“For carbon tetrachloride, a temperature Hugoniot at 7-23 GPa and a distribution of the constant-volume specific heat on the Hugoniot C(V)(T) at 1057-3275 K are simultaneously estimated from the Walsh-Christian (WC) equation such that the Hugoniot fits well to the existing measured data. The estimated C(V)(T) distribution reveals the significance of the contribution of electrons and ions to the specific heat. That is, in contrast to the almost uniform distribution of the specific heat predicted from the Debye equation, the C(V)(T) distribution increases significantly with an increase in the Hugoniot temperature due to thermal excitation
of electrons at 1057-1500 K selleck chemicals llc (7-10.1 GPa), additional activation of the dimerization reaction at 1500-2350 K (10.1-16 GPa), and also additional activation of the polymerization reaction Galardin at 2350-3275 K (16-23 GPa). As an example, evidence is presented that carbon tetrachloride
is a semiconductor at 1500 K. The C(V)(T) distribution in each temperature range is formulated and a temperature Hugoniot is reevaluated from the WC equation using the specific heat equations formulated. It is confirmed by a good fit of the reevaluated Hugoniot to the existing measured data that the specific heat equations express the C(V)(T) distribution appropriately.”
“Background-Familial dilated cardiomyopathy (DCM) is a genetically heterogeneous disease with >30 known genes. TTN truncating variants were recently implicated in a candidate gene study to cause 25% of familial and 18% of sporadic DCM cases.
Methods and Results-We used an unbiased genome-wide approach using both linkage analysis and variant filtering across the exome sequences of 48 individuals affected with DCM from 17 families to identify
genetic cause. Linkage analysis ranked the TTN region as falling under the second highest genome-wide multipoint linkage peak, multipoint logarithm of odds, 1.59. We identified 6 TTN truncating variants carried by individuals affected with DCM in 7 of 17 DCM families (logarithm of odds, 2.99); 2 of these 7 families also had novel missense variants that segregated with disease. Two additional novel truncating TTN variants did not segregate with DCM. Nucleotide diversity at the TTN buy 3-MA locus, including missense variants, was comparable with 5 other known DCM genes. The average number of missense variants in the exome sequences from the DCM cases or the approximate to 5400 cases from the Exome Sequencing Project was approximate to 23 per individual. The average number of TTN truncating variants in the Exome Sequencing Project was 0.014 per individual. We also identified a region (chr9q21.11-q22.31) with no known DCM genes with a maximum heterogeneity logarithm of odds score of 1.74.
Conclusions-These data suggest that TTN truncating variants contribute to DCM cause.