城市市政基础设施投资与经济发展的空间交互影响

通过空间联立方程模型,基于2011和2016年241个城市样本数据,研究城市市政基础设施投资与经济发展的双向互馈及其空间相互作用.结果表明:1)考虑内生性后,基础设施投资的空间滞后项系数显著为正,地方政府在投资行为上模仿彼此;2)基础设施投资与经济发展之间存在双向互促作用.建议加强对基础设施投资的预算管理,改革晋升绩效...     

玉米秸秆纤维复合缓冲包装材料的研究

研究了以聚醚多元醇、聚异氰酸酯为基体,以玉米秸秆纤维为增强体的新型复合缓冲包装材料,通过控制玉米秸秆纤维的添加量、发泡剂用量、交联剂与催化剂用量、反应温度等工艺参数,实验制备了具有可降解性能的缓冲包装材料,并利用静态压缩实验方法对比了该材料与发泡聚苯乙烯的缓冲性能.     

The PDZ2 domain of zonula occludens-1 and -2 is a phosphoinositide binding domain

Zonula occludens proteins (ZO) are postsynaptic density protein-95 discs large-zonula occludens (PDZ) domain-containing proteins that play a fundamental role in the assembly of tight junctions and establishment of cell polarity. Here, we show that the second PDZ domain of ZO-1 and ZO-2 binds phosphoinositides (PtdInsP) and we identified critical residues involved in the interaction. Furthermore, peptide and PtdInsP binding of ZO PDZ2 domains are mutually exclusive. Although lipid binding does not seem to be required for plasma membrane localisation of ZO-1, phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P ₂) binding to the PDZ2 domain of ZO-2 regulates ZO-2 recruitment to nuclear speckles. Knockdown of ZO-2 expression disrupts speckle morphology, indicating that ZO-2 might play an active role in formation and stabilisation of these subnuclear structures. This study shows for the first time that ZO isoforms bind PtdInsPs and offers an alternative regulatory mechanism for the formation and stabilisation of protein complexes in the nucleus.     

Helmholtz's Kant revisited (Once more). The all-pervasive nature of Helmholtz's struggle with Kant's Anschauung

In this analysis, the classical problem of Hermann von Helmholtz's (1821–1894) Kantianism is explored from a particular vantage point, that to my knowledge, has not received the attention it deserves notwithstanding its possible key role in disentangling Helmholtz's relation to Kant's critical project. More particularly, we will focus on Helmholtz's critical engagement with Kant's concept of intuition [Anschauung] and (the related issue of) his dissatisfaction with Kant's doctrinal dualism. In doing so, it soon becomes clear that both (i) crucially mediated Helmholtz's idiosyncratic appropriation and criticism of (certain aspects of) Kant's critical project, and (ii) can be considered as a common denominator in a variety of issues that are usually addressed separately under the general header of (the problem of) Helmholtz's Kantianism. The perspective offered in this analysis can not only shed interesting new light on some interpretive issues that have become commonplace in discussions on Helmholtz's Kantianism, but also offers a particular way of connecting seemingly unrelated dimensions of Helmholtz's engagement with Kant's critical project (e.g. Helmholtz's views on causality and space). Furthermore, it amounts to the rather surprising conclusion that Helmholtz's most drastic revision of Kant's project pertains to his assumption of free will as a formal condition of experience and knowledge.     

Evidence for the intracellular accumulation of anandamide in adiposomes

Anandamide is a lipid messenger that carries out a wide variety of biological functions. It has been suggested that anandamide accumulation involves binding to a saturable cellular component. To identify the structure(s) involved in this process, we analyzed the intracellular distribution of both biotinylated and radiolabeled anandamide, providing direct evidence that lipid droplets, also known as adiposomes, constitute a dynamic reservoir for the sequestration of anandamide. In addition, confocal microscopy and biochemical studies revealed that the anandamide-hydrolase is also spatially associated with lipid droplets, and that cells with a larger adiposome compartment have an enhanced catabolism of anandamide. Overall, these findings suggest that adiposomes may have a critical role in accumulating anandamide, possibly by connecting plasma membrane to internal organelles along the metabolic route of this endocannabinoid. S. Oddi, F. Fezza: These authors contributed equally to the study.     

Common variants near MC4R are associated with fat mass, weight and risk of obesity

To identify common variants influencing body mass index (BMI), we analyzed genome-wide association data from 16,876 individuals of European descent. After previously reported variants in FTO, the strongest association signal (rs17782313, P = 2.9 x 10(-6)) mapped 188 kb downstream of MC4R (melanocortin-4 receptor), mutations of which are the leading cause of monogenic severe childhood-onset obesity. We confirmed the BMI association in 60,352 adults (per-allele effect = 0.05 Z-score units; P = 2.8 x 10(-15)) and 5,988 children aged 7-11 (0.13 Z-score units; P = 1.5 x 10(-8)). In case-control analyses (n = 10,583), the odds for severe childhood obesity reached 1.30 (P = 8.0 x 10(-11)). Furthermore, we observed overtransmission of the risk allele to obese offspring in 660 families (P (pedigree disequilibrium test average; PDT-avg) = 2.4 x 10(-4)). The SNP location and patterns of phenotypic associations are consistent with effects mediated through altered MC4R function. Our findings establish that common variants near MC4R influence fat mass, weight and obesity risk at the population level and reinforce the need for large-scale data integration to identify variants influencing continuous biomedical traits.     

Heterogeneous Forecast Adjustment

There is ample empirical evidence that expert‐adjusted model forecasts can be improved. One way to potential improvement concerns providing various forms of feedback to the sales forecasters. It is also often recognized that the experts (forecasters) might not constitute a homogeneous group. This paper provides a data‐based methodology to discern latent clusters of forecasters, and applies it to a fully new large database with data on expert‐adjusted forecasts, model forecasts and realizations. For the data at hand, two clusters can clearly be identified. Next, the consequences of having clusters are discussed. Copyright © 2016 John Wiley & Sons, Ltd.     

Emerging roles of immunoproteasomes beyond MHC class I antigen processing

The proteasome is a multi-catalytic protein complex whose primary function is the degradation of abnormal or foreign proteins. Upon exposure of cells to interferons (IFNs), the β1i/LMP2, β2i/MECL-1, and β5i/LMP7 subunits are induced and incorporated into newly synthesized immunoproteasomes (IP), which are thought to function solely as critical players in the optimization of the CD8(+) T-cell response. However, the observation that IP are present in several non-immune tissues under normal conditions and/or following pathological events militates against the view that its role is limited to MHC class I presentation. In support of this concept, the recent use of genetic models deficient for β1i/LMP2, β2i/MECL-1, or β5i/LMP7 has uncovered unanticipated functions for IP in innate immunity and non-immune processes. Herein, we review recent data in an attempt to clarify the role of IP beyond MHC class I epitope presentation with emphasis on its involvement in the regulation of protein homeostasis, cell proliferation, and cytokine gene expression.