Objective To explore the role of pseudogene AC106872.1 in maintaining the self-renewal capacity of human embryonic stem cells (hESCs). Methods AC106872.1 was knocked out in hESCs and knockout efficiency was validated by PCR and agarose gel electrophoresis. The colony formation of hESCs was assessed through colony formation assays and alkaline phosphatase (AP) staining. The expression level of pluripotency and differentiation marker genes was analyzed by qPCR and flow cytometry. RNA sequencing (RNA-seq) was performed to assess transcriptomic changes upon AC106872.1 knockout. Results Knockout of AC106872.1significantly inhibited the colony formation of hESCs (P＜0.05). The expression level of pluripotency marker genes was significantly reduced (P＜0.000 1), while the expression of differentiation marker genes was markedly increased (P＜0.000 1). Conclusions The pseudogene AC106872.1 plays a crucial role in maintaining human embryonic stem cell self-renewal through regulation of pluripotency genes expression.

Objective To investigate the role of a novel human-specific long noncoding RNA (lncRNA), MEK6-AS1, and its potential molecular mechanism in improving the osteogenic differentiation of senescent mesenchymal stem cells (MSCs). Methods An in vitro human MSCs replicative senescence model was established by sequential passaging, and then senescence was identified by β staining and senescence-related gene expression. RT-qPCR was used to detect the expression of MEK6-AS1 during senescence and osteogenic differentiation of human MSCs (hMSCs); Lentiviral knockdown technology was used to regulate the expression of MEK6-AS1 in the MSCs replicative senescence model. Transcriptome sequencing technology was utilized to analyze the effects of MEK6-AS1 on the transcriptome of hMSCs especially on genes and pathways related to osteogenic differentiation. The effect of MEK6-AS1 as an intervention target at osteogenic differentiation of human senescent hMSCs was evaluated with alkaline phosphatase staining microscopy. PCR technology was used to detect osteogenic gene expression levels in cells. Results With aging process, the osteogenic differentiation ability of hMSCs decreased significantly while the expression level of MEK6-AS1 was enhanced(P＜0.000 1). Knockdown of MEK6-AS1 significantly enhanced the osteogenic differentiation of MSCs by the up-regulating expression of osteogenic markers and increasing mineralization capacity(P＜0.001). Conclusions Knockdown of human-specific lncRNA MEK6-AS1 improves osteogenic differentiation of senescent MSCs, providing a new target and theoretical basis for the treatment of senescence-associated osteoporosis.

Objective To explore the clinical significance and to investigate the expression of TOMM40L in the tissue of triple-negative breast cancer (TNBC). Methods The expression of TOMM40L in TNBC tissues and normal tissues was analyzed with TCGA and UALCAN databases. Univariate and multivariate Cox regression analysis and Nomogram model were used to evaluate the prognostic value of TOMM40L in TNBC patients. Furthermore, the expression of TOMM40L in breast cancer cell lines was evaluated using Western blot analysis and quantitative real-time PCR. Specific siRNA knockdown was performed to evaluate the migration, and cell proliferation of TOMM40L. The potential signaling pathways of TOMM40L were identified by GO and KEGG and GSEA. Results TOMM40L was highly expressed in the TNBC compared to non-TNBC tumor tissues(P＜0.001). TOMM40L levels were enhanced in TNBC cell lines as compared to other non-TNBC cell lines. CCK-8 and Transwell assay demonstrated that TOMM40L knockdown reduced the proliferation and migration of TNBCcell lines. Functional enrichment analysis showed that TOMM40L was involved in glucose metabolism-related pathways. Conclusions The expression of TOMM40L is increased in TNBC and is correlated with poor prognosis. TOMM40L may promote TNBC migration and proliferation.

