Objective To identify serum metabolic markers served in the clinical diagnosis of ulcerative colitis(UC).Methods Ser-um samples from 29 UC patients,31 Crohn's disease(CD)patients,and 21 matched healthy controls(HC)admitted to Department of Gastroenterology,Nanjing Drum Tower Hospital during September 2022 and March 2024 were collected.The ultra-high-performance liquid chromatography coupled with quadrupole-orbitrap mass spectrometry(UHPLC-Q Exactive HF-X)technology was used to detect and analyze serum metabolites.A partial least squares discrimination analysis(PLS-DA)model was constructed,and the metabolites significantly up-regulated in UC were screened based on the variable importance in projection(VIP)score＞1,P value＜0.05,and fold change(FC)＞1.2.The pathway enrichment analysis was performed using the Kyoto Encyclopedia of Genes and Genomes(KEGG)database to reveal the biological pathways involved in the metabolites.The area under the receiver operating characteristic curve(AUCROC)was calculated to evaluate the diagnostic potential of the differential metabolites.Results A total of 1 522 metabo-lites were identified from the three sample groups.Among them,4 metabolites,namely leucodopachrome(VIP=1.964,P＜0.05,FC=1.916),tetrahydrodipicolinate(VIP=1.74,P＜0.05,FC=2.65),N-ethylmaleimide(VIP=1.519,P＜0.05,FC=1.597),and 5,6-dihydroxyindole(VIP=3.018,P＜0.05,FC=1.575),were significantly up-regulated in UC.Their AUCROC values for distinguishing UC from CD were 0.788(95%CI:0.655-0.921),0.773(95%CI:0.639-0.907),0.834(95%CI:0.720-0.949),and 0.899(95%CI:0.821-0.977),respectively,while those for distinguishing UC from HC were 0.966(95%CI:0.924-1.000),0.926(95%CI:0.857-0.995),0.969(95%CI:0.928-1.000),and 0.910(95%CI:0.830-0.990),respectively.KEGG pathway analysis showed that the up-regulated metabolites in UC were primarily enriched in biological pathways such as tyrosine metabolism,glycerophospholipid me-tabolism,and arachidonic acid metabolism.Conclusion The serum metabolic profile of UC patients is significantly changed,and the four differential metabolites mentioned above may serve as effective biomarkers for the differential diagnosis of UC,CD,and HC.

AIM:This study aimed to investigate the mechanisms by which treadmill exercise ameliorates de-pressive-like behaviors and hippocampal neuronal damage in chronic restraint stress(CRS)mice by regulating mitophagy via the Sirt1/PGC-1α signaling axis.METHODS:Forty C57BL/6J mice were randomly assigned to control,CRS,CRS+exercise(EXE)and EXE groups(n=10).The mice in CRS and CRS+EXE groups underwent 4 h of daily restraint for 28 consecutive days to establish a depression model.The mice in CRS+EXE and EXE groups received 8 weeks of treadmill training(6 sessions per week).Depressive-like behaviors were evaluated using the open field test,sucrose preference test,and tail suspension test.Hippocampal neuronal morphology and pathological changes were examined using hematoxy-lin-eosin and Nissl staining,while neuronal apoptosis was assessed through TUNEL staining.Mitochondrial ultrastructure was examined via transmission electron microscopy.Mitochondrial membrane potential and ATP content were measured using JC-1 assay and ATP assay kits,respectively.The expression levels of silent information regulator 1(Sirt1),peroxi-some proliferator-activated receptor γ coactivator-1α(PGC-1α),PTEN-induced kinase 1(PINK1)and parkin were as-sessed at both mRNA and protein levels by RT-qPCR and Western blot assays,as well as key markers of mitophagy[mi-crotubule-associated protein 1 light chain 3(LC3)and P62]and apoptosis(cleaved caspase-9 and cleaved caspase-3).RESULTS:Compared with control group,CRS mice exhibited significantly reduced central zone entries and time(P<0.01),decreased sucrose preference(P<0.01),increased immobility time(P<0.01),severe hippocampal neuronal damage,elevated apoptosis rate(P<0.01),mitochondrial deterioration;reduced membrane potential and ATP content(P<0.01),decreased mRNA expressions of Sirt1,PGC-1α,PINK1,and parkin(P<0.01),reduced protein levels of Sirt1,PGC-1α,PINK1,parkin and LC3(P<0.01),and increased expression of P62,cleaved caspase-9,and cleaved caspase-3(P<0.01).The mice in CRS+EXE group showed significant improvements in all these parameters compared to CRS group(P<0.05 or P<0.01).CONCLUSION:Treadmill exercise mitigates CRS-induced depressive-like behaviors,mi-tochondrial dysfunction,and neuronal apoptosis in mice by activating the hippocampal Sirt1/PGC-1α/mitophagy axis.

