Background: Meniere's disease is a condition caused by disturbances in the auditory and vestibular systems. It is characterized by symptoms such as dizziness, nausea, vomiting, and tinnitus. In the United States, the prevalence of Meniere's disease has been found to be 84 cases per 100,000 women and 56 cases per 100,000 men. Regionally, it is more common in less populated areas, and research has confirmed that the prevalence increases with higher household income. Aim: To evaluate the effectiveness of traditional medicine treatments and therapies for Meniere's disease. Results: The patient is a 43-year-old male, with symptoms of dizziness, vomiting, and tinnitus. Since 2023, he has sought care at the Central Hospital of Mongolian Medicine, where he received traditional medicine treatments including herbal therapy and other traditional therapies on three occasions. As a result, the frequency of dizziness has decreased and other clinical symptoms have improved. Conclusion Traditional medicine treatments have been shown to be effective in managing Meniere's disease by extending the interval between relapses, improving quality of life, and significantly reducing clinical symptoms.

Background: The craniofacial region is one of the most frequently injured parts of the human body, with mandibular fractures being the most common type of facial skeletal injury. The leading causes of mandibular fractures include traffic accidents, falls, interpersonal violence, and sports-related injuries. In Mongolia, mandibular fractures are prevalent, with a higher incidence among males. However, to date, no national-level analysis of mandibular fractures has been conducted. This study aims to comprehensively examine mandibular fractures in Mongolia by identifying demographic factors and causes of injury. Aim: To determine the incidence and causes of mandibular fractures recorded in Mongolia over the past ten years. Materials and Methods: This study collected data on mandibular fractures recorded in the Health Development Center of Mongolia between 2014 and 2023. Cases were identified using the International Classification of Diseases (ICD-10) code S02.6. Information on patient age, gender, and hospital diagnosis was collected, along with the cause of injury, classified according to ICD-10 codes. Patient age was categorized based on the classification system of the National Statistics Office. Statistical analysis was performed using SPSS 26.00 software, employing the chi-square test for data analysis. Results: During the study period, a total of 2,872 patients were diagnosed with mandibular fractures, with the highest incidence occurring in the 20-40 age group. The average patient age was 31.1±12 years. Males were 5.6 times more likely to sustain mandibular fractures compared to females. The primary causes of injury were interpersonal violence (42%), mechanical trauma (17%), falls (16%), and traffic accidents (15%). Conclusion Between 2014 and 2023, 2,872 cases of mandibular fractures were recorded in Mongolia, with the majority occurring in individuals aged 20-40 years. The leading causes of mandibular fractures were interpersonal violence, mechanical trauma, falls, and traffic accidents. Specialized trauma care services were accessed differently in urban and rural areas.

Introduction: According to epidemiological studies conducted in Mongolia over the past decade, diseases of the digestive system have consistently ranked second in terms of morbidity and fourth in mortality. With the rapid advancement of technology, sedentary lifestyles and unhealthy living habits have become more prevalent among the population, leading to a trend of digestive disorders affecting younger age groups. Therefore, investigating the prevalence, pathological changes, and risk factors associated with gallbladder and pancreatic diseases among university students has become the rationale for this study. Objective: To study the prevalence of gallbladder and pancreatic disorders and determine some of the associated risk factors. Methodology: 200 students from the first to sixth year were selected through random sampling based on the WHO age classification. Data collection included a structured questionnaire and ultrasound examination using the SUN-800D device. Diagnostic criteria followed the national clinical guidelines for acute cholecystitis. Results: Out of 200 participants, 120 (60%) were female and 80 (40%) were male. Among them, 128 students (64%) reported skipping breakfast regularly, and 147 (73.5%) did not consume an adequate amount of fluids daily. Ultrasound examinations revealed that 104 students (52%) had some form of gallbladder or pancreatic abnormality. Additionally, gallstones were detected in 1 student (0.5%), and gallbladder polyps were found in 5 students (2.5%). Conclusion Gallbladder and pancreatic abnormalities were observed in 52% of the participants. Among the associated risk factors, 64% of students reported skipping breakfast, and 73.5% had inadequate daily fluid intake. The ultrasound findings showed that 47% had biliary sludge, 32% had gallbladder kinking, and 48.5% had increased pancreatic echogenicity.