Objective To find specific mechanisms through which immune cell activation affects central nervous system inflammation in Alzheimer′s disease (Alzheimer′s disease, AD). Methods The public single-cell human brain database GSE161045 was applied for analysis. Then bulk RNA sequencing was performed in 5×FAD mice, and the results were validated using immunofluorescence staining microscopy with brain paraffin sections from 5×FAD mice. In the BV2 microglial cell line, AβOs were used to inducing activation and assessed the protein expression of PARP9 and PARP14 with Western blot. Finally, the relationship between PARP9 and PARP14 expression and immune infiltration was examined. Results In AD case, the expression of PARP9 and PARP14 was significantly up regulated (P＜0.000 1) in human brain immune cells, particularly in M2-type microglia. This result was confirmed by sequencing data from 5×FAD mice. Immunofluorescence staining of brain sections from 5×FAD mice showed up regulated expression of PARP9 and PARP14 in microglia surrounding Aβ plaques. Furthermore, in HMC3 cell line, activation induced by AβOs led to a significant increase in the protein expression of PARP9 and PARP14(P＜0.05). Conclusions The expression of PARP14 and PARP9 in microglia of AD patients and 5×FAD mice is significantly increased, and PARP9 and PARP14 positive microglia are significantly aggregated around Aβ plaques, indicating that PARP9 and PARP14 are potentially involved in the immune regulation of microglia on Aβ plaques and promote neuroinflammation in AD.

Objective To construct an in vitro research model for studying human liver regeneration based on human pluripotent stem cells (hPSCs)-derived hepatocyte-like organoid (HLO). Methods The hPSCs-derived HLO was obtained by inducing differentiation and the regeneration model after liver injury was constructed by adding acetaminophen (APAP) at fixed time points in HLO culture conditions to simulate acute liver injury. Subsequently, HLO with catenin/cadherin-associated protein beta 1(CTNNB1) knockout, a key gene regulating liver regeneration, was constructed using CRISPR/Cas9 gene editing technology, and regeneration experiments with APAP injury were performed. HLO as a model for liver regeneration studies was further evaluated by morphological observation, RT-qPCR, Western blot and pathological analysis. Results Morphology evidence as well as expres-sion of marker genes showed that hPSCs-derived HLO was able to initiate a post-injury regeneration response after APAP treatment. CTNNB1-deficient HLO showed delayed recovery in dimension and down-regulated or delayed expression of related genes during post-injury regeneration as compared to control HLO. Conclusions A HLO-based hPSCs-derived human liver regeneration model is successfully constructed, which can be used for gene function studies during liver regeneration.

Objective To target at the NKG2A-HLA-E inhibitory axis, a pluripotent stem cell(iPSC)-derived genetically engineered natural killer cells(NK cells) with NKG2A knockout (NKG2A KO-iNK) were prepared and then their tumor-killing efficacy was evaluated in vitro. Methods NKG2A was knocked out in iPSCs using gene-editing technology. These cells were then differentiated into NKG2A KO-iNK cells. Surface markers at each differentiation stage were analyzed by flow cytometry. Western blot confirmed NKG2A knockout, and flow cytometry assessed expression of activating receptors (NKG2D) and natural cytotoxicity receptors (NKp30, NKp44, NKp46) in NKG2A KO-iNK cells. Cytotoxic activity against tumor cell lines with varying human leukocyte antigen E (HLA-E) expression level was evaluated via lactate dehydrogenase (LDH) release assay. Results Co-transfection of iPSCs with Cas9 protein and three small-guide RNAs (sgRNAs) targeting at exons 1 and 2 of the KLRC1 gene (encoding NKG2A) successfully generated monoclonal NKG2A-knockout iPSCs (NKG2A KO-iPSCs) with a single T-base insertion in exon 1. During iPSC differentiation into NK cells, CD34 expression reached 30%-50% at the embryoid body (EB) stage (day 8), while CD56 and CD16 expression exceeded 80% by day 28. Western blot confirmed complete NKG2A knockout in NKG2A KO-iNK cells. Flow cytometry revealed comparable expression level of activating receptor NKG2D and cytotoxicity receptors (NKp30, NKp44, NKp46) between NKG2A KO-iNK and wild-type iNK (WT-iNK) cells. The LDH assay results indicated that the cytotoxic activity of NKG2A KO-iNK cells against the HLA-E highly-expressed B-cell precursor leukemia cell line Nalm6 cells was significantly higher than that of WT-iNK cells, while there was no significant difference between them and human myeloma cell line H929 cells with low HLA-E expression and human hepatocellular carcinoma cell line HepG2 cells with almost no HLA-E expression. Interferon-γ (IFN-γ) pretreatment up regulated HLA-E expression in Nalm6 cells, further amplifying NKG2A KO-iNK-mediated cytotoxicity. Conclusions By disrupting the NKG2A-HLA-E inhibitory axis, NKG2A KO-iNK cells exhibit markedly enhanced in vitro cytotoxicity against HLA-E-high tumor cells. This result highlights their potential function as a novel adoptive cell therapy strategy for cancers reliant on HLA-E-mediated immune evasion.

