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1.  The Effects of Extra-Somatic Weapons on the Evolution of Human Cooperation towards Non-Kin 
PLoS ONE  2014;9(5):e95742.
Human cooperation and altruism towards non-kin is a major evolutionary puzzle, as is ‘strong reciprocity’ where no present or future rewards accrue to the co-operator/altruist. Here, we test the hypothesis that the development of extra-somatic weapons could have influenced the evolution of human cooperative behaviour, thus providing a new explanation for these two puzzles. Widespread weapons use could have made disputes within hominin groups far more lethal and also equalized power between individuals. In such a cultural niche non-cooperators might well have become involved in such lethal disputes at a higher frequency than cooperators, thereby increasing the relative fitness of genes associated with cooperative behaviour. We employ two versions of the evolutionary Iterated Prisoner's Dilemma (IPD) model – one where weapons use is simulated and one where it is not. We then measured the performance of 25 IPD strategies to evaluate the effects of weapons use on them. We found that cooperative strategies performed significantly better, and non-cooperative strategies significantly worse, under simulated weapons use. Importantly, the performance of an ‘Always Cooperate’ IPD strategy, equivalent to that of ‘strong reciprocity’, improved significantly more than that of all other cooperative strategies. We conclude that the development of extra-somatic weapons throws new light on the evolution of human altruistic and cooperative behaviour, and particularly ‘strong reciprocity’. The notion that distinctively human altruism and cooperation could have been an adaptive trait in a past environment that is no longer evident in the modern world provides a novel addition to theory that seeks to account for this major evolutionary puzzle.
doi:10.1371/journal.pone.0095742
PMCID: PMC4010415  PMID: 24796325
2.  Genetic Polymorphisms of TERT and CLPTM1L and Risk of Lung Cancer – a Case- Control Study in a Chinese Population 
Background/objectives
Genetic variants of Telomerase reverse transcriptase (TERT) and cleft lip and palate trans-membrane 1 like (CLPTM1L) genes in chromosome 5p15.33 region were previously identified to influence the susceptibility to lung cancer. We examined the association of single nucleotide polymorphisms (SNPs) in TERT and CLPTM1L genes with lung cancer and explored their potential modifying effects on the relationship between environmental risk factors and lung cancer in a Chinese population.
Methods
We genotyped rs2736100 (TERT) and rs401681 (CLPTM1L) SNPs in a case-control study with 399 lung cancer cases and 466 controls form Taiyuan, China. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression models. Potential confounders were controlled for in the adjusted models.
Results
We found that the GG genotype of TERT was positively associated with lung cancer (OR = 1.47, 95% CI: 1.00 – 2.16). The association was stronger in participants older than 60 years, exposed to low indoor air pollution and adenocarcinoma and squamous cell carcinoma (SCC) in recessive model analysis. The GA genotype of CLPTM1L was inversely associated with lung cancer (OR = 0.72, 95% CI: 0.54 – 0.97). The association was stronger in participants 60 years old or younger, males, heavy smokers, exposed to low indoor air pollution and SCC in dominant model analysis. Individuals carrying both TERT and CLPTM1L risk genotypes had higher risk of lung cancer (OR = 1.80, 95% CI: 1.15 – 2.82). Significant interaction was observed between CLPTM1L and indoor air pollution in association with lung cancer.
Conclusions
Our results reiterate that genetic variants of TERT and CLPTM1L contribute to lung cancer susceptibility in Chinese population. These associations need to be verified in larger and different populations.
doi:10.1016/j.lungcan.2013.01.021
PMCID: PMC3627395  PMID: 23433592
Lung cancer; TERT; CLPTM1L; SNPs; Susceptibility; Chinese population
3.  TP53 genetic polymorphisms, interactions with lifestyle factors and lung cancer risk: a case control study in a Chinese population 
BMC Cancer  2013;13:607.
