Objective:To explore an initial target rate for resuscitation attempted by bystanders for patients experiencing out-of-hospital cardiac arrest in China.Methods:We searched seven electronic databases, including CNKI, VIP, Wanfang, CBM, PubMed, Cochrane, EMBase, for Utstein-style reports of out-of-hospital cardiac arrest, containing data on bystander resuscitation and survival to discharge or 30 days after arrest. All patients with cardiac arrest diagnosed at prehospital emergency medical services were included. Meta-analysis was performed to pool rate ratios (RR) with 95% confidence intervals (CI) of the rate of survival to discharge or 30 days. The population attributable risk percent (PARP) was calculated with RR, and the growth rate curve of PARP following bystander cardiopulmonary resuscitation rate was plotted. We established a multiple linear regression model to show the change in survival to discharge or 30 days with increasing rates of resuscitation attempted by bystanders.Results:We included 24 cohorts with 279 641 patients experiencing out-of-hospital cardiac arrest. The median rates of bystander cardiopulmonary resuscitation and survival to discharge or 30 days after arrest in seven cohorts from China were 2.8% and 0.47%, respectively, both far below the first tertiles in all cohorts worldwide (10.0% and 2.70%, respectively). The meta-analysis showed that resuscitation attempts by bystanders increased the chance of survival to discharge or 30 days ( RR=5.91, 95% CI 3.28-10.66; I2=0, P=0.990). The growth rate curve on PARP showed a rapid attenuation in the increase of PARP after the bystander resuscitation rate reached 10%. The multiple linear regression showed that resuscitation attempted by bystanders could explain 74.4% of the variation in the rates of survival to discharge or 30 days. By increasing the bystander resuscitation rate to 10%, the rate of survival to discharge or 30 days could increase to 1.40% (95% CI 0.76%-2.05%), and the PARP could increase from 19.7% to 32.9%. Conclusions:Low rate of resuscitation attempted by bystanders is currently the main reason for the poor survival rate of out-of-hospital cardiac arrest in China. It is recommended to increase the rate of resuscitation attempted by bystanders in stages with an initial target rate of 10%.

Objective:To explore the significance of any correlation between the cost of the rehabilitation provided to stroke survivors during their hospitalization and the functional levels attained, and to analyze factors influencing that correlation.Methods:The International Classification of Functioning, Disability and Health Rehabilitation Set (ICF-RS) was used to evaluate the functioning of 304 stroke survivors on their days of hospital admission and discharge, as well as on their 10th day in hospital. The cost of their rehabilitation was computed, and demographic and clinical data were collected. A generalized estimation equation was used to analyze the changes in dysfunction with time and its risk factors. The relationship between functional levels and rehabilitation cost and its influencing factors were analyzed.Results:Length of stay, age≥60 and hemorrhagic stroke were significant risk factors for greater dysfunction among the stroke survivors. On the 10th day in hospital and the day before discharge (the 18th day), the frequency of severe dysfunction had decreased. The significant predictors of increased cost were severe or moderate dysfunction, the stage of stroke (sub-acute stage), and non-first rehabilitation.Conclusion:Functional level is a useful predictor of rehabilitation cost. It is influenced by the stage of stroke and non-first rehabilitation.

Objective:To explore the significance of any correlation between the cost of the rehabilitation provided to stroke survivors during their hospitalization and the functional levels attained, and to analyze factors influencing that correlation.Methods:The International Classification of Functioning, Disability and Health Rehabilitation Set (ICF-RS) was used to evaluate the functioning of 304 stroke survivors on their days of hospital admission and discharge, as well as on their 10th day in hospital. The cost of their rehabilitation was computed, and demographic and clinical data were collected. A generalized estimation equation was used to analyze the changes in dysfunction with time and its risk factors. The relationship between functional levels and rehabilitation cost and its influencing factors were analyzed.Results:Length of stay, age≥60 and hemorrhagic stroke were significant risk factors for greater dysfunction among the stroke survivors. On the 10th day in hospital and the day before discharge (the 18th day), the frequency of severe dysfunction had decreased. The significant predictors of increased cost were severe or moderate dysfunction, the stage of stroke (sub-acute stage), and non-first rehabilitation.Conclusion:Functional level is a useful predictor of rehabilitation cost. It is influenced by the stage of stroke and non-first rehabilitation.

Objective:To explore an initial target rate for resuscitation attempted by bystanders for patients experiencing out-of-hospital cardiac arrest in China.Methods:We searched seven electronic databases, including CNKI, VIP, Wanfang, CBM, PubMed, Cochrane, EMBase, for Utstein-style reports of out-of-hospital cardiac arrest, containing data on bystander resuscitation and survival to discharge or 30 days after arrest. All patients with cardiac arrest diagnosed at prehospital emergency medical services were included. Meta-analysis was performed to pool rate ratios (RR) with 95% confidence intervals (CI) of the rate of survival to discharge or 30 days. The population attributable risk percent (PARP) was calculated with RR, and the growth rate curve of PARP following bystander cardiopulmonary resuscitation rate was plotted. We established a multiple linear regression model to show the change in survival to discharge or 30 days with increasing rates of resuscitation attempted by bystanders.Results:We included 24 cohorts with 279 641 patients experiencing out-of-hospital cardiac arrest. The median rates of bystander cardiopulmonary resuscitation and survival to discharge or 30 days after arrest in seven cohorts from China were 2.8% and 0.47%, respectively, both far below the first tertiles in all cohorts worldwide (10.0% and 2.70%, respectively). The meta-analysis showed that resuscitation attempts by bystanders increased the chance of survival to discharge or 30 days ( RR=5.91, 95% CI 3.28-10.66; I2=0, P=0.990). The growth rate curve on PARP showed a rapid attenuation in the increase of PARP after the bystander resuscitation rate reached 10%. The multiple linear regression showed that resuscitation attempted by bystanders could explain 74.4% of the variation in the rates of survival to discharge or 30 days. By increasing the bystander resuscitation rate to 10%, the rate of survival to discharge or 30 days could increase to 1.40% (95% CI 0.76%-2.05%), and the PARP could increase from 19.7% to 32.9%. Conclusions:Low rate of resuscitation attempted by bystanders is currently the main reason for the poor survival rate of out-of-hospital cardiac arrest in China. It is recommended to increase the rate of resuscitation attempted by bystanders in stages with an initial target rate of 10%.

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.
Humans ; Bone Remodeling ; Cell Differentiation ; Osteogenesis ; Semaphorin-3A/pharmacology* ; Trigeminal Ganglion/metabolism*

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.