Angle-resolved photoemission study of MX-chain compound [Ni(chxn)2_2Br]Br2_2

We report on the results of angle-resolved photoemission experiments on a quasi-one-dimensional $MX$-chain compound [Ni(chxn)$_2$Br]Br$_2$ (chxn = 1$R$,2$R$-cyclohexanediamine), a one-dimensional Heisenberg system with $S=1/2$ and $J \sim 3600$ K, which shows a gigantic non-linear optical effect. A "band" having about 500 meV energy dispersion is found in the first half of the Brillouin zone $(0\le kb/\pi <1/2)$, but disappears at $kb / \pi \sim 1/2$. Two dispersive features, expected from the spin-charge separation, as have been observed in other quasi-one-dimensional systems like Sr$_2$CuO$_3$, are not detected. These characteristic features are well reproduced by the $d$-$p$ chain model calculations with a small charge-transfer energy $\Delta$ compared with that of one-dimensional Cu-O based compounds. We propose that this smaller $\Delta$ is the origin of the absence of clear spin- and charge-separation in the photoemission spectra and strong non-linear optical effect in [Ni(chxn)$_2$Br]Br$_2$.Comment: 4 pages, 3 figure

Randomized Comparison Between Everolimus-Eluting Bioresorbable Scaffold and Metallic Stent: Multimodality Imaging Through 3 Years

Objectives: The aim of this study was to investigate the vascular responses and fates of the scaffold after bioresorbable vascular scaffold (BVS) implantation using multimodality imaging. Background: Serial comprehen

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.</p

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries

Cu 2p core-level photoemission spectrum of Sr₂CuO₃

We measure the Cu 2p X-ray photoemission spectrum (XPS) of Sr2CuO3 and analyze it by means of exact diagonalization calculations for (CunO3n)4n- clusters. In Sr2CuO3, the intensity ratio of the 3d9 satellite to the 3d10 L main line is 0.35–0.4, which is evidently smaller than that in the other high-T c related cuprates. We ascribe it as the smaller charge-transfer energy between the Cu 3d and O 2p. The origin of the broad main-line of Sr2CuO3 is also discussed