_2025__Acta Universitatis Medicinalis Anhui

Evaluation of brain aging in patients with type 2 diabetes mellitus by structural magnetic resonance-driven machine learning model

Wang Jie1 , 2 , Miao Ziyue3 , Chang Jiayue3 , Wu Xingwang1 , Zhu Jiajia1 , Cai Huanhuan1

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.022

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abstract:
To explore the brain-predicted age difference (Brain-PAD) in patients with type 2 diabetes mellitus (T2DM) by a machine learning prediction model based on structural magnetic resonance ( sMRI) in the Southwest University Adult Lifespan Dataset (SALD) , and to reveal the relationship between Brain-PAD and dura- tion of T2DM and cognition . Methods Group comparisons about demographic variables and cognitive function were conducted respectively in local database of 104 T2DM patients and 83 healthy controls (HC) . The prediction model via Gaussian process regression (GPR) was constructed by training sMRI data of 329 healthy volunteers in SALD , then its performance was validated and evaluated . Furthermore , Brain-PAD ( predicted age-chronological age) in the local database was calculated . Group comparisons of Brain-PAD between T2DM patients and HCs were conducted by Mann-Whitney U test. Finally , Pearson correlation coefficient (r) was calculated between Brain-PAD and duration of disease and cognition . Results Poor performance in auditory verbal learning test (AVLT)-delayed recall , AVLT-recognition , symbol digital modalities test (SDMT) (P < 0. 05) , and increased Brain-PAD were ob- served in T2DM patients , compared with HCs [1 . 61 9( - 4. 001 , 8. 272) years vs - 1 . 289 ( - 4. 128 , 4. 134) years , Z = 2. 056 , P = 0. 034] . Notably , the median of Brain-PAD in T2DM group was positive , indicating that the brain of T2DM patient maybe relatively “older”than his chronological age . Brain-PAD in T2DM group was as- sociated with performance in AVLT-immediate recall ( r = 0. 291 , P = 0. 003) , AVLT-delayed recall ( r = 0. 248 , P = 0. 011) , SDMT( r = 0. 376 , P < 0. 001) and trail making test (TMT)-A ( r = - 0. 206 , P = 0. 036) . However , the relationships between Brain-PAD and duration of T2DM were not explored . Conclusion Decreased cognitive function in patients with T2DM is demonstrated in this study . The machine learning prediction model based on sMRI supports the identification of brain aging objectively in patients with T2DM .

Plateau hypoxia induces pyroptosis in mouse kidney cells through NOD-like receptor signaling pathway

Xu Xintong , Chen Xiaochen , Cui Chengling , Wang Xin , Gao Xiang

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.009

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The Mechanism of Glutamine activating autophagy exacerbates muscle loss in cancer-associated cachexia

Ma Dufang1 , 2 , Wang Yong2 , Tian Zhihan1 , Su Xiaoyu1 , Qi Yuanfu3

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.026

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Clinical efficacy of cranial electrotherapy stimulation in chronic insomnia : a research study

Jiao Jiajia , Li Jialu , Sun Xixi , Yin Yunfei , Xie Chengjuan

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.021

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abstract:
To investigate the effects of cranial electrotherapy stimulation (CES) with varying parameter configurations on sleep quality in patients diagnosed with chronic insomnia disorder. Methods Seventy-two partici- pants meeting diagnostic criteria for chronic insomnia disorder were randomly allocated to a four-arm parallel study design . The intervention protocol comprised : Group 1 (G1) received cranial electrotherapy stimulation (CES) at 0. 5 Hz , 300 μA; Group 2 (G2) underwent CES treatment at 1 . 5 Hz , 300 μA; Group 3 (G3) administered 100 Hz , 300 μA stimulation; and Group 4 (G4) received sham stimulation with identical device placement but no cur- rent delivery . Primary outcomes were quantified through polysomnography (PSG) recordings conducted at baseline and post-intervention , whereas secondary outcomes were assessed via standardized sleep questionnaires including the Pittsburgh sleep quality index (PSQI) and Insomnia Severity Index (ISI) . Results Following a 10-day inter- vention protocol , significant clinical improvements were observed across all active treatment groups ( G1 - G3) as evidenced by reductions in PSQI . Insomnia severity index ( ISI) scores quantitative polysomnographic analysis re- vealed that both G2 ( 1 . 5 Hz) and G3 ( 100 Hz) cohorts demonstrated statistically significant enhancements in Flinders Fatigue Scale (FFS) scores , total sleep time (TST) , and sleep efficiency (SE) , accompanied by reduced sleep onset latency ( SOL) compared to baseline measurements . However , no statistically significant differences were detected between the G2 and G3 intervention arms across all measured parameters . CES exerted no significant effect on sleep architecture . Conclusion CES can effectively improve the sleep of patients with chronic insomnia.Within a certain range , a higher frequency of CES leads to better sleep improvement effects .

Antibacterial properties and compatibility of plasma-activated water/bletilla striata polysaccharide composite hydrogel

Ren Wenxue1 , Cheng Cheng2 , Han Wei3 , Liu Taofeng4

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.002

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abstract:
To investigate the antibacterial properties and biocompatibility of a novel hydrogel fabricated by integrating plasma-activated water ( PAW) and bletilla striata polysaccharide ( BSP) . Methods The experi- ments were carried out by dividing the hydrogels into four groups based on their compositions : the deionized water (DW)-Carbomer 940 (CBM940 )-carboxymethyl chitosan (CMCS) hydrogel group ( H group) , the PAW-CBM940 - CMCS hydrogel (PAH) group , the DW-BSP-CBM940 -CMCS hydrogel (BSPH) group , and the PAW-BSP-CBM940 - CMCS hydrogel (PA/BSPH) group . Physical properties of the hydrogels were evaluated by testing water loss rate and water vapor transmission rate . The content of active substances was determined using a microplate reader and an electron spin resonance spectrometer (ESR) . The pH and ORP values were measured using a pH meter and an oxidation-reduction potential (ORP) electrode . The antibacterial mechanism was elucidated by analyzing the integ- rity of bacterial biofilms . Antibacterial activity was evaluated via the zone of inhibition assay . Cytotoxicity testing was performed using the cell counting kit-8 (CCK-8) assay , and combined with the cell scratch assay , to collec- tively evaluate the effects of the hydrogel on cellular biocompatibility and migration ability . Results The water loss rate and water vapor transmission rate of PA/BSPH hydrogel were (32. 3 ±2. 3)% and (2 228. 2 ±1 81 . 1) g/( m2 ·d) . Compared with the H group hydrogel , the contents of hydrogen peroxide ( H2 O2 ) and hydroxyl radicals ( ·OH) in PAH and PA/BSPH groups significantly increased (P < 0. 05) , and the diameters of inhibition zones significantly enlarged (P < 0. 05) . The cell viability in PAH group significantly decreased (P < 0. 05) . The PA/ BSPH group showed non-toxicity and a higher cell migration rate ( P < 0. 05 ) . Conclusion The antibacterial mechanism of the PA/BSPH hydrogel relies on the reactive species H2 O2 and ·OH in PAW. The incorporation of BSP enhances the water retention and breathability of the wound dressing while significantly reducing the cytotoxici- ty of PAW. This modification endows the hydrogel with improved biocompatibility and promotes cell proliferation . The PA/BSPH hydrogel demonstrates clinical potential by offering a novel therapeutic strategy for chronic infected wound management.

Construction of a prognostic model for lung cancer based on acrolein-related genes

Feng Yiting1 , 2 , Ren Liangliang2 , Lou Lijuan2 , Shen Yuxian1 , Jiang Ying1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.001

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abstract:
To construct and validate a prognostic model for lung cancer based on acrolein-related genes using bioinformatics methods . Methods Lung cancer datasets GSE30219 and GSE68465 were obtained from the GEO database , and acrolein-related gene sets were retrieved from the CTD database . Differentially expressed genes (DEGs) between cancer and adjacent tissues were identified in the GSE30219 dataset. The intersection of these DEGs and acrolein-related genes was then used to identify candidate genes . Gene set variation analysis ( GSVA) was performed to assess functional alterations based on the intersection genes . A protein-protein interaction (PPI) network was constructed based on the STRING database to identify core hub genes . Subsequently , support vector machine recursive feature elimination (SVM-RFE) and LASSO-Cox regression analyses were employed to develop a prognostic model based on acrolein-related genes , which was independently validated using the GSE68465 dataset. The CIBERSORT algorithm was applied to evaluate the immune cell infiltration characteristics between high- and low-risk groups , and functional enrichment analysis of DEGs between the two groups was conducted to further ex- plore the potential molecular mechanisms underlying the prognostic model . Results A total of 361 acrolein-related DEGs were identified in lung cancer , and 7 key genes were selected for model construction . Kaplan-Meier survival analysis revealed that patients in the high-risk group had significantly lower survival rates compared to those in the low-risk group (P < 0. 000 1) . Receiver operating characteristic (ROC) curve analysis demonstrated that the mod- el possessed good predictive performance . Moreover , immune infiltration analysis indicated that the risk score was closely associated with multiple immune cell subsets , suggesting a potential role of acrolein-related genes in modula- ting the lung cancer immune microenvironment. Conclusion The prognostic model for lung cancer based on acro- lein-related genes demonstrates significant application value in predicting the prognosis of lung cancer , providing new insights into the potential mechanisms of acrolein in the onset and progression of lung cancer.

Mechanism of Anemoside B4 on glutamine metabolism in oral lichen planus epithelial cells via the NOS3-DHFR axis

Li Min , Yang Menghua , Gao Yi , Zhang Zijian , Jiang Dan

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.010

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abstract:
To investigate the mechanism of Anemoside B4 (AB4) on glutamine metabolism in oral li- chen planus (OLP) epithelial cells via the nitric oxide synthase 3 (NOS3)-dihydrofolate reductase (DHFR) axis . Methods Bioinformatics analysis was performed to identify the intersection of molecular targets of OLP , AB4 , and genes related to glutamine metabolism . A lipopolysaccharide ( LPS)-induced HOK-16B model of OLP was estab- lished . HOK-16B were divided into Ctrl group , OLP group , AB4 group , OLP + oe-NOS3 group , OLP + sh-NOS3 group , OLP + sh-NOS3 + oe-DHFR group , and OLP + sh-NOS3 + AB4 group . Cell proliferation was detected by cell counting kit-8 (CCK-8) ; cell apoptosis was detected by TdT-mediated dUTP Nick-End Labeling ( TUNEL) ; inflammatory factors iInterleukin (IL)-1β, tumor necrosis factors-α ( TNF-α) concentrations in cell supernatants were measured using enzyme-linked immunosorbent assay (ELISA) kits; glutamine uptake and glutamate produc- tion were determined using kits; and the protein expression of alanine-serine-cysteine transporter2 ( ASCT2) and glutamine synthase (GLS) was assessed by Western blotting. Results Bioinformatics analysis of molecular targets of OLP , AB4 , and genes related to glutamine metabolism revealed three intersection targets : NFE2L2 , NOS1 , and NOS3 . Compared with the Ctrl group , the OLP group exhibited decreased HOK-16B cell viability (P < 0. 001) , increased apoptosis rate (P < 0. 01) , upregulated concentrations of IL-1βand TNF-α(P < 0. 001) , elevated glu- tamine uptake and glutamate production (P < 0. 01) , and enhanced expression of ASCPT2 and GLS proteins (P < 0. 001) . Compared with the OLP group , the AB4 group showed improved cell viability (P < 0. 05) , reduced apop- tosis rate and release of IL-1βand TNF-α(P < 0. 05) , decreased glutamine uptake and glutamate production (P < 0. 05) , and downregulated expression of ASCPT2 and GLS proteins ( P < 0. 001) . Compared with the OLP group , the OLP + oe-NOS3 group had increased HOK-16B cell viability (P < 0. 01) , reduced apoptosis rate (P < 0. 05) , decreased concentrations of IL-1βand TNF-α(P < 0. 05) , lowered glutamine uptake and glutamate pro- duction (P < 0. 05) , and weakened expression of ASCPT2 and GLS proteins (P < 0. 01) ; whereas the OLP + sh- NOS3 group had decreased HOK-16B cell viability ( P < 0. 05) , increased apoptosis rate ( P < 0. 05) , elevated concentrations of IL-1βand TNF-α ( P < 0. 01 ) , increased glutamine uptake and glutamate production ( P < 0. 05) , and enhanced expression of ASCPT2 and GLS proteins (P < 0. 001) . Compared with the OLP + sh-NOS3 group , both the OLP + sh-NOS3 + oe-DHFR group and the OLP + sh-NOS3 + AB4 group showed increased HOK- 16B cell viability (P < 0. 001) , reduced apoptosis rate (P < 0. 05) , decreased concentrations of IL-1βand TNF-α (P < 0. 01) , lowered glutamine uptake and glutamate production ( P < 0. 05) , and weakened expression of AS- CPT2 and GLS proteins ( P < 0. 05) . Conclusion AB4 inhibits the progression of OLP by mediating glutamine metabolism via the regulation of the NOS3-DHFR axis .

