基于Shuttleworth-Wallace模型的科尔沁沙地流动半流动沙丘蒸散发模拟

陆面蒸散发在气候调节和维持区域水量平衡中起关键作用.量化蒸散发及其各组分项,对深刻揭示干旱半干旱地区的生态水文过程具有重要意义.本研究基于科尔沁沙地流动半流动沙丘2017年生长季气象监测系统的原位监测数据,利用Shuttleworth-Wallace(S-W)模型对沙丘蒸散发进行模拟,在此基础上,对蒸散各组分进行拆分,并利用涡度相关对模拟蒸散发值进行验证.结果表明: 整个生长季模型模拟蒸散发值为308 mm,涡度相关实测值为296 mm,偏差较小,证明S-W模型适用于该地区的蒸散发模拟.蒸散发整体呈生长旺盛期>生长后期>生长初期,分别为192、71和45 mm,分别占总量的62.3%、23.1%和14.6%.日尺度上模型模拟值与实测蒸散发值一致性较高,模型模拟精度大体表现为: 晴天>阴天>雨天,且阴雨天模型模拟值较涡度相关实测值偏低.经拆分,土壤蒸发和植被蒸腾分别为176和132 mm,分别占总量的57.1%和42.9%,表明沙地水分利用效率较低.持续干旱和降水后,蒸散发规律明显不同,且土壤蒸发对降水的敏感性强于植被蒸腾.     

基于建筑容量的城市建设用地碳汇量核算方法

城市建设中的矿物质材料开发利用活动不仅导致大量碳排放,也产生了碳吸收.以往建筑矿物质材料的碳吸收过程一直没有得到重视和科学量化.本研究采用遥感影像阴影高度反演技术,提取地块的建筑容量,识别建筑类型,以此为依据确定矿物材料用量及碳含量参数,采用热重分析法测定碳化率,基于以上步骤构建城市建筑碳汇量的核算方法,并选取沈阳市蒲河新来测试这一核算方法,同时进行不确定性分析.结果表明: 1996—2016年,沈阳市蒲河新城各类型建筑产生的碳汇总量依次为:居住建筑>公共服务建筑>其他类建筑>商业金融建筑>工业建筑;各类建筑用地的碳汇容积率依次为:商业金融建筑>居住建筑>公共服务建筑>其他类建筑>工业建筑.本研究构建的基于建筑容量提取的城市尺度的建筑碳汇量核算方法,可以快速准确地估算不同类型城市建设用地无机材料产生的碳汇量.在城市自然碳汇有限条件下,利用建筑碳汇增加城市碳汇量,能够为我国城市低碳发展提供新的思路.     

Changes in seasonal precipitation distribution but not annual amount affect litter decomposition in a secondary tropical forest

In the tropics of South China, climate change induced more rainfall events in the wet season in the last decades. Moreover, there will be more frequently spring drought in the future. However, knowledge on how litter decomposition rate would respond to these seasonal precipitation changes is still limited. In the present study, we conducted a precipitation manipulation experiment in a tropical forest. First, we applied a 60% rainfall exclusion in April and May to defer the onset of wet season and added the same amount of water in October and November to mimic a deferred wet season (DW); second, we increased as much as 25% mean annual precipitation into plots in July and August to simulate a wetter wet season (WW). Five single‐species litters, with their carbon to nitrogen ratio ranged from 27 to 49, and a mixed litter were used to explore how the precipitation change treatments would affect litter decomposition rate. The interaction between precipitation changes and litter species was not significant. The DW treatment marginally accelerated litter decomposition across six litter types. Detailed analysis showed that DW increased litter decomposition rate in the periods of January to March and October to December, when soil moisture was increased by the water addition in the dry season. In contrast, WW did not significantly affect litter decomposition rate, which was consistent with the unchanged soil moisture pattern. In conclusion, the study indicated that regardless of litter types or litter quality, the projected deferred wet season would increase litter decomposition rate, whereas the wetter wet season would not affect litter decomposition rate in the tropical forests. This study improves our knowledge of how tropical forest carbon cycling in response to precipitation change.     