Objective To establish an integrated feeder-free platform for in vitro expansion and gene editing to tackle the major challenges in clinical applications of cryopreserved primary human natural killer (NK) cells in terms of low expansion efficiency, technical difficulty in genetic modification and safety concerns. Methods A non-viral CRISPR-Cas9 ribonucleoprotein (RNP)-based multiplex gene editing system was developed through systematic optimization of culture medium and nucleofection conditions. Cell phenotype (CD56⁺CD3^-), viability, editing efficiency, and tumor-killing activity were evaluated via flow cytometry and cytotoxicity assays. Results The number of NK cells achieved 5 000-fold expansion over 25 days while maintaining high purity (CD56⁺CD3^- ＞95%) and viability (＞90%).Post-thawing viability (＞80%) and tumor-killing capacity were preserved.Cas9 RNP delivery enabled efficient dual knockout of NKG2A and CISH immune checkpoint genes (＞80%), significantly enhanced cytotoxicity against K562 tumor cells (P＜0.05). Conclusions Compared to viral vectors, the non-viral strategy eliminates genomic integration risks and reduces off-target effects. This result may provide a safe and efficient technical platform for clinical application of NK cell immunotherapy and potentially encourage application of multiplex gene editing in cancer therapy.

Objective To investigate the effect of Mcart1 knockout on acute inflammation of macrophages in vitro and in vivo. Methods The Mcart1 knockout mice were used to establish a sepsis model induced by lipopolysaccharide(LPS), and the survival period was measured. Bone marrow derived macrophages(BMDM) of LPS-induced inflammation mice were cultured in DMEM high-glucose medium. The mRNA levels of M1 and M2 related cytokines of BMDM after LPS stimulation were detected by RT-qPCR. The expression level of inflammation-related cytokines in serum of sepsis mice was detected by ELISA. Results Compared with wild type mice(Mcart1^flox/flox), the survival time length of sepsis in Mcart1 knockout mice(Mcart1^Lyz2-Cre)was significantly shortened(P＜0.001). After inflammation, the mRNA level of M1-related cytokines was up-regulated in BMDM cells of Mcart1^Lyz2-Cre mice(P＜0.05); The mRNA level of M1-related cytokines was down-regulated(P＜0.05); The expression of M1-related mediators in serum of sepsis Mcart1^Lyz2-Cre mice was up-regulated(P＜0.01). Conclusions Mcart1 knockout can significantly raise the inflammatory response of macrophages and aggravate the pathological symptoms of sepsis mice.

Objective To investigate the function of the glutamic-oxaloacetic transaminase 2(GOT2) gene in acute myeloid leukemia cells. Methods ShRNAs targeting at GOT2 were constructed to suppress GOT2 expression in the THP-1 human monocytic leukemia cell line. GOT2 mRNA level was measured by RT-qPCR, and GOT2 protein expression was measured by Western blot. Intracellular free amino acid level was quantified using colorimetric assays. The impact of GOT2 knockdown in THP-1 cell function was evaluated through cell viability (CCK-8 assay) and apoptosis (flow cytometry). Results After GOT2 knockdown, both GOT2 mRNA and protein were significantly decreased in THP-1 cells(P＜0.05). Compared to the control group, GOT2 knockdown did not affect intracellular glutamate levels(P＞0.05), but led to a marked decrease in aspartate level(P＜0.05). GOT2 knockdown significantly impaired THP-1 cell viability, inhibited cell proliferation(P＜0.05) and promoted apoptosis(P＜0.05). Conclusions Down regulation of GOT2 significantly decreases intracellular aspartate level in acute myeloid leukemia cells, impairs cellular viability and induces apoptosis, which suggests that GOT2 may play a key role in the regulation of amino acid metabolism in acute myeloid leukemia.

