Impact of production strategies and animal performance on economic values of dairy sheep traits

The objective of this study was to carry out a sensitivity analysis on the impact of various production strategies and performance levels on the relative economic values (REVs) of traits in dairy sheep. A bio-economic model implemented in the program package ECOWEIGHT was used to simulate the profit function for a semi-extensive production system with the Slovak multi-purpose breed Improved Valachian and to calculate the REV of 14 production and functional traits. The following production strategies were analysed: differing proportions of milk processed to cheese, customary weaning and early weaning of lambs with immediate sale or sale after artificial rearing, seasonal lambing in winter and aseasonal lambing in autumn. Results of the sensitivity analysis are presented in detail for the four economically most important traits: 150 days milk yield, conception rate of ewes, litter size and ewe productive lifetime. Impacts of the differences in the mean value of each of these four traits on REVs of all other traits were also examined. Simulated changes in the production circumstances had a higher impact on the REV for milk yield than on REVs of the other traits investigated. The proportion of milk processed to cheese, weaning management strategy for lambs and level of milk yield were the main factors influencing the REV of milk yield. The REVs for conception rate of ewes were highly sensitive to the current mean level of the trait. The REV of ewe productive lifetime was most sensitive to variation in ewe conception rate, and the REV of litter size was most affected by weaning strategy for lambs. On the basis of the results of sensitivity analyses, it is recommended that economic values of traits for the overall breeding objective for dairy sheep be calculated as the weighted average of the economic values obtained for the most common production strategies of Slovak dairy sheep farms and that economic values be adjusted after substantial changes in performance levels of the traits.     

Association between the Melatonin Receptor 1B Gene Polymorphism on the Risk of Type 2 Diabetes,Impaired Glucose Regulation: A Meta-Analysis

Background

Melatonin receptor 1B (MTNR1B) belongs to the seven-transmembrane G protein-coupled receptor superfamily involved in insulin secretion, which has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) since it was first identified as a loci associated with fasting plasma glucose level through genome wide association approach. The relationship between MTNR1B and T2D has been reported in various ethnic groups. The aim of this study was to consolidate and summarize published data on the potential of MTNR1B polymorphisms in T2D risk prediction.

Methods

PubMed, EMBASE, ISI web of science and the CNKI databases were systematically searched to identify relevant studies. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Heterogeneity and publication bias were also tested.

Results

A total of 23 studies involving 172,963 subjects for two common polymorphisms (rs10830963, rs1387153) on MTNR1B were included. An overall random effects per-allele OR of 1.05 (95% CI: 1.02–1.08; P<10⁻⁴) and 1.04 (95% CI: 0.98–1.10; P = 0.20) were found for the two variants respectively. Similar results were also observed using dominant or recessive genetic model. There was strong evidence of heterogeneity, which largely disappeared after stratification by ethnicity. Significant results were found in Caucasians when stratified by ethnicity; while no significant associations were observed in East Asians and South Asians. Besides, we found that the rs10830963 polymorphism is a risk factor associated with increased impaired glucose regulation susceptibility.

Conclusions

This meta-analysis demonstrated that the rs10830963 polymorphism is a risk factor for developing impaired glucose regulation and T2D.     

The evolution and ecology of multiple antipredator defences

Prey seldom rely on a single type of antipredator defence, often using multiple defences to avoid predation. In many cases, selection in different contexts may favour the evolution of multiple defences in a prey. However, a prey may use multiple defences to protect itself during a single predator encounter. Such “defence portfolios” that defend prey against a single instance of predation are distributed across and within successive stages of the predation sequence (encounter, detection, identification, approach (attack), subjugation and consumption). We contend that at present, our understanding of defence portfolio evolution is incomplete, and seen from the fragmentary perspective of specific sensory systems (e.g., visual) or specific types of defences (especially aposematism). In this review, we aim to build a comprehensive framework for conceptualizing the evolution of multiple prey defences, beginning with hypotheses for the evolution of multiple defences in general, and defence portfolios in particular. We then examine idealized models of resource trade-offs and functional interactions between traits, along with evidence supporting them. We find that defence portfolios are constrained by resource allocation to other aspects of life history, as well as functional incompatibilities between different defences. We also find that selection is likely to favour combinations of defences that have synergistic effects on predator behaviour and prey survival. Next, we examine specific aspects of prey ecology, genetics and development, and predator cognition that modify the predictions of current hypotheses or introduce competing hypotheses. We outline schema for gathering data on the distribution of prey defences across species and geography, determining how multiple defences are produced, and testing the proximate mechanisms by which multiple prey defences impact predator behaviour. Adopting these approaches will strengthen our understanding of multiple defensive strategies.     

