D ue to the negative autopsy and w ithout cardiac structural abnorm alities, unexpected sudden cardiac death (U SC D ) is alw ays a tough issue for forensic pathological expertise. U SC D m ay be asso-ciated w ith parts of fatal arrhythm ic diseases. T hese arrhythm ic diseases m ay be caused by disorders of cardiac ion channels or channel-related proteins. C aveolin can com bine w ith m ultiple m yocardial ion channel proteins through its scaffolding regions and plays an im portant role in m aintaining the depolar-ization and repolarization of cardiac action potential. W hen the structure and function of caveolin are af-fected by gene m utations or abnorm al protein expression, the functions of the regulated ion channels are correspondingly im paired, w hich leads to the occurrence of m ultiple channelopathies, arrhythm ia or even sudden cardiac death. It is im portant to study the effects of caveolin on the functions of ion channels for exploring the m echanism s of m alignant arrhythm ia and sudden cardiac death.

Objective T o explore the genetic variation sites of caveolin (C A V ) and their correlation w ith sudden unexplained death (SU D ).Methods The blood sam ples w ere collected from SU D group (71 cases), coronary artery disease (C A D ) group (62 cases) and control group (60 cases), respectively. T he genom e D N A w ere extracted and sequencing w as perform ed directly by am plifying gene coding region and exon-intron splicing region of CAV1 and CAV3 using PC R . T he type of heritable variation of CVA w as con-firm ed and statistical analysis w as perform ed. Results A total of 4 variation sites that m aybe significa-tive w ere identified in SU D group, and tw o w ere new found w hich w ere CAV1: c.45C>T (T 15T ) and CAV1:c.512G>A (R 171H ), and tw o w ere SN P loci w hich w ere CAV1:c.246C>T (rs35242077) and CAV3:c.99C>T (rs1008642) and had significant difference (P<0.05) in allele and genotype frequencies betw een SU D and control groups. Forem entioned variation sites w ere not found in C A D group. Conclu-sion T he variants of CAV1 and CAV3 m ay be correlated w ith a part of SU D group.

Objective:To explore the effect and possible mechanism of Zexie Tang(ZXT)regulate the balance of M1/M2 polarization in macrophage cells.Methods:Lipid metabolism disorder mouse model was induced by Western diet(WD)in vivo,RAW264.7 cell M1/M2 macrophage model was induced by LPS/IL-4 in vitro,set up blank group,model group and ZXT group.The flu-orescence intensity of M1 and M2 macrophage markers in adipose tissue and RAW264.7 cells was observed by immunofluorescence staining;protein levels of p-AKT,AKT and COX-2 were measured by Western blot;levels of macrophage marker gene mRNAs of M1 and M2 were analysed by qPCR;IL-1β and IL-10 were measured by ELISA;content of NO was detected by Griess;binding of active components of Alismatis Rhizoma and Atractylodes Macrocephala with PI3K protein was analyzed by Docking.Results:Compared with WD group,expression of CD11c was significantly decreased in ZXT group,while expression of CD206 was significantly up-regulated;ZXT reversed LPS-induced increased in CD80 expression,down-regulated mRNA levels of M1 macrophage marker gene iNOS,etc,decreased the expression of COX-2 protein,and inhibited the secretion of IL-1β(P<0.001);ZXT promoted IL-4-induced CD206 expression,up-regulation of M2 macrophage marker gene Arg-1 and other mRNAs levels and secretion of IL-10;ZXT reversed the LPS-induced increased in NO release;p-AKT/AKT protein level increased in vivo and in vitro after ZXT administration;Docking re-sults show that many active ingredients in Alismatis Rhizoma and Atractylodes Macrocephala could form hydrogen bonds stably with PI3K protein.Conclusion:ZXT regulates the M1/M2 polarization balance of macrophages,and its mechanism may be related to the regulation of PI3K/AKT pathway.