The medical-industrial fusion training model combines the knowledge and technology of medical and engineering disciplines in the training of oncology graduate students, which can help accurate diagnosis and treatment of tumors, promote cooperation and innovation in oncology research, as well as promote the cultivation and exchanges of composite and innovative medical talents in oncology, promote the innovation and development of oncology diagnostic and treatment technology, and improve the survival rate and quality of life of oncology patients. This paper discusses the application of medical-industrial fusion training model in the training of o ncology professionals, and explores the new teaching mode of medical-industrial fusion thinking in the cultivation of complex and innovative medical talents in oncology under the background of "new medical science".

With the deepening of China's medical reform, people's demand for health is growing, which promotes the construction of "new medicine" and puts forward higher requirements for the cultivation and education of medical students. Undergraduate medical education is a crucial period for the growth of medical students, and how to do a good job in undergraduate teaching under the background of "new medicine" is currently a research hotspot. The clinical teaching stage is an important period for medical students to fully understand clinical disciplines and cultivate their understanding of specialties. Therefore, we should explore new teaching methods and means to adapt to the needs of the new era. In the context of "new medicine", the medical-engineering fusion diagnosis and treatment technology has become an important trend in the clinical diagnosis and treatment of oncology. In order to adapt to this change, clinical teaching and teaching management in oncology also need new exploration and research. Taking the clinical teaching of oncology as an example, this article discusses how to cultivate medical students' thinking of medical-engineering fusion.

Background and objective Isoliquiritigenin(ISL)is an important pharmacological constituent of Glycyrrhiza glabra,which possesses a range of physiological and pharmacological activities,as well as significant antitumor ac-tivity,and can be used as a potential drug for targeted cancer therapy.LINC01503 is an oncogene,which has been closely asso-ciated with the malignant biological processes of many cancers.The aim of this study was to investigate the effects of ISL on the proliferation,apoptosis,invasion and migration oflung squamous carcinoma cells by regulating LINC01503.Methods Plasma was collected from lung squamous carcinoma patients and healthy individuals treated at Tangshan People's Hospital from Janu-ary 2021 to December 2022.The expression of LINC01503 in lung squamous carcinoma plasma,tissues and cells was detected by real-time quantitative fluorescence polymerase chain reaction(qRT-PCR).Lung squamous carcinoma cells were treated with different concentrations of ISL for 24 h,and LINC01503 expression was detected by qRT-PCR.The cells were treated in groups:si-NC group,si-LINC01503 group,DMSO(0.1％dimethyl sulfone)group,ISL group,pc DNA3.1(+)-NC group,pc DNA3.1(+)-LINC01503 group,ISL+pc DNA3.1(+)-NC group and ISL+pc DNA3.1(+)-LINC01503 groups.CCK-8 assay,clone formation assay,flow cytometry,Transwell assay and scratch assay were used to explore the effect of LINC01503 on the functional phenotype of lung squamous carcinoma cells.Results Fluorescence in situ hybridization results showed that the average fluorescence intensity of LINC01503 in tissue microarrays of lung squamous carcinoma patients was higher than that in paracancerous tissues(P＜0.05).The expression of LINC01503 in the plasma of patients with lung squamous carcinoma was higher than that in the plasma of healthy individuals(P＜0.05).Knockdown of LINC01503 inhibited the proliferation,invasion and migration of lung squamous carcinoma cells and promoted apoptosis(P＜0.05).ISL inhibited the proliferation,invasion,migration and promoted apoptosis of lung squamous carcinoma cells(P＜0.05).Overexpression of LINC01503 followed by intervention with ISL reversed the promotional effect of overexpression of LINC01503 on the proliferation,invasion and migration of lung squamous carcinoma cells as well as the inhibitory effect on apoptosis(P＜0.05).Conclusion LINC01503 was highly expressed in lung squamous carcinoma,and LINC01503 could promote the proliferation,invasion and migra-tion of lung squamous carcinoma cells and inhibit the apoptosis,ISL could inhibit the proliferation,invasion and migration of lung squamous carcinoma cells and promote apoptosis of lung squamous carcinoma cells by regulating the expression of LINC01503.

