Personalized approaches to the treatment of hemophilia A and B.

The recognition that individuals respond differently to the same medication is not new and dates almost to the founding of western medicine. In the last century it came to be recognized that genetic factors influence the heterogeneity of individual responses to medications with respect to both toxicity and effectiveness. Nonetheless, it has been challenging to integrate pharmacogenetic approaches in the routine practice of medicine as the identification of biomarkers is difficult due to the inherent complexity of biological systems.

T-bet modulates the antibody response and immune protection during murine malaria.

CD4(+) T-cell subtypes govern the synthesis of different Ab isotypes and other immune functions. The influence of CD4(+) T-cell differentiation programs on isotype switching and other aspects of host immunological networks during malaria infection are currently poorly understood. Here, we used Tbx21(-/-) mice deficient for T-bet, a regulator of Th1 CD4(+) T-cell differentiation, to examine the effect of Th1 CD4(+) T cells on the immune protection to nonlethal murine malaria Plasmodium yoelii 17XNL.

Epstein-Barr virus latent membrane protein-2A alters mitochondrial dynamics promoting cellular migration mediated by Notch signaling pathway.

Recently, migration and invasion of breast cancer cells have been linked with dysregulated mitochondrial dynamics. Mitochondria are essential cellular organelles that undergo continuous dynamic cycles of fission and fusion. It has been proposed that a delicate balance between these two processes is important for many pathophysiological outcomes including cancer.

Epstein-Barr virus-encoded small non-coding RNAs induce cancer cell chemoresistance and migration.

Epstein-Barr virus (EBV) encoded small, non-coding, non-polyadenylated RNAs, known as EBERs are the most abundantly expressed viral transcripts in latently EBV infected cells. We found the specific role of EBERs in cell cycle progression, resistance against chemotherapeutic drug and cellular invasion in gastric cancer cells in vitro. Ectopic expression of EBERs upregulates the expression of IL-6 and activate its downstream STAT3, which is significantly involved in downregulating the expression of cell cycle inhibitor genes p21 and p27.