Analysis of risk factors for pulmonary artery hypertension in patients with maintenance peritoneal dialysis and establishment and verification of a nomogram

Zu Shuang1 , Yan Qiqi2 , Yang Le1 , Li Huixian1 , Li Xiude1 , Fan Yunshan1 , Zhang Bao1 , Wang Deguang2

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.023

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abstract:
To identify the risk factors for pulmonary arterial hypertension (PAH) in maintenance peri- toneal dialysis (MPD) patients and to develop and validate a nomogram-based risk-prediction model . Methods A total of 168 hospitalized MPD patients from the Department of Nephrology were enrolled . Body-fluid composition was measured by bioelectrical impedance analysis , and pulmonary-artery systolic pressure (PASP) was assessed by echocardiography . Patients were randomly allocated into a training set and a validation set at 1 : 1 ratio . Variables with P < 0. 05 in multivariable Logistic regression in the training set were incorporated to construct a nomogram . The validation set was used to test the model ’s predictive performance . ROC curves , calibration curves , and deci- sion-curve analysis were applied to evaluate accuracy , consistency , and clinical usefulness of the model . Results Dialysis vintage ( OR : 1 . 038 , 95% CI: 1 . 008 - 1 . 069 , P = 0. 012) , hemoglobin level ( OR : 0. 961 , 95% CI: 0. 929 - 0. 994 , P = 0. 021) , and extracellular water/intracellular water ratio (E/I) (OR : 1 . 069 , 95% CI: 1 . 024 - 1 . 115 , P = 0. 002) were independent risk factors for PAH . ROC analysis yielded area under curve as 0. 867 (95% CI: 0. 782 - 0. 953) and 0. 808 (95% CI: 0. 714 - 0. 902) in the training and validation sets , respectively . Calibration plots showed that the predicted curves for both the training and validation sets closely overlapped with the ideal reference line , indicating that the nomogram risk-prediction model had good predictive performance . Deci- sion-curve analysis demonstrated that , within threshold ranges of 0. 13 - 0. 76 ( training set ) and 0. 20 - 0. 76 (val- idation set ) , clinical net benefit was substantial when interventions were guided by the nomogram . Conclusion Dialysis vintage , hemoglobin level , and fluid-overload index (E/I) are independent risk factors for PAH in MPD patients . The nomogram based on these parameters reliably predicts PAH risk and may aid clinical decision-mak- ing.

Effect of ribosomal protein L26 on apoptosis and proliferation of gastric cancer cells

Wang Qian1 , Yang Fang2 , Nie Wei2 , Hu Lihua1 , Zhang Maolin1 , Zhao Lixiang1 , Jin Xiangren3 , Yan Zhiqiang1 , 3

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.008

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abstract:
To investigate the expression of Ribosomal protein L26 ( RPL26) in gastric cancer cells (GC) and its effect on cell apoptosis and proliferation . Methods The expression of RPL26 in GES-1 and GC cell lines was detected by Western blot. GC cell line HGC-27 was used to construct RPL26 overexpression cell line , and GC cell lines HGC-27 and AGS cells were used to construct RPL26 knockdown cell line . The overexpression and knockdown efficiency of RPL26 were detected by Western blot. Cell counting kit-8 (CCK-8) , colony formation assay and Transwell assay were used to detect the effects of the overexpression and knockdown of RPL26 on the pro- liferation and migration of GC cells . Western blot was used to detect the expression of Phosphatidylinositol-3-kinase (PI3K) / protein kinase B (AKT) signaling pathway related factors PI3K , AKT , phosphorylated phosphatidylinosi- tol-3-kinase (p-PI3K) , phosphorylated protein kinase B ( p-AKT) and downstream factors B-Cell lymphoma-2 (Bcl-2) , Bcl-2 associated X protein (Bax) and Cyclin A , G1 /S-specific Cyclin D1(Cyclin D1) , Cyclin-depend- ent kinases (CDK)4 and CDK2 in overexpression and knockdown of RPL26 stably transfected cell lines . Results Compared with GES-1 , RPL26 was highly expressed in HGC-27 cells ( tHGC-27 = 4. 97 ; P < 0. 05) and elevated in AGS , but the difference was not statistically significant. In HGC-27 and AGS cells , CCK-8 and colony formation assays showed that the proliferation ability of cells decreased after the knockdown of RPL26. Transwell assay showed that the migration ability of cells decreased after the knockdown of RPL26. Western blot showed that Bcl-2 expression was decreased in HGC-27 , AGS cells after the knockdown of RPL26 ( tHGC-27 = 11 . 50 , tAGS = 4. 77 ; P < 0. 05) , and Bax expression increased ( tHGC-27 = 9. 63 , tAGS = 4. 05 ; P < 0. 05) . In HGC-27 cells , the ratios of p- PI3K/PI3K and p-AKT/AKT significantly decreased after the knockdown of RPL26 ( tp-PI3K/PI3K = 3 . 86 , tp-AKT/AKT = 8. 29 ; P < 0. 05) . Cyclin A , Cyclin D1 , CDK4 , CDK2 protein expressions decreased ( tCyclin A = 9. 61 , tCyclin D1 = 5 . 10 , tCDK4 = 11 . 64 , tCDK2 = 7 . 81 ; P < 0. 05) , while the overexpression of RPL26 in HGC-27 cells showed the op- posite trend . Conclusion The knockdown of RPL26 may arrest the cell cycle in G1 /S phase by inhibiting the PI3K/AKT signaling pathway , thereby inhibiting cell proliferation and promoting apoptosis .

Geniposide alleviates ulcerative colitis in mice through IL-6/JAK2/STAT3 signaling pathway

Li Kexun1 , Zhao Yuxiang2 , Zeng Qiang3 , Huang Guixiang1 , Yu Hongtao1

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.013

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abstract:
To explore the alleviating effect of geniposide on ulcerative colitis (UC) and to investigate its potential mechanism . Methods A UC mouse model was induced using 5% dextran sulfate sodium ( DSS) . These mice were randomly divided into 6 groups ( n = 8) : control group , model group , sulfasalazine group[ 100 mg/(kg ·d) ] , low-dose geniposide group[ 10 mg/(kg ·d) ] , medium-dose geniposide group[20 mg/(kg ·d) ] , and high-dose geniposide group[40 mg/( kg · d) ] . The mice were orally administered for consecutive 10 days . The colon length and mouse body mass were measured , and the colon mucosal damage index (CMDI) and disease activity index (DAI) were scored . The pathological changes in colon tissue were observed using hematoxylin-eosin (HE) staining. The reagent kits were used to measure the levels of malondialdehyde ( MDA) , myeloperoxidase (MPO) , catalase ( CAT) , and glutathione ( GSH) in colon tissue . The enzyme linked immunosorbent assay (ELISA) was used to analyze the expression levels of tumor necrosis factor-α ( TNF-α) , interleukin-6 ( IL-6) , and IL-1βin colon tissue . Western blot was used to detect the protein expression of mucin 1 (MUC-1) , occludin , IL-6 , p-JAK2 , and p-STAT3 in colon tissue . Results Compared with the normal control group , the body mass and colon length of the model group mice significantly decreased . The expression of MUC-1 and occludin proteins significantly reduced (P < 0. 01) . The activities of CAT and SOD significantly reduced . DAI score and CMDI score significantly increased (P < 0. 01) . The expression levels of TNF-α, IL-6 , and IL-1βsignificantly increased (P < 0. 01) . The content of MPO and MDA significantly increased (P < 0. 01) . The expression of IL-6 , p-JAK2 and p- STAT3 proteins significantly increased ( P < 0. 01) . Compared with the model group , the body mass and colon length of mice in sulfasalazine group and geniposide medium and high-dose groups significantly increased (P < 0. 05 or P < 0. 01) , the expression of MUC-1 and occludin proteins increased (P < 0. 05 or P < 0. 01) , as well as the activity of CAT and SOD (P < 0. 05 or P < 0. 01) . DAI score and CMDI score in Sulfasalazine group and genipo- side medium and high-dose groups significantly reduced (P < 0. 05 or P < 0. 01) , as well as the expression levels of TNF-α, IL-6 , and IL-1β(P < 0. 05 or P < 0. 01) . MPO and MDA content in Sulfasalazine group and genipo- side medium and high-dose groups significantly reduced (P < 0. 05 or P < 0. 01) , as well as the expression of IL- 6 , p-JAK2 , and p-STAT3 proteins (P < 0. 05 or P < 0. 01) . Conclusion Geniposide maintaines intestinal home- ostasis by regulating the structure of the intestinal flora and improves colitis injury in UC mice by inhibiting the acti- vation of the IL-6/JAK2/STAT3 pathway .

Extraction , Purification and Identification Technologies of Exosomes Derived from Polygonum cuspidatum

Wu Jiayu1 , Zhang Hong1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.012

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The correlation between Chemerin levels and intestinal mucosal inflammation in IBS-D model mice

Xing Zhuoyue , Bai Juan , Gao Xin , Huang Jiarui , Xu Lihong , Gao Yinfeng

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.014

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Generation of a FAM50A knockout Beta-TC-6 cell line using CRISPR/Cas9 technology and preparation of a FAM50A polyclonal antibody

Qiu Yaxuan1 , Meng Xiangrui 1 , Xie Xiaoyan2 , Cheng Sitong1 , Peng Yufan2 , Liu Siqi 1 , Zhao Xue2 , 3 , Hu Zhangfeng2 , 3 , Xing Junqiao2 , 3 , Wang Weihua2 , 3

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.016

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The relationship between ectopic fat and iron deposition in muscle and glucose metabolism in patients with elderly obese patients

Nie Hao1 , Liu Min2 , Duan Junhong3 , Liu Hong2

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.019

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Risk factors for hepatocellular carcinoma in patients with HBeAg-negative hepatitis B cirrhosis

Liu Xiaoyan , Gan Xinyi , Li Cheng , Du Wenjun

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.020

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abstract:
To investigate hepatocellular carcinoma ( HCC ) risk factors in hepatitis B e antigen (HBeAg)-negative cirrhotics , and to develop and validate a predictive model using these indicators . Methods A total of 649 hospitalized patients with HBeAg-negative hepatitis B cirrhosis and HBeAg-negative primary HCC were enrolled . Patients were randomly divided into a modeling group ( n = 298) and a validation group ( n = 351) at a 7:3 ratio . Logistic regression analysis was used to screen for independent predictors of HCC occurrence . A predic- tive model was constructed and validated using receiver operating characteristic ( ROC) curves . The clinical net benefit of the prediction model was assessed via decision curve analysis . Results Univariate analysis showed sig- nificant statistical differences between the modeling and validation groups in serum alanine aminotransferase (ALT) , aspartate aminotransferase ( AST) , triglycerides ( TG) , gamma-glutamyl transferase ( GGT) , red blood cell count (RBC) , hemoglobin (Hb) , platelet count (PLT) , international normalized ratio (INR) , alpha-feto- protein (AFP) , serum calcium (Ca2 + ) , serum cholinesterase (CHE) , and HBV DNA levels . Multivariate logistic regression analysis identified AST , GGT , Hb , PLT , Ca2 + , CHE , and HBV DNA as independent influencing fac- tors for HCC occurrence (P < 0. 05) , with ORs (95% CI) of 1 . 002 ( 1 . 000 - 1 . 005) , 1 . 006 ( 1 . 003 - 1 . 008) , 0. 994 (0. 988 - 0. 999) , 0. 984 (0. 981 - 0. 988) , 9. 624 (3 . 821 - 24. 245 ) , 0. 999 (0. 802 - 0. 998) , and 7. 530 (4. 143 - 13 . 687) , respectively . A nomogram prediction model was established based on these seven indi- cators . The area under the ROC curve (AUC) was 0. 936 in the modeling group and 0. 941 in the validation group . Calibration curves demonstrated high predictive accuracy of the nomogram . Conclusion AST , GGT , Hb , PLT , Ca2 + , CHE , and HBV DNA are independent risk factors for HCC development in patients with HBeAg-negative hepatitis B-related cirrhosis . The established non-invasive prediction model exhibits good discriminative ability and clinical utility , providing an experimental basis for early detection and preventive screening of HCC in this patient population .

