Objective To investigate the expression of the histone deacetylase SIRT7 in glioma cells and its impact on epithelial-mesenchymal transformation (EMT), as well as its effects on proliferative, migratory and invasive capabilities of glioma cells. Methods Bioinformatics analysis was conducted on data from glioma patients in the Cancer Genome Atlas (TCGA) and the Chinese glioma Genome Atlas (CGGA) databases to explore the expression of SIRT7 gene in gliomas and its correlation with tumor grading, molecular characteristics and patient clinical prognosis. Glioma cells were randomly divided into control, SIRT7 knockdown, SIRT7 overexpression, drug treatment (10 μmol/L hydrochlorothiazide) and drug (10 μmol/L hydrochlorothiazide)+SIRT7 overexpression groups. The CCK-8 assay, cell scratch assay and Transwell assay were used to observe the effects of upregulating and downregulating SIRT7 expression on glioma cell proliferation, migration and invasion. RT-qPCR and Western blotting were employed to detect the effects of SIRT7 on the expression of neural cadherin (N-cadherin), Vimentin, E-cadherin, transforming growth factor-β (TGF-β), Ki-67, and Smad3 protein in glioma cells. Nude mouse tumor-bearing experiments were conducted to observe the effect of SIRT7 knockdown on glioma growth. Results Higher expression levels of SIRT7 gene were associated with poorer clinical prognosis (P<0.0001). SIRT7 expression levels were significantly correlated with tumor grading and 1p19q coding status (P<0.01). Compared with normal HA cells, glioma cells showed significantly increased SIRT7 expression levels (P<0.01). CCK-8 assay results indicated that, compared with control group, the proliferation activity of glioma cells in SIRT7 knockout group was significantly decreased (P<0.01), while SIRT7 overexpression group showed significantly increased proliferation activity (P<0.01). EdU assay results showed that, compared with control group, the proportion of glioma cells in the proliferative stage was significantly decreased in SIRT7 knockdown group (P<0.01), and significantly increased in SIRT7 overexpression group (P<0.01). Western blotting results revealed that, compared with control group, the protein expression levels of TGF-β, Smad3, N-cadherin and Vimentin were significantly decreased in SIRT7 knockdown group (P<0.01), while the expression level of E-cadherin protein was significantly increased (P<0.05). SIRT7 overexpression group showed significantly increased protein expression levels of TGF‑β, Smad3, N-cadherin and Vimentin (P<0.05), and a significantly decrease in E-cadherin protein expression level (P<0.05). Scratch assay results indicated that, compared with control group, the migration ability of cells in SIRT7 knockdown group and drug group was significantly decreased (P<0.01), and SIRT7 overexpression group showed significantly increased cell migration ability (P<0.05). Compared with drug group, drug+SIRT7 overexpression group exhibited significantly increased cell migration ability (P<0.01). Transwell assay results showed that, compared with control group, the migration and invasion abilities of cells in SIRT7 knockdown group and drug group were significantly decreased (P<0.01), and SIRT7 overexpression group exhibited significantly increased migration and invasion abilities (P<0.01). Compared with drug group, drug+SIRT7 overexpression group showed significantly increased migration and invasion abilities (P<0.01). Nude mouse tumor-bearing assay results indicated that the volume and weight of glioma in SIRT7 knockdown group were significantly reduced compared with control group (P<0.01). Conclusions Glioma patients with high SIRT7 expression have poorer clinical prognosis. SIRT7 can regulate the TGF-β/Smad3 pathway to mediate EMT, promoting the proliferation and migration of glioma cells. SIRT7 knockdown can inhibit the growth of transplanted gliomas in nude mice.

