Aim To study the effect of genistein on contractility of isolated papillary muscles in guinea pig and its mechanisms.Methods Isolated guinea pig papillary muscles were suspended in organ baths containing KH solution,and the effect of genistein on contractility of myocardium was observed after an equilibration period.Results Genistein and isoprenaline hydrochloride showed positive inotropic effects on contractility of myocardium in a dose-dependent manner(1～100 ?mol?L~(-1)) Propranolol(1 ?mol?L~(-1)) and verapamil hydrochloride(0.5 ?mol?L~(-1)) attenuated the positive inotropic effect of isoprenaline hydrochloride(2 ?mol?L~(-1)),but did not change the effect of genistein(100 ?mol?L~(-1)).Furthermore,the enhancement of the contractility induced by elevation of extracellular Ca~(2+) concentration in papillary muscles did not show any change after pretreatment with genistein(1,10 ?mol?L~(-1)).Finally,the positive inotropic effect of genistein was attenuated partially by tamoxifen(1 ?mol?L~(-1)),however,was not influenced by sodium orthovanadate(1 ?mol?L~(-1)).Conclusions Genistein has the positive inotropic effect on guinea pig papillary muscles,which is not related to the activation of Ca~(2+) channel on cell membrane,? adrenoceptor and tyrosine kinase pathway,but this effect may involve in uptake and utilization of sarcoplasmic reticulum Ca~(2+).

Objective To explore the changes of resting state default mode network (DMN) in patients with chronic pain caused by cervical spondylosis (CPCS). Methods 8 healthy controls and 10 patients accepted functional MRI scanning. Surface based DMN was extracted with independent component analysis (ICA). The functional connectivity of the components of DMN were discriminated with support vector machine (SVM) algorithm from the patients to the controls. Results The DMN connectivity was different in the patients from the controls in some of the component areas. Conclusion DMN of CPCS patients is disorder in multiple brain areas, which may be involved with dysfunction of perception processing, emotion and memory.

AIM:To investigate the role of phosphoenolpyruvate carboxykinase 1(PCK1)in the proliferation and migration of mouse vascular smooth muscle cells(VSMCs)and the underlying mechanism.METHODS:The prolif-eration and migration of mouse VSMCs were induced by platelet-derived growth factor(PDGF)-BB.The cells were divided into a vehicle group and a PDGF-BB group.The expression of PCK1 was detected by Western blot and immunofluores-cence staining.The mouse Pck1 siRNA(si Pck1)were transfected into mouse VSMCs to silence PCK1.The cells were di-vided into the vehicle,si Pck1+vehicle,PDGF-BB and si Pck1+PDGF-BB groups.The protein level of PCK1 was detected by Western blot.The proliferation was explored by Ki-67 immunofluorescence staining and the viability was detected by CCK-8 assay.The migration was determined by a scratch test.Mitochondrial dynamics were observed via transmission electron microscopy.A lentivirus carrying dynamin-related protein 1(Drp1)gene(lenti-Drp1)was transfected into VSMCs to induce them to overexpress DRP1.The cells were divided into the PDGF-BB,si Pck1+PDGF-BB,lenti-Drp1+PDGF-BB and lenti-Drp1+si Pck1+PDGF-BB groups.Proliferation,migration and mitochondrial dynamics were measured as described above.RESULTS:PDGF-BB increased the protein expression of PCK1 and DRP1,cell viability,the per-centage of Ki-67-positive cells,the wound healing rate and mitochondrial division in VSMCs.These effects were sup-pressed when PCK1 protein expression was silenced.After DRP1 was overexpressed,the inhibitory effects of PCK1 silenc-ing on cell viability,the percentage of Ki-67-positive cells,the wound healing rate and mitochondrial division were signifi-cantly reversed.CONCLUSION:PCK1 promotes the mitochondrial division,proliferation and migration of VSMCs in mice by upregulating the expression of DRP1.