Background: and Purpose The pathogenesis of neurovascular diseases and various types of dementia is tightly connected to cerebral circulation. An area that requires further exploration is the system of deep cerebral perforating arteries—arteries branching directly from high-pressure intracranial arteries, supplying vital neural structures such as the internal capsule, and characterized by a diameter of well below 1 mm, which makes them difficult to visualize with standard radiological examinations. This study aimed to analyze the morphology of the perforator origins, which constitute connection points between high-pressure intracranial arteries and microcirculation. Methods: Twenty-three human basal ganglia specimens with the middle cerebral artery (MCA, including 172 perforating arteries) and ten brainstem specimens with the basilar artery (BA, including 162 perforating arteries) were prepared and scanned using microcomputed tomography. The geometry and structure of the perforating arteries were analyzed using radiological images and additional histological studies. Results: The ostia of the perforating arteries were ellipsoidal in shape with median stenosis severity of 23% and 20% for MCA and BA perforators, respectively. The local narrowing structure was typical of neointimal hyperplasia. Statistical analysis revealed that the severity of stenosis may be related to age and cardiovascular health. Conclusion Origins of the deep cerebral perforators are locally narrowed by neointimal hyperplasia, which may be a protective mechanism to adjust high blood pressure to the microcirculation. The narrowings may lead to chronic hypoperfusion and play a role in the pathophysiology of cerebral small vessel disease.

Background: The annual incidence of stroke in different regions of the world ranges from 100 to 336 per 100,000 pop ulation, and mortality ranges from 36 to 136, and in Mongolia there are 220 new cases of stroke per 100,000 people and 113 deaths annually, making it one of the countries with the high stroke incidence rate. Aim: To conduct a systematic review of published sources on the epidemiology, causes, and risk factors of ischemic stroke in young people. Materials and Methods: The research sources were searched using keywords such as “Stroke”, “Definition”, “Epidemi ology”, “Etiology”, “Risk factors”, “Young Adult”, “Ischemia”, “Hemorrhage”, “Silent stroke” from the works published in international platforms such as Cochrane Library, Datebase, Medline, PubMed, Google Scholar, and Web of Science, and relevant information and data were selected from the collected sources and a review article was developed. Results: According to the WHO MONICA project report, stroke incidence was reported in 16 countries, with 101–285 men and 47–198 women per 100,000 people aged 35–64 years, while in the United States it was 113.8 per 100,000 people under 55 years, of which 73.1 were cerebral infarctions per 100,000 people, and more than 10 percent were under 55 years. A recent study in Mongolia found that 21–26% of stroke patients were young people (20-50 year old), compared with 10–13% in Western countries. Among the traditional causes and risk factors for stroke in young people, arterial hypertension accounts for 45-60%, smoking 40-60%, alcoholism 40-50%, heart disease 18-30%, dyslipidemia 30%, diabetes 13%, obesity 7-36%; among the specific risk factors, migraine accounts for 10-35%, taking hormonal contraceptives 10-22%, vasculitis 6-10%, blood clotting disorders 2-10%, vascular dissection 6-40%. According to the TOAST classification, large vessel disease accounts for 16-17%, small vessel occlusion 14-15%, cardiac embolism 19-20%, other determined etiologies 22-23% and undetermined 26-27%. Conclusion Epidemiological indicators of stroke vary significantly depending on the level of development of the country, geographical characteristics of the region, lifestyle, age, and gender (stroke incidence rate range: 100–336 per 100,000 population; mortality: 36–136 per 100,000 population). Mongolia is among the countries with high rates of stroke incidence and mortality (incidence rate 220 per 100 000, mortality 113 per 100 000 population). While stroke among young people accounts for 10–13% of all cases in Western countries, this figure reaches 21–26% in Mongolia, which is explained by a combination of traditional and specific risk factors. As stroke is becoming more common among younger populations, it is essential to study its causes and risk factors in detail and to intensify efforts in diagnosis, treatment, and prevention.