Dysregulation of p53 and phosphoinositide (PIPn) signaling are both key drivers of oncogenesis and metastasis. Our recent findings reveal a previously unrecognized interaction between these pathways, converging in the nucleus to form a PIPn-p53 signalosome that modulates nuclear AKT activation and downstream signaling, thereby influencing cancer cell survival and motility. This review examines recent insights into nuclear PIPn signaling in the context of established roles for p53 in cell dynamics and migration while also deliberating current research on how nuclear PIPns interact with p53 to form signalosomes that affect cell motility. We emphasize the critical role of PIPns in stabilizing p53 and activating de novo nuclear AKT signaling, which subsequently modulates key motility-related pathways. Understanding the unique operation and function of the PIPn-p53 signalosome in nuclear phosphatidylinositol 3-kinase (PI3K)-AKT activation offers novel therapeutic strategies for controlling cancer metastasis by targeting pertinent interactions and events.
Humans ; Tumor Suppressor Protein p53/metabolism* ; Signal Transduction ; Cell Movement ; Cell Nucleus/metabolism* ; Phosphatidylinositols/metabolism* ; Proto-Oncogene Proteins c-akt/metabolism* ; Animals ; Neoplasms/pathology* ; Phosphatidylinositol 3-Kinases/metabolism*

OBJECTIVE: To investigate the predictive value of sphinor kinase 1 (sphk1), D-lactic acid, and intestinal fatty acid binding protein (I-FABP) for gastrointestinal injury in patients with sepsis. METHODS: A prospective observational study was conducted. Sixty-eight patients with sepsis and gastrointestinal dysfunction admitted to the department of critical care medicine of the First Affiliated Hospital of Baotou Medical College Inner Mongolia University of Science and Technology from May 2024 to March 2025 were enrolled (sepsis group), and they were divided into acute gastrointestinal injury (AGI) I-IV groups according to the definition and grading criteria of AGI proposed by the European Society of Intensive Care Medicine in 2012. Twenty non-sepsis patients without AGI admitted to the intensive care unit during the same period were enrolled as the control group (non-sepsis group). Within 30 minutes of patient enrollment, plasma sphk1, D-lactic acid, and I-FABP levels were determined by enzyme linked immunosorbent assay (ELISA). General data such as gender, age were recorded, and levels of procalcitonin (PCT), high-sensitivity C-reactive protein (hs-CRP), lactic acid (Lac), and acute physiology and chronic health evaluation II (APACHEII), sequential organ failure assessment (SOFA) were measured. Spearman method was used to analyze the correlation between sphk1, I-FABP, D-lactic acid and other indicators. The receiver operator characteristic curve (ROC curve) was used to evaluate the predictive value of sphk1, D-lactic acid, I-FABP, APACHEII score, and SOFA score for gastrointestinal injury in patients with sepsis. RESULTS: Among the 68 sepsis patients, 13 were classified as AGI grade I, 16 as AGI grade II, 23 as AGI grade III, and 16 had AGI grade IV. There were no statistically significant differences in gender, age, and abdominal infection rate among the groups. The SOFA score and APACHEII score of the sepsis group were significantly higher than those of the non-sepsis group; and the APACHEII score of the AGI IV group was significantly higher than that of the AGI I and AGI II groups. The levels of sphk1, D-lactic acid, I-FABP, PCT, Lac and hs-CRP in the sepsis group were significantly higher than those in the non-sepsis group, and each indicator gradually increased with the increase of AGI grade. Correlation analysis showed that plasma sphk1, D-lactic acid, and I-FABP in patients with sepsis-induced gastrointestinal injury were positively correlated with PCT, Lac, APACHEII score, and AGI grade (all P < 0.05), and sphk1 was positively correlated with I-FABP and D-lactic acid (r values were 0.773 and 0.782, respectively, both P < 0.05). ROC curve analysis showed that sphk1, D-lactic acid, I-FABP, APACHEII score, and SOFA score had high predictive value for gastrointestinal injury in patients with sepsis, with area under the curve (AUC) of 0.996, 0.987, 0.976, 0.901, and 0.934 (all P < 0.05). When the optimal cut-off value of sphk1 was 60.46 ng/L, the sensitivity and specificity were 95.6% and 100%, respectively; when the optimal cut-off value of D-lactic acid was 1 454.3 μg/L, the sensitivity and specificity were 95.6% and 100%, respectively; when the optimal cut-off value of I-FABP was 0.91 ng/L, the sensitivity and specificity were 95.6% and 100%, respectively; when the optimal cut-off value of APACHEII score was 14.5, the sensitivity and specificity were 80.9% and 85.0%, respectively; when the optimal cut-off value of SOFA score was 3.5, the sensitivity and specificity were 85.3% and 95.0%, respectively. CONCLUSIONS The levels of plasma sphk1, I-FABP, and D-lactic acid were significantly elevated in patients with sepsis and gastrointestinal injury. These indicators can serve as sensitive and relatively specific serological markers for early prediction of intestinal mucosal damage.
Humans ; Lactic Acid/blood* ; Fatty Acid-Binding Proteins/blood* ; Sepsis/complications* ; Prospective Studies ; Male ; Female ; Middle Aged ; Predictive Value of Tests ; Adult ; Aged ; Gastrointestinal Diseases/blood* ; Prognosis