Objective To investigate the effects of HIF1A-AS1 on the proliferation and apoptosis of gastric cancer cells lines BGC-823 and MKN28 and its possible mechanism. Methods The expression of HIF1A-AS1 in gastric cancer tissues was analyzed by bioinformatics. HIF1A-AS1 over expression and silenced BGC-823 and MKN28 cell strains were constructed. HIF1A-AS1 expression was detected by real-time PCR, cell proliferation was detected by CCK-8 assay, and apoptosis was detected by flow cytometry. Western blot was used to detect the expression of HIF1A protein in cytoplasm and nucleus and cellular immunofluorescence was used to detect HIF1A protein into nucleus. Results Models of BGC-823 and MKN28 gastric cancer cells with HIF1A-AS1 over-expression and silence were successfully constructed.HIF1A-AS1 over-expression decreased cell proliferation (P＜0.05), while HIF1A-AS1 over-expression significantly increased cell proliferation (P＜0.05). HIF1A-AS1 silencing significantly increased the apoptosis (P＜0.05), and HIF1A-AS1-over expression significantly decreased the apoptosis (P＜0.05). HIF1A-AS1 silencing inhibited the nucleation of HIF1A protein and over-expression promoted the nucleation of HIF1A protein. HIF1A-AS1 silencing significantly decreased the expression of HIF1A cytoplasmic protein (P＜0.05) and over-expression of HIF1A-AS1 significantly increased the expression of HIF1A cytoplasm protein (P＜0.05). HIF1A-AS1 silencing significantly decreased the expression of HIF1A nuclear protein (P＜0.05) while HIF1A-AS1 over-expression significantly increased the expression of HIF1A nuclear protein (P＜0.05). Conclusions HIF1A-AS1 may promote the proliferation and inhibit apoptosis of BGC-823 and MKN28 gastric cancer cells by regulating the expression of parental gene HIF1A.

Objective To investigate the effect of mutation human proprotein convertase subtilism/kexin type 9(hPCSK9^D374Y) in PCSK9 gene on methionine choline deficiency diet (MCD)-induced nonalcoholic steato-hepatitis (NASH) in mice. Methods Sixteen C57BL/6J wild-type mice were selected and randomly divided into the hPCSK9^D374Y group and the control GFP group. MCD was fed for 6 weeks, and then the serum level of hepatic triglyceride, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) was examined. Oil Red O and Sirius Red staining microscopy were used to identify hepatic lipid infiltration and fibrosis severity. F4/80-positive cell infiltration was analyzed using immunohistochemistry. Lipid synthesis and inflammatory response-related proteins were detected by Western blot and related mRNA expression was analyzed by RT-qPCR. Results Hepatic hPCSK9 protein and mRNA were significantly up-regulated, LDLR protein expression was down-regulated, and serum level of ALT and AST was significantly elevated in the hPCSK9^D374Y group of mice(P＜0.05). The degree of hepatic steatosis and fibrosis increased and F4/80-positive cells were significantly increased (P＜0.01). FASN and SCD1 proteins were significantly up-regulated and PPARα was down-regulated in the hPCSK9^D374Y group; The expression of TLR4 and p-P65 was elevated, whereas the expression of IκBα was decreased (P＜0.001). RT-qPCR results showed a significant increase of mRNA coding inflammatory factors TNF-α, IL-1β, IL-6, and MCP-1, and a significant up-regulation of fibrosis-associated mRNAs (collagen Ⅰα and collagen Ⅲα) was found (P＜0.001). Conclusions Functionally acquired mutation in the PCSK9 gene (hPCSK9^D374Y) exacerbates MCD-induced hepatic steatosis, inflammatory response and fibrosis in mice.