Background: Currently, colorectal cancer (CRC) ranks as the third most common cancer and the second leading cause of cancer-related mortality worldwide. CRC frequently metastasizes to the liver (50%), lungs (10–15%), peritoneum (4%), bones (10.7%–23.7%), brain (0.3%–6%), and spinal cord. Approximately 35% of CRC cases are diagnosed before distant metastasis, 36% upon lymph node involvement, and 23% after distant organ metastasis. Although several studies have established primary tumor models in mice in our country, there are limited studies on experimental lung metastasis models, prompting the need for this research. Aim: To establish and evaluate a lung metastasis model of colorectal cancer in C57BL/6J mice using the MC38 cell line. Materials and Methods: This study was conducted at the Institute of Biomedical Sciences, Mongolian National University of Medical Sciences. Approval was obtained from the Ethics Review Board of the Mongolian National University of Medical Sciences (2023/3-09) and all laboratory safety regulations and protocols were strictly followed. Male C57BL/6J mice bred at the Experimental Animal Center of Mongolian National University of Medical Sciences were used. MC38 murine colorectal carcinoma cells were cultured and injected intravenously (via the tail vein) at a concentration of 0.25×10⁶ cells per mouse (n=12) to induce lung metastasis. Histological analysis was subsequently performed. Results: Histological examination revealed significant alterations in lung tissue architecture, characterized by areas of dense infiltration by pleomorphic, hyperchromatic cells, disrupting the normal alveolar structure. No histological abnormalities were observed in other organs. Conclusion Intravenous injection of MC38 colorectal adenocarcinoma cells into the tail vein of C57BL/6J mice successfully induced lung metastases, characterized by hyperchromatic, pleomorphic cell infiltrates forming glandular structures within the lung parenchyma.

Background: In recent years, scientists have found that certain natural compounds have significant potential in cancer prevention and early-stage cancer treatment. Flavanones, a class of polyphenolic compounds found in plants, vegetables, seeds, fruit peels, and flowers, have been identified to possess anticancer, antioxidant, anti- inflammatory, and antibacterial bioactivities. Cancer has become a major global challenge in terms of both economic and public health concerns. Global statistics indicate that 22.8% of deaths are attributed to non-communicable diseases, and 16.8% are caused by cancer, accounting for one in four and one in six deaths, respectively. Aim : To investigate anticancer effects of Iris Tenuifolia-derived flavanone on cancer cell lines. Materials and Methods : The study was conducted at the Bio-Medical Research Institute of the Mongolian National Uni versity of Medical Sciences, investigating the effect of flavanones on cancer cell viability under in vitro conditions using the MTT assay. In the study, colon, liver, and lung cancer cells were cultured, stabilized, and used for the experiments. Colorectal cancer cells (MC38), liver cancer cells (HepG2), and lung cancer cells (A549) were revived, cultured, and stabilized for use in the experimental procedures. Statistical analysis of the results was performed using Microsoft Excel 2010, and graphs were generated using GraphPad Prism 8. Differences between groups were analyzed using Student’s t-test, and a p-value of <0.05 was considered statistically significant. Results : We treated MC38, HepG2, and A549 cancer cells with different concentrations of flavanone (2.5 µM, 5 µM, and 10 µM) for 24 to 48 hours to evaluate cell viability. Flavanone inhibited A549 cell viability by 2.5 μM-10%, 5 μM-25%, and 10 μM-38%, respectively. For HepG2 cells, flavanone treatment at concentrations of 5-10 µM reduced cell viability by 28–58%. No statistically significant effect on the viability of MC38 cells was observed following treatment with flavanone at concentrations ranging from 2.5 to 10 µM. Additionally, although MC38 inhibited cell viability in a dose-de pendent manner in cell cultures, it had a statistically significant effect at higher concentrations of 30-200 μM (p<0.01). Conclusion Flavanone inhibits the cancer cell viability in a dose and time dependent manner