Research progress on the role and mechanism of C/EBPβin female reproduction

Liu Shuzhen1 , Peng Jiahua1 , 2 , Xiao Min1 , Liang Ruining1 , 2 , 3

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.025

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Mechanism of protection of motor neurons in spinal cord anterior horn of SNI rats by acellular nerve allografts via the Bcl-2/Cyt-C/Apaf-1 signalling pathway

Zheng Mengyuan1 , 2 , Hao Zitong1 , 2 , Zhu Qinghua1 , 2 , Tian Zhuangzhuang1 , Guo Xingda1 , Zheng Yuhe1 , Li Cheng1 , Fu Xiumei 1 , 3

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.007

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abstract:
To investigate the protective effects and mechanisms of acellular nerve allografts (ANA) on motor neurons in the spinal cord anterior horn of sciatic nerve injury ( SNI) rats . Methods SPF grade male SD rats were randomly divided into normal , model , ANA-bridged (bridge group) , and autologous nerve transplantation groups (autograft group) , with 6 rats in each group . The SNI rat model was established using the right sciatic nerve clamp method for 10mm . In the bridge group , the ANA was bridged to the two severed ends of the injured sciatic nerve , and in the autograft group , the autologous nerves were flipped head to tail and then bridged to the two se- vered ends . A spectrophotometer was applied to determine the DNA content in normal nerves and ANA . The foot- print test was used to determine the sciatic nerve function index (SFI) of the rats in each group , the wet weight ra- tio of the anterior tibialis muscle was calculated . The morphology and structure of the anterior horn motor neurons of the spinal cord of each group were observed by HE staining. The immunofluorescence and Western blot were used to detect Apaf-1 , Caspase-3 , Bcl-2 , Bax , and Cyt-C proteins expression in the L4-6 segment of the spinal cord . Results The DNA content in the ANA prepared in this study was significantly lower than that in normal nerves (P < 0. 05) . Compared with the normal group , the SFI and wet weight ratio of the anterior tibialis muscle were re- duced in the model group (P < 0. 001) ; compared with the model group , both SFI and wet weight ratio of the ante- rior tibialis muscle significantly increased in the bridge group and the autografts group ( P < 0. 05 , P < 0. 001) , and the SFI and wet weight ratio of the anterior tibialis muscle in the autograft group were higher than those in the bridge group (P < 0. 001 , P < 0. 01) . The results of HE staining showed that the motor neurons in the anterior horn of the spinal cord of the normal group were structurally intact and had clear cytosolic boundaries; the neurons in the model group were lysed and necrotic , with blurred cytosolic boundaries; the neurons in the bridge group were less lysed and necrotic , but the nuclear translocation phenomenon could still be seen; the neurons in the autograft group were morphologically and structurally intact with clear cytosolic boundaries . Compared with the normal group , the expression of Apaf-1 , Caspase-3 , Bax and Cyt-C proteins significantly increased in the model group (P < 0. 001 , P < 0. 01 , P < 0. 01 , P < 0. 05) , but the difference of Bcl-2 protein expression was not statistically sig- nificant. Compared with the model group , the expression of Apaf-1 , Caspase-3 , Bax , and Cyt-C proteins signifi- cantly decreased (P < 0. 001 , P < 0. 05) ; but the expression of Bcl-2 protein significantly increased in the bridge group and the autograft group (P < 0. 05) . The expression of Apaf-1 , Caspase-3 , Bax and Cyt-C proteins in the autografts group was lower than that in the bridge group (P < 0. 001 , P < 0. 05) . Conclusion ANA can exert a protective effect on motor neurons in the anterior horn of the spinal cord of SNI rats by improving the morphology and structure of neurons , increasing the expression of Bcl-2 protein , but decreasing the expression of Cyt-C , Bax , Caspase-3 , and Apaf-1 proteins in the spinal cord . The mechanism of ANA may be related to the Bcl-2/Cyt-C/ Apaf-1-mediated mitochondrial apoptosis signaling pathway .

Sesamin induced ferroptosis in triple negative breast cancer cells through P53/SLC7A11/GPX4 pathway

Zhu Mingmei 1 , Yu Wanlu1 , Xu Hongyue1 , Cui Xinhua1 , Peng Danping2 , Yu Lu1

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.005

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abstract:
To investigate the ferroptosis induced by sesamin in triple-negative breast cancer ( TNBC) 4T1 cells and its underlying mechanism . Methods The binding energy of sesamin with glutathione peroxidase 4 (GPX4) , solute carrier family 7 member 11 ( SLC7A11) , and P53 was analyzed by molecular docking. Mouse TNBC cell line 4T1 was used as a model . Different concentrations of sesamin were administered to 4T1 cells . The effect of sesamin on cell viability was assessed using the cell counting kit 8 (CCK-8) . Transwell assay was used to evaluate the effect of sesamin on cell migration and invasion . The contents of Fe2 + , malondialdehyde (MDA) , and reduced glutathione (GSH) in the cells were measured using kits . 2 ′,7 ′-dichlorofluorescein diacetate (DCFH-DA) probe was employed to detect the content of reactive oxygen species (ROS) in cells . Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot were performed to evaluate the expression of GPX4 , SLC7A11 , and P53 at mRNA and protein levels . Results The binding energies of sesamin with GPX4 , SLC7A11 and P53 were - 21 . 46 , - 21 . 67 , and - 27 . 03 kJ/mol , respectively . Compared with the control group , the viability of 4T1 cells in different concentrations of sesamin groups decreased gradually ( P < 0. 001) , and the migration and invasion ability of 4T1 cells in 20 , 40 , and 80 μmol/L sesamin groups decreased gradually (all P < 0. 001) . Compared with the control group , the contents of Fe2 + , MDA , and ROS in 4T1 cells of 20 , 40 , and 80 μmol/L sesamin groups increased , and the content of GSH decreased . Compared with the control group , the mRNA and protein expression of GPX4 and SLC7A11 in 4T1 cells in the sesamin treatment group decreased , and the mRNA and protein expression of P53 increased ( all P < 0. 001) . Conclusion Sesamin may induce the ferroptosis in 4T1 cells through P53/SLC7A11 /GPX4 pathway .

The role and mechanism of IQGAP1 in oxygen-glucose deprivation/reoxygenation induced microglial polarization

Chao Bo1 , Ren Junhao1 , Guo Ruoyu1 , Su Youle1 , Ma Ying2

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.004

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abstract:
To investigate the role and mechanism of IQ motif containing GTPase activating protein 1 (IQGAP1) in oxygen-glucose deprivation/reoxygenation (OGD/R) -induced polarization of BV-2 microglia cells . Methods The IQGAP1 overexpression plasmid ( oe-IQGAP1 ) and its negative control plasmid ( Vector) were transfected into BV-2 cells , and then the polarization of BV-2 cells was induced by OGD/R , and exogenous inter- feron-γ(IFN-γ) recombinant protein was used for intervention . Cell proliferation rate was detected by cell counting kit-8 (CCK-8) assay . The level of lactate dehydrogenase (LDH) in the supernatant was detected using a test kit. The mRNA expression levels of IQGAP1 , IFN-γand microglial polarization markers inducible nitric oxide synthase (iNOS) , CD86 , CD206 and arginase1 (Arg1) were detected by quantitative real-time polymerase chain reaction (RT-qPCR) . The levels of IFN-γ, tumor necrosis factor-α(TNF-α) , interleukin (IL)-1β, IL-4 and IL-10 in the cell supernatant were detected by enzyme-linked immunosorbent assay (ELISA) . The protein expression levels of IQGAP1 and IFN-γwere detected by Western blot. Results Following OGD/R treatment , the proliferation rate of BV-2 cells , the levels of IL-4 and IL-10 in the supernatant , and the mRNA expression levels of CD206 and Arg1 were significantly reduced (all P < 0. 05) . In contrast , the levels of LDH , TNF-αand IL-1βin the supernatant , as well as the mRNA expression levels of iNOS and CD86 in the cells significantly increased (all P < 0. 05) . More- over , both the mRNA and protein expression levels of IQGAP1 in the cells significantly decreased ( P < 0. 05) . Following IQGAP1 overexpression , the levels of IL-4 and IL-10 in the supernatant of BV-2 cells , along with the mRNA expression levels of CD206 and Arg1 in the cells , were significantly elevated under OGD/R conditions (all P < 0. 05) . Meanwhile , the levels of TNF-αand IL-1βin the supernatant and the mRNA expression levels of iNOS and CD86 in the cells significantly decreased (all P < 0. 05) . Additionally , both the intracellular expression and secretion of IFN-γprotein were reduced ( all P < 0. 05) , whereas the mRNA expression of IFN-γremained un- changed . However , combined intervention with exogenous IFN-γrecombinant protein obviously reversed the inhibi- tory effect of IQGAP1 overexpression on OGD/R-induced M1 polarization of microglia. Conclusion IQGAP1 over- expression inhibits M1 polarization of microglia under OGD/R conditions through the suppression of IFN-γexpres- sion and secretion .

Experimental research on LIF promoting lipopolysaccharide-induced pulpal inflammatory response

Liu Hao1 , 2 , Zhu Youming1 , 2 , Li Song1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.018

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Differential expression and prognostic significance of exosomal miRNA derived from bone marrow stromal cells in the bone marrow supernatants of patients with AML

Dai Wei 1 , Wang Xiaoting1 , Fu Wenjuan2 , Li Qiushuang2 , Zhou Tianhui2 , Lu Mengyuan2 , Huang Huifang1

DOI: 10.19405/j.cnki.issn1000-1492.2025.11.017

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abstract:
To investigate the aberrant alterations of microRNAs ( miRNAs) in exosomes derived from bone marrow stromal cells ( BMSCs) in the bone marrow supernatants of patients with acute myeloid leukemia (AML) and their impact on the prognosis of AML patients . Methods Bone marrow supernatant samples were col- lected from three AML patients and three healthy donors . Exosomes were isolated using a commercial kit , identif- ying the morphology and marker expression , and subjected to miRNA sequencing to determine differentially ex- pressed miRNAs (DE-miRNAs) . The DE-miRNAs were then intersected with the exosomal miRNA expression pro- files of primary AML cells (GSE64029) to exclude AML cell — derived signals and to identify BMSC-derived DE - miRNAs . Subsequently , candidate miRNAs were identified through Cox regression and Lasso regression analyses based on data from The Cancer Genome Atlas (TCGA) . A prognostic risk model for AML was constructed , and pa- tients were stratified into high-risk and low-risk groups according to the median risk score . The prognostic value and clinical relevance of the model were further validated . Finally , the target genes of the candidate miRNAs were pre- dicted , followed by pathway enrichment analysis , construction of key regulatory networks , and correlation analysis between the expression levels of key miRNAs and their corresponding target genes . Results Isolated exosomes ex- hibited a typical cup-shaped morphology with intact structures with particle size of 30 - 150 nm , and expressed exo- somal markers CD63 , ALIX , and TSG101 . miRNA sequencing identified 103 DE-miRNAs in AML patients com- pared with healthy donors; after intersection with the GSE64029 dataset , 83 BMSC-derived DE-miRNAs were re- tained . Among these , five candidate miRNAs ( miR-25-3p , miR-532-5p , miR-194-5p , miR-10a-5p , and miR- 20a-5p) were used to construct the prognostic model . Kaplan — Meier survival analysis demonstrated significantly longer overall survival in the low-risk group compared with the high-risk group ( P < 0. 05) . The areas under the ROC curve for the training/validation cohorts were 0. 80/0. 74 , 0. 80/0. 78 , and 0. 79/0. 64 at 1 , 2 , and 3 years , respectively . The prognostic model was significantly associated with risk stratification , patient age , and FAB classi- fication (P < 0. 05) . KEGG pathway enrichment revealed that target genes of the candidate miRNAs were closely linked to cancer-related signaling pathways , including hepatocellular carcinoma , breast cancer , and non-small cell lung cancer. Correlation analysis indicated that the candidate miRNAs were significantly associated with key genes such as HIF1A , CREB1 , PIK3CA , IGF1R , PIK3R1 , TIAM1 , CRK , and PTEN (P < 0. 05) . Conclusion AML patients exhibit distinct miRNA expression profiles in BMSC-derived exosomes . A five-miRNA signature ( miR-25 - 3p , miR-532-5p , miR-194-5p , miR-10a-5p , and miR-20a-5p) demonstrates robust prognostic performance , sup- porting its potential clinical utility in risk stratification and outcome prediction for AML.

