客家菜馆与社会变迁

客家菜馆的变迁反映出战后香港社会的文化发展和饮食方式的变化 ,它是洞悉传统习俗和社会阶级关系变化时一个重要参数 ,对客家菜馆的研究有助于说明香港社会生活方式的变迁和社会发展     

TRAPPI tethers COPII vesicles by binding the coat subunit Sec23

The budding of endoplasmic reticulum (ER)-derived vesicles is dependent on the COPII coat complex. Coat assembly is initiated when Sar1-GTP recruits the cargo adaptor complex, Sec23/Sec24, by binding to its GTPase-activating protein (GAP) Sec23 (ref. 2). This leads to the capture of transmembrane cargo by Sec24 (refs 3, 4) before the coat is polymerized by the Sec13/Sec31 complex. The initial interaction of a vesicle with its target membrane is mediated by tethers. We report here that in yeast and mammalian cells the tethering complex TRAPPI (ref. 7) binds to the coat subunit Sec23. This event requires the Bet3 subunit. In vitro studies demonstrate that the interaction between Sec23 and Bet3 targets TRAPPI to COPII vesicles to mediate vesicle tethering. We propose that the binding of TRAPPI to Sec23 marks a coated vesicle for fusion with another COPII vesicle or the Golgi apparatus. An implication of these findings is that the intracellular destination of a transport vesicle may be determined in part by its coat and its associated cargo.     

An improved test method and numerical analysis for crack opening resistance of FRC round determinate panels

This paper presents a numerical analysis of a material test program investigating the crack opening properties of fibre reinforced concrete (FRC) round determinate panels (RDP). The objective of this research is to set up a modified RDP test method to improve the current ASTM C1550 test method for FRC and fibre reinforced shotcrete (FRS) composite. By this test method, a kind of light small-diameter panels are applied and more crack information can be obtained by a new rotation angle measuring technique. It is shown that this modified test method can be used to effectively evaluate the crack opening resistance of FRC. The finite element analysis was then performed to clarify the crack propagations and failure mode of FRC RDP panels. It helps establish a reasonable theoretical method to predict the structural response of RDP, combining with this modified testing technique. Foundation item: Supported by the National Natural Science Foundation of China (50708084) and Wuhan Chenguang Science and Technology Project for Young Experts (20035002016-30)     

Oestrogen protects FKBP12.6 null mice from cardiac hypertrophy

FK506 binding proteins 12 and 12.6 (FKBP12 and FKBP12.6) are intracellular receptors for the immunosuppressant drug FK506 (ref. 1). The skeletal muscle ryanodine receptor (RyR1) is isolated as a hetero-oligomer with FKBP12 (ref. 2), whereas the cardiac ryanodine receptor (RyR2) more selectively associates with FKBP12.6 (refs 3, 4, 5). FKBP12 modulates Ca2+ release from the sarcoplasmic reticulum in skeletal muscle and developmental cardiac defects have been reported in FKBP12-deficient mice, but the role of FKBP12.6 in cardiac excitation-contraction coupling remains unclear. Here we show that disruption of the FKBP12.6 gene in mice results in cardiac hypertrophy in male mice, but not in females. Female hearts are normal, despite the fact that male and female knockout mice display similar dysregulation of Ca2+ release, seen as increases in the amplitude and duration of Ca2+ sparks and calcium-induced calcium release gain. Female FKBP12.6-null mice treated with tamoxifen, an oestrogen receptor antagonist, develop cardiac hypertrophy similar to that of male mice. We conclude that FKBP12.6 modulates cardiac excitation-contraction coupling and that oestrogen plays a protective role in the hypertrophic response of the heart to Ca2+ dysregulation.     

Programmed population control by cell-cell communication and regulated killing

De novo engineering of gene circuits inside cells is extremely difficult, and efforts to realize predictable and robust performance must deal with noise in gene expression and variation in phenotypes between cells. Here we demonstrate that by coupling gene expression to cell survival and death using cell-cell communication, we can programme the dynamics of a population despite variability in the behaviour of individual cells. Specifically, we have built and characterized a 'population control' circuit that autonomously regulates the density of an Escherichia coli population. The cell density is broadcasted and detected by elements from a bacterial quorum-sensing system, which in turn regulate the death rate. As predicted by a simple mathematical model, the circuit can set a stable steady state in terms of cell density and gene expression that is easily tunable by varying the stability of the cell-cell communication signal. This circuit incorporates a mechanism for programmed death in response to changes in the environment, and allows us to probe the design principles of its more complex natural counterparts.     

Environmental Paradigms,Biodiversity Conservation,and Critical Systems Thinking

In 1994 Gerald Midgley addressed the issue of the boundary implications of two different paradigms of thought about the environment, namely, humanis and the ecological perspective The distinction that he makes is important because it draws attention to the value implications of an uncritical acceptance of boundaries around human interests that serves to marginalize the environment. It is argued here, however, that Midgley does not go far enough. Just as an uncritical acceptance of humanis marginalizes the environment, so an uncritical acceptance of the environmental perspectiv runs the risk of prioritizing some elements of the environment over others, e.g., the interests of individual animals over species or over ecosystems. This paper seeks to correct this limitation in Midgleys account by developing a more sophisticated framework of environmental paradigms: a framework that can be used to clarify the values of stakeholders in critical systems interventions involving the management of biodiversity.