Janus kinase 2（JAK2）/signal transducer and activator of transcription 3（STAT3） signaling pathway regulates multiple processes in neurons， including growth， development， proliferation and differentiation， and is closely associated with the onset， progression and treatment of cerebral ischemia-reperfusion injury （CIRI）. This article provides an overview of the JAK2/ STAT3 signaling pathway and its relationship with CIRI， followed by a comprehensive review of the current research status on the regulation of the JAK2/STAT3 signaling pathway by traditional Chinese medicine （TCM） to ameliorate CIRI. Among them， TCM monomers and compound prescriptions such as glycyrrhetinic acid， triptolide， and Taohong siwu decoction can inhibit inflammatory responses， enhance cellular autophagy， and suppress apoptosis by inhibiting the JAK2/STAT3 signaling pathway， thereby alleviating CIRI. In addition， TCM monomers and compound prescriptions like astragaloside Ⅳ， ginkgolide K， and Qingnao dripping pills can mitigate CIRI by activating the JAK2/STAT3 signaling pathway to inhibit oxidative stress， promote angiogenesis， and enhance neuronal survival rates.

Objective: To investigate the incidence trend and epidemic characteristics of notifiable infectious diseases in Nanjing City from 2004 to 2022, so as to provide the basis for improving the prevention, control, and monitoring strategies of infectious diseases. Methods: Data pertaining to notifiable infectious diseases reported in Nanjing City from 2004 to 2022 were retrieved from the Infectious Disease Surveillance System of Chinese Disease Prevention and Control Information System. Infectious diseases were classified by law and transmission routes. Temporal distribution incidence of notifiable infectious diseases were descriptively analyzed. The trends in incidence of notifiable disease were analyzed using annual percent change (APC) and average annual percent change (AAPC). Results: A total of 33 types of notifiable infectious diseases with 505 275 cases were reported in Nanjing City from 2004 to 2022. The average annual reported incidence was 347.45/105, showing a decreasing trend from 2018 to 2022 (APC=-13.499%, P<0.05), and there was no significant trend overall (AAPC=-1.586%, P>0.05). A total of 203 235 cases of 25 types of class A and B notifiable infectious diseases were reported, with an average annual reported incidence of 139.75/100 000, showing an overall decreasing trend (AAPC=-4.954%, P<0.05). Eight types of class C notifiable infectious diseases with 302 042 cases were reported, with an average annual reported incidence of 207.69/100 000. The reported incidence showed an increasing trend from 2004 to 2018 (APC=10.117%, P<0.05), and a decreasing trend from 2018 to 2022 (APC=-27.467%, P<0.05). There was no trend overall (AAPC=-0.360%, P>0.05). The reported incidence of blood-borne and sexually transmitted infectious diseases was the highest in class A and B infectious diseases, with an average annual reported incidence of 69.88/100 000, which was at a high epidemic level throughout the year, except February. The reported incidence of respiratory infectious diseases was 51.30/100 000, with a high reported incidence in April and December. The reported incidence of intestinal infectious diseases was the highest (178.06/100 000) in class C infectious diseases, with a high reported incidence in June and November. Conclusions The reported incidence of notifiable infectious diseases in Nanjing City was generally stable from 2004 to 2022. The peak incidence of respiratory infectious diseases occurred in winter and spring, and that of intestinal infectious diseases was in summer and autumn. It is necessary to strengthen the surveillance and intervention of blood-borne and sexually transmitted infectious diseases, respiratory infectious diseases, and intestinal infectious diseases to reduce the risk of infectious diseases.

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.

Aim To investigate the impact of bakuchiol(BAK)on lipid accumulation in macrophage-derived foam cell and explore the underlying mechanisms.Methods MTT assay was used to determine the non-toxic concen-tration of BAK on foam cell.Oil red O staining,NBD cholesterol,and Dil-ox-LDL were used to assess lipid accumulation in foam cell.RT-qPCR and Western blot were utilized to measure mRNA and protein expression,respectively.Re-sults BAK promoted cholesterol effux and reduced lipid accumulation in foam cell.BAK upregulated the mRNA and protein expression levels of ATP-binding cassette transporter A1(ABCA1)and concurrently downregulated the phosphoryl-ation levels of extracellular signal-regulated kinase 1/2(ERK1/2).Treatment with the ERK1/2 activator Ro 67-7476 re-sulted in decreased ABCA1 protein expression compared with the BAK-treated group.Conclusion BAK reduced lipid accumulation in foam cell by inhibiting ERK1/2 phosphorylation,upregulating ABCA1 expression,and promoting choles-terol efflux,thereby suppressing foam cell 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.