Functions and pathologies of BiP and its interaction partners

The endoplasmic reticulum (ER) is involved in a variety of essential and interconnected processes in human cells, including protein biogenesis, signal transduction, and calcium homeostasis. The central player in all these processes is the ER-lumenal polypeptide chain binding protein BiP that acts as a molecular chaperone. BiP belongs to the heat shock protein 70 (Hsp70) family and crucially depends on a number of interaction partners, including co-chaperones, nucleotide exchange factors, and signaling molecules. In the course of the last five years, several diseases have been linked to BiP and its interaction partners, such as a group of infectious diseases that are caused by Shigella toxin producing E. coli. Furthermore, the inherited diseases Marinesco-Sj?gren syndrome, autosomal dominant polycystic liver disease, Wolcott-Rallison syndrome, and several cancer types can be considered BiP-related diseases. This review summarizes the physiological and pathophysiological characteristics of BiP and its interaction partners. Received 20 November 2008; received after revision 09 December 2008; accepted 12 December 2008     

Bitter peptides and bitter taste receptors

Bitter peptides are a structurally diverse group of oligopeptides often generated in fermented, aged, and hydrolyzed food products that make them unfavorable for consumption. Humans perceive bitterness by a repertoire of 25 human bitter receptors, termed T2Rs. Knowledge of the structural features of bitter receptors and of the factors that stimulate bitter receptors will aid in understanding the mechanism responsible for bitter taste perception. This article reviews the current knowledge regarding structural features of bitter peptides and bitter taste receptors. Received 24 November 2008; received after revision 11 December 2008; accepted 16 December 2008     

Apolipoprotein M affecting lipid metabolism or just catching a ride with lipoproteins in the circulation?

Apolipoprotein M (apoM) is a novel apolipoprotein found mainly in high-density lipoproteins (HDL). Its function is yet to be defined. ApoM (25 kDa) has a typical lipocalin ?-barrel fold and a hydrophobic pocket. Retinoids bind apoM but with low affinity and may not be the natural ligands. ApoM retains its signal peptide, which serves as a hydrophobic anchor to the lipoproteins. This prevents apoM from being lost in the urine. Approximately 5% of HDL carries an apoM molecule. ApoM in plasma (1 μM) correlates strongly with both low-density lipoprotein (LDL) and HDL cholesterol, suggesting a link to cholesterol metabolism. However, in casecontrol studies, apoM levels in patients with coronary heart disease (CHD) and controls were similar, suggesting apoM levels not to affect the risk for CHD in humans. Experiments in transgenic mice suggested apoM to have antiatherogenic properties; possible mechanisms include increased formation of pre-? HDL, enhanced cholesterol mobilization from foam cells, and increased antioxidant properties. Received 28 November 2008; received after revision 15 December 2008; accepted 16 December 2008     

The response of human skeletal muscle tissue to hypoxia

Hypoxia refers to environmental or clinical settings that potentially threaten tissue oxygen homeostasis. One unique aspect of skeletal muscle is that, in addition to hypoxia, oxygen balance in this tissue may be further compromised when exercise is superimposed on hypoxia. This review focuses on the cellular and molecular responses of human skeletal muscle to acute and chronic hypoxia, with emphasis on physical exercise and training. Based on published work, it is suggested that hypoxia does not appear to promote angiogenesis or to greatly alter oxidative enzymes in skeletal muscle at rest. Although the HIF-1 pathway in skeletal muscle is still poorly documented, emerging evidence suggests that muscle HIF-1 signaling is only activated to a minor degree by hypoxia. On the other hand, combining hypoxia with exercise appears to improve some aspects of muscle O₂ transport and/or metabolism.     