Objective To investigate the effect of miR-373-3p in diabetic retinopathy (DR), as well as the underlying mechanisms. Methods Serum samples from 35 DR patients and 35 non-DR patients visiting Tianjin Fifth Central Hospital from February 2021 to February 2022 were collected, and expression levels of miR-373-3p and vascular endothelial growth factor A (VEGFA) mRNA were detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR). An in vitro DR model was constructed using high glucose (HG)-treated human retinal microvascular endothelial cells (HRMEC). HRMECs were divided into control group (5 mmol/L glucose and 25 mmol/L mannitol treatment), HG group (30 mmol/L glucose treatment), HG+miR-373-3p mimic-negative control (miR-con) group (30 mmol/L glucose treatment after transfection with miR-con), HG+miR-373-3p mimic group (30 mmol/L glucose treatment after transfection with miR-373-3p), HG+miR-373-3p+vector group (30 mmol/L glucose treatment after co-transfection with miR-373-3p and vector), and HG+miR-373-3p+vascular endothelial growth factor A (VEGFA) group (30 mmol/L glucose treatment after co-transfection with miR-373-3p and VEGFA). The expression levels of miR-373-3p, VEGFA mRNA and protein were analyzed by qRT-PCR and Western blotting. CCK-8, immunofluorescence, Transwell assay, angiogenesis assay, and Western blotting were used to evaluate HRMEC proliferation, migration and angiogenesis abilities. The relationship between miR-373-3p and VEGFA was determined by dual luciferase reporter assay. Results Compared with non-DR patients, DR patients exhibited significantly lower expression levels of miR-373-3p (P<0.05) and higher expression levels of VEGFA mRNA (P<0.05) in serum. Compared with control group, HG group showed decreased expression of miR-373-3p (P<0.05), increased expressions of the mRNA and protein of VEGFA (P<0.05), higher cell viability, proliferation rate, proliferating cell nuclear antigen (PCNA) and Cylin D1 protein, and numbers of migrating cells and angiogenesis ability (P<0.05) in HRMECs. Compared with HG+miR-con group, HG+miR-373-3p group showed increased expression of miR-373-3p (P<0.05), decreased expressions of VEGFA (P<0.05), lower cell viability, proliferation rate, PCNA and Cylin D1 protein (P<0.05), and lower numbers of migrating cells and angiogenesis ability (P<0.05) in HRMECs. Compared with HG+miR-373-3p+vector group, HG+miR-373-3p+VEGFA group showed increased expression of VEGFA (P<0.05), higher cell viability, proliferation rate, PCNA and Cylin D1 protein, and numbers of migrating cells and angiogenesis ability (P<0.05) in HRMECs. The results of dual luciferase reporter assay showed decreased enzymatic activity of luciferase after cotransfection of miR-373-3p and VEGFA sequence (P<0.05). Conclusion MiR-373-3p is lowly expressed in the serum of DR patients, and its potential mechanism may involve targeting VEGFA to inhibit HG-induced HRMEC dysfunction.

Objective To report the diagnosis, treatment, and verification process of a patient with sex development disorder whose chromosomal karyotype and genetic test results are inconsistent, and conduct a literature review to improve the understanding of the mosaic status of sexual development disorders. Methods A 14-year-old patient presented with primary amenorrhea on April 3, 2020, at the First Affiliated Hospital of Hebei North University, exhibiting female sexual characteristics. The patient underwent ultrasonic/magnetic resonance imaging of gonads, assessment of gonadal axis function, chromosomal karyotype, and molecular genetic testing, as well as pelvic exploration, malignant gonads resection, and hormone replacement therapy, resulting in drug-induced menstruation. During the diagnosis and treatment, it was found that the patient's chromosomal karyotype analysis was inconsistent with the molecular genetic test results. Subsequently, samples from the three germ layer cells were taken, and fluorescence in situ hybridization (FISH) was used to detect the sex chromosomes in each germ layer cell. XY probes were used to label the gonadal pathological sections to explore the distribution differences of the Y chromosome in the gonads, and changes in anti-Müllerian hormone (AMH) levels before and after surgery were compared. Databases such as Wanfang and PubMed were searched to summarize relevant cohort study literature and understand the current status of research on this disease. Results The patient's body exhibited a significant differences between the 45,X and 46,XY cell lines in different germ layers and within the same layer tissues. The proportion of 45,X in buccal mucosal cells derived from the ectoderm was 30% (6/20), in peripheral blood lymphocytes derived from the mesoderm was 9.7% (11/114), and in bladder shed cells derived from endoderm was 20.4% (22/108). The gonadal pathological sections labeled with XY probes indicated a mosaic state with a reduced Y-chromosome; where the epididymal structure area had a 45,X cell line mosaic of 50.0%, and the malignant area had a normal "Y" content. After gonadal resection, AMH levels significantly dropped from 7.28 pmol/L to <0.07 pmol/L. Literature review revealed that patients with 45,X/46,XY have a complex phenotype spectrum, most with features of Turner syndrome, and female phenotypes are at risk of gonadal tumors. Conclusions In the diagnosis of difficult cases of sex development disorders, when performing peripheral blood karyotype testing, the number of counted cells and analyzed cells should be increased as much as possible, and multi-germ layer cell sampling should be performed. Gonads with a high "Y" mosaic rate are more prone to malignancy in the abdominal cavity. Detecting AMH levels can distinguish cryptorchidism and anorchidism in sexual development disorders with Y chromosomes.

