气相多环芳烃的吸附净化技术研究进展

多环芳烃(PAHs)是近年来在大气污染问题中逐渐受到关注的一类污染物,不仅其自身严重威胁着人体健康,还可作为低挥发性物质促进二次颗粒物的生长.世界多国开始不断通过各种技术手段对废气中PAHs的排放进行控制,PHAs已成为大气环境领域共同关注的热点问题.吸附法是最具潜力且已被工业应用认可的一类PAHs控制净化关键技术,吸附剂对PAHs的吸、脱附性能是其中的关键.目前国内外学者无论是基于传统碳类吸附剂,还是新型的介孔吸附剂,都针对此类特殊低挥发性气体的吸附相平衡、动力学以及脱附特性做了相关研究,探悉了获取PAHs吸脱附最优平衡的关键因素以及最适吸附剂.本文针对这些结果及相关应用进行了综述,对比分析了介孔吸附剂较传统吸附剂在PAHs吸脱附特性上呈现的优势,旨在为PAHs及其他低挥发性气体吸附净化的相关工作提供有效参考.     

The social brain: Insights from cognitive neuroscience

Cognitive neuroscience has provided powerful tools that now permit the investigation of human social cognition and behavior with unprecedented accuracy. This review summarizes some of the features of the human brain that differentiate it from the brains of other animals, some of the methods used in cognitive neuroscience, and concludes with an example of research from the author’s own lab that implicates the amygdala in emotion recognition, social judgment, and autism.     

A mechanism for impaired fear recognition after amygdala damage

Ten years ago, we reported that SM, a patient with rare bilateral amygdala damage, showed an intriguing impairment in her ability to recognize fear from facial expressions. Since then, the importance of the amygdala in processing information about facial emotions has been borne out by a number of lesion and functional imaging studies. Yet the mechanism by which amygdala damage compromises fear recognition has not been identified. Returning to patient SM, we now show that her impairment stems from an inability to make normal use of information from the eye region of faces when judging emotions, a defect we trace to a lack of spontaneous fixations on the eyes during free viewing of faces. Although SM fails to look normally at the eye region in all facial expressions, her selective impairment in recognizing fear is explained by the fact that the eyes are the most important feature for identifying this emotion. Notably, SM's recognition of fearful faces became entirely normal when she was instructed explicitly to look at the eyes. This finding provides a mechanism to explain the amygdala's role in fear recognition, and points to new approaches for the possible rehabilitation of patients with defective emotion perception.     

Functional characterization of the human α-cardiac actin mutations Y166C and M305L involved in hypertrophic cardiomyopathy

Inherited cardiomyopathies are caused by point mutations in sarcomeric gene products, including α-cardiac muscle actin (ACTC1). We examined the biochemical and cell biological properties of the α-cardiac actin mutations Y166C and M305L identified in hypertrophic cardiomyopathy (HCM). Untagged wild-type (WT) cardiac actin, and the Y166C and M305L mutants were expressed by the baculovirus/Sf9-cell system and affinity purified by immobilized gelsolin G4-6. Their correct folding was verified by a number of assays. The mutant actins also displayed a disturbed intrinsic ATPase activity and an altered polymerization behavior in the presence of tropomyosin, gelsolin, and Arp2/3 complex. Both mutants stimulated the cardiac β-myosin ATPase to only 50?% of WT cardiac F-actin. Copolymers of WT and increasing amounts of the mutant actins led to a reduced stimulation of the myosin ATPase. Transfection of established cell lines revealed incorporation of EGFP- and hemagglutinin (HA)-tagged WT and both mutant actins into cytoplasmic stress fibers. Adenoviral vectors of HA-tagged WT and Y166C actin were successfully used to infect adult and neonatal rat cardiomyocytes (NRCs). The expressed HA-tagged actins were incorporated into the minus-ends of NRC thin filaments, demonstrating the ability to form hybrid thin filaments with endogenous actin. In NRCs, the Y166C mutant led after 72?h to a shortening of the sarcomere length when compared to NRCs infected with WT actin. Thus our data demonstrate that a mutant actin can be integrated into cardiomyocyte thin filaments and by its reduced mode of myosin interaction might be the basis for the initiation of HCM.