Paclitaxel (PTX), a valuable natural product derived from Taxus species, exhibits remarkable anti-cancer properties. It penetrates nanopores in microtubule walls, interacting with tubulin on the lumen surface and disrupting microtubule dynamics, thereby inducing cytotoxic effects in cancer cells. PTX and its derivatives have gained approval for treating various diseases due to their low toxicity, high efficiency, and broad-spectrum application. The widespread success and expanding applications of PTX have led to increased demand, raising concerns about accessibility. Consequently, researchers globally have focused on developing alternative production methods and applying nanocarriers in PTX delivery systems to enhance bioavailability. This review examines the challenges and advancements in PTX sourcing, production, physicochemical properties, anti-cancer mechanisms, clinical applications, trials, and chemo-immunotherapy. It aims to provide a comprehensive reference for the rational development and effective utilization of PTX.
Humans ; Paclitaxel/pharmacology* ; Antineoplastic Agents, Phytogenic/pharmacology* ; Neoplasms/drug therapy* ; Animals ; Taxus/chemistry*

Objective: To investigate the protective effects of the combined concentrated liquid extract of Pueraria lobata (Willd.) Ohwi root (P. lobata, Ge Gen) and Hovenia dulcis Thunb. (H. dulcis, Zhi Ju Zi) against ethanol-induced liver damage in vitro, using a human hepatoma cell line G2 (HepG2) cell model. Methods: HepG2 cells were cultured in medium containing 4% ethanol to establish a model of alcoholic liver damage. The cells were then treated with the combined extract obtained via cryogenic extraction. Biochemical assays and Western blot analyses were performed to assess the levels of oxidative stress markers, antioxidant enzymes, and inflammatory cytokines. In addition, activation of the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway was examined to elucidate the mechanisms underlying the effects of the extract. Results: Treatment with the extract contributed to a significant reduction in the release of nitric oxide and reactive oxygen species in the ethanol-treated HepG2 cells; promoted the elevated expression of superoxide dismutase, catalase, and glutathione, indicating enhanced antioxidant defenses; and showed strong free radical-scavenging activity against 1,1-diphenyl-2-picrylhydrazyl radicals. In addition, by activating the PI3K/AKT pathway, treatment promoted increases in the expression of nuclear factor erythroid 2-related factor 2 and its downstream targets, subsequently inhibiting apoptosis. Moreover. inflammatory responses were mitigated, as indicated by reductions in the expression of tumor necrosis factor-alpha and interleukin-6, and we detected reduction in the levels of alanine aminotransferase and aspartate aminotransferase, thereby indicating hepatoprotective effects. Conclusion The combined P. lobata root and H. dulcis extract was established to have notable antioxidative and anti-inflammatory properties, effectively alleviating ethanol-induced liver damage in vitro. These findings highlight the potential applicability of this extract as a candidate for treating alcoholic liver disease.

