ABSTRACT
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.
ABSTRACT
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.
ABSTRACT
Objective To understand the correlation of enterovirus 71 (EV71), P-selectin glycoprotein ligand-1 (PSG L-1), and scavenger receptor B2 (SCARB2) and to explore the possible pathway and mechanismof EV71 infection by observing the expression of EV71, PSG L-1 and SCARB2 in tissues of infants with brain stemencephalitis. Methods T he organs and tissues of infants with EV71-VP1 positivi-ty in their brain stems were chosen. Expression and distribution of EV71-VP1, PSG L-1, and SCARB2 were detected and compared by immunohistochemistry. Results Strong staining of EV71-VP1 was ob-served in the neuron, glial cells, the inflammatory cells of perivascular cuffing, parietal cells of the gas-tric fundus gland while alveolar macrophages, intestinal gland epitheliumcells, mucosa lymphoid nodule and lymphocyte of palatine tonsil showed moderate staining and weak staining were displayed in mesen-teric lymph nodes and lymphocyte of spleen. PSG L-1 expression was detected in parietal cells of the gastric fundus gland, tonsillar crypt squamous epithelium, alveolar macrophages and leukocytes in each tissue. SCARB2 expression was observed in all the above tissues except the intestines and spleen. Con-clusion T he distribution of EV71 correlates with SCARB2 expression. SCARB2 plays an important role in virus infection and replication. Stomach may be an important site for EV71 replication.
ABSTRACT
Objective To research the role of matrix metalloproteinase-9(MMP-9), transforming growth factor ?1(TGF-?1) in viral myocarditis(VM) and their relationships with myocardial fibrosis, and to explore the forensic significance on sudden death due to viral myocarditis. MethodsSelected 30 cases of VM as experimental group,there cases were divided into definite VM group(n=18) and borderline VM group (n=12);Non-VM(n=10) were selected as control group. Collagen hyperplasia was observed by Masson staining. The expression and localization of MMP-9 and TGF-?1 in viral myocarditis were quantified by immunohistochemical method. Image analysis systems and statistical methods were used for quantitative analysis. ResultsThe amount of collagen fibre in the viral myocarditis group was more than that in the control group. The expression of MMP-9 and TGF-?1 were increased obviously. MMP-9、TGF-?1 expression were positively correlated with the collagen hyperplasis. ConclusionsThe MMP-9 and TGF-?1 may contributes to myocardial fibrosis, and may act as the assistant diagnostic indexes of sudden death due to viral myocarditis.