BACKGROUND:Studies have shown that there is a close relationship between dendritic spine plasticity and Alzheimer's disease,and that resistance or aerobic exercise has some efficacy in improving cognitive dysfunction,but the mechanism of action is unclear.OBJECTIVE:To investigate the effect of aerobic exercise or resistance exercise on dendritic spine plasticity in the hippocampal CA1 region of APP/PS1 transgenic mice.METHODS:Thirty 3-month-old male APP/PS1 mice were selected and randomly divided into three groups:a model group,a resistance exercise group,and an aerobic exercise group.The same litter of 3-month-old C57BL/6J mice were selected as a blank group.Mice in the resistance exercise group were subjected to ladder-climbing exercise and those in the aerobic exercise group were subjected to treadmill exercise for 12 weeks.At the end of the exercise intervention,the water maze experiment and the new arm of the Y maze were used to assess behavioral changes in mice.Hematoxylin-eosin staining,Nissl staining,Golgi staining,and electron microscopy were performed to observe neuronal morphology,Nissl bodies,dendritic spines,and ultrastructural changes in the synapses of the hippocampal region of the mouse brain.The protein expression levels of hippocampal amyloid-beta1-42,Ras,and Drebrin were measured using Western blot analysis.RESULTS AND CONCLUSION:Mice in the model group exhibited a prolonged escape latency over 5 consecutive days(P＜0.05,P＜0.01)and significantly fewer entries into the new arm of the Y maze(P＜0.01).Dendritic spine density in the CA1 region of the hippocampus,as well as Ras and Drebrin expression in the hippocampal tissues of mice in the model group,were lower than those in the normal group(P＜0.01),and amyloid-beta1-42 expression in the hippocampal tissues was higher in the model group compared with the normal group(P＜0.01).Mice in the resistance exercise group and the aerobic exercise group displayed a shortened escape latency over the same 5-day period(P＜0.05,P＜0.01)and showed a significantly greater number of entries into the new arm of the Y maze compared with the normal group(P＜0.01).Dendritic spine density in the CA1 region of the hippocampus,as well as Ras and Drebrin expression in the hippocampal tissues,were higher in both the resistance exercise group and the aerobic exercise group compared with the model group(P＜0.01).Amyloid-beta1-42 expression in the hippocampal tissue was lower in both exercise groups than in the model group(P＜0.01).To conclude,long-term regular aerobic or resistance exercise interventions can increase dendritic spine density and synaptic plasticity in the CA1 region of the hippocampus,enhancing spatial learning and memory abilities in a mouse model of Alzheimer's disease.These effects may be associated with increased expression of Ras and Drebrin proteins in the hippocampus.