Vaults and the major vault protein: Novel roles in signal pathway regulation and immunity

The unique and evolutionary highly conserved major vault protein (MVP) is the main component of ubiquitous, large cellular ribonucleoparticles termed vaults. The 100 kDa MVP represents more than 70% of the vault mass which contains two additional proteins, the vault poly (ADP-ribose) polymerase (vPARP) and the telomerase-associated protein 1 (TEP1), as well as several short untranslated RNAs (vRNA). Vaults are almost ubiquitously expressed and, besides chemotherapy resistance, have been implicated in the regulation of several cellular processes including transport mechanisms, signal transmissions and immune responses. Despite a growing amount of data from diverse species and systems, the definition of precise vault functions is still highly complex and challenging. Here we review the current knowledge on MVP and vaults with focus on regulatory functions in intracellular signal transduction and immune defence. Received 27 June 2008; received after revision 25 July 2008; accepted 30 July 2008     

氮磷加富对山东长岛养殖坛紫菜的生长及营养成分的影响

为探究山东长岛养殖坛紫菜(Pyropia haitanensis)的最适营养盐条件,对不同氮、磷浓度下坛紫菜的生长、光合色素含量、营养成分(粗蛋白、粗脂肪、灰分)和氨基酸组成进行测定分析,并评价其营养价值。结果显示：山东长岛养殖的坛紫菜在氮、磷加富浓度分别为50μmol·L^-1、3.13μmol·L^-1时生长速率最快,叶绿素a、类胡萝卜素、藻红蛋白及藻蓝蛋白含量均显著升高,但在氮、磷浓度分别高于200μmol·L^-1、12.5μmol·L^-1时其生长减缓。坛紫菜对氮、磷的吸收速率受营养盐浓度的显著影响,在氮、磷浓度分别高于200μmol·L^-1、12.5μmol·L^-1时,其对NH⁺₄-N的吸收速率显著高于NO^-₃-N。氮、磷加富培养使坛紫菜营养成分的含量呈显著变化,其中粗蛋白和灰分含量显著增加,而粗脂肪的含量则显著降低;氨基酸总量以及呈味氨基酸占总氨基酸的比值(DAA...     

用MATLAB求解Butterworth最优传递函数

采用MATLAB语言编写函数bwden,通过主程序调用该函数可求出任意阶Butterworth最优传递函数分母多项式的系数,绘制出Butterworth最优传递函数的极点分布图,阶跃响应曲线及波德图.8阶Butter-worth最优传递函数的求解和仿真表明,可有效且简便地用MATLAB求解Butterworth最优传递函数.     

旋流压力式喷嘴低压喷淋特性

以自来水为喷淋介质,对旋流压力式喷嘴低压喷淋特性进行试验研究.分析喷嘴流量和喷孔直径对喷淋角、液滴Sauter平均直径(SMD)的影响规律,研究旋流压力式喷嘴喷淋液滴尺寸分布、喷淋介质径向通量分布及喷淋周相均匀度.结果表明,喷嘴流量越大,喷淋角越大,液滴尺寸越小;喷孔直径增加,喷淋角和液滴尺寸均增大.低压喷淋液滴SMD集中在250～550μm之间,属于大颗粒,得出计算液滴SMD的关联式.喷淋通量在中心最大,喷嘴流量增大,边缘区喷淋通量逐渐增加,介质喷淋周相均匀性较好.实验结果可以为旋流压力式喷嘴,以及惰性粒子流化床干燥器的设计和改进,提供实验依据.     

Prion protein cleavage fragments regulate adult neural stem cell quiescence through redox modulation of mitochondrial fission and SOD2 expression

Neurogenesis continues in the post-developmental brain throughout life. The ability to stimulate the production of new neurones requires both quiescent and actively proliferating pools of neural stem cells (NSCs). Actively proliferating NSCs ensure that neurogenic demand can be met, whilst the quiescent pool makes certain NSC reserves do not become depleted. The processes preserving the NSC quiescent pool are only just beginning to be defined. Herein, we identify a switch between NSC proliferation and quiescence through changing intracellular redox signalling. We show that N-terminal post-translational cleavage products of the prion protein (PrP) induce a quiescent state, halting NSC cellular growth, migration, and neurite outgrowth. Quiescence is initiated by the PrP cleavage products through reducing intracellular levels of reactive oxygen species. First, inhibition of redox signalling results in increased mitochondrial fission, which rapidly signals quiescence. Thereafter, quiescence is maintained through downstream increases in the expression and activity of superoxide dismutase-2 that reduces mitochondrial superoxide. We further observe that PrP is predominantly cleaved in quiescent NSCs indicating a homeostatic role for this cascade. Our findings provide new insight into the regulation of NSC quiescence, which potentially could influence brain health throughout adult life.