Background: The study of small-molecule compounds with antitumor activity involves several crucial steps. These include determining their selective effects on cancer cells, understanding the type of cell death they induce, identifying the activated signaling pathways, pinpointing the target molecules, and elucidating the mechanisms of action. Among the plant-derived compounds with anticancer properties, flavonoids are notable for their ease of isolation and their abundance in food. Apigetrin, a representative flavonoid, is a secondary metabolite found in plants, and our previous study indicated that its anticancer selectivity index was 13.1. However, the specific mechanism by which apigetrin inhibits leukemia cell growth remains unclear. Aim: To study of the inhibitory action of apigenin on leukemia cell culture Materials and Methods: In this study, we evaluated the apoptosis of cells using flow cytometry and investigated the in volvement of the caspase pathway through the use of pancaspase inhibitors to explore the effects of apigetrin on leukemia cell growth. Results: After incubating leukemia RAW264.7 cells with 30 μM apigetrin for 24 and 48 hours, we did not detect any apoptosis through Annexin V and PI staining by flow cytometry. We compared the number of viable cells using the MTT assay after 24-hour treatment of apigetrin with or without pretreatment of Z-VAD, a pancaspase inhibitor, for 30 minutes. The results indicated that the pancaspase inhibitor did not reduce the inhibitory effect of apigetrin on the growth of RAW264.7 cells. In contrast, the positive control group, treated with doxorubicin—which induces apoptosis—showed not only significant apoptosis but also a reduction of the pancaspase inhibitor on the cell growth inhibition. Therefore, these data suggested that apigetrin likely has a cytostatic effect or inhibits the cell cycle rather than being cytotoxic. Future research should focus on determining which stage of the cell cycle RAW264.7 cells treated with apigetrin are in, as well as studying the signaling pathways involved in the cell cycle. Conclusions Apigetrin inhibits the proliferation of RAW264.7 leukemia cells in a caspase-independent and non-apoptotic manner.

Background: The corneal endothelium, the innermost layer of the cornea, is composed of hexagonal cells that maintain corneal transparency and provide essential nutrients to the stroma. These cells play a critical role in preserving visual acuity. Previous studies have demonstrated that endothelial cells do not regenerate, and their density progressively declines with age, accompanied by morphological alterations. Given the individual variability in corneal thickness and endothelial morphology, establishing normative reference values is crucial for diagnosing corneal diseases, planning corneal transplantation, and optimizing surgical strategies for cataract surgery. However, there is a scarcity of data regarding central corneal thickness, endothelial cell density, and cell morphology among Mongolian adults. This knowledge gap provided the rationale for the present study. Aim: To study the central corneal thickness and endothelial cell morphology in Mongolian adults. Materials and Methods: This study was conducted using an analytical cross-sectional design. A total of 198 individuals aged 20 to 79 years were randomly selected, and comprehensive ophthalmic examinations were performed. Corneal parameters—including central corneal thickness, endothelial cell density, mean cell area, coefficient of variation of cell size, and the percentage of hexagonal cells—were quantitatively assessed using a non-contact specular microscope. Ethical approval was obtained from the Research Ethics Committee of the Mongolian National University of Medical Sciences (Approval No. 2024/3-06), and written informed consent was obtained from all participants prior to enrollment. Results: The mean age of the study participants was 48.4±14.5 years, with 48.9% (n=97) being male and 51.1% (n=101) female. In the central cornea, the mean endothelial cell density (ECD) was 2857.14±291.49 cells/mm², the mean central corneal thickness (CCT) was 526.25±33.67 µm, the mean cell area was 335.11±37.82 µm², the percentage of hexagonal cells was 64.81±3.94%, and the coefficient of variation (CV) in cell size was 0.31±0.04. With increasing age, both ECD and the percentage of hexagonal cells showed a statistically significant decline, while the mean cell area and CV demon strated a significant inverse correlation (P=0.0001). No statistically significant differences were observed in corneal thickness or endothelial morphometric parameters between the right and left eyes or between sexes. Among the Mongolian adults, the endothelial cell density decreases by approximately 0.3% annually (r=0.2107, p<0.0001). Conclusion 1. The mean central corneal thickness (CCT) in adult Mongolian individuals was 526.25±33.67 μm, which is comparable to reported averages from other populations. However, the mean endothelial cell density (ECD) was relatively higher, measured at 2857.14±291.49 cells/mm². 2. With advancing age, a progressive decline in central endothelial cell density and the proportion of hexagonal cells was observed, whereas the coefficient of variation (CV) in cell size and the mean cell area showed a corresponding increase

