During narrative comprehension, inference-related priming was reliable and

equally strong in Verubecestat mw both hemispheres. In contrast, during conversation comprehension, inference-related priming was only reliable for target words presented to lvf-RH. This work demonstrates that priming for inference-related concepts can be measured with input in conversational form and suggests the language processing style of the RH is advantageous for comprehending conversation. (C) 2012 Elsevier Ltd. All rights reserved.”
“Radon and radon progeny inhalation exposure are recognized to induce lung cancer. To explore the role of mitochondria in radon-induced carcinogenesis in humans, an in vitro partially depleted mitochondrial Entinostat price DNA (mtDNA) cell line (rho-) was generated by treatment of human bronchial epithelial (HBE) cells (rho+) with ethidium bromide (EB). The characterization of rho- cells indicated the presence of dysfunctional mitochondria and might thus serve a reliable model to investigate the role of mitochondria. In a gas inhalation chamber, rho-

and rho+ cells were exposed to radon gas produced by a radium source. Results showed that apoptosis was significantly increased both in rho- and rho+ cells irradiated by radon. Moreover, apoptosis in rho- cells showed a lower level than in rho+ cells. Radon was further found to depress mitochondrial membrane potential (MMP) of HBE cells with knockdown mtDNA. Production of reactive oxygen species (ROS) was markedly elevated both in rho- and rho+ Sclareol cells exposed to radon. The distribution of phases of cell cycle was different in rho- compared to rho+ cells. Radon irradiation induced a rise in G2/M and decrease in S phase in rho+ cells. In rho- cells, G1, G2/M, and S populations remained similar to cells exposed to radon. In conclusion, radon-induced changes

in ROS generation, MMP and cell cycle are all attributed to reduction of apoptosis, which may trigger and promote cell transformation, leading to carcinogenesis. Our study indicates that the use of the rho- knockdown mtDNA HBE cells may serve as a reliable model to study the role played by mitochondria in carcinogenic diseases.”
“Atherosclerosis results from a metabolic imbalance and chronic arterial inflammation and macrophages are key during the initiation and progression of atherosclerotic lesions. A number of macrophage subsets have been identified in atherosclerotic plaques. Arginase 1 (Arg1), a marker for the M2 anti-inflammatory subset, hydrolyzes L-arginine into urea and omithine, a precursor to L-proline and polyamines, which are implicated in tissue repair and wound healing. Additionally, Arg1 inhibits nitric oxide-mediated inflammatory pathways by competing with iNOS for the same substrate, L-arginine. Therefore, changes in Arg1 expression in macrophages may affect the development of atherosclerosis.