Background: The first confirmed case of COVID-19 in Mongolia was reported on November 11, 2020. In response, the government imposed a nationwide lockdown, which significantly impacted the population’s mental health. Heightened levels of stress, anxiety, loneliness, and depression during the pandemic altered individuals’ psychological stability and behavior. Personality traits—defined as relatively stable patterns of emotion, cognition, and behavior—play a key role in stress responses and emotional regulation under pressure. Emerging evidence suggests that these psychological factors may influence the immune system’s responsiveness, including vaccine-induced antibody production. Aim: To evaluate the association between post-vaccination antibody responses and personality types following two doses of COVID-19 vaccines. Materials and Methods: A total of 738 participants who received two doses of COVID-19 vaccines (AstraZeneca ChAdOx1, n=29; Pfizer-BioNTech, n=119; Sinopharm BBIBP, n=590) and had no prior SARS-CoV-2 infection were enrolled. Serum samples were collected 21–28 days after the second dose, and SARS-CoV-2 RBD (S) IgG antibodies were measured using ELISA (Proteintech Inc., USA). Personality types were assessed using a 56-item temperament questionnaire developed by A. Belov, categorizing individuals into classical temperament types (choleric, phlegmatic, sanguine, melancholic). Logistic regression and ROC analysis were used to examine associations between personality types and antibody response. Results: The presence of an antibody response was significantly higher among individuals with a melancholic temperament, and significantly lower among those with a phlegmatic temperament. Furthermore, antibody titers were higher in participants with melancholic and sanguine temperaments and lower in those with a phlegmatic type. Conclusions 1. During the early period following the second dose of COVID-19 vaccination, the antibody response was higher in individuals with a pure melancholic temperament, while it was lower in those with a phlegmatic temperament. 2. After the second dose of the Sinopharm BBIBP COVID-19 vaccine, antibody titers were higher in individuals with pure melancholic and sanguine temperaments, and lower in those with a phlegmatic temperament.

Background: Children with developmental disabilities benefit from support in motor skills, sensory processing, cognitive development, and social skills. Mongolia has trained occupational therapists for a decade, with 37% specializing in pediatrics, but long-term therapy facilities remain limited. Aim: This study provides a case report on a child with developmental disabilities who received occupational therapy to evaluate improvements in sensory processing, social communication, and daily living skills. Materials and Methods: The study participants were purposively selected from children undergoing occupational therapy at the “Enerel” Child Development Center. Participant A is a 16-year-old male with hearing and speech impairments, as well as an intellectual disability. The initial assessment showed poor sensory processing and behavioral problems and communication difficulties. A tailored program incorporating sensory-based therapies, communication cards, and sign language was developed with caregiver collaboration. Occupational therapy was conducted five times weekly for 11 weeks. Pre and post test assessments included goal attainment scaling (GAS) and Sensory profile 2 (Child). Results: The participant showed improved communication using cards and sign language, better emotional regulation, enhanced sensory processing, and reduced hyperactivity to external stimuli. Goal Achievement (GAS) +2, meaning the goal was achieved better than expected and positive changes were found on the Sensory profile 2, with large effect sizes. Conclusion The study found that sensory- based occupational therapy and sign language training improved occupational performance and goal achievement in children with sensory, behavioral, and communication difficulties.

Background: Hypokalemia is considered when the serum potassium level is less than 3.5 mmol/L. Clinical research indicates that hypokalemia affects 20% of hospitalized patients, and in 24% of these cases, inadequate interventions result in life-threatening complications. At present, there is no research available on the prevalence, management, and outcomes of hypokalemia in hospitalized patients, which justifies the need for this study. Aim: The study aimed to examine the prevalence of hypokalemia and the effectiveness of its management in hospitalized patients within the internal medicine department, in relation to the knowledge of doctors and resident physicians. Materials and Methods: This hospital-based retrospective study included a total of 553 cases of patients hospitalized in the Internal Medicine Department of the Mongolia Japan Hospital between January 2024 and August 2024. Patients with a potassium level of <3.5 mmol/L were diagnosed with hypokalemia, and the effectiveness of potassium replacement therapy was evaluated according to the method of supplementation employed. Results: The prevalence of hypokalemia among hospitalized patients in the Internal Medicine Department was 9.8% (54 cases). Based on the study criteria, 42 cases of hypokalemia were selected for further analysis, and a total of 118 potassium replacements were performed through oral, intravenous, and mixed methods. Following potassium replacement therapy, 37.3% (44) of patients achieved normalized potassium levels, while 62.7% (74) still had persistent hypokalemia. Conclusion According to the study results, the prevalence of hypokalemia among hospitalized patients in the Internal Medicine Department is 9.8%. The method of potassium replacement and the severity of hypokalemia do not impact the normalization of potassium levels, with the critical factor being the proper dosage of supplementation. The knowledge of doctors and resident physicians regarding hypokalemia is insufficient, and there is a need to implement guidelines and protocols for potassium replacement therapy in daily clinical practice.