Objective To investigate the effect of dexmedetomidine (Dex) on propofol-induced nerve injury in neonatal rats. Methods The rats were divided into control group, intra-peritoneally injected propofol to construct nerve injury model group (50 mg/kg), Low, medium and high dose dexmedetomidine intervention model groups (Dex-L, Dex-M and Dex-H with femoral vein injection of 0.25, 0.5 and 1 μg/kg Dex, respectively), and Dex-H+anti-BDNF (10 0μg/kg) group, with 12 animals in each group. The neurological deficit score, number of platform jumping errors, and changes in brain index were detected in rats. HE staining microscopy was applied to measure pathology in the hippocampal CA1 region. ELISA was applied to detect level of interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor-α (TNF-α) in the hippocampal CA1 region. TUNEL staining microscopy was used to measure neuronal apoptosis in the hippocampal CA1 region. Western blot was applied to measure the cleaved caspase-3, proBDNF, mature brain-derived neurotrophic factor (mBDNF), phosphorylated tyrosine kinase B (p-TrkB), and phosphorylated phosphatidylinositol 3 kinase (p-PI3K) proteins in the hippocampal CA1 region. Results Compared with model group, the neuronal damage in rats was improved in Dex-L group, Dex-M group, and Dex-H group, the neurological deficit score, number of platform jumping errors, brain index, level of IL-6, MCP-1, TNF-α in hippocampal CA1 region, neuronal apoptosis rate, and level of cleaved caspase-3 and pro BDNF proteins all reduced, mBDNF, p-TrkB, and p-PI3K proteins in the hippocampal CA1 region raised(P＜0.05). Anti-BDNF inhibited the effect of 1 μg/kg Dex pretreatment on propofol induced nerve injury in neonatal rats. Conclusions Dex pretreatment inhibits neuro-inflammation and neuronal apoptosis, thereby reduces propofol induced nerve injury in neonatal rats. Its mechanism may be related to the activation of the mBDNF/TrkB/PI3K pathway.

Objective To detect Serum metabolites with label-free surface-enhanced Raman spectroscopy (SERS) for quickly distinguishing the metabolic profiles of breast cancer patients and healthy subjects. Methods A kind of Plasma nano-material was synthesized as a probe for SERS, which has also been used to detect Raman reporter molecules to assess its detection capability. Serum samples from breast cancer patients and healthy subjects were collected and the proteins were precipitated with methanol and removed to collect serum metabolites. Probe-based SERS was used to analyze the serum metabolites of patients and explore the changes in the metabolic profiles of breast cancer patients. Results The SERS probe was synthesized and validated. An analytical method based on SERS probe was established, which achieved a linear range (LR) of 4 orders of magnitude and a limit of detection (LOD) up to 10 nmol/L. Raman spectra of serum metabolites from 5 breast cancer patients and 5 healthy subjects were analyzed to study differences in metabolite changes. Conclusions In this study, the molecular spectrum differences of serum metabolites in breast cancer patients were screened by probe-based SERS method, which provides a technology support research on the metabolic changes caused by breast cancer so potentially provide a new method for fast breast cancer screening.

Objective To explore the changes in serum epidermal growth factor receptor (EGFR) and cancer antigen 125 (CA125) levels in pregnant women with adenomyosis (AM) and their relationship with pregnancy outcomes. Methods A total of 108 pregnant women with AM(AM pregnant women group) admitted to Baoding Maternal And Child Health Hospital from June 2021 to August 2023 were collected and divided into a good pregnancy group (n=43) and a poor pregnancy group (n=65) based on pregnancy outcomes. Meanwhile, AM patients were selected as AM group and 108 pregnant women with normal pregnancy test were selected as control group. ELISA was applied to detect the serum level of EGFR and CA125. Pearson correlation was applied to analyze the correlation between serum EGFR and CA125 in AM pregnant women. Multivariate logistic regression was applied to analyze the factors that affected the outcome of AM pregnancy. Receiver operating characteristic (ROC) curve was applied to analyze the predictive value of serum EGFR and CA125 levels for AM pregnancy outcomes. Results Compared with the control group, serum level of EGFR and CA125 in AM group and AM pregnant women group were significantly increased and serum level of EGFR and CA125 in AM pregnant women group was higher than that in AM group (P＜0.05). As the depth grading of endometrial invasion increased, serum level of EGFR and CA125 increased sequentially; The serum level of EGFR and CA125 was obviously elevated in diffuse type and proliferate phase (P＜0.05). The expression level of EGFR and CA125 in the serum of AM pregnant women with premature rupture of membranes, premature birth, placenta previa, and miscarriage was significantly increased(P＜0.05). According to Pearson correlation analysis, there was a positive correlation between serum EGFR and CA125 in AM pregnant women (r=0.487, P＜0.05). The serum level of EGFR and CA125 in good pregnancy group was lower than that in poor pregnancy group (P＜0.05). The area under the curve (AUC) of serum EGFR, CA125, and their combined prediction for AM pregnancy outcome was 0.880, 0.835, and 0.955, respectively and the combined prediction of AUC for AM pregnancy outcome was significantly higher than that of serum EGFR and CA125 alone prediction (Z_{combination-EGFR}=2.279, Z_{combination-CA125}=3.304, both P＜0.05). Conclusions Serum level of EGFR and CA125 in AM pregnant women is elevated, which is closely related to pregnancy outcomes and is potential risk factor for poor pregnancy in AM. The combination of the two is more effective in predicting pregnancy outcomes in AM.

