Daily ingestion of fresh tomato fruits more than 1.5 kg(about Selleck JNK inhibitor 100 g DM)caused soft faeces in goats. (C) 2009 Elsevier B.V. All rights reserved.”
“Androgen receptor signaling plays a critical role in prostate cancer pathogenesis. Yet, the regulation of androgen receptor signaling remains elusive. Even with stringent androgen deprivation therapy, androgen receptor signaling persists. Here, our data suggest that there is a complex interaction between the expression of the tumor suppressor miRNA, miR-31, and androgen receptor

signaling. We examined primary and metastatic prostate cancer and found that miR-31 expression was reduced as a result of promoter hypermethylation, and importantly, the levels of miR-31 expression were inversely correlated with the aggressiveness of the disease. As the expression of androgen receptor and miR-31 was inversely correlated in the cell lines, our study further suggested that miR-31 and androgen receptor could mutually repress each other. Upregulation of miR-31 effectively suppressed androgen DMXAA supplier receptor expression through multiple mechanisms and inhibited prostate cancer growth in vivo. Notably, we found that miR-31 targeted androgen receptor directly at a site located in the coding region, which was commonly mutated in prostate cancer. In addition, miR-31 suppressed cell-cycle regulators including E2F1, E2F2, EXO1,

FOXM1, and MCM2. Together, our findings suggest a novel androgen receptor regulatory mechanism

mediated through miR-31 expression. learn more The downregulation of miR-31 may disrupt cellular homeostasis and contribute to the evolution and progression of prostate cancer. We provide implications for epigenetic treatment and support clinical development of detecting miR-31 promoter methylation as a novel biomarker. Cancer Res; 1-13. (c) 2012 AACR.”
“Networks are increasingly central to modern science owing to their ability to conceptualize multiple interacting components of a complex system. As a specific example of this, understanding the implications of contact network structure for the transmission of infectious diseases remains a key issue in epidemiology. Three broad approaches to this problem exist: explicit simulation; derivation of exact results for special networks; and dynamical approximations. This paper focuses on the last of these approaches, and makes two main contributions. Firstly, formal mathematical links are demonstrated between several prima facie unrelated dynamical approximations. And secondly, these links are used to derive two novel dynamical models for network epidemiology, which are compared against explicit stochastic simulation. The success of these new models provides improved understanding about the interaction of network structure and transmission dynamics.