Static elasticity of cordierite I : effect of heavy ion irradiation on the compressibility of hydrous cordierite

The effect of ion beam irradiations on the elastic properties of hydrous cordierite was investigated by means of Raman and X-ray diffraction experiments. Oriented single crystals were exposed to swift heavy ions (Au, Bi) of various specific energies (10.0-11.1 MeV/u and 80 MeV/u), applying fluences up to 5 7 1013 ions/cm2. The determination of unit-cell constants yields a volume strain of 3.4 7 10-3 up to the maximum fluence, which corresponds to a compression of non-irradiated cordierite at ~480 \ub1 10 MPa. The unit-cell contraction is anisotropic (e1 = 1.4 \ub1 0.1 7 10-3, e2 = 1.5 \ub1 0.1 7 10-3, and e3 = 7 \ub1 1 7 10-4) with the c-axis to shrink only half as much as the axes within the ab-plane. The lattice elasticity for irradiated cordierite (\u3c6{symbol} = 1 7 1012 ions/cm2) was determined from single-crystal XRD measurements in the diamond anvil cell. The fitted third-order Birch-Murnaghan equation-of-state parameters of irradiated cordierite (V0 = 1548.41 \ub1 0.16 \uc53, K0 = 117.1 \ub1 1.1 GPa, 02K/ 02P = -0.6 \ub1 0.3) reveal a 10-11 % higher compressibility compared to non-irradiated cordierite. While the higher compressibility is attributed to the previously reported irradiation-induced loss of extra-framework H2O, the anomalous elasticity as expressed by elastic softening (\u3b2 a-1, \u3b2 b-1, \u3b2 c-1 = 397 \ub1 9, 395 \ub1 28, 308 \ub1 11 GPa, 02(\u3b2-1)/ 02P = -4.5 \ub1 2.7, -6.6 \ub1 8.4, -5.4 \ub1 3.0) appears to be related to the framework stability and to be independent of the water content in the channels and thus of the ion beam exposure

Antithrombin, protein C, and protein S: genome and transcriptome-wide association studies identify 7 novel loci regulating plasma levels

Background:Antithrombin, PC (protein C), and PS (protein S) are circulating natural anticoagulant proteins that regulate hemostasis and of which partial deficiencies are causes of venous thromboembolism. Previous genetic association studies involving antithrombin, PC, and PS were limited by modest sample sizes or by being restricted to candidate genes. In the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium, we meta-analyzed across ancestries the results from 10 genome-wide association studies of plasma levels of antithrombin, PC, PS free, and PS total. Methods:Study participants were of European and African ancestries, and genotype data were imputed to TOPMed, a dense multiancestry reference panel. Each of the 10 studies conducted a genome-wide association studies for each phenotype and summary results were meta-analyzed, stratified by ancestry. Analysis of antithrombin included 25 243 European ancestry and 2688 African ancestry participants, PC analysis included 16 597 European ancestry and 2688 African ancestry participants, PSF and PST analysis included 4113 and 6409 European ancestry participants. We also conducted transcriptome-wide association analyses and multiphenotype analysis to discover additional associations. Novel genome-wide association studies and transcriptome-wide association analyses findings were validated by in vitro functional experiments. Mendelian randomization was performed to assess the causal relationship between these proteins and cardiovascular outcomes. Results:Genome-wide association studies meta-analyses identified 4 newly associated loci: 3 with antithrombin levels (GCKR, BAZ1B, and HP-TXNL4B) and 1 with PS levels (ORM1-ORM2). transcriptome-wide association analyses identified 3 newly associated genes: 1 with antithrombin level (FCGRT), 1 with PC (GOLM2), and 1 with PS (MYL7). In addition, we replicated 7 independent loci reported in previous studies. Functional experiments provided evidence for the involvement of GCKR, SNX17, and HP genes in antithrombin regulation. Conclusions:The use of larger sample sizes, diverse populations, and a denser imputation reference panel allowed the detection of 7 novel genomic loci associated with plasma antithrombin, PC, and PS levels.Clinical epidemiolog