Comparison between ultrafiltration and dextran gel method in the purification ofTfn/PCL micelles

Yu Lingbo1,2, Zhang Yadong2,3, Xu Rui1,2, Sun Yuyu2, Wang Huiyun2, Yang Jinjin1, Cui Yanan2

DOI: 专辑：工程科技Ⅰ辑;医药卫生科技

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abstract:
By using purification efficiency and micelle purity as indicators, the effect of ultrafiltration and dextran gel method for purifying transferrin/polycaprolactone (Tfn/PCL) micelles was compared. Methods Coumarin-6 (C6) was used as a fluorescent probe and was loaded into HOOC-PEG-PCL to form PCL micelles by the film-dispersion method. Tfn was then conjugated to the surface of PCL micelles via an amidation reaction, resulting in two types of micelles: Tfn/PCLH and Tfn/PCLL. The pharmaceutical properties of the two types of micelles were characterized. The micelles were then purified through ultrafiltration method and dextran gel method respectively, and the efficiency of the two methods, along with the purity of the final micelles, was compared. The density of Tfn on the surface of PCL micelles was also calculated. Results The hydrated diameter of PCL micelles was approximately 73 nm, and the C6 loading efficiency was around 0.046%. The size increased to 134 nm and 158 nm for Tfn/PCLL and Tfn/PCLH, respectively. The micelle population was monodisperse. The purification results showed that, for the ultrafiltration method, after two and one rounds of purification, the Tfn/C6 ratio stabilized at 23.6 and 3.4 for Tfn/PCLH and Tfn/PCLL, respectively. For the dextran gel filtration method, the Tfn/C6 ratio reached 23.7 for the Tfn/PCLH group after two rounds of purification. However, for the Tfn/PCLL group, the Tfn/C6 ratio increased during four rounds of dextran gel purification, and a significant difference (P = 0.0424) was observed between the first and last filtrations. The density ofTfn in the final micelles were calculated. For the ultrafiltration method, the Tfn density of Tfn/PCLH and Tfn/PCLL were 94.9% and 13.8%, respectively. For the dextran gel filtration method, the density of the two micelles were 95.6% and 14.4%, respectively. For Tfn/PCLL group, the density results revealing a statistically significant difference (P=0.0002). Conclusion The purification efficiency of the two methods is comparable. However, the purity of the final micelles shows a significant difference, with the dextran gel filtration method resulting in higher purity, particularly for the Tfn/PCLL micelles.

The role of functional near-infrared spectroscopy in predicting postoperative delirium in elderly patients undergoing perioperative joint replacement surgery

Wu Jianxiao1, Zhang Muchun1, Guo Jingyi1, Yang Lizhuang2, Hu Xianwen1

DOI: 专辑：医药卫生科技

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abstract:
To explore the role of neuroimaging features monitored by functional near-infrared spectroscopy (fNIRS) in postoperative delirium (POD) in elderly patients undergoing joint replacement during perioperative period, and to provide a basis for early clinical prediction. Methods A total of 105 elderly patients who underwent joint replacement under general anesthesia were included. The Mini-Mental State Examination (MMSE) scale was used to evaluate the patient's cognition one day before the operation. Before the start of the surgery, fNIRS was used to monitor the changes of cerebral blood oxygen saturation when the patient performed the task state. The 3-minute delirium diagnostic scale (3D-CAM scale) was used to evaluate the occurrence of POD at 24, 48 and 72 h after operation. Brain network analysis was performed and Logistic regression analysis was used to explore the relationship between fNIRS monitoring data and POD in elderly patients undergoing joint replacement surgery during preoperative task state. The receiver operating characteristic curve (ROC curve) was constructed to evaluate the diagnostic efficacy, and the Hosmer-Lemeshow goodness-of-fit test was used to test the goodness of fit of the model. Results Among 105 patients, 100 cases were effectively analyzed, of which 20 cases (20%) had POD. Brain network analysis showed that the r value of functional connectivity correlation coefficient in POD group (0.069±0.118) was lower than that in non-POD group (0.073±0.084). The low channel connectivity of right primary somatosensory cortex-right primary motor cortex (RS1-RM1) and left anterior pole-right Broca's triangle (LFP-RBA44) was an important factor affecting the occurrence of POD (P < 0.05). Based on this result, the area under the ROC curve was 0.797 and 0.784, respectively. The results of Hosmer-Lemeshow goodness-of-fit test showed that the model fitted well (all P>0.5). Conclusion The neuroimaging features extracted from the cerebral oxygen saturation data monitored by fNIRS are significantly correlated with the risk of POD in elderly patients undergoing joint replacement during perioperative period. Among them, the low connectivity of preoperative RS1-RM1 and LFP-RBA44 brain network channels is an important influencing factor of POD occurrence. Predicting the occurrence of POD based on fNIRS is conducive to the early intervention and risk reduction of perioperative complications, improving medical quality and promoting precision medical practice.

Analysis of the changes in intestinal microbiota of patients with moderate to severe acne based on 16S rRNA high-throughput sequencing technology

Jiang Shichao, Wang Xiaomeng, Chen Zheng, Qiao Song, Yang Fan, Guo Birong

DOI: 专辑：医药卫生科技

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Effects of hypoxia at different concentrations on the migration capacity of oligodendrocyte progenitor cells

Wang Qian1,2, Wang Zhaoyan2, Luan Zuo2, Yuan Yuhua1

DOI: 专辑：基础科学;医药卫生科技

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abstract:
To explore the effects of hypoxia on the migration ability of human oligodendrocyte precursor cells (hOPCs) and its regulatory mechanisms. Methods Based on the variations in oxygen concentration within the culture system, three experimental groups were set up: the 21% O₂ group (normoxic control group), the 5% O₂ group, and the 2% O₂ group. The migration ability of hOPCs under normoxia (21% O₂), 5% O₂, and 2% O₂ conditions was detected through the Transwell migration assay. RT-qPCR, transcriptome sequencing, and flow cytometry were used to detect the expression changes of genes and proteins such as hypoxia-inducible factor 1 alpha (HIF-1α) and Chemokine (C-X-C Motif) Receptor 4 (CXCR4). Bioinformatics analysis was combined to analyze the KEGG pathways related to migration, so as to explore the effects of different oxygen concentrations on the migration ability of hOPCs and their possible mechanisms. Results Hypoxia treatments at concentrations of 5% O₂ and 2% O₂ could both promote the in vitro migration of hOPCs, and the promoting effect of migration was more significant at the 2% O₂ concentration (P<0.001). After hypoxia treatment, the mRNA expression levels of HIF-1α, CXCR4, etc. in hOPCs significantly increased (P<0.001). Compared with the 5% O₂ concentration, the expression of CXCR4 in cells was higher at the 2% O₂ concentration (P<0.000 1). Flow cytometry analysis detection showed that the expression of CXCR4 increased significantly after hypoxia treatment (P<0.01), and with the decrease of oxygen concentration, its expression level further increased (P<0.000 1). Ordinary transcriptome sequencing analysis indicated that hypoxia treatment could activate the PI3K-Akt signaling pathway and the Axon guidance pathway. Conclusion In conclusion, hypoxia treatment can enhance the in vitro migration ability of hOPCs, and this effect is negatively correlated with the oxygen concentration. Its mechanism may be related to the up-regulation of the expression of genes such as HIF-1α and CXCR4, and the activation of the migration related signaling pathway including PI3K-Akt signaling pathway and Axon guidance pathway.

Clinical analysis of assisted reproductive technology assisted pregnancy outcome in female patients with thyroid cancer after surgery

Yao Xiang1,2,3 ，Xu Wenjuan1,2,3 ，Wang Jianye1,2,3 ，Gao Qun4 ，Zhao Gang5 ，Zhou Ping1,2,3

DOI: 专辑：医药卫生科技

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abstract:
To evaluate the pregnancy outcomes of assisted reproductive technology (ART) in women with a history of thyroid cancer who retained fertility intentions after completing cancer treatment. Methods A retrospective analysis was performed on 61 patients with a history of thyroid cancer who underwent in vitro fertilization/intracytoplasmic sperm microinjection and embryo transfer (IVF/ICSI-ET). These patients were included as the case group. A total of 122 non-cancer patients who received ART during the same period were selected as the control group using 1:2 matching based on age and oocyte retrieval time. Baseline characteristics, outcomes of the first ART cycle, and cumulative pregnancy outcomes were compared between the two groups. Results There was no significant difference in the basic data, the total amount of gonadotropin (Gn) and the days of use between the case group and the control group (P＞0.05). However, the case group had significantly fewer retrieved oocytes, mature oocytes (MII), lower fertilization and cleavage rates, and fewer transferable and high-quality embryos, as well as fewer embryos transferred during the first cycle (P < 0.05). However, there was no significant difference in the rate of first embryo implantation and first clinical pregnancy between the two groups (P > 0.05). In the analysis of cumulative outcomes, the two groups did not show statistically significant differences in the cumulative pregnancy rate, clinical pregnancy rate per transfer cycle, number of egg retrieval cycles required to achieve each live birth, number of transfer cycles, and number of embryos used (P > 0.05). However, the cumulative live birth rate was significantly lower in the case group compared to the control group (P = 0.005). Conclusion After treatment for thyroid cancer, when ART is used to help pregnant women, the pregnancy outcome is comparable to that of women without tumors. Individualized reproductive management and timely fertility preservation strategies are recommended to optimize reproductive outcomes in this population.

Correlation analysis of inflammatory markers (NLR/PLR/SII) with the severity of intrauterine adhesions

Wang Ying1,2,3 ，Xu Xuan1,2,3 ，Zhang Longyu1,2,3 ，Wu Rong1,2,3 ，Hu Jingjing1,2,3 ，Yang Wenjuan1,2,3 ，Wu Xiao1,2,3 ，Wei Zhaolian1,2,3

DOI: 专辑：医药卫生科技

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Expression of SLC7A11 in esophageal squamous cell carcinoma tissues and its preliminary study on mediating tumor cell metabolism

Zhang Huakun1, Sun Mengfei2, Sun Qi2, Zhou Ziru1, Yu Jie3, Chen Yunzhao3, Cui Xiaobin

DOI: 专辑：医药卫生科技

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abstract:
To investigate the relationship between solute carrier family 7 member 11 (SLC7A11) expression in esophageal squamous cell carcinoma (ESCC) and clinical prognosis, and to determine its effects on ESCC cell growth, migration, and other biological activities. Methods SLC7A11 protein expression was measured in 310 ESCC tissues and 259 adjacent normal tissues using immunohistochemistry to statistically assess the association of SLC7A11 with clinicopathologic characteristics and prognosis in ESCC patients. The expression of SLC7A11 in ESCC cell lines was suppressed through siRNA-mediated knockdown. The specific effects of SLC7A11 knockdown onproliferation and migration were evaluated using CCK-8, clonogenic assay, and Transwell assays. Adenosine triphosphate (ATP), lactic acid and pyruvate assays were used to measure ESCC metabolism. Results SLC7A11 protein expression was localized predominantly in the cytoplasm of ESCC tissues. Significantly higher SLC7A11 expression levels were observed in ESCC tissues compared to adjacent normal tissues (P<0.001). High SLC7A11 expression was associated with poorer differentiation in patients (P<0.01). Kaplan-Meier survival analysis demonstrated significantly shorter overall survival in patients with high SLC7A11 expression compared to those with low expression (P<0.05). CCK-8 and colony formation assays demonstrated that the knockdown of SLC7A11 expression significantly suppressed the proliferative capacity of tumor cells (P<0.001). Furthermore, Transwell assays revealed a marked decline in tumor cell migration capacity following SLC7A11 suppression (P<0.001). Critically, SLC7A11 knockdown also reduced intracellular levels of ATP, lactate, and pyruvate, demonstrating that SLC7A11 modulated metabolic activity in ESCC cells（P<0.001）. Conclusion The expression level of SLC7A11 is relatively high in ESCC and is strongly associated with poor prognosis. Silencing SLC7A11 significantly inhibits esophageal cancer cell growth and migration. SLC7A11 has the ability to regulate glucose, lactic acid and ATP metabolism levels in ESCC, thereby affecting the metabolic microenvironment of ESCC.

The regulatory mechanism ofTLR4 on the inflammatory response in mice with gastric ulcers through autophagy and oxidative stress

Du Jinxuan 1, Feiluore Dilixiati 1, Xuan Qiuyun 2

DOI: 专辑：医药卫生科技

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abstract:
To investigate the effects of Toll-like receptor 4 (TLR4) inhibition on autophagy and oxidative stress, as well as its regulatory role and mechanism in the inflammatory response in a mouse model of gastric ulcer. Methods Sixty adult male Kunming mice were equally divided into five groups: control group, model group, model+TLR4-IN-C34 group, model+TLR4-IN-C34+3-MA group, and model+TLR4-IN-C34+H₂O₂ group. Except for the control group, all groups were administered 40 mg/kg indomethacin via gavage. Treatment groups received injections every three days, and all groups were treated for 30 days. Mice were euthanized by cervical dislocation, and gastric tissues were collected. Gastric ulcer scores were assessed, and pathological changes were evaluated via HE staining and scoring. Serum levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), advanced oxidation protein products (AOPP), and prostaglandin E2 (PGE2), as well as gastric tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH), were measured using ELISA. Western blot analysis was performed to detect the expression of TLR4, microtubule-associated protein 1 light chain 3-I (LC3-I), microtubule-associated protein 1 light chain 3-II (LC3-II), autophagy-related protein 5 (Atg5), Beclin-1, nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H quinone dehydrogenase 1 (NQO1) in gastric tissues. Immunofluorescence staining was used to assess LC3-II fluorescence intensity in gastric tissues. Results Compared with the control group, the model group exhibited upregulation of ulcer scores, HE staining scores, TLR4, IL-1β, IL-6, TNF-α, and AOPP levels, and downregulation of LC3-II fluorescence intensity, PGE2 levels, Atg5, Beclin-1, nuclear Nrf2, HO-1, NQO1 levels, and the LC3-II/I ratio (all P < 0.05). Compared with the model group, the model+TLR4-IN-C34 group showed downregulation of ulcer scores, HE staining scores, TLR4,IL-1β, IL-6, TNF-α, and AOPP levels, and upregulation of LC3-II fluorescence intensity, PGE2 levels, Atg5, Beclin-1, nuclear Nrf2, HO-1, NQO1 levels, and the LC3-II/I ratio (all P < 0.05). Compared with the model+TLR4-IN-C34 group, the model+TLR4-IN-C34+3-MA group exhibited upregulation of ulcer scores, HE staining scores, IL-1β, IL-6, TNF-α, and AOPP levels, and downregulation of LC3-II fluorescence intensity, PGE2 levels, Atg5, Beclin-1, and the LC3-II/I ratio (all P < 0.05). Compared with the model+TLR4-IN-C34 group, the model+TLR4-IN-C34+H2O2 group showed upregulation of ulcer scores, HE staining scores, IL-1β, IL-6, TNF-α, and AOPP levels, and downregulation of PGE2 levels and nuclear Nrf2, HO-1, and NQO1 levels (all P < 0.05). Conclusion Inhibition of TLR4 ameliorates gastric ulcer symptoms and suppresses the inflammatory response in mice by upregulating autophagy and reducing oxidative stress (all P < 0.05).