Background: Identifying reliable biomarkers for early detection, risk stratification, and prognosis of CVD in the context of CKD is, therefore, of critical importance. Cystatin C has emerged as a potential biomarker capable of reflecting both cardiac injury and renal impairment, particularly in patients with arterial hypertension. This study aimed to evaluate the association between serum cystatin C levels, left ventricular hypertrophy, and chronic kidney disease in individuals with hypertension. Objective: To assess serum cystatin C concentrations in patients with left ventricular hypertrophy and chronic kidney disease secondary to arterial hypertension. Materials and Methods: A case-control analytical study was conducted, enrolling 44 patients aged 45 years or older with both left ventricular hypertrophy and chronic kidney disease due to arterial hypertension alongside a control group of apparently healthy individuals. Serum cystatin C levels were measured using immunoturbidimetric assay. Statistical analysis was performed using SPSS version 25.0. Group comparisons were made using independent-sample t-tests, while multivariate regression and receiver operating characteristic (ROC) analyses were employed to explore associations and the predictive value of cystatin C. Results: The mean serum cystatin C concentration in the case group was 1.6±0.1 mg/L, significantly higher than in the control group (0.88±0.03 mg/L, p<0.05). Similarly, the estimated glomerular filtration rate (eGFR) was markedly reduced in the case group (44.88±6.8 mL/min/1.73 m²) compared to the controls (92.88±3.4 mL/ min/1.73 m², p<0.05). In the case group, a statistically significant inverse correlation was observed between serum cystatin C levels and glomerular filtration rate (GFR), with a regression coefficient of β=−0.028 (p<0.006). Conclusion The elevated serum cystatin C levels (1.6±0.1 mg/L) and decreased eGFR (38.99±12.7 mL/min/1.73 m²) observed in the case group suggest that cystatin C may serve as a potential biomarker for the early diagnosis of left ventricular hypertrophy due to arterial hypertension and chronic kidney disease, as well as for predicting related complications.

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: 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.

BACKGROUND. Sensorineural hearing impairment (SNHI) is the most common inherited sensory defect, affecting about 3 per 1000 children. More than 50% of these patients have a genetic cause (i.e. hereditary hearing impairment; HHI). Mutations in certain genes were noted to be extraordinarily popular in the deaf patients across different populations, making molecular screening feasible for these common deafness genes. One of the most important characteristics that we have learned concerning hereditary hearing loss is that common deafness genes and their mutations are usually different according to the ethnic background. As demonstrated in our previous studies performed in Taiwanese patients, the mutation spectrums of common deafness genes, such as the GJB2 gene and the SLC26A4 gene, are different from those in the Caucasian or even other Asian populations. These findings further underscore the indispensability of the collection of local data in terms of genetic counseling. In the collaborative project, we have successfully established a cohort of >100 hearing-impaired families, and clarified the genetic epidemiology of deafness in the Mongolian population. We identified several special deafness mutations such as GJB2 c.23+1G>A, c.559_604dup, and SLC26A4 c.919-2A>G, and our results revealed that Mongolian patients demonstrate a unique genetic profile in deafness as compared to other East Asian populations (paper in preparation). Meanwhile, by organizing a seminar at National Taiwan University Hospital in March 2017, we have transferred crucial concepts and techniques regarding how to perform genetic testing for deafness to the Mongolian colleagues. In the future, we plan to strengthen the mutual collaboration by expanding the clinical cohort and upgrading the genetic examination platform using the NGS techniques.

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.

Regardless the possession of any graduation and qualifications anywhere in order to train the doctors and medical professionals with the capabilities to work in any places there are the needs of the knowledgeable mentors to teach their knowledge, abilities and trends to the students in national, regional and international levels. This survey was started to determine the needs of the skills development of the mentors of the Mongolian National University of Medical Sciences under the mission to make it as one of the best 100 medical universities in the Asia-Pacific region and in order to create the favorable environment to accelerate the development of the university and creating a team consists from qualified mentors and researchers by improving the trainings, researches and clinical favorable environment including the quality improvement of the activities.The total of 333 mentors from the 5 structures and 3 branches of the Mongolian National University of Medical Sciences were surveyed to be developed by the University of Michigan including the use of the widely used questionnaires in the universities consisting from 7 groups and 81 questions to determine the needs of the mentors.The working range of the best medical mentors including their needs of the skills was studied. The 55.7% (50.4-61.0%) of the mentors included in the survey were told that the facilitation of the learning needed, 82.4% (78.3-86.5%) as the role models needed, 79.9% (75.6-84.2%) as the provision of the information is needed, 76.3% (71.7-80.9%) as 82.8% (78.8-86.9%) as the planning needed and 81.0% (76.8-85.2%) as the assessment of the training is needed.There is a need to develop the skills related to the 6 frameworks as the learning facilitation for the mentors, role model providers, information providers, resource developers, planners and assessors.