铝板水热碳吸附工艺制备APC/Al层状复合材料的显微组织、力学性能和摩擦学性能

采用铝板水热碳吸附工艺(HTCAP)和真空热压烧结工艺(VHPS)制备无定形碳(APC)/Al层状复合材料,研究葡萄糖溶液浓度对其显微组织、力学性能和摩擦学性能的影响。结果表明,APC在层间分布均匀,并且通过Al的扩散与基体形成良好的界面结合。随着葡萄糖溶液浓度的增加,层间硬度、极限抗拉强度(UTS)和伸长率先增大后减小,而磨损率则呈现相反的趋势,摩擦因数(COF)逐渐减小。当葡萄糖溶液浓度为0.3 mol/L时,伸长率最大,为16.4%,磨损率最小,为0.344×10^(-5)mm^(3)/(N·m)。粘着磨损是APC/Al层状复合材料的主要磨损机制。耐磨性的提高是由于在磨损表面形成均匀的APC润滑膜。

Micron-sized fiber diamond probe for quantum precision measurement of microwave magnetic field

We present a quantitative measurement of the horizontal component of the microwave magnetic field of a coplanar waveguide using a quantum diamond probe in fiber format.The measurement results are compared in detail with simulation,showing a good consistence.Further simulation shows fiber diamond probe brings negligible disturbance to the field under measurement compared to bulk diamond.This method will find important applications ranging from electromagnetic compatibility test and failure analysis of high frequency and high complexity integrated circuits.

二异丙基苯基和十一烷取代的聚乙烯二酰亚胺薄膜激发态动力学研究

苝二亚胺及其衍生物的堆积模式与其分子结构相密切关,进而影响其激发态动力学.通过调节单体、二聚体、J聚体或H聚体等苝二亚胺分子的堆叠模式,可以有效调控其激发态动力学.本文合成了两种苝二亚胺衍生物,十一烷取代的苝二亚胺和二异丙基苯基取代的苝二亚胺,并用旋涂法制备薄膜.利用时间分辨荧光谱和瞬态吸收光谱,系统地研究了两种苝二亚胺非晶膜的激发态动力学.实验结果表明,由于分子存在强耦合作用,这两种薄膜在光激发后都形成了激基缔合物.有趣的是,二异丙基苯基取代的苝二亚胺中瞬态吸收光谱表现了明显的三线态瞬态吸收信号,由此推断二异丙基苯基取代的苝二亚胺薄膜在光激发后产生单线态裂分.该研究阐明非晶态苝二亚胺薄膜中激发态动力学,并为更好地理解和调控非晶态膜的激发态特性提供了借鉴.

Histone modification landscape and the key significance of H3K27me3 in myocardial ischaemia/reperfusion injury

Histone modifications play crucial roles in the pathogenesis of myocardial ischaemia/reperfusion(I/R)injury.However,a genome-wide map of histone modifications and the underlying epigenetic signatures in myocardial I/R injury have not been established.Here,we integrated transcriptome and epigenome of histone modifications to characterize epigenetic signatures after I/R injury.Disease-specific histone mark alterations were mainly found in H3K27me3-,H3K27ac-,and H3K4me1-marked regions 24 and 48 h after I/R.Genes differentially modified by H3K27ac,H3K4me1 and H3K27me3 were involved in immune response,heart conduction or contraction,cytoskeleton,and angiogenesis.H3K27me3 and its methyltransferase polycomb repressor complex 2(PRC2)were upregulated in myocardial tissues after I/R.Upon selective inhibition of EZH2(the catalytic core of PRC2),the mice manifest improved cardiac function,enhanced angiogenesis,and reduced fibrosis.Further investigations confirmed that EZH2 inhibition regulated H3K27me3 modification of multiple pro-angiogenic genes and ultimately enhanced angiogenic properties in vivo and in vitro.This study delineates a landscape of histone modifications in myocardial I/R injury,and identifies H3K27me3 as a key epigenetic modifier in I/R process.The inhibition of H3K27me3 and its methyltransferase might be a potential strategy for myocardial I/R injury intervention.

