Background: The development of accurate and non-invasive diagnostic tools is essential for improving early detection of cancers. Recent studies have shown that serum biomarkers may be useful for early detection of gastric cancer. Aim: We aimed to evaluate the diagnostic accuracy of PGI and PGR biomarkers for detection of the gastric cancer and atrophic gastritis. Materials and Methods: To identify relevant studies, the MEDLINE (PubMed) database was searched using the keywords (((“Gastritis, Atrophic”[Mesh]) OR “Stomach Neoplasms”[Mesh]) AND “Pepsinogen A”[Mesh]) AND “Sensitivity and Specificity”[Mesh]). Based on the inclusion and exclusion criterias, studies were selected according to the PRISMA guidelines. Meta-analysis was performed using Review Manager 5.4.1 and STATA/IC 15.0 (StataCorp LLC, USA, 2017). Results: According to the PRISMA guidelines, we selected a total of 18 studies in this meta-analysis. The meta-analysis results showed that the sensitivity of the PGI for the detection of atrophic gastritis was 58.5% (95% CI, 44.5-71.3), specificity was 90.2% (95% CI, 68.4-97.5), and DOR was 13.0 (95% CI, 2.6-64.6); the sensitivity of the PGR was 69.9% (95% CI, 58.1-79.5), specificity was 80.9% (95% CI, 52.4-94.2), and DOR was 9.8 (95% CI, 2.6-36.9). However, the sensitivity of the PGI biomarkers for detecting gastric cancer was 72.6% (95% CI, 54.7-85.3), specificity was 66.9% (95% CI, 52.5-78.7), DOR was 5.4 (95% CI, 3.1-9.3); PGR sensitivity was 77.8% (95% CI, 64.4-87.4), specificity was 65.0% (95% CI, 53.2-75.1), DOR was 6.6 (95% CI, 3.7-11.7); PGI+PGR sensitivity was 62.3% (95% CI, 51.1-72.2), specificity was 87.6% (95% CI, 78.0-93.3), DOR was 11.6 (95% CI, 6.8-19.8). Conclusion PGI and PGR tests demonstrated high specificity but moderate sensitivity. Although serum pepsinogen cannot replace endoscopy, it is considered to be an additional test and can be used to select high-risk populations.

Background: Serum natriuretic peptide (NT-proBNP) is a critical biomarker for diagnosing left ventricular dysfunction. Heart failure is the leading cause of mortality in chronic kidney disease (CKD), emphasizing the need for its early detection and prognosis. Objective: This study aimed to determine the serum NT-proBNP levels in participants with CKD and establish a cut-off value for predicting heart failure. Methods: A descriptive cross-sectional study was conducted from April 1 to July 1,2024. This study received approval from the Ethics Committee of the Institute of Medical Sciences (Approval No.24/01). A total of 117 CKD patients hospitalized in the Nephrology and Endocrinology Department of the third state hospital were enrolled based on predefined inclusion and exclusion criteria. Data were collected using questionnaires, laboratory and heart ultrasound test results. Serum NT-proBNP levels were measured using a rapid immunofluorescence quantitative analyzer. Data were analyzed with SPSS 26.0. Results: The mean age of the 117 participants was 57.9 ± 14.7 years, with 51.3% being male. The mean serum NT-proBNP level was 7686 ± 12149 pg/mL. Statistically significant differences were observed in serum creatinine, sodium, calcium, CKD stage, and arterial hypertension between genders (p<0.05). NT-proBNP levels in hemodialysis patients differed significantly between heart failure and non-heart failure groups (p<0.05). Significant differences were also found in hemoglobin, serum albumin, NT-proBNP levels, and CKD stages (p<0.05). NT-proBNP correlated significantly with risk factors such as hemodialysis, diabetes, and decreased systolic blood pressure (p<0.0001). A weak inverse relationship was noted between systolic blood pressure and NT-proBNP (R² = 0.16). The NT-proBNP cut-off value for predicting heart failure was 3027 pg/mL, with an AUC of 61.7% (sensitivity: 74.5%, specificity: 55%). Conclusion Serum NT-proBNP levels are elevated in CKD patients regardless of heart failure. The established cut-off value for NT-proBNP in CKD patients to detect heart failure was 3027 pg/mL, with moderate diagnostic utility (AUC = 61.7%).