Objective To identify the impact of glucose variability (GV) on the development of gestational hypertension (GH) in patients with gestational diabetes mellitus (GDM), and to find the differences between various GV metrics as well as to evaluate their predictive value in management strategy development. Methods A total of 127 pregnant women diagnosed with GDM were included in this study. After the diagnosis of GDM, continuous glucose monitoring (CGM) and blood pressure measurements were performed, and the occurrence of gestational hypertensive disorders was recorded. Indices of glucose variability were calculated using an automated software EasyGV version 9.0. Results The results revealed an association between gestational hypertension and glucose variability in GDM patients. Among the study participants, 2 cases(1.6%) were diagnosed with preeclampsia and 9 cases(7.1%) were diagnosed with gestational hypertension. TBR% (time below range) showed a significantly negative correlation with diastolic blood pressure at 29-32 weeks of gestation and with both diastolic and systolic blood pressure during delivery. TIR% (time in range) showed a negative correlation with the rate of change in systolic blood pressure between two prenatal visits. CONGA (continuous overlapping net glycemic action) emerged as an independent predictor of gestational hypertension (OR: 3.648; 95% CI: 1.046, 12.721; P=0.042). When CONGA exceeded 4.856, the risk of gestational hypertension in GDM patients increased. Conclusions Blood glucose variation is an independent factor affecting the occurrence of pregnancy-induced hypertension in GDM women. This study suggests new targets for the use and management of CGM in pregnant women with GDM. For GDM patients at high risk of hypertensive disease during pregnancy, blood glucose should be kept at a reasonable and stable level.

Objective Compared with endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA), this study aims to explore the diagnostic advantages of endobronchial ultrasound-guided transbronchial node biopsy (EBUS-TBNB) in the diagnosis of mediastinal lymph node metastasis, lymphadenitis, sarcoidosis and other mediastinal lymph node diseases associated with mediastinal enlargement in lung cancer and extra-pulmonary tumors. Methods The detection rate of malignant tumor was(14/35, 40%) by EBUS-TBNA and average amount of bleeding during each operation was 1-2 mL; Compared with EBUS-TBNA, the detection rate of malignant tumors by EBUS-TBNB was(23/35, 66%)(P＜0.01), and 4 cases of granulomas were diagnosed, and the average amount of bleeding during each operation was 3-4 mL. Conclusions Compared with EBUS-TBNA, EBUS-TBNB has a higher detection rate for malignant tumors and has more advantages in the diagnosis of benign proliferative diseases. It can further improve the accuracy and sensitivity of diagnosing mediastinal enlarged lymph nodes so is worthy of clinical promotion and application.

Chimeric antigen receptor-modified T (CAR-T) cell therapy, as a new type of cellular immunotherapy, has shown good clinical efficacy in the treatment of malignant hematological tumors, especially B-cell acute lymphoblastic leukemia. However, there are problems such as antigen loss and immune evasion in single-target selection, so multi-target therapy strategies are gradually gaining attention. Multi-target CAR-T can effectively avoid antigen escape caused by a single target by targeting multiple tumor-associated antigens at the same time, reduce the risk of recurrence, and is expected to improve the therapeutic effect. This paper primarily discusses the structural types of multi-target CAR-T cell therapy and its clinical trial applications in the treatment of B-cell acute lymphoblastic leukemia (B-ALL), aiming to provide future references for the treatment of B-ALL.

