Glucose metabolic reprogramming is important in promoting the occurrence and development of malignant tumors and meeting the high demands of the malignant proliferation of tumor cells. An in-depth investigation of the mechanism of glucose metabolic reprogramming in lung cancer is important for the development of effective therapeutic strategies for lung cancer. Traditional Chinese medicine (TCM) is characterized by multiple components, targets, and pathways and can exert antitumor effects through multiple mechanisms. This article illustrates systematically the mechanism of action of Chinese herbal monomers and compound formulas regulating glucose metabolic reprogramming in lung cancer and explores deeply their regulatory effects on key enzymes of glycolysis and metabolism-related signaling pathways, and their potential in overcoming the drug resistance of lung cancer. It aims to provide a reference basis for the study of therapeutic targets and mechanisms of action of TCM in prevention and treatment of lung cancer and theoretical sources for the research and development of new medicines.

AIM:This study aims to investigate the mechanisms through which Astragaloside IV(AS)pre-vents and treats osteoporosis by regulating intestinal flora.METHODS:Thirty 3-month-old female Sprague-Dawley(SD)rats were selected for the study.Ten rats were randomly assigned to a sham group,while the remaining twenty underwent bilateral ovariectomy(OVX)to simulate osteoporosis.Following the modeling,the twenty OVX rats were randomly divid-ed into two groups:the OVX group and the AS treatment group,which received continuous gavage for 12 weeks.Bone mineral density(BMD)of the femur and lumbar vertebrae was measured using dual-energy X-ray absorptiometry(DXA).Hematoxylin-eosin(HE)staining was employed to assess the microstructure of the femur and colonic mucosa,while immu-nohistochemistry was used to measure the expression of collagen type Ⅰ alpha 1 chain(COL1A1)protein in the femur.Ad-ditionally,RT-qPCR was utilized to analyze the mRNA expression of bone formation-related indicators,including alkaline phosphatase(ALP),COL1A1,and Runt-related transcription factor 2(RUNX2).Fresh fecal samples were collected from the rats for 16S rDNA sequencing to detect changes in intestinal microbiota composition.RESULTS:Compared to the sham group,OVX rats exhibited a significant increase in body weight and a marked decrease in femur and lumbar ver-tebrae bone density.HE staining revealed trabecular bone fractures with a disrupted reticular structure in the OVX group,along with the presence of numerous cavities and fat vacuoles in the bone marrow.The colonic mucosa showed signs of vil-lous shedding and mild crypt atrophy.Immunohistochemistry results demonstrated a substantial reduction in brown-yellow granules and COL1A1 expression in the OVX group.Conversely,in the AS group,there was a reduction in body weight and a significant increase in bone density of the femur and lumbar vertebrae.The trabecular architecture appeared more or-ganized,with less severe fractures compared to the OVX group.In the AS group,the number of cavities and fat vacuoles in the bone marrow was also reduced,and the colonic mucosa exhibited improved villous structure and less crypt atrophy.Immunohistochemical analysis indicated that AS treatment significantly enhanced COL1A1 expression.Furthermore,after AS intervention,the mRNA expression levels of ALP,COL1A1,and RUNX2 were notably increased.16S rDNA sequenc-ing revealed a significant increase in the abundance of Firmicutes,Proteobacteria,f_Pseudonocardiaceae,f_Marinifilace-ae,f_Oscillospiraceae,f_Ruminococcaceae,and f_Peptostreptococcaceae,while p_Euryarchaeota,Bacteroidetes,and f_Muribaculaceae showed significant reductions.Overall,OVX led to increased diversity in the species distribution of in-testinal microbiota,whereas AS treatment helped recalibrate the aforementioned phyla(families)and reduce diversity.CONCLUSION:Astragaloside IV can increase bone density in OVX rats,improve bone microstructure,promote bone formation,and prevent colonic mucosal damage by regulating the relative abundance of intestinal flora.