Objective To identify serum metabolic markers served in the clinical diagnosis of ulcerative colitis(UC).Methods Ser-um samples from 29 UC patients,31 Crohn's disease(CD)patients,and 21 matched healthy controls(HC)admitted to Department of Gastroenterology,Nanjing Drum Tower Hospital during September 2022 and March 2024 were collected.The ultra-high-performance liquid chromatography coupled with quadrupole-orbitrap mass spectrometry(UHPLC-Q Exactive HF-X)technology was used to detect and analyze serum metabolites.A partial least squares discrimination analysis(PLS-DA)model was constructed,and the metabolites significantly up-regulated in UC were screened based on the variable importance in projection(VIP)score＞1,P value＜0.05,and fold change(FC)＞1.2.The pathway enrichment analysis was performed using the Kyoto Encyclopedia of Genes and Genomes(KEGG)database to reveal the biological pathways involved in the metabolites.The area under the receiver operating characteristic curve(AUCROC)was calculated to evaluate the diagnostic potential of the differential metabolites.Results A total of 1 522 metabo-lites were identified from the three sample groups.Among them,4 metabolites,namely leucodopachrome(VIP=1.964,P＜0.05,FC=1.916),tetrahydrodipicolinate(VIP=1.74,P＜0.05,FC=2.65),N-ethylmaleimide(VIP=1.519,P＜0.05,FC=1.597),and 5,6-dihydroxyindole(VIP=3.018,P＜0.05,FC=1.575),were significantly up-regulated in UC.Their AUCROC values for distinguishing UC from CD were 0.788(95%CI:0.655-0.921),0.773(95%CI:0.639-0.907),0.834(95%CI:0.720-0.949),and 0.899(95%CI:0.821-0.977),respectively,while those for distinguishing UC from HC were 0.966(95%CI:0.924-1.000),0.926(95%CI:0.857-0.995),0.969(95%CI:0.928-1.000),and 0.910(95%CI:0.830-0.990),respectively.KEGG pathway analysis showed that the up-regulated metabolites in UC were primarily enriched in biological pathways such as tyrosine metabolism,glycerophospholipid me-tabolism,and arachidonic acid metabolism.Conclusion The serum metabolic profile of UC patients is significantly changed,and the four differential metabolites mentioned above may serve as effective biomarkers for the differential diagnosis of UC,CD,and HC.

AIM:This study aimed to investigate the mechanisms by which treadmill exercise ameliorates de-pressive-like behaviors and hippocampal neuronal damage in chronic restraint stress(CRS)mice by regulating mitophagy via the Sirt1/PGC-1α signaling axis.METHODS:Forty C57BL/6J mice were randomly assigned to control,CRS,CRS+exercise(EXE)and EXE groups(n=10).The mice in CRS and CRS+EXE groups underwent 4 h of daily restraint for 28 consecutive days to establish a depression model.The mice in CRS+EXE and EXE groups received 8 weeks of treadmill training(6 sessions per week).Depressive-like behaviors were evaluated using the open field test,sucrose preference test,and tail suspension test.Hippocampal neuronal morphology and pathological changes were examined using hematoxy-lin-eosin and Nissl staining,while neuronal apoptosis was assessed through TUNEL staining.Mitochondrial ultrastructure was examined via transmission electron microscopy.Mitochondrial membrane potential and ATP content were measured using JC-1 assay and ATP assay kits,respectively.The expression levels of silent information regulator 1(Sirt1),peroxi-some proliferator-activated receptor γ coactivator-1α(PGC-1α),PTEN-induced kinase 1(PINK1)and parkin were as-sessed at both mRNA and protein levels by RT-qPCR and Western blot assays,as well as key markers of mitophagy[mi-crotubule-associated protein 1 light chain 3(LC3)and P62]and apoptosis(cleaved caspase-9 and cleaved caspase-3).RESULTS:Compared with control group,CRS mice exhibited significantly reduced central zone entries and time(P<0.01),decreased sucrose preference(P<0.01),increased immobility time(P<0.01),severe hippocampal neuronal damage,elevated apoptosis rate(P<0.01),mitochondrial deterioration;reduced membrane potential and ATP content(P<0.01),decreased mRNA expressions of Sirt1,PGC-1α,PINK1,and parkin(P<0.01),reduced protein levels of Sirt1,PGC-1α,PINK1,parkin and LC3(P<0.01),and increased expression of P62,cleaved caspase-9,and cleaved caspase-3(P<0.01).The mice in CRS+EXE group showed significant improvements in all these parameters compared to CRS group(P<0.05 or P<0.01).CONCLUSION:Treadmill exercise mitigates CRS-induced depressive-like behaviors,mi-tochondrial dysfunction,and neuronal apoptosis in mice by activating the hippocampal Sirt1/PGC-1α/mitophagy axis.

