Atopic dermatitis （AD） is an atopic disease with a complex etiology and pathogenesis resulting from the interaction of multiple factors. The NOD-like receptor pyrin domain-containing 3 （NLRP3） inflammasome is an important component of innate immunity and is involved in the onset and progression of AD， encompassing multiple processes such as inflammation， pyroptosis， and autophagy. Traditional Chinese medicine （TCM） has shown significant clinical efficacy in the treatment of AD and also offers advantages including flexible compatibility， multi-target effects， and low drug resistance. A large number of studies have shown that single Chinese medicinal components and compound prescriptions can treat atopic diseases by modulating the NLRP3 inflammasome. This article elaborates on the activation of the NLRP3 inflammasome and its influence on the pathogenesis and progression of AD， and summarizes recent studies on the mechanisms by which active constituents， extracts， and compound formulations of Chinese medicine treat AD through regulation of the NLRP3 inflammasome and related signaling pathways， with the aim of providing a reference for the clinical treatment of AD and the development of TCM.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

Objective:To observe any effects of contralateral repeated transcranial magnetic stimulation (rTMS) of the swallowing motor cortex on the swallowing and brainstem auditory evoked potentials (BAEPs) of stroke survivors with dysphagia.Methods:A total of 83 stroke survivors with dysphagia were randomly divided into an ipsilesional stimulation group ( n=22), a contralesional stimulation group ( n=21), a bilateral stimulation group ( n=20), and a control group ( n=20). In addition to their conventional dysphagia training, those in the three stimulation groups received 3Hz rTMS while the control group was given fake stimulation. The treatment was administered daily for 20 minutes, 6 days a week, for 5 consecutive weeks. Before and after the treatment, swallowing function was assessed videofluoroscopically and using the Dysphagia Outcome and Severity Scale (DOSS). The oral and pharyngeal stages of swallowing were evaluated using the videofluoroscopic dysphagia scale (VDS). Brain stem conduction was assessed using BAEPs. Results:After treatment the average DOSS scores of all 4 groups were significantly better than before the treatment. The average DOSS scores of the contralesional and bilateral sti-mulation groups were then significantly better than those of the other two groups. The sub-item and total VDS scores of all 4 groups had decreased significantly, but the average score of the bilateral stimulation group was significantly lower than the control group′s average. Ipsilesional stimulation significantly improved the VDS sub-item scores for the triggering of pharyngeal swallowing, laryngeal elevation, and pharyngeal transit time compared with the control group. In the contralesional stimulation group the average total score and the VDS sub-item scores for apraxia, premature bolus loss, oral transit times, the triggering of pharyngeal swallowing, vallecular residue, laryngeal elevation, coating on the pharyngeal wall, and pharyngeal transit time were significantly lower than those of the control group, on average. After the treatment the latencies of BAEP waves I, III and V and the I-III, III-V and I-V interpeak intervals had decreased significantly in all four groups, but the average latencies and intervals of the bilateral and contralesional groups were significantly shorter than those of the control group. The latencies and intervals of the bilateral stimulation group were then significantly shorter than those in the ipsilesional stimulation group on average. The average latency of wave V in the bilateral stimulation group (6.53±0.73ms) was significantly shorter than that in the contralesional stimulation group after the treatment.Conclusion:Bilateral rTMS over the swallowing motor cortex combined with conventional dysphagia training can significantly improve the swallowing of dysphagic stroke survivors.