrointestinal cancer and to fight against these harmful cancers.

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: 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: 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.

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.