-The world in which we are living is a huge network of networks and should be described by interdependent networks. The interdependence between networks significantly affects the evolutionary dynamics of cooperation on them. Meanwhile, due to the diversity and complexity of social and biological systems, players on different networks may not interact with each other by the same way, which should be described by multiple models in evolutionary game theory, such as the Prisoner's Dilemma and Snowdrift Game. We therefore study the evolutionary dynamics of cooperation on two interdependent networks playing different games respectively. We clearly evidence that, with the increment of network interdependence, the evolution of cooperation is dramatically promoted on the network playing Prisoner's Dilemma. The cooperation level of the network playing Snowdrift Game reduces correspondingly, although it is almost invisible. In particular, there exists an optimal intermediate region of network interdependence maximizing the growth rate of the evolution of cooperation on the network playing Prisoner's Dilemma. Remarkably, players contacting with other network have advantage in the evolution of cooperation than the others on the same network.

Background:Coronary atherosclerotic heart disease (CAD) is mainly caused by atherosclerosis, an inflammatory disease characterized by plaque formation in arteries. Reactive oxygen species caused structural damage and dysfunction of arterial endothelial cells. Thioredoxin-interacting protein (TXNIP) is the endogenous inhibitor and regulator of thioredoxin, a major cellular antioxidant and antiapoptotic system. In order to explore the role of TXNIP in the occurrence and development of CAD, we detected the TXNIP expression and discussed its molecular mechanisms in CAD.Methods:The mRNA levels of TXNIP gene in peripheral leucocytes were detected in CAD and healthy controls (CTR) by quantitative real-time polymerase chain reaction. And TXNIP proteins were detected by western blotting.Results:TXNIP gene expression levels in patients with unstable angina pectoris (UAP, n = 96) were significantly increased compared with those of CTR (n = 192, P < .05). However, the situation is different in acute myocardial infarction (n = 96, P > .05). Logistic regression analysis showed that TXNIP levels were significantly positive correlated with UAP (OR = 1.728, P < .05).Conclusions:TXNIP gene expression in the peripheral leucocytes was increased in patients with UAP, indicating that TXNIP in circulating leucocytes may be involved in the pathogenesis of UAP.

Baicalin showed multifaceted regulation of genes with important roles in tissue growth and differentiation, and thus it has the potential to be a promising candidate for HPLC-based periodontal regeneration therapy.

Background Acute myocardial infarction (AMI) is the most serious type of coronary atherosclerotic heart disease (CAD). The pathological changes are characterized by atherosclerosis. Oxidative stress plays an important role in atherosclerosis. Thioredoxin-interacting protein (TXNIP), an endogenous inhibitor and regulator of thioredoxin, could bind thioredoxin to regulate its expression and antioxidant activity negatively. The NCBI data show that there are two isoforms in TXNIP gene, namely, TXNIP1 and TXNIP2. Our previous studies have shown that TXNIP expression levels in patients with unstable angina pectoris (UAP) were increased compared with controls (CTR). However, no upregulation of TXNIP was detected in AMI patients. Methods The leucocytes were isolated from peripheral venous blood, and total RNA of the leucocytes was extracted. Then, real-time quantitative PCR was performed. Results mRNA levels of TXNIP2 in AMI were significantly increased compared with CTR (P < 0.05). However, the expression of TXNIP1 was downregulated in AMI, but the difference was not statistically significant (P > 0.05). Logistic regression analysis showed that TXNIP2 mRNA levels were significantly associated with AMI (OR = 2.207, P < 0.05). Conclusions The expression of TXNIP2, not TXNIP1, is upregulated in leukocytes of AMI patients, indicating that only TXNIP2 in circulating leucocytes may be involved in the pathogenesis of AMI.

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