Cumulative effects of triadic closure and homophily in social networks.

Social network structure has often been attributed to two network evolution mechanisms-triadic closure and choice homophily-which are commonly considered independently or with static models. However, empirical studies suggest that their dynamic interplay generates the observed homophily of real-world social networks. By combining these mechanisms in a dynamic model, we confirm the longheld hypothesis that choice homophily and triadic closure cause induced homophily. We estimate how much observed homophily in friendship and communication networks is amplified due to triadic closure. We find that cumulative effects of homophily amplification can also lead to the widely documented core-periphery structure of networks, and to memory of homophilic constraints (equivalent to hysteresis in physics). The model shows that even small individual bias may prompt network-level changes such as segregation or core group dominance. Our results highlight that individual-level mechanisms should not be analyzed separately without considering the dynamics of society as a whole.

Pharmacogenetic Variation in Over 100 Genes in Patients Receiving Acenocumarol.

Coumarins are widely prescribed worldwide, and in Mexico acenocumarol is the preferred form. It is well known that despite its efficacy, coumarins show a high variability for dose requirements. We investigated the pharmacogenetic variation of 110 genes in patients receiving acenocumarol using a targeted NGS approach. We report relevant population differentiation for variants on CYP2C8, CYP2C19, CYP4F11, CYP4F2, PROS, and GGCX, VKORC1, CYP2C18, NQO1. A higher proportion of novel-to-known variants for 10 genes was identified on 41 core pharmacogenomics genes related to the PK (29), PD (3), of coumarins, and coagulation proteins (9) including, CYP1A1, CYP3A4, CYP3A5, and F8, and a low proportion of novel-to-known variants on CYP2E1, VKORC1, and SULT1A1/2. Using a Bayesian approach, we identified variants influencing acenocumarol dosing on, VKORC1 (2), SULT1A1 (1), and CYP2D8P (1) explaining 40-55% of dose variability. A collection of pharmacogenetic variation on 110 genes related to the PK/PD of coumarins is also presented. Our results offer an initial insight into the use of a targeted NGS approach in the pharmacogenomics of coumarins in Mexican Mestizos.