Reciprocal influence of connexins and apical junction proteins on their expressions and functions

Membranes of adjacent cells form intercellular junctional complexes to mechanically anchor neighbour cells (anchoring junctions), to seal the paracellular space and to prevent diffusion of integral proteins within the plasma membrane (tight junctions) and to allow cell-to-cell diffusion of small ions and molecules (gap junctions). These different types of specialised plasma membrane microdomains, sharing common adaptor molecules, particularly zonula occludens proteins, frequently present intermingled relationships where the different proteins co-assemble into macromolecular complexes and their expressions are co-ordinately regulated. Proteins forming gap junction channels (connexins, particularly) and proteins fulfilling cell attachment or forming tight junction strands mutually influence expression and functions of one another.     

Lipid droplet proteins and metabolic diseases

Lipid droplets (LDs) are ubiquitous cellular organelles for lipid storage which are composed of a neutral lipid core bounded by a protein decorated phospholipid monolayer. Although lipid storage is their most obvious function, LDs are far from inert as they participate in maintaining lipid homeostasis through lipid synthesis, metabolism, and transportation. Furthermore, they are involved in cell signaling and other molecular events closely associated with human disease such as dyslipidemia, obesity, lipodystrophy, diabetes, fatty liver, atherosclerosis, and others. The last decade has seen a great increase in the attention paid to LD biology. Regardless, many fundamental features of LD biology remain obscure. In this review, we will discuss key aspects of LD biology including their biogenesis, growth and regression. We will also summarize the current knowledge about the role LDs play in human disease, especially from the perspective of the dynamics of the associated proteins. This article is part of a Special issue entitled Cardiac adaptations to obesity, diabetes and insulin resistance, edited by Professors Jan F.C. Glatz, Jason R.B. Dyck and Christine Des Rosiers.     

夜间低温对不同光强下生长的两种沟谷雨林树苗荧光参数的影响

 于雾凉季测定了叶片叶绿素荧光参数,探讨了4～6 ℃夜间低温对4种相对光强下生长的两种西双版纳沟谷雨林树苗光系统Ⅱ（PSⅡ）活性的影响及雾对植物的可能保护机制。随夜间低温处理时间延长,不同光强下生长的团花树（Anthocephalus chinensis）和玉蕊（Barringtonia macrostachya）叶片日间和长期光抑制,以及PSⅡ反应中心的可逆失活或破坏加剧,生长环境光越强夜间低温的效应越明显,弱光下其效应不显著。间接表明雾使光强减弱利于缓解自然夜温降低对本区热带植物的影响。中光强下玉蕊对照植株发生了胁迫诱导的光抑制;相同处理条件下玉蕊的光抑制程度均比团花树重,表明玉蕊对夜间低温引起的光抑制更敏感。夜间低温处理后,中等和低光强下团花树的热耗散多于玉蕊,表明其光保护作用较强。夜间低温处理期间两种植物的光抑制与热耗散增多和PSⅡ反应中心的可逆失活或破坏的加剧有关。     

Wnt3a upregulates transforming growth factor-β-stimulated VEGF synthesis in osteoblasts

It is recognized that Wnt3a affects bone metabolism via the canonical Wnt/β-catenin signalling pathway. We have previously shown that transforming growth factor-β (TGF-β) stimulates the synthesis of vascular endothelial growth factor (VEGF) via p44/p42 mitogen-activated protein (MAP) kinase, stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK) and p38 MAP kinase in osteoblast-like MC3T3-E1 cells. In the present study, we investigated the effect of Wnt3a on TGF-β-stimulated VEGF synthesis in these cells. Wnt3a, which alone had little effect on the VEGF levels, significantly enhanced the TGF-β-stimulated VEGF release. Lithium chloride and SB216763, inhibitors of glycogen synthase kinase 3β, markedly amplified the TGF-β-stimulated VEGF release. Wnt3a failed to affect the TGF-β-induced phosphorylation of Smad2, p44/p42 MAP kinase, p38 MAP kinase or SAPK/JNK. Wnt3a and lithium chloride strengthened the VEGF mRNA expression induced by TGF-β. These results strongly suggest that Wnt3a upregulates VEGF synthesis stimulated by TGF-β via activation of the canonical pathway in osteoblasts.     

内生真菌Colletotrichum sp. B501的寡糖提取物对黄花蒿发根中青蒿素生物合成的诱导

在黄花蒿(Artemisia annua L.)发根液体培养中,黄花蒿内生炭疽菌(Colletotrichum sp. B501)细胞壁寡糖提取物可促进发根青蒿素的合成.经寡糖诱导子(20 mg/L)处理4 d后,发根青蒿素含量达1.15 mg/g, 比对照高出64.29%.诱导作用与诱导子浓度、作用时间相关.诱导处理1 d后,X射线能谱分析表明黄花蒿发根细胞中Ca2+积累量显著增高,电镜观察发现液泡内出现高电子致密物,具活性氧清除作用的过氧化物酶表现出高活性(6.5 unit*min-1*g-1 FW).诱导处理第三天,细胞核DNA呈梯度条带降解,部分细胞出现程序化死亡.内生菌细胞壁寡糖提取物引起的生理反应有利于细胞中青蒿素的生物合成.     

