ABSTRACT
OBJECTIVE@#To compare the distribution characteristics of pressing sensitive acupoints on the body surface between bronchial asthma (BA) patients and healthy subjects, and to analyze the distribution rules of pressing sensitive acupoints in BA patients.@*METHODS@#Seventy BA patients and 70 healthy subjects were selected in this study. The pressing sensitive acupoints were checked with finger pulp and marked on human nerve segment graph. The numbers of pressing sensitive acupoints were counted and the positional relationship between distribution of pressing sensitive acupoints and the position of meridians and nerve segment was observed.@*RESULTS@#(1) The incidence rates of pressing sensitive acupoints in BA patients group and healthy subjects group were 91.4% (64/70) and 15.7% (11/70) respectively, and the BA patients group was higher than the healthy subjects group (<0.01). (2) The top 3 meridians with pressing sensitive acupoints occuring in BA patients were bladder meridian of foot-, lung meridian of hand- and large intestine meridian of hand-, and the most frequent pressing sensitive acupoints were Feishu（BL 13）, Xinshu（BL 15）, Chize（LU 5） and Jueyinshu (BL 14). (3) The pressing sensitive acupoints in BA patients were distributed mainly on C, C and T-T nerve segment.@*CONCLUSION@#Pressing sensitive acupoints have a close correlation with physical condition, and there is a close relation between pressing sensitive acupoints distribution and corresponding meridians and nerve segments in BA patients.
ABSTRACT
Cancer therapeutics-related cardiac dysfunction(CTRCD)is receiving more attention.Risk factors assessment before cancer therapy,cardiac function monitoring during and after cancer therapy,and early detection and treatment of myocardial injury are key to preventing clinical heart failure.The incidence and severity of cardiotoxicity can be reduced by measures such as reducing drug dose,adjusting administration route,and using low toxic drugs.Cardioprotective agents including anti-heart failure drugs and dexrazoxane are important for the prevention and treatment of CTRCD.Patients with advanced heart failure may also benefit from mechanical treatments including cardiac resynchronization therapy and mechanically-assisted ventricular devices.This article reviews the recent advances in the prevention and treatment of CTRCD.
Subject(s)
Humans , Cardiotoxicity , Heart , Heart DiseasesABSTRACT
AIM:To study the protective effect of heat shock factor1(HSF1) on the mice with lipopolysaccha-ride (LPS)-induced acute lung injury(ALI),and to screen the relevant differentially-expressed genes. METHODS:ALI mouse model was established by LPS intracheal instillation. The macroscopic and pathological changes of the lung tissue were observed,and the concentrations of total protein,TNF-α, IL-β, IL-6 and VEGF in the bronchoalveolar lavage fluid (BALF) were analyzed. Differentially-expressed genes in the lung tissues of HSF1 +/ +mice and HSF1 -/- mice with ALI induced by LPS were screened by gene chips. The key gene was verified by real-time qPCR. RESULTS:The macroscopic and pathological changes of the lung injury in HSF1 -/- +LPS mice were more serious than those in HSF1 +/ ++LPS mice.The concentrations of total protein,VEGF,TNF-α,IL-1β and IL-6 in the BALF of HSF1 -/- +LPS mice were significantly higher than those of HSF1 +/ ++LPS mice(P<0.05). Compared with the HSF1 +/ +mice,a total of 918 differentially-ex-pressed genes were indentified in the HSF1 -/- mice, among which the expression levels of 65 genes had obvious diffe-rence,with 28 genes up-regulated,including Atg7,ccr1,cxcr2,Tbl1xr1,Mmp9,Pparg,Plcb2,Arrb2,Cntn1,Col4a6, etc, and 37 genes down-regulated,including Fgfr1,Fgfr2,Map4k4,Ddx58,Tfg,Stat3,Smad4,Lamc1,Sdc3,etc. The results of real-time qPCR showed that the mRNA level of CXCR2 in HSF1 -/- + LPS mice was significantly higher than that in HSF1 +/ ++ LPS mice,which was consistent with the results of gene chips. CONCLUSION:HSF1 has protective effect on the mice with LPS-induced ALI. CXCR2 may be involved in the protective effect of HSF1 on this process.