Objective To investigate the protective effects of paeonol (PAE) on autophagy in human neuroblastoma cells (SH-SY5Y) induced by overexpression of α-synuclein (α-Syn), and to explore its related mechanism. Methods SH-SY5Y cells served as control group, while those induced with A53T-α-Syn mutation were used as model group. Additional groups included PAE (150 μg/ml) group, 3-MA (1 mmol/L) group, and PAE(150 μg/ml)+3-MA (1 mmol/L) group. Cell viability was assessed using CCK-8 method, cell morphology was observed under an optical microscope, and protein expressions of α-Syn, LC3-Ⅱ, p62, Beclin-1, phosphorylated c-Jun N-terminal kinase (p-JNK), and p-Bcl-2 were determined by Western blotting. Results Compared with control group, model control exhibited decreased cell survival (P<0.01), increased α-Syn expression (P<0.001), reduced expression of autophagy-related proteins LC3-Ⅱ and Beclin-1 (P<0.01, P<0.05), elevated autophagy substrate protein p62 (P<0.05), and decreased expression of autophagy pathway-related proteins p-JNK and Bcl-2 (P<0.05, P<0.01). Compared with model group, PAE group showed increased cell survival (P<0.01), decreased α‑Syn and p62 protein expression (P<0.01, P<0.05), and increased expression of LC3-Ⅱ, Beclin-1, p-JNK and Bcl-2 (P<0.05). Compared with PAE group, 3-MA+PAE group demonstrated increased α-Syn expression (P<0.05). Conclusions PAE could attenuate the injury of SH-SY5Y cells induced by A53T-α-Syn and eliminate over-expressed α‑Syn by activating autophagy pathway, which may be associated with the upregulation of JNK/Bcl-2 mediated autophagy pathway.

Objective To evaluate the predictive value of dose-surface histogram (DSH) for radiation proctitis (RP) in prostate cancer (PCa) patients undergoing radiotherapy. Methods This prospective randomized controlled clinical trial included 380 PCa patients who underwent image-guided radiotherapy in the First Affiliated Hospital of Hebei Northern University from January 2018 to January 2023. Patients were randomly divided into observation group (n=200) and control group (n=180). The rectal dose distribution of patients in the two groups was evaluated by using DSH and dose-volume histogram (DVH), respectively. The receiver operating characteristic (ROC) curve was utilized to evaluate the predictive value of DSH for acute RP, with DVH serving as a reference. Results The difference was not statistically significant in clinical information such as age, KPS score, and body mass index (BMI) between the observation and control groups (P>0.05), as well as in acute RP incidence (P>0.05). There were significant differences in S₄₀ and V₄₀, S₅₀ and V₅₀, S₆₀ and V₆₀, S₇₀ and V₇₀, and S₇₈ and V₇₈ between the two groups (P<0.05). S₄₀, S₅₀, V₄₀, and V₅₀ showed low efficacy (P<0.001) in predicting acute RP at each level, with AUC ≤0.700. S₆₀ and V₆₀ showed moderate efficacy (P<0.001) in predicting acute RP at each level, with AUC 0.700-0.900. S₇₀, S₇₈, V₇₀ and V₇₈ showed high efficacy (P<0.001) in predicting acute RP at each level, with AUC >0.900. Conclusions The predictive value of DSH for rectal toxicity in patients with PCa is basically consistent with that of DVH. It is expected to become a novel and valuable tool for evaluating radiotherapy plans in the future.

