RESUMO
[Objective]To summarize Professor LIN Shengyou's experience in the treatment of radiation-induced lung injury based on the theory of pathogenesis evolution.[Methods]Through clinical visits,organizing medical records,studying ancient and modern literature,starting from the evolution of the disease mechanism,this paper summarizes Professor LIN's clinical experience in application of the theory of pathogenesis evolution in the treatment of radiation-induced lung injury,and provides evidence with a clinical trial.[Results]Because of the special effect of radiation on the human body,Professor LIN believes that the basic pathogenesis of radiation-induced lung injury runs through the whole time,that is,heat evil harms the lung.With the development of the disease,the pathogenesis can be divided into three stages:at the beginning,the evil is flourishing,and the heat is damaging the lung;in the middle stage,the evil causes vital Qi decline,and the heat causes Yin injury first,then the lung and kidney deficiency;over time Yin damage affects Yang,leading to Yin and Yang deficiency.In clinic doctors should grasp the basic pathogenesis,identify the present pathogenesis and deduce the potential pathogenesis.Classic formula Maxing Shigan Decoction can be selected as the basic formula of the disease,added or subtracted according to the pathogenesis of each stage.In the case,according to the law of pathogenesis evolution,Maxing Shigan Decoction was added or subtracted as the main formula,and satisfactory curative effect was obtained.[Conclusion]By differentiating the syndrome of radiation-induced lung injury through the theory of pathogenesis evolution,Professor LIN has unique insights and significant curative effect,which is worthy of further clinical promotion and research.
RESUMO
Placental dysplasia increases the risk of recurrent spontaneous abortion (RSA). However, the underlying mechanism regulating placental development remains unclear. In this study, we showed that the expression of CDC42 was decreased in the villous tissue of RSA samples compared to healthy controls. Further examination demonstrated that CDC42 deficiency led to the differentiation of human trophoblast stem cells (hTSCs) and inhibited their proliferation. Genetic manipulation of YAP and EZRIN in hTSCs revealed that CDC42 regulates the stemness and proliferation of hTSCs; this is dependent on EZRIN, which translocates YAP into the nucleus. Moreover, the expression pattern of EZRIN, YAP, and Ki67 was also abnormal in the villous tissue of RSA samples, consistent with in vitro experiments. In summary, these findings suggest that the CDC42/EZRIN/YAP pathway plays an important role in placental development.
Assuntos
Proteínas do Citoesqueleto/metabolismo , Placenta , Trofoblastos , Proteínas de Sinalização YAP/metabolismo , Proteína cdc42 de Ligação ao GTP/metabolismo , Proliferação de Células , Regulação para Baixo , Feminino , Humanos , Placenta/metabolismo , Gravidez , Células-Tronco , Trofoblastos/citologia , Trofoblastos/metabolismoRESUMO
The macrophage scavenger receptor SR-AI binds to host tissue debris to perform clearance and it binds to bacteria for phagocytosis. In addition, SR-AI modulates macrophage activation through cell signaling. However, investigation of SR-AI signaling on macrophages is complicated due to its promiscuous ligand specificity that overlaps with other macrophage receptors. Therefore, we expressed SR-AI on HEK 293T cells to investigate its ligand binding and signaling. On 293Tcells, SR-AI could respond to E. coli DH5α, leading to NF-κB activation and IL-8 production. However, this requires E. coli DH5α to be sensitized by fresh serum that is treated with heat-inactivation or complement C3 depletion. Anti-C3 antibody inhibits the binding of SR-AI to serum-sensitized DH5α and blocks DH5α stimulation of SR-AI signaling. Further analysis showed that SR-AI can directly bind to purified iC3b but not C3 or C3b. By mutagenesis, The SRCR domain of SR-AI was found to be essential in SR-AI binding to serum-sensitized DH5α. These results revealed a novel property of SR-AI as a complement receptor for iC3b-opsonized bacteria that can elicit cell signaling.