BACKGROUND/OBJECTIVES: This study examined the relationship between famine exposure in early life and the risk of type 2 diabetes in adulthood during the 1959–1961 Chinese Famine. SUBJECTS/METHODS: A total of 3,418 individuals aged 35–74 years free of diabetes from two studies in 2006 and 2009 were followed up prospectively in 2009 and 2012, respectively. Famine exposure was classified as unexposed (individuals born in 1962–1978), fetal exposed (individuals born in 1959–1961), child exposed (individuals born in 1949–1958), and adolescent/adult exposed (born in 1931–1948). A logistic regression model was used to assess the relationship between famine exposure and diabetes after adjustment for potential covariates. RESULTS: During a three-year follow-up, the age-adjusted incidence rates of type 2 diabetes were 5.7%, 14.5%, 12.7%, and 17.8% in unexposed, fetal-exposed, child-exposed, and adolescent/adult-exposed groups, respectively (P < 0.01). Relative to the unexposed group, the relative risks (95% confidence interval) for diabetes were 2.15 (1.29–3.60), 1.53 (0.93– 2.51), and 1.65 (0.75–3.63) in the fetal-exposed, child-exposed, and adolescent/adult-exposed groups, after controlling for potential covariates. The interactions between famine exposure and obesity, education level, and family history of diabetes were not observed, except for the urbanization type. Individuals living in rural areas with fetal and childhood famine exposure were at a higher risk of type 2 diabetes, with relative risks of 8.79 (1.82–42.54) and 2.33 (1.17–4.65), respectively. CONCLUSIONS These findings indicate that famine exposure in early life is an independent predictor of type 2 diabetes, particularly in women. Early identification and intervention may help prevent diabetes in later life.

Traditionally, Tripterygium hypoglaucum (Levl.) Hutch (THH) are widely used in Chinese folk to treat rheumatoid arthritis (RA). This study aimed to investigate whether the anti-RA effect of THH is related with the gut microbiota. The main components of prepared THH extract were identified by HPLC-MS. C57BL/6 mice with adjuvant-induced arthritis (AIA) were treated with THH extract by gavage for one month. THH extract significantly alleviated swollen ankle, joint cavity exudation, and articular cartilage destruction in AIA mice. The mRNA and protein levels of inflammatory mediators in muscles and plasma indicated that THH extract attenuated inflammatory responses in the joint by blocking TLR4/MyD88/MAPK signaling pathways. THH extract remarkably restored the dysbiosis of the gut microbiota in AIA mice, featuring the increases of Bifidobacterium, Akkermansia, and Lactobacillus and the decreases of Butyricimonas, Parabacteroides, and Anaeroplasma. Furthermore, the altered bacteria were closely correlated with physiological indices and drove metabolic changes of the intestinal microbiota. In addition, antibiotic-induced pseudo germ-free mice were employed to verify the role of the intestinal flora. Strikingly, THH treatment failed to ameliorate the arthritis symptoms and signaling pathways in pseudo germ-free mice, which validates the indispensable role of the intestinal flora. For the first time, we demonstrated that THH extract protects joint inflammation by manipulating the intestinal flora and regulating the TLR4/MyD88/MAPK signaling pathway. Therefore, THH extract may serve as a microbial modulator to recover RA in clincial practice.ver RA in clincial practice.
Mice ; Animals ; Gastrointestinal Microbiome ; Tripterygium ; Myeloid Differentiation Factor 88/genetics* ; Toll-Like Receptor 4/genetics* ; Mice, Inbred C57BL ; Arthritis, Experimental/drug therapy*