BACKGROUND:Studies have shown that there is a close relationship between dendritic spine plasticity and Alzheimer's disease,and that resistance or aerobic exercise has some efficacy in improving cognitive dysfunction,but the mechanism of action is unclear.OBJECTIVE:To investigate the effect of aerobic exercise or resistance exercise on dendritic spine plasticity in the hippocampal CA1 region of APP/PS1 transgenic mice.METHODS:Thirty 3-month-old male APP/PS1 mice were selected and randomly divided into three groups:a model group,a resistance exercise group,and an aerobic exercise group.The same litter of 3-month-old C57BL/6J mice were selected as a blank group.Mice in the resistance exercise group were subjected to ladder-climbing exercise and those in the aerobic exercise group were subjected to treadmill exercise for 12 weeks.At the end of the exercise intervention,the water maze experiment and the new arm of the Y maze were used to assess behavioral changes in mice.Hematoxylin-eosin staining,Nissl staining,Golgi staining,and electron microscopy were performed to observe neuronal morphology,Nissl bodies,dendritic spines,and ultrastructural changes in the synapses of the hippocampal region of the mouse brain.The protein expression levels of hippocampal amyloid-beta1-42,Ras,and Drebrin were measured using Western blot analysis.RESULTS AND CONCLUSION:Mice in the model group exhibited a prolonged escape latency over 5 consecutive days(P＜0.05,P＜0.01)and significantly fewer entries into the new arm of the Y maze(P＜0.01).Dendritic spine density in the CA1 region of the hippocampus,as well as Ras and Drebrin expression in the hippocampal tissues of mice in the model group,were lower than those in the normal group(P＜0.01),and amyloid-beta1-42 expression in the hippocampal tissues was higher in the model group compared with the normal group(P＜0.01).Mice in the resistance exercise group and the aerobic exercise group displayed a shortened escape latency over the same 5-day period(P＜0.05,P＜0.01)and showed a significantly greater number of entries into the new arm of the Y maze compared with the normal group(P＜0.01).Dendritic spine density in the CA1 region of the hippocampus,as well as Ras and Drebrin expression in the hippocampal tissues,were higher in both the resistance exercise group and the aerobic exercise group compared with the model group(P＜0.01).Amyloid-beta1-42 expression in the hippocampal tissue was lower in both exercise groups than in the model group(P＜0.01).To conclude,long-term regular aerobic or resistance exercise interventions can increase dendritic spine density and synaptic plasticity in the CA1 region of the hippocampus,enhancing spatial learning and memory abilities in a mouse model of Alzheimer's disease.These effects may be associated with increased expression of Ras and Drebrin proteins in the hippocampus.