Background
A pathway-based genotyping analysis suggested rs2078486 was a novel TP53 SNP, but very few studies replicate this association. TP53 rs1042522 is the most commonly studied SNP, but very few studies examined its potential interaction with environmental factors in relation to lung cancer risk. This study aims to examine associations between two TP53 single-nucleotide polymorphisms (SNPs) (rs2078486, rs1042522), their potential interaction with environmental factors and risk of lung cancer.
Methods
A case–control study was conducted in Taiyuan, China. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). Multiplicative and additive interactions between TP53 SNPs and lifestyle factors were evaluated.
Results
Variant TP53 rs2078486 SNP was significantly associated with elevated lung cancer risk among smokers (OR: 1.70, 95% CI: 1.08 - 2.67) and individuals with high indoor air pollution exposure (OR: 1.51, 95% CI: 1.00-2.30). Significant or borderline significant multiplicative and additive interactions were found between TP53 rs2078486 polymorphism with smoking and indoor air pollution exposure. The variant genotype of TP53 SNP rs1042522 significantly increased lung cancer risk in the total population (OR: 1.57, 95% CI: 1.11-2.21), but there was no evidence of heterogeneity among individuals with different lifestyle factors.
Conclusions
This study confirmed that TP53 rs2078486 SNP is potentially a novel TP53 SNP that may affect lung cancer risk. Our study also suggested potential synergetic effects of TP53 rs2078486 SNP with smoking and indoor air pollution exposure on lung cancer risk.
doi:10.1186/1471-2407-13-607
PMCID: PMC3877976  PMID: 24369748
Lung cancer; TP53; Single-nucleotide polymorphism; Chinese population
4.  Effect of telmisartan on the expression of adiponectin receptors and nicotinamide adenine dinucleotide phosphate oxidase in the heart and aorta in type 2 diabetic rats 
Background
Diabetic cardiovascular disease is associated with decreased adiponectin and increased oxidative stress. This study investigated the effect of telmisartan on the expression of adiponectin receptor 2 (adipoR2) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits in the heart and the expression of adiponectin receptor 1 (adipoR1) in aorta in type 2 diabetic rats.
Methods
Type 2 diabetes was induced by high-fat and high-sugar diet and intraperitoneal injection of a low dose of streptozotocin (STZ). Heart function, adipoR2, p22phox, NOX4, glucose transporter 4(GLUT4), monocyte chemoattractant protein-1(MCP-1) and connective tissue growth factor (CTGF)in the heart, and adipoR1, MCP-1 and nuclear factor kappa B (NF-κB) in aorta were analyzed in controls and diabetic rats treated with or without telmisartan (5mg/kg/d) by gavage for 12 weeks.
Results
Heart function, plasma and myocardial adiponectin levels, the expression of myocardial adipoR2 and GLUT4 were significantly decreased in diabetic rats (P <0.05). The expression of myocardial p22phox, NOX4, MCP-1, and CTGF was significantly increased in diabetic rats (P <0.05). The expression of adipoR1 was decreased and the expression of MCP-1 and NF-κB was increased in the abdominal aorta in diabetic rats (P <0.05). Telmisartan treatment significantly attenuated these changes in diabetic rats (P <0.05).
Conclusions
Our results suggest that telmisartan upregulates the expression of myocardial adiponectin, its receptor 2 and GLUT4. Simultaneously, it downregulates the expression of myocardial p22phox, NOX4, MCP-1, and CTGF, contributing so to the improvement of heart function in diabetic rats. Telmisartan also induces a protective role on the vascular system by upregulating the expression of adipoR1 and downregulating the expression of MCP-1 and NF-κB in the abdominal aorta in diabetic rats.
doi:10.1186/1475-2840-11-94
PMCID: PMC3471013  PMID: 22873349
Telmisartan; Adiponectin receptor; NADPH oxidase; Type 2 diabetic; Cardiac; Aorta

Results 1-4 (4)