Effects of magnolol and honokiol blend on performance,egg quality,hepatic lipid metabolism,and intestinal morphology of hens at late laying cycle

Magnolol and its isomer honokiol are polyphenols with anti-oxidative and anti-inflammatory activities. We evaluated the effects of magnolol and honokiol supplementation alone or in combination with hen diets during the late laying cycle. A total of 540 Jingfen pink-shell laying hens (50 weeks old) were randomly assigned to six treatments: a control diet and diets supplemented with 300 mg/kg magnolol (M₃₀₀), honokiol (H₃₀₀), or 300 mg/kg total phenols with a magnolol/honokiol ratio of 2:1 (M₂₀₀H₁₀₀), 1:2 (M₁₀₀H₂₀₀), and 1:1 (M₁₅₀H₁₅₀). Compared with that of the control, all supplementation groups had higher laying rates and the M₃₀₀, M₁₀₀H₂₀₀, and M₁₅₀H₁₅₀ groups showed comparatively lower feed conversion ratios. Magnolol and honokiol supplementation increased the Haugh units of fresh eggs at week 62 and alleviated the decline of the Haugh units of eggs stored for 14 days. Compared with that of the control group, the serum total antioxidant capacity of the M₁₀₀H₂₀₀ and M₁₅₀H₁₅₀ groups significantly increased, and all supplementation groups had higher total antioxidant capacity and lower malondialdehyde content in the liver. With respect to lipid metabolism, the M₂₀₀H₁₀₀ and M₁₅₀H₁₅₀ groups had lower total and relative liver weights compared with those of the control and H₃₀₀ groups. The mRNA expression levels of CCAAT enhancer binding protein alpha, sterol regulatory element binding protein-1, fatty acid synthase and stearyl coenzyme A desaturase 1 involved in lipogenesis; microsomal triglyceride transfer protein and apolipoprotein B involved in fatty acid transport; and the proinflammatory cytokine interleukin-1 beta were lower in all supplementation groups compared with those in the control. With respect to gut health, the heights of the jejunum and ileum villi significantly increased in all supplementation groups compared with those of the control, and the jejunum villus heights of the M₃₀₀ and M₁₅₀H₁₅₀ groups were higher than those of the H₃₀₀ and M₁₀₀H₂₀₀ groups. The H₃₀₀ and M₁₅₀H₁₅₀ groups had higher mRNA expression levels of zonula occludens-1 in the ileum compared with those in the control and M₃₀₀ groups, whereas all supplementation groups had higher mRNA levels of claudin-1 than that of the control group. In conclusion, magnolol and honokiol improved hen performance and the albumen quality of fresh and stored eggs by improving the antioxidant capacity, liver lipid metabolism, and intestinal health of laying hens. The combination of magnolol and honokiol at a 1:1 ratio may be an optimal choice for hen diet supplementation.     

Are regional precipitation–productivity relationships robust to decadal-scale dry period?

降水-生产力的空间关系是否稳定不变？ 降水是全球陆地生态系统中植被生长和净初级生产力的主要驱动因素。因此,探究降水和生产力关系有助于深入了解气候变化如何改变生态系统功能。降水-生产力的空间关系在全球不同草地上非常相似,但在连续多年气候异常的情况下,这种关系是否会发生变化以及如何变化尚不清楚。本研究利用 利用中国北方温带草地长达10年低于多年平均降水的时期,基于遥感植被指数数据,量化了区域尺度上降水-植被生产力关系在持续多年的干湿期之间将如何变化。结果表明,在连续10年的干期,降水-生产力空间相关性急剧下降,而该空间关系的下降主要是由于不同草原类型对干旱的响应在空间上存在高度的异质性,即不同生态系统对干旱的响应程度存在差异。因此,如果未来气候变化进一步加剧全球草地的干旱,那么基于历史时期(平水期)得到的降水-生产力空间关系推测区域尺度植被生产力可能导致误差。     