OBJECTIVE To investigate the role and mechanism of microRNA-125b (miR-125b) in downregulating ion channel-related protein expression in a cardiac hypertrophy model.METHODS① In vivo:Lentiviral vectors for miR-125b overexpression and knockdown were constructed,and male C57BL/6 mice were divided into the following groups:sham group (thoracotomy without virus injection),LV-miR-125b group (mmu-miR-125b mimic),LV-miR-125b-inhibitor group (mmu-miR-125b-inhibitor),and negative control group (LV-NC).The mice were raised under normal conditions for 4 weeks.The ultrastructural changes in myocardium tissue sections of LV-miR-125b mice were observed using trans-mission electron microscopy.The cardiac hypertrophy model in mice was established using thoracic aortic constriction (TAC).Echocardiography was performed to measure ejection fraction (EF) and frac-tional shortening (FS),and the ratio of heart weight to body weight (HW/BW),ratio of heart weight to tibia length (HW/TL),as well as the expression level of the myocardial hypertrophy marker β-myosin heavy chain (β-MHC) were calculated to evaluate the success of the TAC-induced hypertrophy model.Subse-quently,C57BL/6 mice were divided into four groups:Sham group,TAC model group,LV-miR-125b-inhibitor+TAC group,and LV-NC+TAC group.Protein expression levels of cardiac sodium channel (Nav1.5) and calcium channel (Cav1.2) were detected using Western blotting.RT-qPCR was performed to assess the levels of miR-125b and mRNA expression of myocardial hypertrophy markers,including atrial natriuretic peptide (ANP),brain natriuretic peptide (BNP),and β-MHC.② In vitro:Primary cultured neonatal Kunming mouse cardiomyocytes were divided into four groups:cell control group (no treatment),miR-125b overexpression group,miR-125b-inhibitor group,and negative control group (NC).RT-qPCR was used to detect the levels of miR-125b,ANP,BNP,and β-MHC.Western blotting and immunofluorescence were performed to assess the expression levels of Nav1.5 and Cav1.2 in the cardiomyocytes.Luciferase reporter gene assay was used to evaluate the direct effect of miR-125b on the target proteins Nav1.5 and Cav1.2.RESULTS ① In vivo:Compared to the Sham group,the TAC model mice showed significantly increased the ratio of heart weight to body weight (HW/BW),the ratio of heart weight to tibia length (HW/TL),and expression levels of the myocardial hypertrophy marker β-MHC (P＜0.05),indicating the successful establishment of the TAC model.Furthermore,miR-125b expression was significantly elevated in the TAC model group (P＜0.01).In the LV-miR-125b group,compared to the LV-NC group,the expression levels of myocardial hypertrophy markers ANP,BNP,and β-MHC were significantly increased (P＜0.01),while the ejection fraction (EF) and fractional short-ening (FS) values of the mice were significantly reduced (P＜0.01).Additionally,Additionally,myocardium ultrastructure of LV-miR-125b group was damaged.Compared to the LV-NC+TAC group,the LV-miR-125b-inhibitor+TAC group showed a significant increase in ejection fraction (EF) and fractional shortening (FS) values (P＜0.05).Additionally,the levels of Nav1.5 and Cav1.2 in myocardium tissue were signifi-cantly elevated in the LV-miR-125b-inhibitor+TAC group compared to the LV-NC+TAC group (P＜0.05).② In vitro:Compared to the NC group,the miR-125b overexpression group showed a significant increase in miR-125b expression (P＜0.01),as well as elevated levels of ANP,BNP,and β-MHC (P＜0.01).However,miR-125b-inhibitor significantly reversed the increases in ANP,BNP,and β-MHC (P＜0.01).Western blotting and immunofluorescence results showed that,compared to the NC group,the miR-125b mimic group exhibited significantly decreased levels of Nav1.5 and Cav1.2 (P＜0.01),while miR-125b-inhibitor led to an increase in the levels of both Nav1.5 and Cav1.2.Luciferase assay results demon-strated that miR-125b directly binds to the ion channel proteins Nav1.5 and Cav1.2,encoded by the SCN5A and CACNA1C genes.CONCLUSION miR-125b promotes the development of cardiac hyper-trophy by inhibiting the voltage-gated ion channel proteins Nav1.5 and Cav1.2 Inhibition of miR-125b expression improves cardiac hypertrophy.