AIM:This study aims to investigate the mechanisms through which Astragaloside IV(AS)pre-vents and treats osteoporosis by regulating intestinal flora.METHODS:Thirty 3-month-old female Sprague-Dawley(SD)rats were selected for the study.Ten rats were randomly assigned to a sham group,while the remaining twenty underwent bilateral ovariectomy(OVX)to simulate osteoporosis.Following the modeling,the twenty OVX rats were randomly divid-ed into two groups:the OVX group and the AS treatment group,which received continuous gavage for 12 weeks.Bone mineral density(BMD)of the femur and lumbar vertebrae was measured using dual-energy X-ray absorptiometry(DXA).Hematoxylin-eosin(HE)staining was employed to assess the microstructure of the femur and colonic mucosa,while immu-nohistochemistry was used to measure the expression of collagen type Ⅰ alpha 1 chain(COL1A1)protein in the femur.Ad-ditionally,RT-qPCR was utilized to analyze the mRNA expression of bone formation-related indicators,including alkaline phosphatase(ALP),COL1A1,and Runt-related transcription factor 2(RUNX2).Fresh fecal samples were collected from the rats for 16S rDNA sequencing to detect changes in intestinal microbiota composition.RESULTS:Compared to the sham group,OVX rats exhibited a significant increase in body weight and a marked decrease in femur and lumbar ver-tebrae bone density.HE staining revealed trabecular bone fractures with a disrupted reticular structure in the OVX group,along with the presence of numerous cavities and fat vacuoles in the bone marrow.The colonic mucosa showed signs of vil-lous shedding and mild crypt atrophy.Immunohistochemistry results demonstrated a substantial reduction in brown-yellow granules and COL1A1 expression in the OVX group.Conversely,in the AS group,there was a reduction in body weight and a significant increase in bone density of the femur and lumbar vertebrae.The trabecular architecture appeared more or-ganized,with less severe fractures compared to the OVX group.In the AS group,the number of cavities and fat vacuoles in the bone marrow was also reduced,and the colonic mucosa exhibited improved villous structure and less crypt atrophy.Immunohistochemical analysis indicated that AS treatment significantly enhanced COL1A1 expression.Furthermore,after AS intervention,the mRNA expression levels of ALP,COL1A1,and RUNX2 were notably increased.16S rDNA sequenc-ing revealed a significant increase in the abundance of Firmicutes,Proteobacteria,f_Pseudonocardiaceae,f_Marinifilace-ae,f_Oscillospiraceae,f_Ruminococcaceae,and f_Peptostreptococcaceae,while p_Euryarchaeota,Bacteroidetes,and f_Muribaculaceae showed significant reductions.Overall,OVX led to increased diversity in the species distribution of in-testinal microbiota,whereas AS treatment helped recalibrate the aforementioned phyla(families)and reduce diversity.CONCLUSION:Astragaloside IV can increase bone density in OVX rats,improve bone microstructure,promote bone formation,and prevent colonic mucosal damage by regulating the relative abundance of intestinal flora.

The incidence of nonsynostotic plagiocephaly in infants is increasing year by year. This article reviews the etiology, types, early assessment, monitoring and diagnosis, and nursing intervention of nonsynostotic plagiocephaly, aiming to further improve the awareness and attention of medical staff and caregivers of infants to nonsynostotic plagiocephaly and achieve early identification and intervention, so as to improve the adverse outcomes of nonsynostotic plagiocephaly.

Objective:To study the variational trend in disease characteristics of patients with hepatitis B-related primary liver cancer (HBV-HCC) in the past five years.Method:A single-center retrospective cross-sectional analysis was performed to compare patients diagnosed with HBV-HCC from January 2012 to December 2016 (control group) and from January 2017 to December 2021 (observation group). The data of the study variables were extracted from the electronic medical record system of the hospital information system of the Second Hospital of Lanzhou University. The 1:2 propensity score matching was used to adjust potential confounding factors such as gender and age. Multivariate logistic regression analysis was used to study the factors affecting changes in disease characteristics of the HBV-HCC population in the observation group. GraphPad Prism 8.0 software was used to draw forest plots to intuitively display the effect size of the study variables in the logistic regression analysis.The t-test was used to compare normally distributed data between groups. The χ2 test was used for inter-group comparison. Results:A total of 1 717 eligible cases were collected, including 510 in the control group and 1 207 in the observation group. Compared with the control group, the number of newly diagnosed cases in the observation group increased by 2.36 times, and males were still the main onset population (83.3% vs. 82.7%). The median age of onset increased (51.9 vs. 53.5 years, P<0.001). 79.4% of HBV-HCC patients had not received antiviral therapy, and the proportion of HBeAg-negative patients increased (56.4%). The factors affecting HBV-HCC patients included family history of HBV ( OR=1.626, 95% CI: 1.181-2.238), family history of hepatocellular carcinoma ( OR=1.388, 95% CI: 1.013-1.901), hypoviremia ( OR=1.322, 95% CI: 1.046-1.671), abnormal alanine aminotransferase ( OR=1.545, 95% CI: 1.231-1.940), liver fibrosis ( OR=1.478, 95% CI: 1.153-1.894), liver cirrhosis ( OR=1.431, 95% CI: 1.128-1.815), and metabolic-related fatty liver disease ( OR=1.438, 95% CI: 1.116-1.815) after propensity score matching adjustment. The factors affecting HBeAg-positive patients were decreased ( OR=0.390, 95% CI: 0.389-0.617); however, the number of early HBV-HCC diagnoses was increased (12.7% vs. 19.3%, P=0.001). Conclusion:The characteristics of patient disease and occurrence of HBV-HCC are changing over the past five years. The risk of developing hepatocellular carcinoma in middle- to older male patients with chronic hepatitis B is increasing with familial history of HBV and hepatocellular carcinoma, HBeAg negativity, hypoviremia, abnormal alanine aminotransferase, liver fibrosis, cirrhosis, and metabolic-related fatty liver disease.