Objective:To explore the effects and possible mechanisms of Tyrobp gene on neuroinflammation in Tourette's syndrome mice.Methods:Twenty C57BL/ 6J and Tyrobp knock-out male mice aged 6 weeks were randomly divided into 4 groups according to random number table method: WT+ NS group, Tyrobp -/-+ NS group, WT+ IDPN group and Tyrobp -/-+ IDPN group. Mice in WT+ IDPN group and Tyrobp -/-+ IDPN group were injected with IDPN intraperitoneally at a dose of 150 mg/kg·d, while mice in WT+ NS group and Tyrobp -/-+ NS group were injected with equal volume of normal saline, once a day for 7 days. Then stereotypical behavior of mice were evaluated. Western blot was used to detect the levels of Tyrobp, TNF-α, IL-6, IL-1β, TLR4, Myd88, p-NF-κB p65 and p-IκBα in the striatum of mice. Immunofluorescence staining was used to observe the activation of microglia. Statistical analysis was performed using GraphPad Prism 8.0 software, and t-test was used for comparison between two groups. One-way ANOVA was used to compare the means of multiple samples, and LSD test was used for further pairwise comparison. Results:The results of behavior assessment showed that there were significant differences in the motor stereotypic behavior and categorical stereotypic behavior score( F=270.9, 379.7, P<0.01), and the scores in WT+ IDPN group were higher than those in Tyrobp -/-+ IDPN group (motor stereotypic behavior: (3.23±0.26), (2.13±0.21), t=9.02, P<0.05; categorical stereotypic behavior: (45.80±4.29), (26.60±3.48), t=12.00, P<0.05). Western blot results showed that there were significant differences in the protein expression level of TNF-α, IL-6, IL-1β, TLR4, Myd88, p-NF-κB p65 and p-IκBα ( F=29.07, 23.09, 39.36, 57.6, 52.55, 15.50, 40.48, all P<0.05), the level of those in WT + IDPN group was higher than those in WT+ NS group( t=8.31, 7.37, 8.13, 11.43, 10.47, 6.05, 9.96, all P<0.05), Tyrobp -/-+ IDPN group was higher than Tyrobp -/-+ NS group ( t=3.60, 3.00, 5.84, 4.81, 3.59, 2.26, 4.68, all P<0.05), and WT + IDPN group was higher than Tyrobp -/-+ IDPN group ( t=3.97, 3.93, 4.14, 6.40, 7.63, 3.45, 3.03, all P<0.05). Immunofluorescence showed that microglial cells in the striatum region of mice in WT+ IDPN group and Tyrobp -/-+ IDPN group were enlarged and microglial cells were activated, and the activation pattern of microglial cells in WT+ IDPN group was more obvious than that in Tyrobp -/-+ IDPN group. Conclusion:Tyrobp may be involved in the pathogenesis of Tourette's syndrome by promoting neuroinflammation mediated by TLR4/Myd88/NF-κB signaling pathway.

Objective: To explore the clinical effect and safety of minor liver resection for hilar cholangiocarcinoma (HC) of Bismuth-Corlette type Ⅲ and Ⅳ. Methods: From May 2007 to May 2017, the clinical data of 108 patients with Bismuth-Corlette type Ⅲ and Ⅳ HC underwent hepatectomy were collected and analyzed retrospectively.There were 56 males and 52 females, aged (57.2±5.3) years (ranged 48-76 years) .Among the 108 cases, there were 51 cases of type Ⅲa, 40 cases of type Ⅲb and 17 cases of type Ⅳ. Small-scale hepatectomy (≤3 hepatectomy) was performed in 70 cases, including 8 cases of 4b segment resection, 28 cases of 4b segment+5 segment resection, and 34 cases of partial 4 segment+partial 7 segment+partial 1 segment resection. Large-scale hepatectomy was performed in 38 cases (>3 segments) , of which 30 cases were treated with 2 segments+3 segments+4 segments+1 segment, and 8 cases were treated with 5 segments+7 segments+8 segments+1 segment. t′ test was used to analyze the data which did not conform to the normal distribution, and χ² test was used to calculate the incidence of postoperative complications and the 1, 3, and 5-year cumulative overall survival rate. Results: (1) The operation time of minor liver resection group ((180±25)minutes) was shorter than that of major liver resection group ((210±35)minutes) (t′=4.676, P<0.05) , the amount of blooding operation time of minor liver resection group ((310±80)ml) was less than that of major liver resection group ((500±110)ml)in the operation (t′=9.385, P<0.05) , and the difference was statistically significant. (2) The incidence of complications was lower in minor liver resection group and major liver resection group, and the difference was statistically significant (χ²=5.230, P<0.05) . (3) The actual 1-, 3- and 5-year survival rates were 87.1%, 58.4%, 30.0% and 84.2%, 57.9%,31.6%, respectively. There were no significant differences in survival rates in two groups in 1-, 3- and 5-year survival rates (χ²=0.177, P=0.674; χ²=0.005, P=0.946; χ²=0.029, P=0.865) . Conclusions Compared to patients with major liver resection, Minor liver resection for selected patients with HC of Bismuth-Corlette Ⅲ and Ⅳaccording to our criteria achieved better long-term outcomes. Chen′s biliojejunostomy is a simple, effective and safe method, which can be widely used when there are multiple biliary intestinal anastomosese.