Objective This study explores the efficacy and underlying mechanisms of combining rhCYGB with 5-FU to target hypoxia-induced treatment resistance in liver cancer.The aim is to develop a novel combinato-rial therapy strategy for improving outcomes in patients with refractory liver cancer.Methods The half-maximal inhibitory concentration(IC50)of drugs on liver cancer cells under normoxia and hypoxia was determined,and dose-response curves were generated to assess sensitivity to 5-FU.The combined effects of rhCYGB and 5-FU were analyzed withCompuSyn and SynergyFinder 3.0.Tumor stem cell sphere formation assays and flow cytometry for CD133-positive cells were conducted to evaluate the impact on cancer stemness.Wound healing assays assessed the effects on migration.Results The IC50 values under hypoxia exhibited a significant fold change compared to normoxia(P<0.05),specifically a 15.27-fold,4.25-fold,and 2.34-fold increase for Hep3B,Huh7,and HepG2 cells respectively.Assessment of drug combination effects demonstrated a synergistic interaction between 5-FU and rhCYGB.Compared to the 5-FU monotherapy group,the combination of 5-FU and rhCYGB exerted an inhibitory effect on the formation of liver cancer stem cell spheres(P<0.05)and significantly downregulated the proportion of CD133-positive subpopulations in Hep3B cells(P<0.05).Wound healing assay results revealed a synergistic inhibitory effect on the migration of Hep3B cells after 48 hours of treatment with rhCYGB combined with 5-FU undernormoxia(P<0.05).Conclusions The combination of rhCYGB and 5-FU demonstrates syner-gistic effects in liver cancer.The underlying mechanism may involve the modulation of stemness and cell migration capacity.

OBJECTIVE To investigate the role and mechanism of microRNA-125b (miR-125b) in downregulating ion channel-related protein expression in a cardiac hypertrophy model.METHODS① In vivo:Lentiviral vectors for miR-125b overexpression and knockdown were constructed,and male C57BL/6 mice were divided into the following groups:sham group (thoracotomy without virus injection),LV-miR-125b group (mmu-miR-125b mimic),LV-miR-125b-inhibitor group (mmu-miR-125b-inhibitor),and negative control group (LV-NC).The mice were raised under normal conditions for 4 weeks.The ultrastructural changes in myocardium tissue sections of LV-miR-125b mice were observed using trans-mission electron microscopy.The cardiac hypertrophy model in mice was established using thoracic aortic constriction (TAC).Echocardiography was performed to measure ejection fraction (EF) and frac-tional shortening (FS),and the ratio of heart weight to body weight (HW/BW),ratio of heart weight to tibia length (HW/TL),as well as the expression level of the myocardial hypertrophy marker β-myosin heavy chain (β-MHC) were calculated to evaluate the success of the TAC-induced hypertrophy model.Subse-quently,C57BL/6 mice were divided into four groups:Sham group,TAC model group,LV-miR-125b-inhibitor+TAC group,and LV-NC+TAC group.Protein expression levels of cardiac sodium channel (Nav1.5) and calcium channel (Cav1.2) were detected using Western blotting.RT-qPCR was performed to assess the levels of miR-125b and mRNA expression of myocardial hypertrophy markers,including atrial natriuretic peptide (ANP),brain natriuretic peptide (BNP),and β-MHC.② In vitro:Primary cultured neonatal Kunming mouse cardiomyocytes were divided into four groups:cell control group (no treatment),miR-125b overexpression group,miR-125b-inhibitor group,and negative control group (NC).RT-qPCR was used to detect the levels of miR-125b,ANP,BNP,and β-MHC.Western blotting and immunofluorescence were performed to assess the expression levels of Nav1.5 and Cav1.2 in the cardiomyocytes.Luciferase reporter gene assay was used to evaluate the direct effect of miR-125b on the target proteins Nav1.5 and Cav1.2.RESULTS ① In vivo:Compared to the Sham group,the TAC model mice showed significantly increased the ratio of heart weight to body weight (HW/BW),the ratio of heart weight to tibia length (HW/TL),and expression levels of the myocardial hypertrophy marker β-MHC (P＜0.05),indicating the successful establishment of the TAC model.Furthermore,miR-125b expression was significantly elevated in the TAC model group (P＜0.01).In the LV-miR-125b group,compared to the LV-NC group,the expression