Objective To investigate the regulatory mechanism of Notch signaling pathway by YAP in non-alcoholic steatohep-atitis(NASH)liver fibrosis,and assess the intervention effect of Cigu Xiaozhi prescription in detoxification and phlegm treatment.Methods C57BL/6J mice were randomly divided into different groups,including a normal group,NASH liver fibrosis model group,verteporfin(VP)intervention group,VP+Chinese medicine(Cigu Xiaozhi prescription)low-dose group,VP+Chinese medicine high-dose group,and dimethyl sulfoxide control group.The methionine/choline-deficient diet combined with low-dose CCl4 was used to construct the NASH liver fibrosis model.The degree of liver fibrosis was evaluated using hematoxylin and eosin(HE)and Masson staining.Four protein factors associated with liver fibrosis were detected using enzyme-linked immunosorbent assay,and hydroxyproline levels in the mouse liver was determined using the alkaline water method.The localization of α-SMA,ColⅠ,YAP,and Notch1 proteins in the liver was determined using immunohistochemistry.Additionally,the mRNA and protein expression levels of the Notch signaling pathway molecules,namely Notch1/2,J agged1,and DLL4,were assessed using real-time quantitative PCR and Western blotting analyses,respectively.Results The HE and Masson staining results revealed that the liver cells of NASH liver fibrosis mice were swollen and the cytoplasm was transparent.Additionally,evident fibrosis was observed in the hepatic lobule,portal area,and sinus;it was accompanied by heightened levels of inflam-matory cell infiltration,a large number of fat droplets,and instances of local hepatocyte necrosis,dissolution,and cirrhosis.The four factors associated with liver fibrosis showed a substantial increase(P<0.01).α-SMA,ColⅠ,YAP,and Notch1 were localized in the cytoplasm of hepatocytes.YAP,Notch1/2,and Jagged1 were highly expressed in the liver(P<0.01)but were downregulated after intervention with VP and VP+high and low doses of Cigu Xiaozhi prescription(P<0.05).Meanwhile,DLL4 factor was upregulated in the VP+high-dose of Cigu Xiaozhi prescription group(P<0.05).Conclusion YAP may inhibit activation of the Notch pathway by downregulating Notch1/2 and Jagged1 and upregulating DLL4,thereby interfering with the occurrence of liver fibrosis in NASH.Treatment with Cigu Xiaozhi pre-scription may inhibit Notch signaling pathway activation by downregulating YAP,Notch1/2,and Jagged1 and upregulating DLL4 through its multi-components and multi-targets properties,ultimately slow the progression of liver fibrosis in NASH.