The role of S100A2 in the progression of colorectal cancer

Huo Yishan 1, Duan Xiangbing 1, Xu Xiaohui 1, Li Tao 2, Ma Xiumin 1

DOI: 专辑：医药卫生科技

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abstract:
To investigate the role of calcium-binding protein S100A2 in colorectal cancer (CRC) progression and its association with fructose metabolism in CRC cells. Methods Differential expression of S100A2 between CRC patients and healthy individuals was analyzed using the GEPIA2 tumor database. Western blot and qRT-PCR were performed to compare S100A2 expression levels in CRC cell lines (HCT116, SW480, Caco-2) and normal human colonic epithelial cells (NCM460). Immunohistochemical staining was conducted to assess S100A2 expression in CRC tissues and adjacent non-tumor tissues. S100A2-knockdown stable CRC cell lines and negative control cell lines were established via lentiviral transduction. Functional assays, including CCK-8, wound healing and Transwell experiments were utilized to evaluate the effects of S100A2 downregulation on CRC cell proliferation, migration, and invasion. Western blot and immunofluorescence staining were employed to analyze the impact of S100A2 knockdown on the expression levels of fructose transporter 5 (GLUT5) and ketohexokinase (KHK). Intracellular fructose concentration was measured using a fructose assay kit. A nude mouse CRC xenograft model was established using S100A2-knockdown HCT116 cell lines to investigate the role of S100A2 in tumor proliferation in vivo. Tumor tissues from the xenografted mice were analyzed by Western blot and immunofluorescence staining to evaluate the expression levels of GLUT5 and KHK. Results S100A2 expression was significantly elevated in CRC patients compared with healthy individuals. All three CRC cell lines exhibited markedly higher S100A2 expression than normal colonic epithelial cells. S100A2 knockdown significantly inhibited CRC cell proliferation, migration, and invasion capacities. Downregulation of S100A2 suppressed the expression of fructose metabolism-related proteins GLUT5 and KHK, accompanied by reduced cellular fructose uptake. In vivo experiments demonstrated that S100A2 knockdown effectively inhibited tumor growth and decreased GLUT5/KHK expression in xenograft tissues. Conclusion Downregulation of S100A2 inhibits CRC progression by modulating fructose metabolism in CRC cells.

NGR1 modulates mitophagy in human cardiomyocytes via the PINK1/Parkin pathway after hypoxia/reoxygenation

Xiong Xiaoman1, Wu Huan1, Lu Shanglin2, Wang Yong1, Zheng Yuhua1, Xiang Yi1, Zhou Haiyan2, Liu Xingde1

DOI: 专辑：医药卫生科技

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abstract:
To investigate the mechanism by which Notoginsenoside R1 (NGR1) ameliorates hypoxia/reoxygenation (H/R)-induced injury in AC16 human cardiomyocyte cell lines through the regulation of mitophagy. Methods Common genes linked to hypoxia/reoxygenation injury and mitophagy were identified by intersecting data from GeneCards and MitoCarta databases. AC16 cell viability was assessed via CCK-8 assay under varying NGR1 concentrations (0, 6.25, 12.5, 25, 50, 100, 200, 300, 400, 500 μmol/L). AC16 cells were divided into the following groups: control group (Control), model group (H/R), and treatment groups (H/R + NGR1 at 100, 200, and 300 μmol/L). Mitochondrial membrane potential (ΔΨm) was measured using 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) staining. Transcriptional levels of mitophagy-related genes (Parkin, Pink1, P62) were quantified by reverse transcription-quantitative PCR (RT-qPCR). Protein expression of mitophagy-related markers (Parkin, Pink1, P62, and LC3II) was evaluated via Western blot analysis. Mitochondrial ultrastructure was visualized by transmission electron microscopy (TEM). Results Compared to the control group, cell viability in the H/R group significantly decreased (P < 0.01). Treatment with NGR1 at concentrations above 100 μmol/L significantly enhanced the cell viability of AC16 cells compared to the H/R group (P < 0.01). H/R induced a significant decrease in mitochondrial membrane potential (P < 0.01), which was restored by NGR1 treatment (P<0.01). The mRNA levels of Parkin, PINK1, and P62 in the H/R group were upregulated compared to the control group (P<0.05), while NGR1 intervention downregulated their expression (P<0.05). Protein expression levels of Parkin, Pink1, and LC3II in the H/R group significantly increased, while P62 expression decreased compared to the control group (P<0.01). In contrast, different doses of NGR1 treatment significantly reduced the expression of Parkin, Pink1, and LC3II while increasing P62 expression (P<0.05). TEM revealed that the mitochondrial structure in the H/R group was severely disrupted, with fragmented and disorganized cristae, which was alleviated by NGR1. Conclusion NGR1 ameliorates H/R-induced AC16 cell injury, and its mechanism may be associated with modulating the PINK1/Parkin pathway to suppress excessive mitophagy.

Analysis of the incidence and mortality trends of type 2 diabetic nephropathy in China from 1990 to 2021

Dou Xuewei, Cui Wenfei, Niu Ling, Yin Binglei, Wang Jinjin

DOI: 专辑：医药卫生科技

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Analysis of follicular helper T cell percentage and expression levels of functionally related cytokines in a mouse model of incomplete embryo implantation disorders

Wang Peng1 ，Gong Xiaoyun1 ，Zhang Manli1 ，Zhang Yunian1 ，La Xiaolin1,2,3,4

DOI: 专辑：医药卫生科技

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abstract:
To detect the proportion of splenic follicular helper T (Tfh) cells and their functionally related cytokine expression levels in the incomplete embryo implantation disorder (EID) model mice, and to explore the immunological mechanism of Tfh in infertility caused by embryo implantation disorder. Methods Sixteen female Kunming mice were randomly divided into two groups, with eight mice in each group. On day 4 of pregnancy, an incomplete EID mouse model was established by oral gavage of mifepristone suspension, while an equal volume of saline was administered to the control group. On day 8 of pregnancy, the mice were euthanized. Flow cytometry was used to detect the levels of Tfh cells in the spleen lymphocytes of both incomplete EID mice and normal control mice. qRT-PCR was performed to measure the mRNA levels of B-cell lymphoma 6 (Bcl-6) and chemokine receptor 5 (CXCR5) in the spleen lymphocytes of both groups. Western blotting was employed to assess the protein expression levels of Bcl-6 and CXCR5 in the spleen lymphocytes of both groups. Serum levels of interleukin-4 (IL-4), IL-6, and IL-21 were measured by ELISA. Immunohistochemistry (IHC) was used to observe the expression levels of progesterone receptor (PR), Bcl-6, and CXCR5 proteins in the uterine endometrial tissue of mice in both groups. Results Incomplete-type EID mice had a reduced number of embryo implantation points and reduced endometrial PR receptor expression. Flow assay results showed that the proportion of CD4+CXCR5+Tfh cells in splenic lymphocytes of incomplete-type EID mice was significantly higher than that of normal controls (P<0.05).Compared with the normal control group, Bcl-6 and CXCR5 mRNA levels and protein levels were elevated in splenic lymphocytes of incomplete EID mice, with statistically significant differences(P<0.05); serum IL-4, IL-6, and IL-21 levels were elevated in incomplete EID mice, and Bcl-6 and CXCR5 proteins in the endometrium were significantly elevated (P<0.05). Conclusion The increase of Tfh cells and their associated cytokines Bcl-6 and CXCR5 is associated with the development of incomplete EID, and may be involved in the development of female immune infertility.

Research progress of urea-containing PET tracers targeting prostate specific membrane antigen1

Zhu Hong1,2, Wang Hui2, Si Hongwei2, Zhang Dan2, Chen Dengyun2, Dai Pengfei1,2

DOI: 专辑：医药卫生科技

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Astragalus polysaccharide regulates exosomes derived from breast cancer cells and its effects on macrophage polarization and antitumor effects

Guan Chenjuan1 , Xie Caixia2 , Zheng Xiaojiao2 , Bao Nana2 , Wang Lu2 , Bai Wenhui2 , Qiao Shu2 , Zhang Haonan3

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.003

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abstract:
To investigate the effects and mechanisms of Astragalus Polysacharin (APS) on the prolifer- ation and metastasis of breast cancer cells by regulating miR-107 and miR-346-mediated macrophage polarization in breast cancer-derived exosomes . Methods Forty 8-week-old female BALB/c mice were selected and breast cancer xenograft models and 4T1 transplanted tumor models were established . The mice were divided into the control group and the APS group . The APS group mice received daily intragastric administration of APS for 25 days , while the control group mice were given the same amount of normal saline . After all treatments were completed , the mice were euthanized , and tumor tissues were isolated . Western blot and flow cytometry were used to detect the expres- sions of proliferating cell nuclear antigen (PCNA) , Ki-67 , CD206 , CD163 , inducible nitric-oxide synthase (iN- OS) , and CD86 . The apoptosis of single-cell suspensions in tumor tissues was analyzed . Human breast cancer cell line MDA-MB-231 was cultured and stimulated with APS , and exosomes from the cell culture medium were collect- ed . The proliferation , migration , and invasion of cells were detected by CCK-8 assay , scratch assay , permeability chamber cell invasion assay , and qRT-PCR . Differentially expressed genes were screened by bioinformatics . Re- sults By measuring the expressions of molecules related to breast cancer cell proliferation and metastasis , it was shown that APS treatment reduced the expressions of proliferation-related proteins (PCNA and Ki-67) and metasta- sis-related proteins (Vimentin) in MDA-MB-231 xenograft tumor tissues; and the polarization of tumor-associated macrophages was observed . APS treatment of 4T1 transplanted tumor tissues could reduce the number of M2 macro- phages and increase the number of M1 macrophages , resulting in a decrease in the ratio of M2/M1 macrophages and an increase in cell apoptosis in 4T1 transplanted tumor tissues . The expressions of related proteins iNOS and CD86 increased , and CD206 and CD163 decreased . After APS treatment , the exosomes produced by MDA-MB- 231 reduced the polarization of M2 macrophages and affected the expressions of miR-107 and miR-346 . Conclusion APS inhibits the polarization of M2 macrophages by regulating the expression of miR-107 or miR-346 in breast cancer cell-derived exosomes , ultimately inhibiting the proliferation and metastasis of breast cancer cells .

