Complete androgen insensitivity syndrome (CAIS), also known as Morris syndrome, is a rare X-linked recessive disorder characterized by a 46XY karyotype and a female external phenotype. We present the case of a 32-year-old patient who presented to Unimed International Hospital in 2024 with primary amenorrhea, infertility, and chronic pelvic pain. Clinical examination, imaging, and laboratory investigations led to the diagnosis of CAIS. Laparoscopic surgery was performed to remove bilateral gonadal structures and a cystic mass on the left side. Histopathological analysis revealed testicular tissue and a serous cystadenoma originating from the left mesonephric remnant. Following gonadectomy, hormone replacement therapy was initiated, resulting in stabilization of hormone levels. This rare case highlights the possibility of mesonephric remnant-derived cystadenoma in CAIS and underscores the diagnostic value of cytogenetic and histological evaluations, especially in distinguishing between ovarian and testicular tissue when imaging findings are inconclusive.

Background: A drug related problem is defined by the Pharmaceutical Care Network Europe Association as an an event or circumstance involving drug therapy that actually or potentially interferes with desired health outcomes. One critical aspect of preventing such errors is proper dose adjustment, which plays a vital role in the diagnosis and treatment of disease. For instance, adjusting the dose of warfarin based on the patient’s INR level is essential. In a 1995 study conducted in England, clinical pharmacists recommended target doses of angiotensin-converting enzyme (ACE) inhibitors for patients with chronic heart failure. As a result, patients experienced a significant reduction in pulmonary and peripheral edema, along with improved exercise test outcomes. At the Mongolian-Japanese Hospital of the Mongolian Medical University of Science and Technology, it is important to analyze dosage-related issues identified by clinical pharmacists and inform healthcare professionals about common dosage selection errors and associated risks. Aim: We analyzed issues related to medication dosage. Materials and Methods: A retrospective study was conducted to examine problem related to dosage detected through prescription monitoring at the Mongolian Japanese Hospital of the Mongolian National University of Health Sciences from 2023 to 2024. Results: Out of a total of 2340 drug-related problem identified across five inpatient wards during this period, 581 (100%) were related to dosage. Clinical pharmacists performed prescription review on approximately 67% of all inpatients, which was consistent between years. However, medication-related problems tended to decrease from 41.1% (n=1499) in 2023 to 22.3% (n=841) in 2024 (p=0.05). The majority of dose-related problems, 75.6% (n=440), were overdoses. Medication-related problems were most common in the surgical department, with 59.5% (n=346) (p=0.001). The most frequent dosage-related errors involved exceeding the daily dose of diclofenac, administering higher- than-recommended doses of ceftriaxone, failing to adjust cefotaxime for renal function, and using inappropriate doses of metronidazole in patients with impaired liver function. The leading cause of these errors was failure to adhere to guideline-recommended dosing, which accounted for 71.3% (n=415) of cases (p=0.001). When dosage-related recommendations were provided to physicians before of treatment, acceptance rates increased by 14% (p=0.001). These interventions resulted in an estimated cost saving of 1.267.219₮ and a reduction of 363 injections. Conclusion Therefore, clinical pharmacist-led prescription review can help reduce the risk of dosage errors, lower associated healthcare costs, and alleviate the burden on medical staff.

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: 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.

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: 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.

The present study was conducted to assess relationship between drinking water fluoride levels and dental caries among 12 years old school children of 2 districts of Ulaanbaatar city, Mongolia. A cross-sectional analytical study was conducted on 533 school children aged 12 years, selected from 6 schools of 2 districts of Ulaanbaatar city. 533 children were divided into 2 groups according to the fluoride concentration of the waters. The all children were examined oral examination, dental caries was assessed by the DMF-T index. The result of the present study revealed that the caries prevalence in the study population was about 68,9%, and mean DMF-T was 3.05. Water fluoride concentration was highest in Khan-Uul district with 0.622ppm. There was highest prevalence of caries in children who consume water from filtration system in both districts.

The present study was conducted to assess relationship between drinking water fluoride levels and dental caries among 12 years old school children of 2 districts of Ulaanbaatar city, Mongolia.A cross-sectional analytical study was conducted on 533 school children aged 12 years, selected from 6 schools of 2 districts of Ulaanbaatar city. 533 children were divided into 2 groups according to the fluoride concentration of the waters. The all children were examined oral examination, dental caries was assessed by the DMF-T index.The result of the present study revealed that the caries prevalence in the study population was about 68,9%, and mean DMF-T was 3.05. Water fluoride concentration was highest in Khan-Uul district with 0.622ppm.There was highest prevalence of caries in children who consume water from filtration system in both districts.

Background Diabetes is a metabolic disorder that is characterized by chronic high blood glucose levels that causes complications in the eyes, kidneys, heart, vessels and nerves. Currently diabetic nephropathy is the most significant long-term complications in terms of morbidity and mortality for individual patients with diabetes. Honey bee venom can be considered as a natural remedy for diabetes due to its blood glucose levels lowering and lipid-regulating effect on diabetic rabbits. Aim The aim of this study was to investigate the effect of Mongolian honey bee venom (Apis mellifera) on renal dysfunction in alloxan induced diabetic rabbits. Material and Method Twenty two Chinchilla rabbits were divided into three groups: control (n=6), diabetic (n=8), and bee venom treated (n=8). The diabetic group was injected with 5% solution of Alloxan monohydrate 100 mg/kg intravenously behind the ear for 2 minutes to induce diabetes. The bee venom treated group received a bee sting (a sting contains 0.2-0.5 ml of bee venom) on their hind paw every day after their diagnosis of diabetes. Result Bee venom treatment (BVT) led to the following changes: compared to the diabetic group, the bee venom treated group’s blood glucose levels lowered between 14.9% and 26.5%; the plasma creatinine and urea levels were decreased respectively by 19,8% and 14.8%. Blood urea nitrogen (BUN) levels were reduced by 14.8%. Conclusion: Treatment with Mongolian bee venom lowered the blood glucose levels and prevents the renal dysfunction in alloxan induced diabetic rabbits