Background: In recent years, the incidence of liver diseases due to complications of non-alcoholic fatty liver disease (NAFLD) has shown a significant upward trend in Southeast Asian countries. NAFLD is a hepatic disorder characterized by lipid accumulation in the microstructure of the liver in individuals who consume little to no alcohol. It is often associated with insulin resistance and is diagnosed when steatosis affects more than 5% of hepatocytes histologically, or when the fat signal intensity on MRI exceeds 5.6%, based on fat-to-water ratio measurements. In Mongolia, histological studies using frozen liver sections with routine and special staining techniques are limited, highlighting the necessity of this study. Aim: To determine and compare the degree of steatosis and fibrosis in frozen liver tissue samples of patients with NAFLD through histological analysis. Materials and Methods: This study was conducted at the the Department of Anatomy, School of Biomedicine and Bio medical Research Institute of MNUMS in collaboration with the Second State Central Hospital. Ethical approval was obtained from the Research Ethics Committee of MNUMS (Protocol No. 2024/3-06). All procedures adhered strictly to laboratory biosafety protocols. Participants were selected among patients undergoing elective laparoscopic cholecystectomy, from whom informed consent was obtained. Based on inclusion criteria, five participants were grouped as follows: healthy control (n=1), NAFLD without fibrosis (n=2), and NAFLD with fibrosis (n=2). Liver biopsies (approx. 1 cm in size) were obtained intraoperatively, immediately deep-frozen in liquid nitrogen, and prepared for histological evaluation. Results: In patients with NAFLD compared to the healthy liver group, disruption of hepatocyte columnar architecture and mild periportal lymphocytic infiltration were observed. Oil Red O staining revealed 34–66% micro- and macrovesicular steatosis, corresponding to grade 2 steatosis. Masson’s trichrome staining showed no fibrotic changes in perivenular or periportal areas (Ishak grade 0/4) at this stage. However, upon progression to grade 3 steatosis, early-stage fibrosis was observed in both perivenular and periportal regions (Ishak grade 1/4). Further progression to stage 4 fibrosis was characterized by the development of connective tissue septa, although no significant changes in droplet size were observed. Conclusions 1. Increasing stages of fibrosis are not directly influenced by the severity of hepatic steatosis in NAFLD. 2. Although the degree of steatosis increases, the absence of corresponding fibrotic changes in early stages indicates a complex progression pattern of NAFLD requiring further investigation.

Background: Alloxan is a chemical compound commonly used in experimental animal models of diabetes. In 1943, Shaw Dunn and Mc- Letchie reported that alloxan causes specific necrosis of pancreatic β-cells in experimental animals, which led to the study of alloxan in relation to diabetes. In this study, we evaluated the structural changes in the pancreatic tissue of diabetic mice induced by alloxan. Aim: To study the structural changes in the pancreatic tissue of diabetic mice induced by alloxan. Materials and Methods: According to the protocol for establishing a diabetic model, alloxan monohydrate was injected intraperitoneally into 6- to 8-week-old C57BL/6 mice to develop a diabetic model and evaluate the structure of pancreatic tissue. Results: Alloxan induced severe degenerative changes in the centers of the pancreatic islets of mice in the diabetic group. The islet shape was irregular, and the central part was relatively sparse; dead (karyolysis) cells were observed. In the exocrine part of the pancreas, the acinar structure was preserved; the nuclei of acinar cells were stained bright blue. The plasma-particle ratio of some acinar cells was lost, the plasma contained vacuoles, and the interstitial spaces were enlarged and appeared pale. On the 7th day of the experiment, the positive expression of β-cells in the pancreatic islets of mice in the diabetic group was reduced compared to the control group, and a necrotic area was observed. On the 28th day, the positive expression of β-cells was visible in the central part of the islet. When the qualitative characteristics of the positively stained cells of the islets of Langerhans were converted into quantitative values, the percentage of the area of insulin-positive stained cells was 13.37% ± 0.89% in the control group and 6.01% ± 0.39% in the diabetic group. The percentage of glucagon-positive stained cells in the control group was 15.27% ± 1.11%, and in the diabetic group was 5.01% ± 0.58%. The islet area of the pancreatic islets of Langerhans in the diabetic group was observed to be increased compared to the control group. This is thought to be due to the swelling of the islet cells and the formation of empty spaces created by necrotic cells. Conclusion The results of the functional assay showed that glucose- dependent insulin secretion was still active after 28 days of the experiment. Alloxan-induced necrosis and apoptosis reduced the percentage of insulin- and glucagon-positive cells in the islets of Langerhans.

