Objective To analyze the pathogenic bacteria and drug resistance of peritoneal dialysis-associated peritonitis(PDAP),and provide a clinical reference for the rational use of antibiotics.Methods The demographic data of PDAP patients admitted to the peritoneal dialysis(PD)Center of the First Affiliated Hospital of Soochow University from July 1,2015 to December 30,2021 were collected,and the pathogens,drug resistance and prognosis were retrospectively analyzed.Results A total of 150 episodes of PDAP occurred in 92 patients.The positive rate of PD fluid culture was 61.33％,including 65 cases(70.65％)of Gram-positive(G+)bacteria,mainly Staphylococcus and Streptococcus.Gram-negative(G-)bacteria were in 16 cases(17.39％),mainly Escherichia coli and Enterobacter cloacae.There were 11 cases(11.96％)of multiple infections,including 5 cases of combined fungal infection.From 2016 to 2021,the incidence of G+bacteria-related PDAP decreased from 14 to 8 cases.G+strains were resistant to methicillin(35.00％),and were sensitive to linezolid(100.00％),teicoplanin(100.00％)and rifampicin(100.00％).The sensitivity rate to vancomycin was 98.59％.G-strains were sensitive to ceftazidime(86.36％),ceftizoxime(88.89％)and amikacin(100.00％).The MIC of vancomycin against Staphylococcus showed an upward trend in 2019-2021.The overall cure rate of PDAP was 81.33％in patients who responded to antibiotic treatment,and the cure rate of G+bacteria was higher than that of multiple infections(89.23％vs.36.36％,P＜0.01).The outcome of patients with multiple infections,especially those with concurrent fungal infection was poor.Conclusion The incidence of PDAP in the PD center has shown a decreasing trend in recent years.G+bacteria are still the main pathogenic bacteria causing PDAP,and they are highly resistant to methicillin,so vancomycin should be used as empirical therapy.For G-bacteria,cefotaxime and amikacin can be chosen as empirical therapy.There is a drift in the MIC values of vancomycin against Staphylococcus in the study period,so it is necessary to monitor the MIC of vancomycin against Staphylococcus and its changing trend.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To assess the prevalence of dentinal hypersensitivity (DH) and related factors in urban adults in China.Methods:The study was designed as an observational, cross-sectional epidemiological study carried out in adults aged 18-69 years old in seven cities (Beijing, Shanghai, Wuhan, Chengdu, Xi′an, Guangzhou, and Harbin) of China. The study was conducted from March 2021 to May 2023. Patients were required to complete a questionnaire regarding the subjects′ socio-economic factors, dietary behavior, oral health behavior and personal antecedent factors. DH was clinically diagnosed by judging whether the tooth cold air stimulation provoked DH or not, and recorded by investigator pain rating Schiff score. Compare the findings of six cities (Harbin excluded) with a similar study conducted in 2008.Results:In total, 11 622 subjects from seven cities in China participated the study. Fifty two point two percent (6 072/11 622) of subjects reported DH in questionnaire, 36.7% (4 266/11 622) of subjects reported experiencing DH in response to cold air stimulation for at least one study tooth. Risk factors including age, sex, city, toothbrush method and acid reflux showed marked associations with DH ( P<0.05). The prevalence of DH of urban residents in six cities (Harbin excluded) was 33.7% (3 335/9 882), higher than that in 2008 [29.7%(2 354/7 939)]. Conclusions:Overall, DH was common among urban adults in China and the prevalence increased in recent years. Better understanding of DH and its associated factors should be considered in its prevention and management by dental professionals.