OBJECTIVES: To explore the association between GPSM2 expression level and gastric cancer progression and analyze the functional pathways and action mechanism of GPSM2. METHODS: We analyzed GPSM2 expression levels in gastric cancer tumors based on data from the GEPIA database and the clinical data of 109 patients. Public databases enrichment analysis were used to assess the impact of GPSM2 expression level on survival outcomes and the functional pathways and action mechanism of GPSM2. We further observed the effects of GPSM2 knockdown and overexpression on proliferation, migration and apoptosis of MGC803 cells using CCK-8 assay, colony formation assay, flow cytometry and immunoblotting and on the growth of MGC803 cell xenografts in nude mice. RESULTS: Bioinformatic analysis and immunohistochemical staining of the clinical specimens both revealed high GPSM2 expressions in gastric cancer (P<0.01). A high GPSM2 expression was significantly correlated with T3-4 stages, N2-3 stages, a carcinoembryonic antigen (CEA) level ≥5 μg/L, and a carbohydrate antigen (CA) 19-9 level ≥37 kU/L (P<0.05). Cox regression analysis identified high GPSM2 expression as an independent risk factor affecting 5-year survival of the patients (P<0.05). Gene ontology (GO) analysis suggested that GPSM2 was involved in cell cycle regulation. In MGC803 cells, GPSM2 overexpression significantly promoted cell proliferation and G1/S transition and xenograft growth in nude mice. KEGG pathway enrichment analysis indicated that GPSM2 executed its biological functions by regulating the p53 signaling pathway, which was confirmed by the results of immunoblotting experiments showing suppression of p53 signaling pathway activity in GPSM2-over expressing MGC803 cells. CONCLUSIONS GPSM2 is highly expressed in gastric cancer to affect patient prognosis by promoting tumor cell proliferation and G1/S transition possibly via inhibiting the p53 pathway.
Stomach Neoplasms/metabolism* ; Humans ; Cell Proliferation ; Prognosis ; Animals ; Mice, Nude ; Cell Line, Tumor ; Mice ; Apoptosis ; Tumor Suppressor Protein p53/metabolism* ; Cell Movement

OBJECTIVES: To analyze MYO1B expression in gastric cancer, its association with long-term prognosis and its role in regulating biological behaviors of gastric cancer cells. METHODS: We analyzed MYO1B expression in gastric cancer and its correlation with tumor grade, tumor stage, and patient survival using the Cancer Public Database. We also examined MYO1B expression with immunohistochemistry in gastric cancer and paired adjacent tissues from 105 patients receiving radical surgery and analyzed its correlation with cancer progression and postoperative 5-year survival of the patients. GO and KEGG enrichment analyses were used to explore the biological functions of MYO1B and the key pathways. In cultured gastric cancer cells, we examined the changes in cell proliferation, migration and invasion following MYO1B overexpression and knockdown. RESULTS: Data from the Cancer Public Database showed that MYO1B expression was significantly higher in gastric cancer tissues than in normal tissues with strong correlations with tumor grade, stage and patient prognosis (P<0.05). In the clinical tissue samples, MYO1B was significantly overexpressed in gastric cancer tissues in positive correlation with Ki67 expression (r=0.689, P<0.05) and the parameters indicative of gastric cancer progression (CEA ≥5 μg/L, CA19-9 ≥37 kU/L, G3-4, T3-4, and N2-3) (P<0.05). Kaplan-Meier analysis and multivariate Cox regression analysis suggested that high MYO1B expression was associated with decreased postoperative 5-year survival and was an independent risk factor (HR: 3.522, 95%CI: 1.783-6.985, P<0.05). MYO1B expression level was a strong predictor of postoperative survival (cut-off value: 3.11, AUC: 0.753, P<0.05). GO and KEGG analyses suggested that MYO1B may regulate cell migration and the mTOR signaling pathway. In cultured gastric cancer cells, MYO1B overexpression significantly enhanced cell proliferation, migration, and invasion and promoted the phosphorylation of Akt and mTOR. CONCLUSIONS High MYO1B expression promotes proliferation, migration and invasion of gastric cancer cells and is correlated with poor patient prognosis.
Humans ; Stomach Neoplasms/metabolism* ; Cell Proliferation ; Prognosis ; Cell Movement ; Myosin Type I/genetics* ; Neoplasm Invasiveness ; Cell Line, Tumor ; Female ; Male