Background: Hyperferritinemia, characterized by elevated serum ferritin levels, affects approximately 5–25% of the general population. Given the frequent coexistence of liver iron overload syndrome and metabolic syndrome—both of which significantly contribute to global morbidity and mortality—it is essential to investigate their interconnections. However, there is a lack of sufficient evidence, both in Mongolia and internationally, regarding the relationship between iron storage indicators, metabolic syndrome, and its components. A deeper understanding of iron’s role in disease progression is needed. Aim: This study aims to assess the association between hyperferritinemia and metabolic syndrome parameters. Materials and Methods: A cross-sectional analytical observational study was conducted on 159 male participants who met the inclusion criteria. Data were collected using a standardized questionnaire, and anthropometric measurements were taken. Blood samples were analyzed to determine glucose, triglyceride, total cholesterol, and high-density lipoprotein (HDL) levels using an automated biochemical analyzer. Serum ferritin concentrations were measured via the ELISA method (DRG Instruments GmbH, Germany), with hyperferritinemia defined as a serum ferritin level exceeding 400 ng/ ml. Metabolic syndrome was diagnosed based on the Harmonized criteria. Statistical analyses included the chi-square test and Fisher’s exact test for categorical variables, the Mann-Whitney U test for non-normally distributed data, and Spearman’s correlation test to assess relationships between glycemic levels, lipid parameters, and metabolic syndrome components. Results: The findings indicate that 59 participants (37.1%) had metabolic syndrome, while 33 (20.8%) presented with hyperferritinemia. The presence of metabolic syndrome and hyperglycemia increased the likelihood of developing hyperferritinemia by 3.4 and 3.7 times, respectively, whereas abdominal obesity raised the risk by 2.2 times. Conclusion There was a significant correlation between serum ferritin levels and certain parameters of metabolic syndrome among the male participants in this study.

Background: Cervical cancer is a common disease among women. Treatment for cervical cancer includes surgery, radiation therapy, chemotherapy, or a combination of chemotherapy and radiation therapy. Cisplatin is the first-line chemotherapy drug for cervical cancer. Research has shown that about 20% of cervical cancer patients become resistant to chemotherapy, which results in decreased results, tumor recurrence, and poor prognosis. Therefore, researching new drugs, improving the sensitivity of cervical cancer cells to cisplatin, and improving the effectiveness of cervical cancer treatment is the basis of this research. Aim: To investigate the inhibitory effect of curcumin on cisplatin-resistant cervical cancer Hela/DDP and SiHa/DDP cell lines. Materials and Methods: The study utilized cisplatin-resistant cervical squamous carcinoma (SiHa/DDP) and adenocarcinoma (Hela/DDP) cell lines. The cells in the experimental group were treated with 8.5 μM of curcumin, while the control group received only the culture medium. A colony formation assay was conducted to assess cell proliferation, with colonies stained using crystal violet; the number of colonies was then counted and compared between the two groups. Results : 1. In the Hela/DDP cell line, the control group formed an average of 507.7±15.70 colonies, whereas the experimental group, treated with curcumin, formed 112.3±16.17 colonies. The difference between the groups was statistically significant (p < 0.0001). 2. In the SiHa/DDP cell line, the control group had an average of 450.3±17.95 colonies, while the experimental group treated with curcumin had 198.3±13.05 colonies. This difference was also statistically significant (p < 0.0001). Conclusions 1. Curcumin significantly reduces the proliferation of cisplatin-resistant cervical squamous cell carcinoma (Hela/DDP) cells. 2. Curcumin significantly reduces the proliferation of cisplatin-resistant cervical adenocarcinoma (SiHa/DDP) cells.