The gut microbiota is generally thought in regulating the body′s metabolism and immune function. The imbalance of gut microbiota is related to the occurrence and development mechanisms of acute and chronic lung diseases, resulting from lung injury. The “gut-lung axis” pays a main role in various ways in the occurrence of lung injury, including intestinal barrier dysfunction, reduced diversity of gut microbiota, decreased secretion of beneficial metabolites, translocation of gut microbiota and metabolites to the lungs, immune damage to the body and lungs, increased inflammatory response in the lungs.

Objective To explore the methods of continuing education for advanced endoscope operations by digestive specialists through the establishment and teaching effect evaluation of the ERCP (endoscope retrograde cholangiopancreatography) introductory training mode. Methods A total of 26 trainees from 3 sessions of the ERCP introductory training courses at Peking Union Medical College Hospital from September 2023 to September 2024 were included. The teaching effects of the training courses and its 5 modules were subjectively and objectively evaluated by questionnaires, on - site tests and evaluations by senior ERCP operators. Results Through the ERCP introductory training courses, the trainees′ self-evaluated proficiency in duodenoscope structure (pre-training: 2.4±2.4, post- training: 8.2±1.5, P＜0.001), duodenoscope operation (pre-training: 1.2±2.2, post-training: 6.6±1.8, P＜0.001), papillary cannulation (pre-training: 0.5±1.3, post-training: 5.4±1.8, P＜0.001), intra-bile duct operation (pre-training: 0.2±0.6, post-training: 4.9±2.1, P＜0.001), and identification of intra-bile duct lesions (pre-training: 1.7±2.1, post-training: 6.0±2.0, P＜0.001) was significantly improved. The accuracy rate of the trainees′ theoretical tests and picture recognition before training was 37.2% and then increased up to 62.8% after training. Before training, all trainees were considered by senior operators as not ready to start ERCP training on real patients, while after training, 69.2% (18/26) of the trainees were considered ready to start ERCP training on real patients. Conclusions The multi-module ERCP introductory training courses have a significant effect in terms of laying a foundation for trainees to start ERCP training on patients and of providing a reference for the continuing education mode of advanced endoscope operations for digestive specialists in China.

Objective To explore the effectiveness of multimodal comprehensive diabetes management teaching in the standardized training of endocrinology residents. Methods Fifty-nine resident physicians rotating through the endocrinology department from March to October 2024 were selected. They underwent a multimodal comprehensive diabetes management teaching model that integrated standardized theoretical instruction, case discussions, teaching ward rounds, practical operations, and interdisciplinary pharmaceutical education. The effectiveness of this teaching model was evaluated through multiple dimensions using a comprehensive diabetes management evaluation form, Mini-Clinical Evaluation Exercise (Mini-CEX) scale, and satisfaction surveys. Results After two months of multimodal standardized training, the results showed: 1) The resident physicians demonstrated significant improvements in all aspects of comprehensive diabetes management (P＜0.05). 2) The Mini-CEX scores of the resident physicians generally reached excellent levels (P＜0.05). 3) Both the resident physicians and teaching faculty showed significantly higher satisfaction with the comprehensive diabetes management program after the training (P＜0.05). Conclusions Multimodal comprehensive diabetes management teaching is effective in enhancing the standardized diagnosis and treatment abilities of resident physicians in the endocrinology department regarding diabetes.

With the rapid development of information technology, digitization of education has become an important driving force to promote education reform. In the education system of medical colleges, the construction and implementation of professional curriculum courses play an important role in the cultivation of qualified medical talents. Emergence of education digitization has brought unprecedented opportunities but also some challenges to the curriculum construction by teachers in medical school. This paper aims to explore how to effectively promote construction of professional curriculums with information technology(IT) guided by education digitization strategy and to recommend a series of methods in terms of strategy implementation in medical schools.