OBJECTIVES: To investigate the impact of high expression of transmembrane and coiled helix structural domain 1 (TMCO1) on prognosis of gastric cancer and the possible mechanisms. METHODS: TMCO1 expression in gastric cancer and its effect on gastric cancer progression and prognosis were analyzed using publicly available databases and clinical data of patients undergoing radical surgery in our hospital, and its possible biological functions were explored using KEGG and GO analyses. In gastric cancer HGC-27 cells, the effects of lentivirus-mediated TMCO1 overexpression and TMCO1 silencing on cell apoptosis, proliferation, invasion and migration were examined. RESULTS: TMCO1 expression was significantly elevated in gastric cancer tissues (P<0.05), and its high expression was positively correlated with cancer progression (P<0.001) and a lowered postoperative 5-year survival rate of the patients (P<0.05). Bioinformatic analyses suggested that TMCO1 may affect gastric cancer cell apoptosis via Wnt signaling. In HGC-27 cells, TMCO1 overexpression significantly promoted tumor cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion, whereas TMCO1 silencing produced the opposite effects. Western blotting showed that β-catenin levels were significantly upregulated in TMCO1-overexpressing cells and downregulated in cells with TMCO1 silencing. CONCLUSIONS TMCO1 is overexpressed in gastric cancer tissues, and its high expression promotes gastric cancer progression and affects long-term prognosis of the patients possibly by activating the Wnt/ β-catenin signaling pathway to inhibit apoptosis of gastric cancer cells.
Humans ; Stomach Neoplasms/metabolism* ; Apoptosis ; Prognosis ; Cell Line, Tumor ; Cell Proliferation ; Cell Movement ; Wnt Signaling Pathway ; beta Catenin/metabolism* ; Gene Expression Regulation, Neoplastic

OBJECTIVES: To investigate the effect of hypaphorine (HYP) on Crohn's disease (CD)‑like colitis in mice and its molecular mechanism. METHODS: Thirty male C57BL/6J mice were equally randomized into WT, TNBS, and HYP groups, and in the latter two groups, mouse models of CD-like colitis were established using TNBS with daily gavage of 15 mg/kg HYP or an equivalent volume of saline. The treatment efficacy was evaluated by assessing the disease activity index (DAI), body weight changes, colon length and histopathology. The effect of HYP was also tested in a LPS-stimulated Caco-2 cell model mimicking intestinal inflammation by evaluating inflammatory responses and barrier function of the cells using qRT-PCR and immunofluorescence staining. GO and KEGG analyses were conducted to explore the therapeutic mechanism of HYP, which was validated in both the cell and mouse models using Western blotting. RESULTS: In the mouse models of CD-like colitis, HYP intervention obviously alleviated colitis as shown by significantly reduced body weight loss, colon shortening, DAI and inflammation scores, and expressions of pro-inflammatory factors in the colon tissues. HYP treatment also significantly increased the TEER values, reduced bacterial translocation to the mesenteric lymph nodes, liver, and spleen, lowered serum levels of I-FABP and FITC-dextran, increased the number of colonic tissue cup cells, and upregulated colonic expressions of MUC2 and tight junction proteins (claudin-1 and ZO-1) in the mouse models. In LPS-stimulated Caco-2 cells, HYP treatment significantly inhibited the expressions of pro-inflammatory factors and increased the expressions of tight junction proteins. Western blotting showed that HYP downregulated the expressions of the key proteins in the TLR4/MyD88 signaling pathway in both the in vitro and in vivo models. CONCLUSIONS HYP alleviates CD-like colitis in mice possibly by suppressing intestinal epithelial inflammation and improving gut barrier function.
Animals ; Male ; Mice, Inbred C57BL ; Crohn Disease/drug therapy* ; Mice ; Humans ; Caco-2 Cells ; Intestinal Mucosa/metabolism* ; Colitis/drug therapy* ; Disease Models, Animal ; Inflammation ; Toll-Like Receptor 4/metabolism* ; Myeloid Differentiation Factor 88/metabolism* ; Intestinal Barrier Function

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

Objective:To analyze and validate the reliability and validity of the social skills improvement system-rating scales Chinese version (parent version) (SSIS-RS-C) in middle school students.Method:A total of 1 486 parents of middle school students were recruited according to the cluster sampling method.The social responsiveness scale and strengths and difficulties questionnaire were used as criterion validity tools.A retest was conducted one month later.SPSS 27.0 was used for descriptive statistics, item analysis, internal consistency test, test-retest reliability test and criterion validity test. AMOS 24.0 was used to perform confirmatory factor analysis .Results:Item analysis indicated significant positive correlations between each item and the subscales ( r=0.293-0.782, all P<0.01), with significant differences in scores between high and low groups ( t=10.079-37.038, all P<0.01).Confirmatory factor analysis supported a seven-factor structure for the social skills subscale(communication, cooperation, assertion, responsibility, empathy, engagement and self control) and a five-factor structure for the problem behavior subscale (externalizing, bullying, hyperactivity/inattention, internalizing and autism spectrum) of the SSIS-RS-C.There was a positive correlation between the social skills subscale and prosocial behavior ( r=0.637, P<0.001), and between the problem behavior subscale and social impairments and difficult behaviors ( r=0.765, 0.688, both P<0.001).The Cronbach's α coefficients for the total scale, social skills subscale and problem behavior subscale were 0.934, 0.972 and 0.963, respectively.The test-retest correlation coefficients for the total score and the two subscales were 0.665, 0.871 and 0.598, respectively (all P<0.001). Conclusion:The SSIS-RS-C demonstrated good reliability and validity in the Chinese adolescent population.