Objective To determine the expression profile of serum microRNAs(miRNAs) in early-onset familial Alzheimer's disease (EO-FAD) patients. methods miRNA microarrays were performed to detect the expression profile of serum miRNAs in 2 cases of EO-FAD patients,2 cases of EO-FAD carriers and 2 cases of normal controls.Preliminary bioinformatic analysis was conducted. Result sIt was found that 21 miRNAs were up-regulated and 22 miRNAs were down-regulated in serum of EO-FAD patients,the differences were statistically significant(P<0.05).miR-5704(P=0.0002),miR-4639-3p(P=0.0195),miR-107(P=0.0204) were markedly up-regulated,miR-5572(P=0.0008),miR-204-3p(P=0.0014),miR-542-5p(P=0.0106) and miR-155-5p(P=0.0240) were markedly down-regulated.Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis suggested that the dysregulated miRNAs may be involved in the mechanism of EO-FAD by affecting neurotrophin signaling pathway.Conclusion miR-5704,miR-4639-3p,miR-107,miR-5572,miR-204-3p,miR-542-5p and miR-155-5p may be used as potential biomarkers of EO-FAD,and involved in the mechanism of EO-FAD by affecting neurotrophin signaling pathway.

Objective:To discuss the influence of ALDH1+and CD133+phenotypic breast cancer stem-like cells in TA2 triple negative breast cancer on promoting epithelial-mesenchymal transition (EMT) occurrence in TA2 mice with triple-negative breast cancer and on their biological behavior. Methods:Flow cytometry was performed to analyze the markers ALDH1 and CD133 in TA2 mice triple nega-tive breast cancer and breast cancer stem-like cells with ALDH1+, ALDH1?, CD133+, and CD133?phenotypes, which were sorted out. Then, the TA2 mice were inoculated with sorted tumor cells according to cell type. The mice were divided into ALDH1+, ALDH1?, CD133+, and CD133-groups. The tumor-growing conditions were observed. A tumor tissue was sliced for the immunohistochemical testing of ALDH1?, CD133?, and EMT-related Twist1, E-cadherin, and VE-cadherin proteins. The expression difference of breast cancer stem cell surface markers ALDH1 and CD133 in triple-negative breast cancer and EMT-related proteins Twist1, E-cadherin, and VE-cad-herin was analyzed. Results:The expression rates of breast cancer stem cell markers ALDH1 and CD133 in TA2 mice triple negative breast cancer were 31.2%and 6.5%, respectively. The tumor growth ability of TA2 mice from ALDH1+group was obviously stronger than that from ALDH1?group. The CD133+group was evidently stronger than CD133?group. The immunohistochemical results showed that ALDH1, Twist1, and VE-cadherin expression levels in the ALDH1+group were evidently higher than that in the ALDH1?group (all P<0.05). E-cadherin expression decreased (P<0.05). CD133?, Twist1, and VE-cadherin expression levels in CD133+group were higher than that in CD133?group (all P<0.05). Conclusion:In TA2 mice triple negative breast cancer, ALDH1+and CD133+phenotypic breast cancer stem-like cells may influence the expression of EMT-related proteins, and promote the formation of triple-negative breast cancer.

Objective:To investigate the clinical significance of epithelial-to-mesenchymal (EMT) in lung squamous cell carcino-ma (LSCC) and to examine the effect of EMT on the invasive and migration abilities of LSCC. Methods:Immunohistochemical stain-ing was performed to determine the expression of E-cadherin, Vimentin, and TGF-β1 in 79 LSCC patients, and the clinical significance was explored. SK-MES-1 lung squamous carcinoma cells were cultured in conditioned medium containing various concentrations of transforming growth factor-β1 (TGF-β1) for 5 and 10 days. The expression levels of E-cadherin and Vimentin were detected via West-ern blot and reverse transcription-polymerase chain reaction (RT-PCR). With different concentrations and induction times, invasion and wound healing assays were performed to evaluate the invasion and migration abilities. Results:E-cadherin expression was significantly lower, whereas Vimentin expression was significantly higher in LSCC with lymph node metastasis than in that without noda metastasis (P<0.05). In the tissues of 79 LSCC patients, TGF-β1 expression was significantly related to lymph node metastasis (P<0.05). Western blot showed that Vimentin expression was higher, whereas E-cadherin expression was lower in TGF-β1 inducing medium with 10 ng/mL SK-MES-1 cells than in the other media. RT-PCR showed similar results. Scratch test and invasion assay both showed that treat-ment of cells with cytokines markedly enhanced the migration and invasion of the cells. Conclusion:Lymph node metastasis of LSCC correlates with EMT. SK-MES-1 cells undergo EMT via TGF-β1 induction, which enhances invasion and migration.