Experimental study on the improvement of non-alcoholic fatty liver disease by regulating G0S2 and ATGL expression with polydatin

Sheng Luguang1 , 2 , Liu Dandan3 , Liu Weibin3 , Lei Tao3 , Chen Qingguang4 , Lu Hao4 , Xu Bilin1 , 2 , 3

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.010

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abstract:
To investigate the effects of polydatin on a high-fat diet-induced non-alcoholic fatty liver dis- ease (NAFLD) mouse model and hepatoma G2 (HepG2) cell model , and to reveal its potential molecular mecha- nisms . Methods Thirty 6-week-old male SPF C57BL/6J mice were randomly divided into a normal diet group and a high-fat diet group . After the NAFLD mouse model was established in the high-fat diet group , they were further divided into a model group and a polydatin treatment group . The polydatin treatment group was administered poly- datin by gavage at a dose of 250 mg/(kg ·d) for 10 weeks , during which body weight was monitored and oral glu- cose and insulin tolerance tests were performed . At the end of the experiment , a series of tests to evaluate the effects of polydatin on mouse liver weight , blood lipids , liver lipid accumulation , and liver injury markers were per- formed . The expression of G0 /G1 switch gene 2(G0S2) and adipose triglyceride lipase (ATGL) was measured by qRT-PCR and Western blot , and gene expression was further verified using immunohistochemical staining. The effects of polydatin on HepG2 cell activity was assessed by CCK-8 assay , lipid accumulation was observed by oil red O staining , and the expression of G0S2 and ATGL was detected by qRT-PCR and Western blot. Results Polydatin significantly reduced the body weight , liver weight , and serum and liver tissue levels of aspartate aminotransferase (AST) , alanine aminotransferase (ALT) , triglyceride (TG) , and total cholesterol (TC) in mice (P < 0. 05) , al- leviated pathological liver damage , decreased G0S2 expression (P < 0. 05) , and increased ATGL expression (P < 0. 05) . At the cellular level , polydatin reduced lipid droplet accumulation , improved lipid metabolism , decreased G0S2 expression ( P < 0. 05 ) , and increased ATGL expression ( P < 0. 05 ) . Even in cells with knockdown of G0S2 , polydatin still promoted fat decomposition (P < 0. 01) . Conclusion Polydatin promotes hepatic fat break- down by regulating the expression of G0S2 and ATGL , helping to alleviate metabolic disorders and liver damage in the NAFLD mouse model caused by a high-fat diet , offering a new strategy for treating NAFLD .

Correlation between small intestinal bacterial overgrowth and cognitive function in peritoneal dialysis patients

Xu Hongting , Wang Liangjing , Li Dashan , Qi Xiangming

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.021

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abstract:
To explore the correlation between small intestinal bacterial overgrowth (SIBO) and cogni- tive impairment in patients undergoing peritoneal dialysis (PD) . Methods 60 PD patients and 46 non-dialysis pa- tients with end-stage renal disease (ESRD) were included in this study . SIBO was detected by lactulose hydrogen methane breath test (LHMBT) . The cognitive function levels of the subjects were evaluated using the Montreal cog- nitive assessment (MoCA) and mini-mental state examination (MMSE) . The emotional states of the patients were assessed by self-rating anxiety scale (SAS) and self-rating depression scale (SDS) . The gastrointestinal symptoms were evaluated using gastrointestinal symptom rating scale (GSRS) . According to the results of LHMBT , the PD patients were further divided into two subgroups : SIBO-positive and SIBO-negative . The general conditions , labora- tory data , and scores of each scale were compared between the two groups . Furthermore , according to the MoCA scores , the PD patients were divided into two groups : those with normal cognitive function and those with cognitive dysfunction . The positive rates of SIBO between the two groups were compared . Binary Logistic stepwise regression was used to explore whether SIBO was an independent risk factor for cognitive impairment in PD patients . At the same time , other independent influencing factors for cognitive impairment in PD patients were analyzed . Results The positive rate of SIBO in PD patients was 40. 00% . Among them , the positive rate of SIBO in the group with normal cognitive function during peritoneal dialysis was 27. 27% , and the positive rate of SIBO in the group with cognitive dysfunction during peritoneal dialysis was 55 . 56% . There was a statistically significant difference in the positive rate of SIBO between the two groups (P = 0. 026) . Further analysis by multivariate Logistic stepwise re- gression showed that in addition to age (OR = 1 . 118 , 95% CI 1 . 007 - 1 . 242 , P = 0. 037) , educational attainment (OR = 0. 655 , 95% CI 0. 442 - 0. 972 , P = 0. 036) , and hemoglobin( OR = 0. 946 , 95% CI 0. 895 - 0. 998 , P = 0. 044) , SIBO (OR = 7 . 613 , 95% CI 1 . 160 - 49. 979 , P = 0. 034) was also an independent risk factor for cognitive impairment in PD patients . Conclusion The incidence of SIBO in PD patients is relatively high and is associated with multiple factors , among which SIBO may be closely related to cognitive dysfunction in PD patients .

Establishment of the EMT model of CoCl2 -induced NRK-52E cells

Ni Lei, Sun Qingqing,Cheng Jiangrui,Wei Wei, Wang Chun

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.014

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abstract:
To establish an in vitro cell model of Cobalt dichloride (CoCl2)-induced epithelial-mesenchymal transition (EMT) in rat renal tubular epithelial cells (NRK-52E). Methods NRK-52E cells were cultured in vitro and randomly divided into a blank control group (NC group) and a CoCl2 treatment group. The CoCl2 treatment group underwent 1, 2, 3, and 4 cycles of treatment, with each cycle consisting of CoCl2 treatment for 9 h followed by recovery in CoCl2-free medium for 3 h. The optimal concentration and time of CoCl2-induced EMT were screened using the CCK-8 assay. Morphological changes in cells were observed using light microscopy and phalloidin staining. The expression levels of EMT marker proteins were detected by Western blot and immunofluorescence. Results Compared with the NC group, stimulation by 100 μmol/L CoCl2 for 48 h significantly induced apoptosis (P<0.01), meeting the requirements for subsequent experiments. Western blot results showed that the expression of hypoxia-inducible factor-1α (HIF-1α) and α-smooth muscle actin (α-SMA) significantly increased in the 3-cycle group treated with 100 μmol/L CoCl2 for 9 h followed by recovery for 3 h (P<0.001), indicating the most pronounced fibrotic response. Observations under light microscopy and rhodamine-labeled phalloidin staining revealed that the morphological changes and cytoskeletal rearrangement of NRK-52E cells were most significant in the 3-cycle group treated with 100 μmol/L CoCl2 for 9 h followed by recovery for 3 h, demonstrating the best model stability. Immunofluorescence results showed that compared with the NC group, the fluorescence intensity of the fibrous matrix protein Collagen I significantly increased in the 3-cycle group treated with 100 μmol/L CoCl2 for 9 h followed by recovery for 3 h (P<0.001). Conclusion The protocol involves treating NRK-52E cells with 100 μmol/L CoCl₂ for 9 h, following 3 h of recovery in CoCl₂-free medium. Repeating this cycle three times can establish an in vitro EMT model.

Screening and validation of chemoresistance marker in lung adenocarcinoma based on gene expression profile

Wei Handong1 , Chen Shuxing2 , Liu Linting2 , Jing Zihan3 , Yang Yiting1 , Song Qiong1 , Wang Wenchu1 , Zou Chunlin1 , Wang Lihui 1

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.006

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abstract:
To discover molecular markers associated with lung adenocarcinoma diagnosis/prognosis and drug resistance through screening of differentially expressed genes based on published chip data in gene expression databases using bioinformatics methods . Methods Comprehensive analysis was performed in available mRNA mi- croarray datasets including lung adenocarcinoma tissues dataset GSE32863 and lung adenocarcinoma taxane-platin resistance dataset GSE77209 from the gene expression omnibus (GEO) database . Gene ontology enrichment analy- sis , gene pathway enrichment analysis and protein interaction network analysis were performed based on significant- ly correlated genes . The expression level of genes was validated in the cancer genome atlas (TCGA) dataset. Sur- vival differences were assessed by the log-rank test in TCGA lung adenocarcinoma dataset. Based on the publica- tions genomics of drug sensitivity in cancer (GDSC) database in CellMiner cross database (CellMiner CDB) , Pear- son correlation analysis was used to analyze the correlation between differentially expressed genes and the half-maxi- mal inhibitory concentration (IC50 ) of anticancer drugs . Results There were a total of 77 genes which had a dif- ferent expression in resistance lung adenocarcinoma cells and lung adenocarcinoma cancer tissues . The functional enrichment analysis showed that these co-different expression genes were mainly enriched in microtubule , extracel- lular exosome , cell cycle and signaling by nuclear receptors . Protein-protein interactions (PPI) network screened 6 most connected genes as molecular complex (MCODE) . Among the MCODE , overexpressed ubiquitin conjugating enzyme E2 T (UBE2T) , kinesin family member 20A(KIF20A) , PCNA clamp associated factor (KIAA0101) , pi- tuitary tumor-transforming gene 1 ( PTTG1) and NIMA related kinase 2 ( NEK2) were associated with poor out- comes . Survival analysis results showed that these five genes were upregulated in lung adenocarcinoma tissues and drug-resistant cells and were significantly associated with poor prognosis in lung adenocarcinoma patients . Drug sen- sitivity analysis results suggested that high expression of PTTG1 and UBE2T was significantly associated with sensi-tivity to multiple anticancer drugs , including paclitaxel and docetaxel . RT-PCR validation showed that PTTG1 and UBE2T were highly expressed in docetaxel-resistant cells A549-TXR and H358-TXR. Conclusion PTTG1 and UBE2T holds the potential to be chemoresistance markers in lung adenocarcinoma.

Porphyromonas gingivalis promotes esophageal squamous cell carcinoma progression and enhances cetuximab resistance via EGFR/GSK3 βpathway induced EMT

Lang Yaowu , Chen Pan , Zhang Zichao , Liu Ke , Shi Linlin , Gao Shegan

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.017

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abstract:
To investigate the regulatory role of Porphyromonas gingivalis (Pg) infection on the EGFR/ GSK3 βsignaling axis , and its impact on epithelial-mesenchymal transition (EMT) and cetuximab (Ctx) resistance in esophageal squamous cell carcinoma (ESCC) . Methods Single cell RNA sequencing was employed to perform differential analysis of cellular subpopulations , identifying differentially expressed genes in ESCC tissues infected and non-infected with Pg. IHC was conducted to assess the expression of Pg and epidermal growth factor receptor ( EGFR) in ESCC tissues . Western blot , RT-PCR , and IF staining were performed to evaluate EGFR expression in Pg infected ESCC cell lines KYSE70 and TE1 . ESCC cells were treated with Pg and EGFR inhibitor Ctx , and di- vided into four groups : control (NC) group , Pg group , Ctx group , Pg + Ctx group . Cell proliferation , migration and invasion abilities were evaluated using CCK-8 , plate cloning , wound healing and Transwell assay . Western blot analysis was performed to detect the expression of EMT and EGFR/GSK3 βsignaling pathway-associated proteins and their phosphorylation levels . Transforming growth factor-β1 ( TGF-β1) was used to induce EMT in ESCC cells , promoting a transition from the epithelial phenotype to mesenchymal-like phenotype . The differential effects of Ctx on these two phenotypic states were subsequently compared . Results Epithelial cells were predominantly enriched in Pg-positive tissues , and Pg infection promoted the upregulation of EGFR expression in ESCC cells . Compared to the NC group , Pg treatment significantly enhanced the proliferation , invasion and migration capabili- ties of ESCC cells , and also increased chemoresistance to Ctx and reduced its antitumor efficacy . Pg induced EMT in ESCC cells via the EGFR/GSK3 βsignaling pathway . Notably , Ctx exhibited markedly weaker inhibitory effects on mesenchymal-like cells compared to epithelial ESCC cells . Conclusion Pg promotes ESCC cells prolif- eration , invasion and migration by regulating EMT through the EGFR/GSK3 βsignaling pathway , and enhances chemoresistance to Ctx .

Study on CTRP3-mediated UCHL1 enhancing SeVGMT reprogramming of CFs to protect cardiac function in MI mice

Song Yanbin1 , Zhang Yunqing2 , Liu Huiyu3 , Chen Junmin1

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.016

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abstract:
To investigate the effects of C1q tumor necrosis factor-related protein 3 (CTRP3)-enhanced Sendai virus (SeV) vector-overexpressing Gata4 , Mef2c , and Tbx5 (SeVGMT) in the treatment of myocardial in- farction (MI) mice and to analyze whether ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) mediates this thera- peutic pathway. Methods The mice were divided into 7 groups ( n = 12) : Sham group , MI group , SeVGMT group , CTRP3-Lv group , UCHL1-sh group , SeVGMT + CTRP3-Lv group , and SeVGMT + CTRP3-Lv + UCHL1-sh group . In the Sham group , only the skin was incised without ligation , while the coronary artery was ligated 2 - 3 mm below the left atrial appendage in mice in other groups . PBS was injected at three points in the myocardial in- farction boundary in the Sham and MI groups 30 minutes after ligation . Mice in other groups were injected with level of METTL14 mRNA was positively correlated with the level of m6A in placental tissue . The results of the CCK-8 experiment showed that compared with the control group , knockdown of METTL14 expression in trophoblast cells significantly reduced the cell proliferation rate , while the proliferation ability of trophoblast cells with overex- pressed METTL14 was enhanced . The results of the scratch test showed that compared with the control group , the relative healing rate of scratches was significantly reduced after METTL14 knockdown , while it increased after the overexpression of METTL14 . The results of the Transwell assay and invasion assay showed that compared with the control group , after knockdown of METTL14 , the number of trophoblast cells passing through the chamber was sig- nificantly reduced , while the number of trophoblast cells with overexpressed METTL14 passing through the chamber increased . Conclusion The total RNA m6A modification level in placental tissue of ePE is lower than that in the normal pregnancy group . The down-regulation of methyltransferase METTL14 is involved in the regulation of the to- tal RNA m6A modification level . The overexpression of METTL14 can enhance the proliferation , migration and in- vasion abilities of trophoblast cells . It provides a new perspective for exploring the pathogenesis of early-onset pre- eclampsia.