Objective:To analyze and validate the reliability and validity of the social skills improvement system-rating scales Chinese version (parent version) (SSIS-RS-C) in middle school students.Method:A total of 1 486 parents of middle school students were recruited according to the cluster sampling method.The social responsiveness scale and strengths and difficulties questionnaire were used as criterion validity tools.A retest was conducted one month later.SPSS 27.0 was used for descriptive statistics, item analysis, internal consistency test, test-retest reliability test and criterion validity test. AMOS 24.0 was used to perform confirmatory factor analysis .Results:Item analysis indicated significant positive correlations between each item and the subscales ( r=0.293-0.782, all P<0.01), with significant differences in scores between high and low groups ( t=10.079-37.038, all P<0.01).Confirmatory factor analysis supported a seven-factor structure for the social skills subscale(communication, cooperation, assertion, responsibility, empathy, engagement and self control) and a five-factor structure for the problem behavior subscale (externalizing, bullying, hyperactivity/inattention, internalizing and autism spectrum) of the SSIS-RS-C.There was a positive correlation between the social skills subscale and prosocial behavior ( r=0.637, P<0.001), and between the problem behavior subscale and social impairments and difficult behaviors ( r=0.765, 0.688, both P<0.001).The Cronbach's α coefficients for the total scale, social skills subscale and problem behavior subscale were 0.934, 0.972 and 0.963, respectively.The test-retest correlation coefficients for the total score and the two subscales were 0.665, 0.871 and 0.598, respectively (all P<0.001). Conclusion:The SSIS-RS-C demonstrated good reliability and validity in the Chinese adolescent population.

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

Strengthening the comprehensive leadership of the Party in public hospitals requires continuous exploration of new models that integrate Party building with business.This paper uses SWOT analysis to dynamically analyze the internal com-petitive advantages and disadvantages,as well as the external environmental opportunities and threats of the hospital.It explores the development of party building brands such as"Party Member Service Studios"with party members serving at the grassroots level as the core,"Party Member Reception Rooms"with party building and co-construction as the core,"Digital Discipline In-spection 2.0"with integrity as the core,and"Care Projects"with employee care as the core.Through the research on the devel-opment path of party building brands,this paper fully explores the potential value and profound significance of high-quality devel-opment in the hospital,providing references for the construction of party building brands in other hospitals.

Objective To explore the regulatory role of Abelson interactor 2(ABI2)in progression and prognosis of gastric cancer.Methods TIMER2.0,GEPIA,Kaplan-Meier Plotter and DAVID databases were used to analyze ABI2 expression in pan-cancer and its association with the prognosis of gastric cancer.Gastric cancer and adjacent tissues from 120 patients undergoing radical gastrectomy in our hospital between January,2016 and October,2018 were examined for ABI2 expression and its correlation with disease progression and prognosis.MGC-803 cell models of ABI2 knockdown and overexpression were established for observing the changes in cell proliferation,migration,and invasion,and the impact of ABI2 expression modulation on xenograft growth was evaluated in nude mice.Results Database analysis and examination of the clinical samples showed that ABI2 was highly expressed in gastric cancer tissues.Survival analysis suggested that gastric cancer patients with a high expression of ABI2 had a reduced postoperative 5-year survival rate(P<0.0001),and further Cox univariate and multivariate survival analyses indicated that a high ABI2 expression was an independent risk factor affecting the patients survival outcomes(P=0.022,HR=1.887,95%CI:1.096-3.249).Enrichment analysis suggested the involvement of ABI2 in Wnt signaling.In MGC-803 cells,ABI2 overexpression promoted cell proliferation and xenograft growth in nude mice,increased the expressions of vimentin and N-cadherin,and lowered E-cadherin expression,while ABI2 knockdown produced the opposite effects.Mechanistic analysis revealed that ABI2 overexpression promoted the expressions of Wnt2 and β-catenin in both MGC-803 cells and the xenografts,and their expressions were significantly lowered by ABI2 knockdown.Conclusion ABI2 is highly expressed in gastric cancer,which affects long-term prognosis of the patients,possible due to its regulatory effect on Wnt signaling to promote proliferation,migration and invasion of gastric cancer cells.