[摘 要] 目的：探讨精氨酸-甘氨酸-天冬氨酸（RGD）修饰对肿瘤抑素19肽（T-19）抗肝癌活性的影响，比较分析T-19及RGD修饰的T-19（RGD-T-19）对肝癌SK-Hep-1细胞增殖、侵袭和迁移能力的影响。方法：用Fmoc固相法合成T-19及RGD-T-19，用高效液相色谱仪和质谱进行分离、鉴定。常规培养SK-Hep-1细胞，用0、50、100、150、200、250 mg/mL的T-19及RGD-T-19分别处理细胞，分为0 mg/mL（对照）组、50 mg/mL组、100 mg/mL组、150 mg/mL组、200 mg/mL组、250 mg/mL组。CCK-8法、克隆形成实验、划痕愈合实验和Tanswell小室实验、WB法和qPCR法分别检测SK-Hep-1细胞的增殖、迁移、侵袭能力，以及环氧合酶-2（COX-2）、基质金属蛋白酶-2（MMP-2）、MMP-9、组织基质金属蛋白酶抑制剂-1（TIMP-1）、TIMP-2蛋白和MMP-1、MMP-2 mRNA的表达。结果：经质谱鉴定，用Fmoc固相法合成的T-19及RGD-T-19纯度高。T-19和RGD-T-19均能显著抑制SK-Hep-1细胞的增殖、迁移、侵袭能力，抑制COX-2蛋白、MMP-2和MMP-9蛋白及mRNA的表达、促进TIMP-1、TIMP-2蛋白的表达（P < 0.05, P < 0.01, P < 0.001），RGD-T-19的抑制或促进效应均明显强于T-19（均P < 0.05）。结论：利用Fmoc固相法合成了纯度高、活性好的T-19及RGD-T-19，两种肽均能抑制SK-Hep-1细胞增殖、侵袭和迁移能力，RGD-T-19作用明显强于T-19。

Inflammatory bowel disease (IBD) is characterized by chronic relapsing intestinal inflammation and encompasses ulcerative colitis (UC) and Crohn's disease (CD). IBD has emerged as a global healthcare problem. Clinically efficacious therapeutic agents are deficient. This study concentrates on models of ulcerative colitis with the objective of discovering novel therapeutic strategies. Previous investigations have established that schisandrin A demonstrates anti-inflammatory effects in vitro, concurrently enhancing the transcriptional activity of farnesoid X receptor (FXR). FXR inversely modulates the transcriptional activity of NF-κB, which has an important role in regulating inflammatory responses. Consequently, the current study was to explore the safeguarding influence of schisandrin A on ulcerative colitis and delineate the mechanism by which it regulates this effect through the FXR signaling pathway. The effect of schisandrin A on the mRNA levels of inflammatory factors was evaluated in RAW264.7 cells. The dual luciferase reporter gene assay was used to verify the relationship between schisandrin A and FXR targeting. The animal experiments were performed in accordance with the regulations of the Animal Ethics Committee of Shanghai University of Traditional Chinese Medicine (approval No. PZSHUTCM2304250005). Acute ulcerative colitis was induced in wild-type or FXR knockout C57BL/6 mice by drinking 3% dextran sodium sulfate (DSS) for 7 days, and schisandrin A was administered via gavage for a continuous treatment period of 7 days. The body weight and faecal were monitored daily. The mRNA levels of inflammatory factors in colon tissue and FXR target genes were measured by RT-qPCR. The findings revealed that schisandrin A, in vitro, impeded the lipopolysaccharide (LPS)-induced elevation in mRNA levels of inflammatory factors and schisandrin A could augment transcriptional activity of FXR. In wild-type mice, schisandrin A significantly improved weight loss, colon shortening, loose stools and blood in stools in mice with acute ulcerative colitis, and schisandrin A significantly reduced the expression of pro-inflammatory factors genes and significantly increased the expression of FXR target genes in colon tissues. In FXR knockout mice, the administration of schisandrin A failed to yield ameliorative effect on acute ulcerative colitis in mice. In conclusion, schisandrin A can reduce intestinal inflammation through the FXR signaling pathway to alleviate acute ulcerative colitis in mice. Implications arise that Schisandra lignans could serve as lead compounds for drug development aimed at inflammatory bowel disease.