Epidermal endoplasmic reticulum stress induced by UVB radiation and therapeutic interventions

Lin Boyang, Qiang Lei

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.025

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Expression of m6A methyltransferase METTL14 in trophoblast cells and its effect on the development of early-onset preeclampsia

Tang Xiong , Chen Fan , Xie Siyu , Guo Yafei , He Ye , Zhang Ying

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.015

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abstract:
To explore the role of N6-methyladenosine ( m6A) modification of RNA and Methyltrans- ferase like Protein 14 methyltransferase (METTL14) in the pathogenesis of early-onset preeclampsia (ePE) . Meth- ods Placental tissues of 15 pregnant women with early-onset preeclampsia and 15 normal pregnant women were collected . The level of m6A was determined by colorimetry , and the expression of METTL14 was determined by RT-qPCR , Western blot and immunohistochemistry ( IHC ) experiments . By transfecting siRNA and plasmid , METTL14 levels of trophoblast cells were knocked down and overexpressed , and cell phenotype experiments were carried out in vitro . The effects of METTL14 on the proliferation , migration and invasion of trophoblast cells were investigated by CCK-8 , scratch assay , Transwell assay and invasion assay . Results The level of m6A in placental tissue of ePE was lower than that of normal pregnancy . METTL14 was mainly expressed in the nuclei of trophoblast cells . Compared with normal pregnancy , the expression of METTL14 in placental tissue of ePE decreased , and the level of METTL14 mRNA was positively correlated with the level of m6A in placental tissue . The results of the CCK-8 experiment showed that compared with the control group , knockdown of METTL14 expression in trophoblast cells significantly reduced the cell proliferation rate , while the proliferation ability of trophoblast cells with overex- pressed METTL14 was enhanced . The results of the scratch test showed that compared with the control group , the relative healing rate of scratches was significantly reduced after METTL14 knockdown , while it increased after the overexpression of METTL14 . The results of the Transwell assay and invasion assay showed that compared with the control group , after knockdown of METTL14 , the number of trophoblast cells passing through the chamber was sig- nificantly reduced , while the number of trophoblast cells with overexpressed METTL14 passing through the chamber increased . Conclusion The total RNA m6A modification level in placental tissue of ePE is lower than that in the normal pregnancy group . The down-regulation of methyltransferase METTL14 is involved in the regulation of the to- tal RNA m6A modification level . The overexpression of METTL14 can enhance the proliferation , migration and in- vasion abilities of trophoblast cells . It provides a new perspective for exploring the pathogenesis of early-onset pre- eclampsia.

Expression of COL1A2 in cervical cancer and its relationship with tumor immune infiltration

Zhang Yu1 , 2 , Zhu Xiaoyu1 , 2 , Xu Dianqin1 , 2 , Chen Xiaowei2 , Zhong Mingyan2 , Zhou Xinzhu1 , 2 , Tan Yujie1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.005

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abstract:
To explore the expression of collagen type 1 alpha 2 (COL1A2) in cervical cancer and its correlation with immune infiltration . Methods Bioinformatics techniques were used to analyze the expression of COL1A2 in cervical cancer. Western blot and RT-qPCR were used to detect the expression of COL1A2 in cervical cancer tissues and cell lines . The correlation between the expression of COL1A2 and tumor immune cell infiltration was analyzed by tumor immune estimation resource (TIMER2 . 0) . Gene set enrichment analysis (GSEA) was used to analyze the possible mechanism of COL1A2 in cervical cancer. Jaspar database was used to predict the transcrip- tion factors of COL1A2 . Western blot and RT-qPCR were used to detect the expression of transcription factors in cervical cancer tissues and cell lines . Results The expression of COL1A2 was down-regulated in cervical cancer (P < 0. 05) . The expression of COL1A2 was positively correlated with the levels of macrophages and myeloid den- dritic cells (P < 0. 01) . The proportions of 22 types of immune cells were different in different cervical cancer pa- tients . In addition , compared with the high expression group of COL1A2 , the proportion of M0 macrophages , M2 macrophages and resting memory CD4 + T cells increased in the low expression group of COL1A2 , while the propor- tion of CD8 + T cells , activated memory CD4 + T cells , follicular helper T cells , activated NK cells and activated myeloid dendritic cells decreased (P < 0. 05) . GSEA analysis showed that COL1A2 was related to immune-related signaling pathways , including Notch signaling pathway , interleukin-6/janus kinase/signal transducer and activator of transcription 3 (IL6/JAK/STAT3) , Wnt/β-catenin signaling pathway , etc . (P < 0. 01) . Jaspar database pre- dicted that the transcription factor of COL1A2 was paired box protein 5 (PAX5) , and the expression of PAX5 de- creased in cervical cancer (P < 0. 05) . Conclusion COL1A2 is expected to become a potential diagnostic biomar- ker and immunotherapy target for cervical cancer.

Preparation and in vitro study of baicalin combined with gelatin/chitosan coaxial electrospinning membrane

Fang Hui, Wang Chenbing

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.024

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An association study between ALOX15 gene polymorphisms and non-cardia gastric carcinogenesis

Chu Ning1 , 2 , Dong Wenjie1 , Gao Fang3 , Li Yingze4 , Chen Yaru1 , Zhang Bin5 , Jia Yanbin1

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.012

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abstract:
To explore the association between single nucleotide polymorphism (SNP) in the arachido- nate 15-lipoxygenase (ALOX15) gene and Helicobacter pylori (H. pylori) infection as well as the risk of non-cardi- a gastric cancer in Baotou Han population , and to provide experimental evidence and data support for the screening of susceptible population for non-cardia gastric cancer. Methods A total of 458 cases with non-cardia gastric canc- er and 460 healthy examination people were collected . The 14 C urea breath test (UBT) and enzyme-linked immu- nosorbent assay (ELISA) were used to detect H. pylori infection in the 460 healthy individuals . The genotypes of ALOX15 rs2619112 , rs2619118 , rs2664593 , rs7220870 were detected by polymerase chain reaction-restriction fragment length polymorphism , and the association of SNP with H. pylori infection as well as the risk of non-cardia gastric cancer was statistically analyzed . Results The positive rate of H. pylori infection was 42. 4% . ALOX15 rs2619112 , rs2619118 , rs2664593 , and rs7220870 had no association with H. pylori infection . ALOX15 rs2619112 , rs2664593 , and rs7220870 were not associated with the risk of non-cardia gastric cancer. Compared with the carriers of (CC + CT) genotype , the carriers of rs2619118 TT genotype had an increased onset risk of non-cardia gastric cancer [ OR (95% CI) = 1 . 512 ( 1 . 110 - 2. 060 ) ] . The haplotype ACCC constructed by ALOX15 rs2619112 , rs2619118 , rs2664593 , and rs7220870 could reduce the onset risk of non-cardia gastric cancer . The second-order interaction of ALOX15 rs2619112 and rs2619118 was associated with the risk of non-car- dia gastric cancer ( P < 0. 05) . Conclusion ALOX15 rs2619112 , rs2619118 , rs2664593 , rs7220870 may not play a major role in H. pylori infection . ALOX15 rs2619118 TT genotype is a risk factor for the development of non-cardia gastric cancer. The haplotype ACCC constructed by ALOX15 rs2619112 , rs2619118 , rs2664593 , and rs7220870 reduces the onset risk of non-cardia gastric cancer. The interaction of ALOX15 rs2619112 and rs2619118 has a synergistic effect in the development of non-cardia gastric cancer.

Prohibitin 2 exacerbates lipopolysaccharide-induced periodontal bone inflammation via the NF-κB signaling pathway

Zhao Jingxin , Hu Jiamin , Gao Jike , Cheng Ming , Zhu Youming , Sun Xiaoyu

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.002

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abstract:
To elucidate the molecular mechanism by which prohibitin 2 (PHB2) mediates periodonti- tis-induced bone tissue inflammation through regulating the nuclear factor kappa B (NF-κB) signaling pathway and its role in irreversible alveolar bone resorption . Methods Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) were used to detect the expression differences of in- flammatory factors and PHB2 in healthy and inflamed alveolar bone tissues of mice in vivo . In vitro , an inflammato- ry model was established using lipopolysaccharide ( LPS)-induced a mouse calvaria-derived preosteoblastic cell line , subclone E1 (MC3T3-E1) cells . Western blot and qRT-PCR were used to clarify the regulatory relationship between PHB2 and inflammatory factors , and immunofluorescence staining was performed to observe changes in PHB2 subcellular localization . PHB2 overexpression plasmids were constructed using molecular cloning , and RNA interference was employed to knock down PHB2 expression to assess its regulatory role in inflammation . Based on RNA-seq data , differential expression analysis based on the negative binomial distribution , version 2 ( DESeq2) was used for differential expression analysis , and kyoto encyclopedia of genes and genomes (KEGG) pathway en- richment along with gene ontology ( GO) functional annotation were performed to identify key signaling pathways and differentially expressed genes . Results In the mouse periodontitis model , PHB2 expression was significantly upregulated in alveolar bone tissues . In the in vitro inflammatory cell model , PHB2 levels positively correlated with interleukin (IL)-6 , IL-1β, and tumor necrosis factor-alpha (TNF-α) levels , and its subcellular localization shifted during inflammation . RNA-seq data and the detection of the level of phosphorylation of p65 protein (p-p65) dem- onstrated that PHB2 exacerbated inflammatory responses through the NF-κB signaling pathway and was mechanisti- cally linked to upregulation of the upstream chemokine C-X-C motif chemokine ligand 10 (CXCL10) . Conclusion PHB2 aggravates LPS-induced periodontitis inflammation via the NF-κB signaling pathway , providing new in- sights into the molecular mechanisms underlying the development of periodontitis .

Evaluation of the effect of puerarin on rheumatoid arthritis in rats based on AKT-FOXO1-IL-9 pathway

Liu Xiaoyu1 , Yu Han1 , Yu Jie2 , Gao Jingru1 , Ma Qingqing1 , Shi Jihai3 , Dong Xiangli4 , Hao Jinqi 1 , Yin Ruolan1 , Yu Yanqin1 , 5

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.009

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abstract:
To explore the therapeutic mechanism of puerarin in treating rheumatoid arthritis (RA) rats based on the serine/tyrosine protein kinase B (AKT)-phosphorylated forkhead box protein O1 (FOXO1)-interleu- kin-9 (AKT-FOXO1-IL-9) signaling pathway . Methods 36 rats were randomly divided into a blank group , a model group , a positive control group , and low , medium , and high dose groups of puerarin . Except for the blank group , the other groups were induced with type Ⅱ collagen to establish a RA rat model . After successful modeling , different doses of puerarin and methotrexate were given to treat the rats . The body mass and toe thickness of the rats were measured , and biochemical indicators of rat blood rheology were detected . X-ray was used to observe changes in rat joint morphology . Safranin green staining were used to observe the pathology of rat joint tissue . ELISA was used to detect the levels of IL-9 and rheumatoid factors in rat serum , and Western blot was used to detect changes in levels of AKT and FOXO1 . Results Compared with the blank group , the model group had the lowest toe thick- ness , and X-ray images showed more obvious segmental stenosis and more severe marginal bone invasion; scaly like changes appeared at the edges of joints stained with safranin green , accompanied by the exudation of inflammatory cells and increased proliferation and secretion of chondrocytes; the expression levels of inflammatory factors IL-9 and rheumatoid factors were the highest , and the expression levels of AKT and FOXO1 proteins were the highest (P < 0. 05) . Compared with the model group , the toe thickness of rats treated with different doses of puerarin de- creased ; X-ray images showed that the puerarin treatment group of rats showed improvement in plantar joint stenosis and marginal bone invasion; the results of safranin green staining showed that after treatment with different doses of puerarin , the infiltration of inflammatory cells decreased , and the expression levels of inflammatory factor IL-9 , rheumatoid factors , AKT , and FOXO1 proteins decreased significantly ( P < 0. 05) , with the high-dose puerarin group showing the most significant difference . Compared with the high-dose puerarin group , the positive control group showed a significant decrease in the above results and statistical differences (P < 0. 05) . Conclusion Puer- arin has a good therapeutic effect on rats with RA by inhibiting the AKT-FOXO1-IL-9 pathway . The high-dose pu- erarin group (60 mg/kg) has the best therapeutic effect and the results show a dose-response relationship .