Abdominal war trauma is a common and high-risk type of injury in the modern battlefield, with rapid changes in condition and a high mortality rate. There is an urgent need for emerging medical technologies to improve the efficiency and success rate of first aid for military casualties. With the development of artificial intelligence (AI), 5G, and other emerging technologies, the concept of intelligent medical treatment is gradually forming and can assist in the diagnosis and treatment of abdominal trauma. This paper reviews the characteristics of abdominal war trauma in modern wars, discusses the application of intelligent medical treatment for abdominal war trauma and its drawbacks to be solved, aiming to provide reference for research related to abdominal war trauma.

Knee osteoarthritis (KOA) is a chronic degenerative joint disease, which poses a major challenge particularly among the elderly population due to its high incidence and high disability. Imaging examination has been used commonly to diagnose KOA. However, it faces imitations in predicting disease progression due to the lack of prior information and constraints in manpower and time. With the rapid evolution of big data and computational technologies, artificial intelligence (AI) is progressively integrating into various healthcare domains. Therefore, the integration of artificial intelligence (AI) into healthcare holds promise for revolutionizing KOA diagnosis and treatment. AI-assisted diagnostic models have demonstrated the potential to automate diagnosis, classify disease severity, and predict disease progression with improved efficiency and accuracy. In addition, these models provide personalized diagnosis and treatment options, as well as accurate disease progression risk assessment. Despite these promising outcomes, challenges such as high costs associated with data annotation and limitations in model generalization capabilities persist. This paper reviews recent advancements in AI applications and summarizes the potential value of utilizing AI applications for KOA. To further enhance the utilization of AI in KOA management to overcome current limitations, future efforts should focus on standardizing clinical sample databases, optimizing AI algorithms, and enhancing external verification sets.

Diagnosis and treatment of digestive tract tumors is not optimistic with high incidence and mortality. Early diagnosis is conducive to improving the survival rate and quality of life of the patients. A variety of endoscopic imaging techniques have been applied in the diagnosis of digestive tract tumors, each with its own advantages and disadvantages. Optical coherence tomography (OCT) has emerged as a non-invasive and high-resolution imaging technique with unique advantages in staging and diagnosis of superficial digestive tract tumors. The complexity of massive image processing has also been effectively addressed with the development of artificial intelligence (AI), and AI-assisted OCT imaging, especially in the diagnosis of digestive tract tumors, has shown good prospects. This review summarizes the principle and development of OCT, and discusses the potential of AI-assisted OCT for deep learning in the diagnosis of digestive tract tumors.