Objective:To explore any effect of electroacupuncture (EA) at the Baihui (DU20) and Dazhui (GV14) acupoints on the learning and memory of rats modeling cerebral palsy (CP), and on the miR-126 regulated VEGF/Notch1 pathway.Methods:Fifty-four male Sprague-Dawley rats 7 days old with an average weight of (20±5g) were randomly divided into a sham operation group, a model group, and an electroacupuncture group, each of 18. All except the sham operation group had a model of CP induced using left common carotid artery ligation combined with hypoxia. Twenty-four hours after successful modelling, the EA group received 14 sessions of electroacupuncture at the DU20 and GV14 acupoints, once every other day. On the 29th day, learning and memory ability were evaluated using a Morris Water Maze. The expression of vascular endothelial growth factors (VEGF and VEGFR-2) was detected using immunohistochemical staining. The levels of notch1 and hes1 protein were quantified using western blotting, and the expression of miR-126 RNA was quantified using reverse transcription polymerase chain reactions (RT-qPCRs).Results:Compared with the sham group, there was a significant decrease in the average learning and memory, and the level of miR126 in the model group, but a significant increase in the expression of VEGF and VEGFR-2 and the levels of notch1 and hes1. Significant improvement was observed in all of the measurements of the EA group compared with the model group.Conclusions:Electroacupuncture at the DU20 and GV14 acupoints can improve the ability of learning and memory of rats modeling CP. The mechanism may be related to regulation of the VEGF/notch1 pathway by miR-126 and its promotion of angiogenesis.

Objective:To construct and validate a risk prediction model for major complications 30 days after surgery in the elderly patients with hip fracture.Methods:A retrospective study was conducted to analyze the clinical data of 276 elderly patients with hip fracture who had been admitted to Department of Trauma and Orthopaedics, The Hospital Affiliated to Chengde Medical University from June 2019 to December 2021. There were 96 males and 180 females with an age of (74.5±9.3) years, and 139 femoral neck fractures and 137 intertrochanteric fractures. The outcome of this study was whether major complications occurred within 30 days after surgery. Multiple logistic regression analysis identified the risk factors for major complications in the elderly patients with hip fracture within 30 days after surgery. The forward step-by-step method and likelihood ratio test were used to screen the best prediction model. A nomogram was constructed to display the model. The stability and effectiveness of the model were evaluated by the receiver operating characteristic curve (ROC), Hosmer-Lemeshow goodness-of-fit test, clinical decision curve and clinical impact curve analysis.Results:Logistic regression analysis showed that decreased preoperative hemoglobin ( P< 0.05), time from admission to surgery >72 hours ( OR=3.001, 95% CI: 1.564 to 5.758, P<0.001), control of nutritional status (CONUT) score >4 points ( OR=3.394, 95% CI: 1.724 to 6.680, P<0.001), and age-adjusted modified frailty index (aamFI) >2 points ( OR=2.875, 95% CI: 1.548 to 5.339, P= 0.001), increased operation time ( OR=1.016, 95% CI: 1.006 to 1.025, P=0.001), and surgical bleeding >60 mL ( OR=2.373, 95% CI: 1.016 to 5.540, P=0.046) were independent risk factors for major complications within 30 days after surgery in the elderly patients with hip fracture. The area under the ROC curve in the logistic risk prediction model was 0.846 (95% CI: 0.799 to 0.889), and the results of Hosmer-Lemeshow goodness-of-fit test showed ( χ2=8.080, P=0.426). The clinical decision curve and clinical impact curve showed that the prediction model was accurate and effective. Conclusion:Based on the patients' preoperative hemoglobin, time from admission to surgery, control of nutritional status score, age-adjusted modified frailty index, operation time and surgical blood loss, this study has constructed successfully a risk prediction model for complications 30 days after surgery in the elderly patients with hip fracture which enables medical staff to predict the occurrence of major postoperative complications.

