The association of the NOD2 SNPs with CD susceptibility was found in both our initial discovery cohort from the University Hospital Munich-Grosshadern (Supplemental Table S3) and the replication cohort from the University Hospital Munich, Campus Innenstadt and from Ruhr-University Bochum (Supplemental Table S4).
Rong and Perelson [4, 11, 12] developed a kind of mathematical models with latent infection and antiretroviral therapy, examined the relationships among combination drug therapy, viral blips, and the number of latent infected T-cells, and showed that the viral replication from the latent reservoir might result in low-level persistence of viraemia during combination drug therapy.
This genotype-phenotype association was also restricted to lean individuals in the replication cohort from the EUGENE2 consortium (N = 827), comprising individuals from Sweden, Italy, Denmark, Finland, and Germany.
(a) 3D triangulation of DEM (b) overlaying the texture Figure 19 3D triangulation of the replication example from Figure 15(b).
According to their model, the replication initiates from the plus-strand RNA, which passes through the template entry channel of RdRps.
The replication starts from derivation of the energy use distribution for a building stock in a specific location from the survey data.
In mammals, the replication begins from the replication origin of H-strand (OH) and DNA synthesis proceeds unidirectionally.
There was evidence that chromosomal inversions in H. pylori are symmetric around the replication axis from replication origin to replication terminus [14], [44], as shown in Figure S2.
volcanii, it is possible that the genome rearrangement leading to the deletion of the replication origin from pHV4 was mediated by IS element transposition.