Objective To investigate whether axillary lymph node dissection (ALND) can be exempted for young breast cancers with reference to the inclusion criteria of American College of Surgeons Oncology Group (ACOSOG) Z0011 trial. Methods A retrospective analysis was conducted on 134 cases of young breast cancer patients admitted to the Second Affiliated Hospital of Nanchang University and the Affiliated Hospital of Jiujiang College from February 28, 2013 to February 28, 2018 who met the inclusion criteria of the ACOSOG Z0011 trial. Patients were divided into case group [n=63, with sentinel lymph node biopsy (SLNB)] and control group (n=71, with SLNB and ALND). General clinicopathologic data, including age, tumor TNM stage, pregnancy or breastfeeding status, estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), Ki-67, vessel carcinoma embolus, and tumor Nottingham grade, were collected and compared between the two groups. The 5-year disease-free survival (DFS) and 5-year overall survival (OS) of the two groups were analyzed using the Kaplan-Meier method with log-rank tests. A multifactorial Cox proportional hazards regression model was used to analyze the effect of SLNB implementation alone on the DFS and OS in young breast cancer. Results There were no statistically significant differences in age, pregnancy or breastfeeding status, tumor T classification, tumour molecular classification, tumor Nottingham grade and vessel carcinoma embolus between the two groups (P>0.05). The 5-year DFS rate for the 134 young breast cancer patients was 74.6% and the 5-year OS rate was 83.6%. A statistically significant difference was observed in the 5-year DSF rate between case and control groups (66.7% vs. 81.7%, P=0.033), while there was no statistically significant difference in the 5-year OS rate (77.8% vs. 88.7%, P=0.085). The multifactorial Cox proportional hazards regression model analysis showed that performing SLNB alone was an independent risk factor for DFS in young breast cancer patients (HR=2.261, 95%CI 1.097-4.660, P=0.027), but not for OS (HR=1.976, 95%CI 0.789-4.946, P=0.146). Conclusions Young breast cancers exempted from ALND according to the ACOSOG Z0011 trial inclusion criteria had a higher rate of local recurrence, but their OS was not significant affected. Therefore, whether young breast cancers can be exempted from ALND still requires further clinical trial validation.

Objective To investigate the viability of Runt-related transcription factor 1 (RUNX1) as a biomarker for gastric cancer and to assess the impact of the small molecule inhibitor Ro24-7429 on the proliferation, migration, and invasion of gastric cancer cells following targeted modulation. Methods Through the GEPIA database, we analyzed RUNX1 mRNA expression in gastric cancer or normal gastric tissues. Utilizing RUNX1 expression data from the TCGA database, a receiver operating characteristic (ROC) curve was constructed to appraise the potential of RUNX1 as a gastric cancer biomarker. In September 2022, we collected tissue samples from 6 patients with gastric cancer from the Department of General Surgery at the Second Hospital of Lanzhou University. After extracting tissue proteins, Western blotting was employed to compare RUNX1 protein expression in tumor and adjacent tissues. Gastric cancer cell lines with high RUNX1 expression were identified and the suppressive effect of the small molecule inhibitor Ro24-7429 on RUNX1 protein expression was verified by Western blotting. the effect of Ro24-7429 was validated by using CCK-8, colony formation, cell scratch, and Transwell assays. RUNX1 protein levels in gastric cancer tissues were quantified using immunohistochemical staining. An organoid model of gastric cancer was then established from the high-expression samples and verified by both HE and immunization analyses. Lastly, the impact of Ro24-7429 on the growth of gastric cancer organoids with meticulous tracking was evaluated using a biological microscope within a designated area. Results The analysis from the GEPIA database revealed a heightened expression of RUNX1 mRNA in gastric cancer tissues compared with normal tissues (P<0.05). The ROC curve derived from the RUNX1 expression data in the TCGA database boasts an area under the curve (AUC) of 0.956, underscoring RUNX1's potential as a robust diagnostic marker. Western blotting results revealed significantly higher RUNX1 protein expression in gastric cancer tissues than in adjacent tissues (P<0.001). Among 5 gastric cancer cell lines studied, AGS and HGC27 exhibited pronounced RUNX1 protein expression (P<0.001). The small molecule inhibitor Ro24-7429, targeting RUNX1, potently suppressed RUNX1 expression in gastric cancer cells. The results from CCK-8, colony formation, scratch, and Transwell assays showed that Ro24-7429 effectively inhibited proliferation, migration, and invasion of gastric cancer cells (P<0.001). In a gastric cancer organoid model derived from high RUNX1 expression samples, the RUNX1 expression was remarkably consistent with its originating tissue. As expected, upon the targeted inhibition of RUNX1 using Ro24-7429, the cancer organoids significantly reduced growth capacity. Conclusions RUNX1 shows potential as a biomarker for gastric cancer. Ro24-7429 specifically inhibits RUNX1 expression and suppresses tumor cell proliferation, migration, and invasion in gastric cancer cell lines and organoid models.