Analysis of protein adduction kinetics by quantitative mass spectrometry: competing adduction reactions of glutathione-S-transferase P1-1 with electrophiles

Defining the mechanisms and consequences of protein adduction is crucial to understanding the toxicity of reactive electrophiles. Application of tandem mass spectrometry and data analysis algorithms enables detection and mapping of chemical adducts at the level of amino acid sequence. Nevertheless, detection of adducts does not indicate relative reactivity of different sites. Here, we describe a method to measure the kinetics of competing adduction reactions at different sites on the same protein. Adducts are formed by electrophiles at Cys14 and Cys47 on the metabolic enzyme glutathione-S-transferase P1-1 and modification is accompanied by a loss of enzymatic activity. Relative quantitation of protein adducts was done by tagging N-termini of peptide digests with isotopically labeled phenyl isocyanate and tracking the ratio of light-tagged peptide adducts to heavy-tagged reference samples in liquid chromatography-tandem mass spectrometry analyses using a multiple reaction monitoring method. This approach was used to measure rate constants for adduction at both positions with two different model electrophiles, N-iodoacetyl-N-biotinylhexylenediamine and 1-biotinamido-4-(4'-[maleimidoethyl-cyclohexane]-carboxamido)butane. The results indicate that Cys47 was approximately two- to three-fold more reactive toward both electrophiles than was Cys14. This result was consistent with the relative reactivity of these electrophiles in a complex proteome system and with previously reported trends in reactivity of these sites. Kinetic analyses of protein modification reactions provide a means of evaluating the selectivity of reactive mediators of chemical toxicity.     

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCzeta

Prostaglandins are lipid signaling intermediates released by keratinocytes in response to ultraviolet irradiation (UVR) in the skin. The main prostaglandin released following UVR is PGE(2), a ligand for 4 related G-protein-coupled receptors (EP(1), EP(2), EP(3) and EP(4)). Our previous work established that PGE(2) stimulates melanocyte dendrite formation through activation of the EP(1) and EP(3) receptors. The purpose of the present report is to define the signaling intermediates involved in EP(1)- and EP(3)-dependent dendrite formation in human melanocytes. We recently showed that activation of the atypical PKCzeta isoform stimulates melanocyte dendricity in response to treatment with lysophosphatidylcholine. We therefore examined the potential contribution of PKCzeta activation on EP(1)- and EP(3)-dependent dendrite formation in melanocytes. Stimulation of the EP(1) and EP(3) receptors by selective agonists activated PKCzeta, and inhibition of PKCzeta activation abrogated EP(1)- and EP(3)-receptor-mediated melanocyte dendricity. Because of the importance of Rho-GTP binding proteins in the regulation of melanocyte dendricity, we also examined the effect of EP(1) and EP(3) receptor activation on Rac and Rho activity. Neither Rac nor Rho was activated upon treatment with EP(1,3)-receptor agonists. We show that melanocytes express only the EP(3A1) isoform, but not the EP(3B) receptor isoform, previously associated with Rho activation, consistent with a lack of Rho stimulation by EP(3) agonists. Our data suggest that PKCzeta activation plays a predominant role in regulation of PGE(2)-dependent melanocyte dendricity.     

Regulation of the epithelial calcium channel TRPV6 by the serum and glucocorticoid-inducible kinase isoforms SGK1 and SGK3

Epithelial calcium (re)absorption is mediated by TRPV5 and TRPV6 channels. TRPV5 is modulated by the SGK1 kinase, a process requiring the PDZ-domain containing scaffold protein NHERF2. The present study explored whether TRPV6 is similarly regulated by SGKs and the scaffold proteins NHERF1/2. In Xenopus oocytes, SGKs activate TRPV6 by increasing its plasma membrane abundance. Deletion of the putative PDZ binding motif on TRPV6 did not abolish channel activation by SGKs. Furthermore, coexpression of neither NHERF1 nor NHERF2 affected TRPV6 or potentiated the SGKs stimulating effect. The present observations disclose a novel TRPV6 regulatory mechanism which presumably participates in calcium homeostasis.