Background: Skin wounds can occur for many reasons, including UV radiation, mechanical burns, trauma, and chronic inflammation caused by metabolic factors. In Mongolia, as of 2022, household burns were the top 5 causes of injuries, the leading cause of injuries in children aged 0-5, and accounted for 18.4% of all illnesses in children aged 0-5. Skin burns and wounds take a long time to heal, which causes emotional, aesthetic, and economic stress for doctors. Developing in novative, effective, and low-side effects therapeutic products to improve wound healing is of great clinical and economic importance. The lack of research on the effects of bacterial metabolites and aloe vera (Aloe barbadensis Miller) on burn wounds was the basis for our research. Aim: To determine the effects of a mixture of bacterial metabolites and aloe vera on burn wounds in experimental animals. Materials and Methods: Eight-week-old BALB/c mice were divided into three groups: control group, bacterial metabo lite group, and aloe vera group. The mice were anesthetized, and the dorsal hair was shaved over a 2×2 cm area using an electric clipper. A second-degree burn wound model was created by exposing the shaved dorsal skin to hot air at 200°C for 10 seconds. A total of 100 μL of a bacterial metabolite suspension mixed with aloe vera at a 1:1 ratio was applied evenly to the center of the wound. Wound images were captured daily, and wound areas were measured using ImageJ software. Healing was evaluated on days 7, 14, and 21 of treatment and compared with the control group. The initial wound size was defined as 100%, and wound closure percentages were calculated accordingly. Burn skin tissues from both experimen tal and control groups were subjected to immunofluorescence staining for the vascular marker α-SMA (Thermo Fisher Scientific). Statistical analysis: The differences between the control and experimental groups were analyzed using an independent t-test using GraphPad Prism 10 software, and the mean, standard deviation, and statistical correlation were calculated. Results: The effect of the mixture of bacterial metabolites and aloe vera (Aloe barbadensis Miller) on the healing of burn wounds in experimental mice was compared with the control group. The wound size at 7 days was 82.1% in the control group and 83.7% in the experimental group (p<0.197), at 14 days was 62.6% in the control group and 58.1% in the exper imental group (p<0.0001), at 21 days was 50.7% in the control group and 32.7% in the experimental group (p<0.0001). No statistically significant difference in wound healing was observed between the groups at day 7; however, significant differences were observed at days 14 and 21. Immunofluorescence analysis revealed uniform expression of α-SMA-pos itive cells in the experimental group at 7, 14, and 21 days of treatment, whereas α-SMA expression was not detected in the control group. Conclusion The combination of bacterial metabolites and aloe vera promotes wound healing in experimental mouse burn wounds.

Postmenopausal estrogen deficiency can lead to genitourinary syndrome of menopause (GSM), which manifests as vaginal dryness, dyspareunia, and sexual dysfunction, among other clinical symptoms. These complications often result in emotional distress and a decline in overall quality of life (7). Several studies estimate that 25–50% of postmenopausal women experience symptoms such as pain during intercourse, burning, itching, and dysuria due to vaginal atrophy and inflammation (9). Menopause is commonly diagnosed based on the absence of menstruation and hormone levels (10), but one of the simplest diagnostic methods is the evaluation of the vaginal microenvironment. There is limited data in Mongolia regarding the vaginal microenvironment of perimenopausal and postmenopausal women and the factors influencing its changes. This gap in knowledge formed the basis of our study. The aim of this research was to assess the vaginal microenvironment in menopausal women and to analyze its relationship with various influencing factors. We conducted a cross-sectional observational study using a descriptive research design. A total of 110 women aged 45–55 years, presenting with menopausal symptoms at “Santmaral” Women’s Clinic and the Women’s Outpatient Department of Songinokhairkhan Health Center, were selected for the study. Both quantitative and qualitative research methods were employed, including surveys and physical examinations. Participants completed a 10-minute questionnaire consisting of 8 open-ended and 12 closed-ended questions. The vaginal microenvironment was assessed using special pH test strips applied to vaginal secretions. Data were analyzed using Excel 21 and SPSS 23, comparing the vaginal microenvironment with various influencing factors. The results showed that the average vaginal microenvironment pH among menopausal women was 5.18 ± 0.45 (n=110). In married women, the average pH was 5.1 ± 0.45; among women with a history of pregnancy, it was 4.10 ± 1.58; and among those who had given birth, it was 2.8 ± 0.98 — indicating an abnormal vaginal microenvironment. Women who were using hormone replacement therapy had an average pH of 5.05 ± 0.45, while those using non-hormonal contraceptive methods had an average pH of 5.3 ± 0.43. These findings were statistically significant (p = 0.0001****)

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: 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.