Introduction: Cases of gastric cancer have been declining worldwide in recent years. However, gastric cancer incidence increased in the last decade in Mongolia. In Mongolia, over 80% of gastric cancer cases are diagnosed during the late stage. Several studies have revealed that serum pepsinogens (PGs) level reflects, indirectly, histological and functional characteristics of the gastric mucosa. Goal: We aimed to evaluate the risk of gastric cancer and its precancerous condition based on serum PGI, PGI/II biomarkers. Materials and Methods: This case-control study enrolled 114 subjects, including patients with gastric cancer (n=36), atrophic gastritis (n=40) and healthy controls (n=138). The questionnaires were obtained to determine risk factors. Serum PGI, PGII, and H. pylori IgG levels were measured by ELISA (Pepsinogen I ELISA; Pepsinogen II ELISA; H.Pylori IgG ELISA; BIOHIT Plc, Helsinki, Finland). PGI to PGII ratio was calculated. Patients were classified into the ABC(D) group according to Miki K approach. Also, we developed new scoring system based on some risk factors and serum PGI, PGI/II ratio. Logistic regressions were performed to evaluate risk and expressed by odds ratio (OR) and 95% confidence intervals (95%CI). Results: Mean age of the subjects was 60±10.9 years. H.Pylori was positive in 67 subjects. The serum PGI and PGI/II ratio levels were significantly decreased in gastric cancer and atrophic gastritis groups compared to the healthy control. According to classification ABC(D), group D (OR 5.04, 95% CI 1.13-22.50) had higher proportion of atrophic gastritis cases, group C (OR 6.19, 95% CI 1.04-36.78) had higher proportion of gastric cancer cases than others. Additionally, we created a risk prediction scoring system with a score ranging from 0 to 7, based on variables age, family history of gastric cancer, prior disease history, PGI and PGI/II ratio levels. For the atrophic gastritis patients, 17 (42.5%) were classified into medium-risk category (OR 4.49, 95% CI 1.38-14.58) and 17 (42.5%) were classified into high-risk category (OR 7.69, 95% CI 2.16-27.43). Whereas, 11 (30.6%) patients with gastric cancer were classified into medium-risk category (OR 4.35, 95% CI 1.13-16.85), 21 (58.3%) were classified into high-risk category (OR 14.25, 95% CI 3.60-56.43). Conclusion The methods based on serum PGI and PGI/II may identify a high risk population of gastric cancer and atrophic gastritis.

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: 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: 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 : Low triglycerides and cholesterol was associated with hepatitis C virus (HCV) infection. Chronic HCV infection is the main cause of liver injury and it may influence to serum lipid levels. We aimed to evaluate the effect of antiviral treatment on the change of lipid profiles during interferon-based anti-HCV treatment. Material and Methods : Totally 863 patients who completed the interferon-based antiviral therapy in Kaohsiung Medical University Hospital were included in this present study. The lipid profile measured and assessed in the baseline of the treatment and after 6 months of completion of the treatment. Results : The most of the patients (81.2%) were achieved sustained virological response (SVR) by antiviral therapy. There was no significant difference between baseline triglycerides (TG) levels in the SVR group and non SVR groups. The TG levels at 6 months after completion of the treatment was significantly elevated in SVR group (102.9±57.0 mg/dL, p=0.0001) but did not elevated in non SVR group (94.5±45.6 mg/dL, p=0.690) compared with baseline TG levels.
After adjusting patients by four indexes for fibrosis (FIB4) in cut-off point 3.25, serum TG levels significantly increased in low FIB4 group (103.2±57.9 mg/dL, p=0.0001) but not in high FIB4 group (98.1±49.6 mg/dL, p=0.095) after 6 months end of the treatment. Serum TG level was increased greater in patients who had low FIB4 score and patients who achieved SVR (baseline 89.1±34.8 mg/dL; 6 months after treatment 104.3±59.3 mg/dL, paired T test p=0.0001). Conclusion The eradication of HCV is the main cause of the increase of lipids after Pegylated Interferon and Ribavirin treatment.
However advanced fibrosis also has an effect in increase of TG after the treatment.

Familial hypercholesterolemia (FH) (OMIM#143890) is the most common metabolic autosomal disorder. The prevalence of the homozygous FH has been reported as 1 in a million in the general population, compared to much more mild form heterozygous FH with prevalence of 1 in 200-500. Mutations in the low-density lipoprotein receptor (LDLR), apolipoprotein B (ApoB), proprotein convertase subtilin/kexin9 (PCSK9), and low-density lipoprotein receptor adapter protein 1 (LDLRAP1) genes have been linked to FH. These mutations result in a disorder in low-density lipoprotein cholesterol (LDL-C) catabolism, and significantly increasing the levels of LDL-C, total cholesterol in serum, leading to specific clinical signs such as tendon xanthoma, corneal arcus, cardiovascular diseases, and early death from coronary heart disease if left unattended. Therefore, there is an ardent need for early diagnosis followed by aggressive therapeutic intervention and lifestyle modification. Currently, FH can be diagnosed either clinically or genetically. There have three main clinical diagnostic criteria for FH: the US MedPed Program, the Simon Broom Register Group in the UK, and the Netherland’s criteria. The occurrence of so many different LDLR mutations and their widespread distribution throughout the gene imposes severe practical limitations on simple genetic screening. Indeed, exon by exon sequencing of LDLR and other genes in each patient is the best screening genetic methods of choice. Although the hypercholesterolemia associated with FH can be controlled with cholesterol-lowering drug therapy (statins and other), patient response can vary quite widely.

Gastric cancer has been and still considered one of the most common causes of cancer-related mortality and it continues to be a major public health issue. The incidence and mortality of gastric cancer in Mongolia is the highest in the world. For this reason, this paper provides the information about current status of gastric cancer in Mongolia in the first section. Morbidity and mortality of gastric cancer increased steadily during the last decade. In the second section we overview the most important factors that can accelerate the risk of gastric cancer. Evidence from case-control, cohort studies and meta-analysis have suggested that the risk of gastric cancer is related to several factors including genetics, Helicobacter pylori, other factors related to the environment and lifestyle. Risk factors could have different effects on the onset and the evolution of gastric cancer.