AIM:This study aims to investigate the effects of Osthole(OST)on inflammation and cartilage-de-grading proteases in an interleukin 1β(IL-1β)-induced chondrocyte inflammation model.METHODS:Prediction:we collected target genes for OST and those related to knee osteoarthritis(KOA)from four databases.After standardizing the target genes obtained from the UniProt database,two overlapping genes were identified using the Venny tool.Additional-ly,protein interaction relationships were obtained from the STRING database,and core target genes were screened and vi-sualized using Cytoscape software.Enrichment analysis for the overlapping genes was performed through Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways.Finally,the active drug components and target proteins were validated and visualized through computational analysis.Validation:primary rabbit chondrocytes were iso-lated and cultured in vitro.Cell morphology and toluidine blue staining were employed to confirm chondrocyte identity.An inflammatory injury model was induced using IL-1β.The cells were divided into control,model,low-dose,medium-dose,high-dose OST,and celecoxib groups.Chondrocyte viability was assessed using the CCK-8 method.Western blot and im-munofluorescence techniques were utilized to detect the proteins IL-1β,tumor necrosis factor-alpha(TNF-α),matrix me-talloproteinase 13(MMP-13),and a disintegrin and metalloproteinase with thrombospondin motifs(ADAMTS-4).Gene expression levels of IL-1β,IL-6,TNF-α,and MMP-13 were measured via RT-qPCR.RESULTS:A total of 80 potential OST targets were identified for treating KOA,with 10 core target genes(CASP3,TNF,HIF1A,IL-1β,NFKB1,PARP1,NFE2L2,JAK2,MAPK1,and GSK3B)screened.GO and KEGG analyses further elucidated the molecular mechanisms of OST in KOA treatment,highlighting multiple biological processes and signaling pathways involved.Molecular docking simulations confirmed stable binding of OST to key targets TNF and IL-1β within the IL-17 signaling pathway.Chondro-cytes exhibited long spindle and pavement-like shapes.Based on the effects of varying OST concentrations on chondro-cytes,2.5,5,and 10 μmol/L OST were selected for pharmacodynamic testing.Compared to the model group,OST signif-icantly reduced inflammation in the chondrocyte inflammation model and inhibited the expression of cartilage matrix-de-grading enzymes,showing no statistically significant difference from the celecoxib group.CONCLUSION:OST promotes chondrocyte proliferation and differentiation.It effectively inhibits inflammation in the IL-1β-induced chondrocyte model and mitigates chondrocyte injury.The underlying mechanism may involve the degradation of chondroproteoglycans and the protection of the extracellular matrix.

AIM:This study aims to investigate the effects of Osthole(OST)on inflammation and cartilage-de-grading proteases in an interleukin 1β(IL-1β)-induced chondrocyte inflammation model.METHODS:Prediction:we collected target genes for OST and those related to knee osteoarthritis(KOA)from four databases.After standardizing the target genes obtained from the UniProt database,two overlapping genes were identified using the Venny tool.Additional-ly,protein interaction relationships were obtained from the STRING database,and core target genes were screened and vi-sualized using Cytoscape software.Enrichment analysis for the overlapping genes was performed through Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways.Finally,the active drug components and target proteins were validated and visualized through computational analysis.Validation:primary rabbit chondrocytes were iso-lated and cultured in vitro.Cell morphology and toluidine blue staining were employed to confirm chondrocyte identity.An inflammatory injury model was induced using IL-1β.The cells were divided into control,model,low-dose,medium-dose,high-dose OST,and celecoxib groups.Chondrocyte viability was assessed using the CCK-8 method.Western blot and im-munofluorescence techniques were utilized to detect the proteins IL-1β,tumor necrosis factor-alpha(TNF-α),matrix me-talloproteinase 13(MMP-13),and a disintegrin and metalloproteinase with thrombospondin motifs(ADAMTS-4).Gene expression levels of IL-1β,IL-6,TNF-α,and MMP-13 were measured via RT-qPCR.RESULTS:A total of 80 potential OST targets were identified for treating KOA,with 10 core target genes(CASP3,TNF,HIF1A,IL-1β,NFKB1,PARP1,NFE2L2,JAK2,MAPK1,and GSK3B)screened.GO and KEGG analyses further elucidated the molecular mechanisms of OST in KOA treatment,highlighting multiple biological processes and signaling pathways involved.Molecular docking simulations confirmed stable binding of OST to key targets TNF and IL-1β within the IL-17 signaling pathway.Chondro-cytes exhibited long spindle and pavement-like shapes.Based on the effects of varying OST concentrations on chondro-cytes,2.5,5,and 10 μmol/L OST were selected for pharmacodynamic testing.Compared to the model group,OST signif-icantly reduced inflammation in the chondrocyte inflammation model and inhibited the expression of cartilage matrix-de-grading enzymes,showing no statistically significant difference from the celecoxib group.CONCLUSION:OST promotes chondrocyte proliferation and differentiation.It effectively inhibits inflammation in the IL-1β-induced chondrocyte model and mitigates chondrocyte injury.The underlying mechanism may involve the degradation of chondroproteoglycans and the protection of the extracellular matrix.