老年急性脑梗死患者血清CRP, FG, LP(a)变化研究

目的:探讨老年急性脑梗死患者检测血清C反应蛋白(CRP)、纤维蛋白原(FG)及脂蛋白(a)(LP(a))的变化及意义。方法:选择2013年12月-2014年12月在我院就诊的年龄≥60岁的急性脑梗死患者90例作为实验组,根据中国脑卒中患者临床神经功能缺损程度评分标准(NDS),分为轻型、中型和重型;根据病灶直径及Adama分型法分为腔隙性脑梗死、小梗死和大梗死,另外选择90例健康老人为对照组。测定所有受试者血清中的CRP、FG及LP(a)的水平,并比较它们在实验组与对照组、实验组不同严重程度和不同病变类型的患者中的差异。结果:实验组血清CRP、FG和LP(a)的水平高于对照组,且差异具有统计学意义(P0.05);重型患者血清CRP、FG和LP(a)水平明显高于中型患者,中型患者显著高于轻型患者,且差异均有统计学意义(P0.05);大梗死患者血清CRP、FG和LP(a)水平明显高于小梗死患者,小梗死患者显著高于腔隙性梗死患者,且差异均有统计意义(P0.05)。结论:血清CRP、FG和LP(a)水平异常升高与老年急性脑梗死的发生发展密切相关。     

低钾型周期性麻痹相关的Cchl1a3基因R528H敲入小鼠模型的构建

目的：构建低钾型周期性麻痹相关的Cchl1a3基因R528H敲入小鼠模型。方法将 Cchl1a3-knock-in打靶载体电转染ES细胞,经过G418和Ganciclovoir筛选阳性ES细胞克隆并用PCR和DNA测序法鉴定。将阳性ES克隆注射到小鼠囊胚,获得嵌合体小鼠。通过杂交获得的杂合子小鼠与FLP小鼠交配繁育获得去neo杂合子小鼠,并用PCR和DNA测序进行鉴定。将去neo杂合子小鼠交配得到纯合子后代,进行生长发育等方面的观察。结果打靶载体成功转染ES细胞,PCR和DNA测序法证实9个ES细胞克隆发生正确的同源重组。通过显微注射获得7只嵌合体小鼠。将嵌合体小鼠交配繁育的杂合子小鼠和FLP小鼠交配获得9只去neo杂合子小鼠,最终得到15只去neo纯合子小鼠。该小鼠在发育至性成熟阶段,精神、饮食及活动状态良好,但是在4个月龄时逐渐出现脱毛,皮肤破溃甚至死亡。结论成功构建Cchl1a3基因 R528H 突变的纯合子小鼠,为研究人类CACNA1S基因功能和阐明低钾型周期性麻痹发生的分子机制奠定了基础。     

Plasma lipoproteins are important components of the immune system

Plasma lipoproteins (VLDL, LDL, Lp[a] and HDL) function primarily in lipid transport among tissues and organs. However, cumulative evidence suggests that lipoproteins may also prevent bacterial, viral and parasitic infections and are therefore a component of innate immunity. Lipoproteins can also detoxify lipopolysaccharide and lipoteichoic acid. Infections can induce oxidation of LDL, and oxLDL in turn plays important anti‐infective roles and protects against endotoxin‐induced tissue damage. There is also evidence that apo(a) is protective against pathogens. Taken together, the evidence suggests that it might be valuable to introduce the concept that plasma lipoproteins belong in the realm of host immune response.     

A Microfluidic Platform for Precision Small-volume Sample Processing and Its Use to Size Separate Biological Particles with an Acoustic Microdevice

A major advantage of microfluidic devices is the ability to manipulate small sample volumes, thus reducing reagent waste and preserving precious sample. However, to achieve robust sample manipulation it is necessary to address device integration with the macroscale environment. To realize repeatable, sensitive particle separation with microfluidic devices, this protocol presents a complete automated and integrated microfluidic platform that enables precise processing of 0.15–1.5 ml samples using microfluidic devices. Important aspects of this system include modular device layout and robust fixtures resulting in reliable and flexible world to chip connections, and fully-automated fluid handling which accomplishes closed-loop sample collection, system cleaning and priming steps to ensure repeatable operation. Different microfluidic devices can be used interchangeably with this architecture. Here we incorporate an acoustofluidic device, detail its characterization, performance optimization, and demonstrate its use for size-separation of biological samples. By using real-time feedback during separation experiments, sample collection is optimized to conserve and concentrate sample. Although requiring the integration of multiple pieces of equipment, advantages of this architecture include the ability to process unknown samples with no additional system optimization, ease of device replacement, and precise, robust sample processing.     

Inactivation of chloroplast photosynthetic electron-transport activity by Ni

Ni²⁺ inhibits electron-transport activity of isolated barley chloroplasts and this inhibition of electron transport by Ni²⁺ is distinctly different from other heavy metal ion (e.g., Pb²⁺, Cd²⁺, Zn²⁺)-induced inhibition of chloroplast function. Ni²⁺ inactivates Photosystem II (PS II) activity at a lower concentration than that required for the same extent of inhibition of Photosystem I (PS I)-mediated electron flow. Ni²⁺ induces changes in chlorophyll a (Chl a) emission characteristics and brings about a lowering of the Chl a fluorescence yield, and this lowering of Chl a fluorescence intensity is not relieved by the exogenously supplied electron donor NH₂OH which donates electrons very close to the PS II reaction centres. Immobilization of the chloroplast membrane structure with glutaraldehyde fails to arrest the Ni²⁺-induced loss of PS II activity. Also, Ni²⁺-treated chloroplasts do not regain the ability to photoreduce 2,6-dichlorophenolindophenol even after washing of chloroplasts with buffer. These results indicate that unlike Zn²⁺ or Pb²⁺, Ni²⁺ induces alterations in the chloroplast photosynthetic apparatus resulting in an irreversible loss of electron-transport activity.