levels of myocardial hypertrophy markers ANP,BNP,and β-MHC were significantly increased (P＜0.01),while the ejection fraction (EF) and fractional short-ening (FS) values of the mice were significantly reduced (P＜0.01).Additionally,Additionally,myocardium ultrastructure of LV-miR-125b group was damaged.Compared to the LV-NC+TAC group,the LV-miR-125b-inhibitor+TAC group showed a significant increase in ejection fraction (EF) and fractional shortening (FS) values (P＜0.05).Additionally,the levels of Nav1.5 and Cav1.2 in myocardium tissue were signifi-cantly elevated in the LV-miR-125b-inhibitor+TAC group compared to the LV-NC+TAC group (P＜0.05).② In vitro:Compared to the NC group,the miR-125b overexpression group showed a significant increase in miR-125b expression (P＜0.01),as well as elevated levels of ANP,BNP,and β-MHC (P＜0.01).However,miR-125b-inhibitor significantly reversed the increases in ANP,BNP,and β-MHC (P＜0.01).Western blotting and immunofluorescence results showed that,compared to the NC group,the miR-125b mimic group exhibited significantly decreased levels of Nav1.5 and Cav1.2 (P＜0.01),while miR-125b-inhibitor led to an increase in the levels of both Nav1.5 and Cav1.2.Luciferase assay results demon-strated that miR-125b directly binds to the ion channel proteins Nav1.5 and Cav1.2,encoded by the SCN5A and CACNA1C genes.CONCLUSION miR-125b promotes the development of cardiac hyper-trophy by inhibiting the voltage-gated ion channel proteins Nav1.5 and Cav1.2 Inhibition of miR-125b expression improves cardiac hypertrophy.

Objective:To explore the classification performance of combined model constructed from CT signs combined with radiomics for discriminating COVID-19 pneumonia and other viral pneumonia.Methods:The clinical and CT imaging data of 181 patients with viral pneumonia confirmed by reverse transcription-polymerase chain reaction in 15 hospitals of Yunnan Province from March 2015 to March 2020 were analyzed retrospectively. The 181 patients were divided into COVID-19 group (89 cases) and non-COVID-19 group (92 cases), which were further divided into training cohort (126 cases) and test cohort (55 cases) at a ratio of 7∶3 using random stratified sampling. The CT signs of pneumonia were determined and the radiomics features were extracted from the initial unenhanced chest CT images to build independent and combined models for predicting COVID-19 pneumonia. The diagnostic performance of the models were evaluated using receiver operating characteristic (ROC) analysis, continuous net reclassification index (NRI) calibration curve and decision curve analysis.Results:The combined models consisted of 3 significant CT signs and 14 selected radiomics features. For the radiomics model alone, the area under the ROC curve (AUC) were 0.904 (sensitivity was 85.5%, specificity was 84.4%, accuracy was 84.9%) in the training cohort and 0.866 (sensitivity was 77.8%, specificity was 78.6%, accuracy 78.2%) in the test cohort. After combining CT signs and radiomics features, AUC of the combined model for the training cohort was 0.956 (sensitivity was 91.9%, specificity was 85.9%, accuracy was 88.9%), while that for the test cohort was 0.943 (sensitivity was 88.9%, specificity was 85.7%, accuracy was 87.3%). The AUC values of the combined model and the radiomics model in the differentiation of COVID-19 group and the non-COVID-19 group were significantly different in the training cohort ( Z=-2.43, P=0.015), but difference had no statistical significance in the test cohort ( Z=-1.73, P=0.083), and further analysis using the NRI showed that the combined model in both the training cohort and the test cohort had a positive improvement ability compared with radiomics model alone (training cohort: continuous NRI 1.077, 95 %CI 0.783-1.370; test cohort: continuous NRI 1.421, 95 %CI 1.051-1.790). The calibration curve showed that the prediction probability of COVID-19 predicted by the combined model was in good agreement with the observed value in the training and test cohorts; the decision curve showed that a net benefit greater than 0.6 could be obtained when the threshold probability of the combined model was 0-0.75. Conclusion:The combination of CT signs and radiomics might be a potential method for distinguishing COVID-19 and other viral pneumonia with good performance.