Sinoatrial node pacemaker cells share dominant biological properties with glutamatergic neurons

Activation of the heart normally begins in the sinoatrial node(SAN).Electrical impulses spontaneously released by SAN pacemaker cells(SANPCs)trigger the contraction of the heart.However,the cellular nature of SANPCs remains controversial.Here,we report that SANPCs exhibit glutamatergic neuron-like properties.By comparing the single-cell transcriptome of SANPCs with that of cells from primary visual cortex in mouse,we found that SANPCs co-clustered with cortical neurons.Tissue and cellular imaging confirmed that SANPCs contained key elements of glutamatergic neurotransmitter system,expressing genes encoding glutamate synthesis pathway(G/s),ionotropic and metabotropic glutamate receptors(Grina,Gria3,Grm1 and Grm5)t and glutamate transporters(Slc17a7).SANPCs highly expressed cell markers of glutamatergic neurons(Snap25 and S/-c17a7)t whereas Gad1,a marker of GABAergic neurons,was negative.Functional studies revealed that inhibition of glutamate receptors or transporters reduced spontaneous pacing frequency of isolated SAN tissues and spontaneous Ca2+transients frequency in single SANPC.Collectively,our work suggests that SANPCs share dominant biological properties with glutamatergic neurons,and the glutamatergic neurotransmitter system may act as an intrinsic regulation module of heart rhythm,which provides a potential intervention target for pacemaker cell-associated arrhythmias.

Prevalence of cardiovascular diseases in China

Cardiovascular diseases(CVD)cause one third of all deaths in China,and the number is anticipated to double by 2020.They also greatly result in disability and adjusted life year loss.The prevalence of CVD has become a new burden for China,due to an aging population,smoking,and changes in dietary habits and lifestyles.As the largest developing country,China needs to tailor her own national policies for managing CVD with full consideration of epidemiology,local needs,and afford-ability.Smoking cessation,increased physical activity,control of hypertension and hypercholesterolemia,and maintenance of a“traditional Chinese”diet should be important strategies for reducing the burden of CVD in China.Health officials in China should take their responsibilities to implement educational and preventive measures seriously.

Mechanistic and therapeutic perspectives for cardiac arrhythmias：beyond ion channels

Cardiac arrhythmias are among the most common causes of death in the world. Foundational studies established the critical role of ion channel disorders in arrhythmias, yet defects in ion channels themselves, such as mutations, may not account for all arrhythmias. Despite the progress made in recent decades, the antiarrhythmic drugs currently available have limited effectiveness,and the majority of these drugs can have proarrhythmic effects. This review describes novel knowledge on cellular mechanisms that cause cardiac arrhythmias, focuses on the dysfunction of subcellular organelles and intracellular logistics, and discusses potential strategies and challenges for developing novel, safe and effective treatments for arrhythmias.

Nucleoporin 35 regulates cardiomyocyte pH homeostasis by controlling Na^(+)-H^(+)exchanger-1 expression

The mammalian nuclear pore complex is comprised of∼30 different nucleoporins(Nups).It governs the nuclear import of gene expression modulators and the export of mRNAs.In cardiomyocytes,Na1-H1 exchanger-1(NHE1)is an integral membrane protein that exclusively regulates intracellular pH(pHi)by exchanging one intracellular H1 for one extracellular Na1.However,the role of Nups in cardiac NHE1 expression remains unknown.We herein report that Nup35 regulates cardiomyocyte NHE1 expression by controlling the nucleo-cytoplasmic trafficking of nhe1 mRNA.The N-terminal domain of Nup35 determines nhe1 mRNA nuclear export by targeting the 5′-UTR(2412 to2213 nt)of nhe1mRNA.Nup35 ablationweakensthe resistance of cardiomyocytes to an acid challenge by depressingNHE1 expression.Moreover,we identify thatNup35 andNHE1 are simultaneously downregulated in ischemic cardiomyocytes both in vivo and in vitro.Enforced expression of Nup35 effectively counteracts the anoxia-induced intracellular acidification.We conclude that Nup35 selectively regulates cardiomyocyte pHi homeostasis by posttranscriptionally controlling NHE1 expression.This finding reveals a novel regulatory mechanism of cardiomyocyte pHi,and may provide insight into the therapeutic strategy for ischemic cardiac diseases.