Inhibition of thrombin-induced microglial activation and NADPH oxidase by minocycline protects dopaminergic neurons in the substantia nigra in vivo

The present study shows that activation of microglial NADPH oxidase and production of reactive oxygen species (ROS) is associated with thrombin-induced degeneration of nigral dopaminergic neurons in vivo. Seven days after thrombin injection in the rat substantia nigra (SN), tyrosine hydroxylase immunocytochemistry showed a significant loss of nigral dopaminergic neurons. This cell death was accompanied by localization of terminal deoxynucleotidyl transferase-mediated fluorecein UTP nick-end labelling (TUNEL) staining within dopaminergic neurons. This neurotoxicity was antagonized by the semisynthetic tetracycline derivative, minocycline, and the observed neuroprotective effects were associated with the ability of minocycline to suppress NADPH oxidase-derived ROS production and pro-inflammatory cytokine expression, including interleukin-1beta and inducible nitric oxide synthase, from activated microglia. These results suggest that microglial NADPH oxidase may be a viable target for neuroprotection against oxidative damage.     

近金线属的分类地位及金线属的鉴别特征(鲤形目:鲤科:亚科)

本文根据系统学原理,提出了建立新类元的依据;并据此从分类和系统发育上论证了近金线属ＡｎｃｈｉｃｙｃｌｏｃｈｅｉｌｕｓＬｉｅｔＬａｎ独立成属的可能性,认为应将近金线属归于金线属;修订了金线属ＳｉｎｏｃｙｃｌｏｃｈｅｉｌｕｓＦａｎｇ的鉴别特征。     

Resveratrol effects in bladder cancer: A mini review

Bladder cancer has a high incidence worldwide and is the most common genitourinary cancer. The treatment of bladder cancer involves surgery and chemotherapy; however high failure rates and toxicity are observed. In this context, the search of new drugs aiming a more effective treatment is extremely necessary. Natural products are an important source of compounds with antiproliferative effects. Resveratrol is a naturally occurring plant polyphenol whose anticancer activity has been demonstrated in different types of cancer. This review summarizes the in vitro and in vivo studies using models of bladder cancer treated with resveratrol and discusses its different mechanisms of action.     

Suppression of FOXO1 attenuates inflamm-aging and improves liver function during aging

The liver is a key metabolic organ that maintains whole-body nutrient homeostasis. Aging-induced liver function alterations contribute to systemic susceptibility to aging-related diseases. However, the molecular mechanisms of liver aging remain insufficiently understood. In this study, we performed bulk RNA-Seq and single-cell RNA-Seq analyses to investigate the underlying mechanisms of the aging-induced liver function changes. We found that liver inflammation, glucose intolerance, and liver fat deposition were aggravated in old mice. Aging significantly increased pro-inflammation in hepatic macrophages. Furthermore, we found that Kupffer cells (KCs) were the major driver to induce pro-inflammation in hepatic macrophages during aging. In KCs, aging significantly increased pro-inflammatory levels; in monocyte-derived macrophages (MDMs), aging had a limited effect on pro-inflammation but led to a functional quiescence in antigen presentation and phagosome process. In addition, we identified an aging-responsive KC-specific (ARKC) gene set that potentially mediates aging-induced pro-inflammation in KCs. Interestingly, FOXO1 activity was significantly increased in the liver of old mice. FOXO1 inhibition by AS1842856 significantly alleviated glucose intolerance, hepatic steatosis, and systemic inflammation in old mice. FOXO1 inhibition significantly attenuated aging-induced pro-inflammation in KCs partially through downregulation of ARKC genes. However, FOXO1 inhibition had a limited effect on aging-induced functional quiescence in MDMs. These results indicate that aging induces pro-inflammation in liver mainly through targeting KCs and FOXO1 is a key player in aging-induced pro-inflammation in KCs. Thus, FOXO1 could be a potential therapeutic target for the treatment of age-associated chronic diseases.