The expression and function of STAT4 in lung adenocaroma

Chai Qian1 , Zhang Yanke2 , Wu Min1 , Zhao Lei 1

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.004

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Research on the effect of miHA-TM in enhancing donor bone marrow transplantation outcomes under low-intensity conditioning

Pu Yajing , Zhou Meng

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.001

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Analysis of lower limb alignment and gait after TKA for varus knees

Zhou Jian1 , Hua Xingyi 1 , Lu Junqin2 , Tang Kang1 , Fang Wei3

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.020

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abstract:
To investigate the relationship between lower limb alignment and knee functional gait after total knee arthroplasty (TKA) for varus knee deformity . Methods A total of 94 patients with knee osteoarthritis and varus deformity underwent mechanically aligned TKA . The knee society score ( KSS) , hip-knee-ankle angle (HKA) , medial proximal tibial angle ( mMPTA) , and gait parameters ( step length , gait speed , cadence , thigh jerk acceleration , and thigh swing work) were assessed preoperatively and one month postoperatively . The correla- tion between KSS scores and changes in lower limb alignment was also analyzed . Results The KSS clinical score of the operated knee significantly improved from 39. 19 ±9. 55 preoperatively to 73 . 01 ±6. 90 postoperatively (P < 0. 001) . The KSS functional score increased from 41 . 12 ±10. 66 to 56. 33 ±7 . 41(P < 0. 001) . Postoperative gait analysis revealed significant improvements in step length , gait speed , cadence , and thigh swing work ( P < 0. 001) , while thigh jerk acceleration showed no significant change (P = 0. 525) . The HKA angle of the affected limb increased from 170. 61 ±4. 39 preoperatively to 177. 30 ±3 . 49 postoperatively ( P < 0. 001) . Similarly , the mMPTA angle increased from 83 . 95 ±3 . 32 to 89. 15 ±1 . 94 (P < 0. 001) . Correlation analysis indicated that The KSS clinical score was positively correlated with HKA ( P < 0. 001) and mMPTA ( P < 0. 05) of the lower limb force line . The KSS functional score was positively correlated with HKA (P < 0. 05) but not with mMPTA (P > 0. 05) . Conclusion In patients with severe knee osteoarthritis due to varus deformity , TKA significantly alleviates pain and improves both clinical and functional KSS scores within one month postoperatively . Restoring lower limb mechanical alignment is positively associated with joint functional recovery and enhances gait performance .

Research advances on centromere proteins shaping immunosuppressive tumor microenvironment to promote immune escape

Wang Suqin , Tan Jiayan , Li Ya

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.027

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The study on the relationship between transgingival characteristics of implant restorations and peri-implant health

Li Xinya , Xia Rong

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.023

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Experimental study on the effect of different surface treatment methods on the anti staining ability of lithium disilicate glass ceramics

Ji Zhibo1 , Li Xiaowen1 , Xu Xinyi 1 , Song Guoyi2 , Ma Kun3 , Sun Lei 1 , 4

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.022

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Research progress on application of cell co-culture technology in respiratory diseases

Song Yuwei 1 , Yang Jingfan1 , Li Haibo1 , Qin Yanqin1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.026

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Role of TFEB-autophagy pathway in rifampicin-induced liver injury and its mechanism

Xu Hongmei , Song Yulin

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.007

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abstract:
To investigate the role of transcription factor EB (TFEB) -autophagy pathway in rifampicin- induced liver injury and its possible mechanism . Methods Forty 6-8-week-old C57/BL6 mice were randomly di- vided into five groups : control group , model group , TFEB low-dose agonist group , TFEB high-dose agonist group , and autophagy agonist group , with 8 mice in each group . Except for the control group , the other four groups were given rifampicin 200 mg/(kg ·d) by gavage daily . TFEB agonist was administered intraperitoneally at a low dose of 20 mg/kg and a high dose of 50 mg/kg for 7 days at 1 h after rifampicin administration . Autophagy agonist was administered by gavage at a dose of 10 mg/kg 6 h before rifampicin administration on day 1 . The experiment was completed 7 days after modeling. The degree of liver injury was evaluated by detecting liver function indexes and liver pathological changes . Western blot was used to detect the protein expression total TFEB , chelator 1( p62) , microtubule-associated protein light chain 3(LC3) , benzyl chloride 1(Beclin-1) , sodium taurocholate co-transpor- ting polypeptide(NTCP) and bile salt export pump(BSEP) levels in liver nucleus/liver tissue were quantified . Re- sults Compared with the control group , the serum levels of alanine aminotransferase ( ALT) , aspartate amin- otransferase (AST) , total bilirubin ( TBIL) , direct bilirubin ( DBIL) , and total bile acid ( TBA) in the model group increased (P < 0. 05) , and obvious pathological changes were observed in the liver. Compared with the mod- el group , the high dose and low dose of TFEB agonist and autophagy agonist groups had reductions in the above in- dicators (P < 0. 05) . Compared with the low-dose TFEB agonist group , the high-dose TFEB agonist group had re- ductions in the above indicators (P < 0. 05) . The proportion of TFEB in the nucleus was ( 1 . 0 ±0. 10) in the con- trol group , (0. 6 ±0. 05) in the model group , (0. 8 ±0. 08) in the low-dose agonist group , and (0. 9 ±0. 07) in the high-dose agonist group (P < 0. 05) . Autophagy agonist group (0. 7 ±0. 06) (P < 0. 05) . Compared with the control group , the levels of NTCP and BSEP in the liver of the model group decreased (P < 0. 05) , and the expres- sion of NTCP and BSEP in the TFEB low-dose and high-dose agonist groups were restored , and the expression of NTCP and BSEP in the autophagy agonist group also increased (P < 0. 05) . Compared with the control group , the protein expression levels of TFEB , LC3-Ⅱ/LC3 - Ⅰand Beclin-1 in the liver tissue of the model group significantly decreased (P < 0. 05) , while the protein expression level of p62 significantly increased ( P < 0. 05) . Compared with the model group , the protein expression levels of TFEB , LC3-Ⅱ/LC3 - Ⅰand Beclin-1 in the liver tissue of the TFEB agonist high-dose group , low-dose group and autophagy agonist group increased (P < 0. 05) , while the pro- tein expression level of p62 decreased (P < 0. 05) . Conclusion TFEB can improve rifampicin-induced liver inju- ry by activating autophagy pathway , and the main mechanism may be related to the up-regulation of NTCP and BSEP expression .

Predictive value of methylation of RUNX3 promoter region in 28-day prognosis of patients with sepsis

Ying Liunian1, Liu Lei1,2, Zhang Ying1，2,Yin Yongqiang1, Zhong Yi2

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.019

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abstract:
To investigate the methylation status of the RUNX family transcription factor 3 (RUNX3) promoter and its mRNA expression in sepsis patients, and to analyze their relationship with the prognosis of sepsis.Methods Differentially expressed genes related to sepsis, including RUNX3, were identified from multiple datasets obtained from the gene expression omnibus (GEO) database. The gene expression and methylation sites were validated. A total of 120 patients with sepsis were included. Clinical data were recorded, and blood samples were collected at enrollment. Relative expression levels of RUNX3 in blood samples and promoter methylation status were detected using qPCR and methylation-specific PCR (MSP), respectively. Pearson correlation coefficients were used to analyze the correlation between RUNX3 levels in patient blood and clinical indicators. Kaplan-Meier analysis was performed to plot survival curves, and Cox proportional hazards regression analysis was conducted to identify factors affecting the prognosis of sepsis patients. Results Data set analysis revealed that RUNX3 was a differentially methylated gene associated with the prognosis of sepsis. The mRNA expression level of RUNX3 was lower in the non-survivor group compared to the survivor group (P < 0.05), and the methylation ratio of RUNX3 was higher in the non-survivor group than in the survivor group (P < 0.05). In sepsis patients, RUNX3 mRNA expression levels were negatively correlated with Interleukin-6 (IL-6), Procalcitonin (PCT), C-reactive protein (CRP), Acute Physiology and Chronic Health Evaluation (APACHE II) score, and Sequential Organ Failure Assessment（SOFA）score. Kaplan-Meier analysis showed that the 28-day survival rate in the methylated group was lower than that in the unmethylated group (P < 0.05). Cox regression analysis results indicated that RUNX3 promoter methylation was an independent risk factor for predicting the 28-day prognosis of sepsis patients. Conclusion In sepsis patients, the mRNA levels of RUNX3 were reduced, and the degree of promoter methylation was higher. RUNX3 promoter methylation was an independent risk factor for the 28-day prognosis of sepsis patients and could serve as a prognostic biomarker for sepsis.

Research progress on bone morphogenetic proteins and oral squamous cell carcinoma

Xing Fu’ao1, Tian Faming2, Lian Qiangqiang2, Fan Xinhao3

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.028

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Ginkgo biloba extract down-regulates TLR4/NLRP3 signaling to protect airway inflammation in COPD rats

Pan Ying1，Mo Xueni1，Wang Gerui1，Feng Yuqing2，Xie Fang2，Mao Meiling1，Wei Tingting1， Xiang Jing1 ，Huang Lianjian1 ，Wei Fanbo1 ，Yang Yibao2

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.008

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abstract:
To explore the regulatory effects of ginkgo biloba extract on airway inflammatory injury and Toll-like receptor 4(TLR4)/nucleotide-binding oligomerization domain-containing 3(NLRP3) pathway in rats with chronic obstructive pulmonary disease (COPD). Methods Thirty-six male SD rats were selected and randomly divided into four groups: the normal control group, the model group, the prednisone treatment group, and the ginkgo biloba extract treatment group, with 9 rats in each group. Except for the normal control group, the COPD rat models in the other groups was constructed by intratracheal instillation of lipopolysaccharide (LPS) combined with cigarette smoke exposure. After successful modeling, the rats were continuously administered drugs for 12 weeks, followed by sampling. The general conditions and respiratory symptoms of the rats were observed. The pathological changes of lung tissues were observed by hematoxylin-eosin (HE) staining technique; the mRNA and protein expression levels ofTLR4, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and NLRP3 in rat lung tissues were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. Results Compared with the normal control group, the lung tissues of rats in the model group were significantly damaged, and the protein and mRNA expression of TLR4, TNF-α, IL-1β, and NLRP3 increased (P < 0.05). Compared with the model group, lung tissue damage was reduced in the prednisone group and the ginkgo biloba extract group, and TLR4, TNF-α, IL-1β, NLRP3 protein and mRNA expression decreased (P < 0.05). Conclusion Ginkgo biloba extract may reduce TLR4, TNF-α, IL-1β, and NLRP3 expression in lung tissues of COPD rats and alleviate their airway inflammatory response by inhibiting the TLR4/NLRP3 signaling pathway.

Application of metagene next-generation sequencing of alveolar lavage fluid in the detection of pathogenic bacteria of pulmonary infection

Zhang He, Luo Xinyue, Heng Xin, Zhang Yun, Wang Songping, Deng Jun

DOI: 10.19405/j.cnki.issn1000-1492.2025.10.018

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abstract:
To investigate the value of metagene next-generation sequencing (mNGS) in the detection of pathogens in patients with pulmonary infection. Methods A retrospective analysis was performed on clinical data from 434 patients with pulmonary infections admitted over the past four years. Based on the presence of underlying comorbidities, patients were divided into underlying disease group (n=262) and non-underlying disease group (n=172). Pathogen detection was conducted using both mNGS and conventional tests. Clinical and laboratory parameters, radiographic findings, and pathogen detection results were systematically analyzed. The diagnostic performance of the two methods in identifying causative pathogens of pulmonary infections was compared. Results The positive rate of mNGS in 434 patients was higher than that of conventional tests, and the difference was statistically significant (P<0.05). The efficacy of mNGS in detecting bacteria and viruses was significantly higher than that of conventional tests, and the difference was statistically significant (P<0.05). Although the fungal detection rate of mNGS was higher than that of conventional tests, the difference was not statistically significant. Among them, the detection rates of Mycobacterium tuberculosis, Mycoplasma pneumoniae, Haemophilus influenzae, Streptococcus pneumoniae, Streptococcus constellation, Staphylococcus aureus and Aspergillus fumigatus were significantly higher than those of conventional tests, and the difference was statistically significant (P<0.05). Subgroup analysis showed that the proportion of males, hospital stay, smoking prevalence and average age in the underlying disease group were higher than those in the non-underlying disease group, and the difference was statistically significant (P<0.05), while there were no significant differences in antibiotic use and endotracheal intubation rate between the two groups. The most common pathogens detected by mNGS in the underlying disease group were Mycobacterium tuberculosis, Haemophilus influenzae, Streptococcus pneumoniae, Pseudomonas aeruginosa, human herpesvirus type 4 and Aspergillus fumigatus, while the most common pathogens in the non-underlying disease group were Mycobacterium tuberculosis, Haemophilus influenzae, Streptococcus pneumoniae, Mycoplasma pneumoniae and Klebsiella pneumoniae. The positive rate of mNGS in the two groups was significantly higher than that of conventional tests, and the difference was statistically significant (P<0.05), while the difference in the positive rate of mNGS between the two groups was not statistically significant. Conclusion mNGS has significant advantages over conventional tests of pathogen in lung infection, and is less affected by underlying diseases, which can provide an etiological basis for lung infection.

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