Objective:To establish an evaluation index system for patient safety education targeted at undergraduate nursing interns.Methods:Based on the CIPP (Context, Input, Process, Product) evaluation model, a preliminary draft of the index system was developed using a literature review and semi-structured interviews. The Delphi method and the Analytic Hierarchy Process were applied to finalize the index system.Results:Two rounds of Delphi expert consultation were conducted. In the first round, 23 questionnaires were distributed, and 20 valid responses were received (effective response rate: 86.96%) . Among them, 15 experts (75.00%) provided revision suggestions. In the second round, 20 questionnaires were distributed, and 19 valid responses were received (effective response rate: 95.00%) , with two experts (10.53%) offering suggestions. The expert authority coefficients for the two rounds were 0.900 and 0.921, respectively. Kendall's coordination coefficients were 0.272 and 0.273 ( P<0.01) . The final evaluation system consisted of four first-level indicators, eight second-level indicators, and 18 third-level indicators. Conclusions:The evaluation index system constructed in this study is scientifically grounded and reliable. However, its practical utility and applicability require further validation.

Objective:To establish an evaluation index system for patient safety education targeted at undergraduate nursing interns.Methods:Based on the CIPP (Context, Input, Process, Product) evaluation model, a preliminary draft of the index system was developed using a literature review and semi-structured interviews. The Delphi method and the Analytic Hierarchy Process were applied to finalize the index system.Results:Two rounds of Delphi expert consultation were conducted. In the first round, 23 questionnaires were distributed, and 20 valid responses were received (effective response rate: 86.96%) . Among them, 15 experts (75.00%) provided revision suggestions. In the second round, 20 questionnaires were distributed, and 19 valid responses were received (effective response rate: 95.00%) , with two experts (10.53%) offering suggestions. The expert authority coefficients for the two rounds were 0.900 and 0.921, respectively. Kendall's coordination coefficients were 0.272 and 0.273 ( P<0.01) . The final evaluation system consisted of four first-level indicators, eight second-level indicators, and 18 third-level indicators. Conclusions:The evaluation index system constructed in this study is scientifically grounded and reliable. However, its practical utility and applicability require further validation.

Objective: To investigate the late identification and its influencing factors of newly reported HIV/AIDS cases in Shangcheng District, Hangzhou City, so as to provide insights into the development of strategies for early detection and identification of HIV/AIDS cases. Methods: Basic information, identification routes and CD4+T lymphocyte counts among newly reported HIV/AIDS cases in Shangcheng District from 2013 to 2022 were collected through the Chinese Disease Prevention and Control Information System. The proportion of late identification of newly reported HIV/AIDS cases was analyzed, and factors affecting late identification was analyzed by a multivariable logistic regression model. Results: Totally 1 052 HIV/AIDS cases were newly reported in Shangcheng District from 2013 to 2022, including 1 011 males (96.10%), and had a mean age of (32.90±12.39) years. There were 333 cases with late identification, accounting for 31.65%. The proportions of late identification have no significant changing trend from 2013 to 2022 (P>0.05). Multivariable logistic regression analysis showed that HIV/AIDS cases aged 25 years and older (25 to 49 years, OR=1.894, 95%CI: 1.350-2.658; 50 years and older, OR=3.010, 95%CI: 1.838-4.928) had a higher risk of late identification, while HIV/AIDS cases with college degree and above (OR=0.655, 95%CI: 0.459-0.936) and identified by voluntary counseling and testing (OR=0.542, 95%CI: 0.380-0.772) had a lower risk of late identification. Conclusions The proportion of late identification of newly reported HIV/AIDS cases in Shangcheng District from 2013 to 2022 was 31.65%. Age, educational level and identification route were important factors affecting late identification of HIV/AIDS cases in Shangcheng District.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling.Here,we focused on the role of Semaphorin 3A(Sema3A),expressed by sensory nerves,in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement(OTM)model.Firstly,bone formation was activated after the 3rd day of OTM,coinciding with a decrease in sensory nerves and an increase in pain threshold.Sema3A,rather than nerve growth factor(NGF),highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM.Moreover,in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells(hPDLCs)within 24 hours.Furthermore,exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload.Mechanistically,Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway,maintaining mitochondrial dynamics as mitochondrial fusion.Therefore,Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation,both as a pain-sensitive analgesic and a positive regulator for bone formation.