The asymmetric relationships of the distribution of conspecific saplings and adults in forest fragments

随着土地利用方式变化的加剧,生境片段化已成为影响植物多样性的主要因子之一。通常,当成年树个体的密度越高,其周边同种幼树个体的存活率可能会下降,从而为其它物种提供了空间和资源,进而可以维持较高的局域物种多样性。因此,同种成年树和幼树个体的空间分布格局关系和作用强度可以调节植物多样性。然而,对于在片段化森林中,同种成年树和幼树个体空间分布关系的研究却很少报道,迄今尚不清楚片段化景观中同种个体的空间分布关系与物种多样性之间的联系。本研究选择千岛湖陆桥岛屿系统中的27个岛屿,基于岛屿上幼树和成年树个体的空间分布数据,利用混合效应模型分析它们之间的作用强度。同种幼树和成年树个体的空间作用强度越大,说明它们之间的负相互作用越强,即幼树和成年树个体空间分布越分散。此外,本研究分析了岛屿属性(岛屿面积、与大陆的距离和与最近岛屿的距离)与同种个体空间作用强度及物种多样性之间的关系。结果表明,同种个体的空间作用强度随着与最近岛屿距离的增加而增加。同时,物种多样性随着同种个体的空间作用强度的增加而显著增加,且岛屿面积和同种个体的空间作用强度分别解释了岛屿间物种多样性差异的26%和6%,共同解释了8%。耐阴种和非常见种比非耐阴种和常见种的同种幼树和成年树的空间分布更为分散。本研究表明,同种个体的空间分布可能会影响多度较低物种在片段化森林中的生存,反映了生物相互作用对于维持片段化森林中的植物多样性具有重要作用。 本研究也强调在检验同种密度制约时应考虑森林之间的连接度。     

Distinct genomic traits of acral and mucosal melanomas revealed by targeted mutational profiling

The incidence of melanoma is rising globally including China. Comparing to Caucasians, the incidence of non‐cutaneous melanomas is significantly higher in Chinese. Herein, we performed genomic profiling of 89 Chinese surgically resected primary melanomas, including acral (n = 54), cutaneous (n = 22), and mucosal (n = 13), by hybrid capture‐based next‐generation sequencing. We show that mucosal melanomas tended to harbor more pathogenic mutations than other types of melanoma, though the biological significance of this finding remains uncertain. Chromosomal arm‐level alterations including 6q, 9p, and 10p/q loss were highly recurrent in all subtypes, but mucosal melanoma was significantly associated with increased genomic instability. Importantly, 7p gain significantly correlated with unfavorable clinical outcomes in non‐cutaneous melanomas, representing an intriguing prognostic biomarker of those subtypes. Furthermore, focal amplification of 4q12 (KIT, KDR, and PDGFRα) and RAD51 deletion were more abundant in mucosal melanoma, while NOTCH2 amplification was enriched in acral melanoma. Additionally, cutaneous melanomas had higher mutation load than acral melanomas, while mucosal melanomas did not differ from other subtypes in mutation burden. Together, our data revealed important features of acral and mucosal melanomas in Chinese including distinctive driver mutation pattern and increased genomic instability. These findings highlight the possibilities of combination therapies in the clinical management of melanoma.     

Four cypermethrin isomers induced stereoselective metabolism in H295R cells

Cypermethrin (CP) is widely used for controlling agricultural and indoor vermin. Previous studies have reported the stereoselective difference of CP in biological activities. However, little is known about their potential mechanisms between metabolic phenotypes and endocrine-disrupting effects. Herein, nuclear magnetic resonance (NMR)-based metabolomics combining metabolite identification and pathway analysis were applied to evaluate the stereoselective metabolic cdisorders induced by CP isomers in human adrenocortical carcinoma cells (H295R) culture medium. Then, gene expression levels related to disturbed metabolic pathways were assessed to verify according to metabolic phenotypes. Metabolomics profiles showed that [(S)-cyano(3-phenoxyphenyl)methyl](1R,3R)-3-(2,2-dichloroethenyl)-2,2-dimethylcyclopropane-1-carboxylate [(1R,3R,αS)-CP] induced the most significant changes in metabolic phenotypes than did the other stereoisomers. There are 10 differential metabolites (isoleucine, valine, leucine, ethanol, alanine, acetate, aspartate, arginine, lactate, and glucose) as well as two significantly disturbed pathways, including “pyruvate metabolism” and “alanine, aspartate, and glutamate metabolism,” that were confirmed in H295R cells culture medium of (1R,3R,αS)-CP compared with other stereoisomers. Polymerase chain reaction (PCR) array also confirmed the results of metabolomics. Our results can help to understand the potential mechanisms between the isomer selectivity in metabolic phenotypes and endocrine-disrupting effects. Data provided here not only lend authenticity to the cautions issued by the scientists and researchers but also offer a solution for the balance between environment and political regulations.     

Cross-scale drivers of plant trait distributions in a fragmented forest landscape

During community assembly, plant functional traits are under selective pressure from processes operating at multiple spatial scales. However, in fragmented landscapes, there is little understanding of the relative importance of local-, patch- and landscape-scale processes in shaping trait distributions. Here, we investigate cross-scale influences of landscape change on traits that dictate plant life history strategies in re-assembling plant communities in a fragmented landscape in eastern China. Using forest dynamics plots (FDPs) on 29 land-bridge islands in which all woody plants have been georeferenced and identified to species, we characterized and derived two composite measures of trait variation, representing variation across the leaf economics spectrum and plant size. We then tested for trait shifts in response to local-, patch- and landscape-scale factors, and their potential cross-scale interactions. We found substantial community-wide trait changes along local-scale gradients (i.e. forest edge to interior): more acquisitive leaf economic traits and larger sized species occurred at edges, with a significant increase in trait means and trait range. Moreover, there were significant cross-scale interaction effects of patch and landscape variables on local-scale edge effects. Altered spatial arrangement of habitat in the surrounding landscape (i.e. declining habitat amount and increasing patch density), as well as decreasing area at the patch level, exacerbated edge effects on traits distributions. We suggest that synergistic interactions of landscape- and patch-scale processes, such as dispersal limitation, on local-scale environmental filtering at edges, together shape the spatial distributions of plant life history strategies in fragmented plant communities.     

Ferroptosis is involved in alcohol-induced cell death in vivo and in vitro

ABSTRACT

A critical pathogenic factor in the development of lethal liver failure is cell death induced by the accumulation of lipid reactive oxygen species. In this study, we discovered and illuminated a new mechanism that led to alcoholic liver disease via ferroptosis, an iron-dependent regulated cell death. Study in vitro showed that both necroptosis inhibitor and ferroptosis inhibitors performed significantly protective effect on alcohol-induced cell death, while apoptosis inhibitor and autophagy inhibitor had no such effect. Our data also indicated that alcohol caused the accumulation of lipid peroxides and the mRNA expression of prostaglandin-endoperoxide synthase 2, reduced the protein expression of the specific light-chain subunit of the cystine/glutamate antiporter and glutathione peroxidase 4. Importantly, ferrostatin-1 significantly ameliorated liver injury that was induced by overdosed alcohol both in vitro and in vivo. These findings highlight that targeting ferroptosis serves as a hepatoprotective strategy for alcoholic liver disease treatment.