大面积烧伤患者早期红细胞膜胆固醇变化与红细胞变形性的关系

目的研究大面积烧伤患者早期红细胞膜胆固醇与红细胞变形指数的变化及意义。方法利用核孔滤膜法测量红细胞变形指数,使用化学修饰电极测量红细胞膜胆固醇。结果大面积烧伤患者早期与正常对照组比较红细胞变形指数显著下降,分别为7.826±0.53及6.541±0.61,而红细胞膜胆固醇则显著升高,分别为(0.645±0.062)mmol/g膜蛋白及(0.891±0.051)mmol/g膜蛋白(P＜0.01),且二者呈高度负相关(r=-0.801)。结论红细胞膜胆固醇能够有效反映大面积烧伤患者早期红细胞变形能力,并成为反映大面积烧伤的早期微循环状态的新型量化指标。     

大面积烧伤患者早期红细胞膜胆固醇变化与红细胞变形性的关系

目的研究大面积烧伤患者早期红细胞膜胆固醇与红细胞变形指数的变化及意义。方法利用核孔滤膜法测量红细胞变形指数 ,使用化学修饰电极测量红细胞膜胆固醇。结果大面积烧伤患者早期与正常对照组比较红细胞变形指数显著下降 ,分别为 7.82 6± 0 .5 3及 6 .5 41± 0 .6 1,而红细胞膜胆固醇则显著升高 ,分别为(0 .6 45± 0 .0 6 2 ) mm ol/ g膜蛋白及 (0 .891± 0 .0 5 1) m mol/ g膜蛋白 (P<0 .0 1) ,且二者呈高度负相关 (r=- 0 .80 1)。结论红细胞膜胆固醇能够有效反映大面积烧伤患者早期红细胞变形能力 ,并成为反映大面积烧伤的早期微循环状态的新型量化指标     

G6PD缺乏红细胞膜磷脂含量有其不对称性改变的研究

目的：通过测定葡萄糖－６－磷酸脱氢酶（Ｇ６ＰＤ）缺乏红细胞膜磷脂的含量及其不对称性的变化，研究Ｇ６ＰＤ缺乏对红细胞膜结构的影响，方法：不对称性实验采用磷脂酶Ａ２处理完整红细胞，磷脂的测定采用高效液相色谱法。结果：正常红细胞膜磷脂酰乙醇胺（ＰＥ），磷脂酰丝氨酸（ＰＳ），磷脂酰胆碱（ＰＣ）含量分别为５．５９±１．１６，２．９２±０．５０，６．６４±０．９２ｍｇ／ｍｇ膜蛋白；Ｇ６ＰＤ缺乏红细胞膜ＰＥ，Ｐ     

遗传性球形红细胞增多症的分子病理学

遗传性球形红细胞增多症是一种较常见的红细胞膜遗传性缺陷所致的溶血性贫血,主要是膜骨架蛋白的缺陷所致。本文就本病膜蛋白异常的四种类型概述近年来相关分子病理学方面的进展。     

遗传性球形红细胞增多症的分子病理学

遗传性球形红细胞增多症是一种较常见的红细胞膜遗传性缺陷所致的溶血性贫血，主要是膜骨架蛋白的缺陷所致。本文就本病膜蛋白异常的四种类型概述近年来相关分子病理学方面的进展。     

G6PD缺乏红细胞膜磷脂含量及其不对称性改变的研究

目的：通过测定葡萄糖－６－磷酸脱氢酶（Ｇ６ＰＤ）缺乏红细胞膜磷脂的含量及其不对称性的变化，研究Ｇ６ＰＤ缺乏对红细胞膜结构的影响。方法：不对称性实验采用磷脂酶Ａ２处理完整红细胞，磷脂的测定采用高效液相色谱法。结果：正常红细胞膜磷脂酰乙醇胺（ＰＥ）、磷脂酰丝氨酸（ＰＳ）、磷脂酰胆碱（ＰＣ）含量分别为５．５９±１．１６，２．９２±０．５０，６．６４±０．９２ｍｇ／ｍｇ膜蛋白；Ｇ６ＰＤ缺乏红细胞膜ＰＥ、ＰＳ、ＰＣ分别为５．１８±１．８６，１．５１±０．５８，５．７０±１．９１ｍｇ／ｍｇ膜蛋白，两组中ＰＳ有显著性差异（Ｐ＜０．００１），说明Ｇ６ＰＤ缺乏红细胞膜ＰＳ含量降低。在正常人红细胞膜中有１７．６％±２．５％ＰＥ，５７．９％±４．７％ＰＣ在外层，外层未发现ＰＳ，在Ｇ６ＰＤ缺乏红细胞膜中有３０．２％±５．７％ＰＥ，５３．８％±７．４％ＰＣ，２７．２％±５．８％ＰＳ在外层，两组中ＰＥ和ＰＳ有显著性差异（Ｐ＜０．０１和Ｐ＜０．００１），外层的ＰＣ无明显变化，说明ＰＥ、ＰＳ均向外层移动。结论：由于Ｇ６ＰＤ缺乏，红细胞膜磷脂结构发生改变，是红细胞溶血的重要机制之一。     

联合诱导法对K562细胞红系分化及其相关基因和膜蛋白表达的影响

目的优化K562细胞体外红系诱导分化条件,分析红系相关基因和膜蛋白的表达,探讨K562细胞的分化潜能。方法采用红系诱导联合培养法,优化丁酸钠、促红细胞生成素、氯化高铁血红素、枸橼酸铁等成分组合和剂量组合。鉴定指标选用红系血红素合成酶(eALAS)mRNA和粒系bcr/ablmRNA表达丰度分析、细胞形态学观察、联苯胺染色阳性率计数。红系分化进一步鉴定指标选用Real-timePCR检测10种红系分化相关基因的表达;流式细胞术测定红系细胞膜标志物。结果K562细胞诱导120h后,联苯胺染色阳性率达100%;α、β收缩蛋白(spectrinα、β)、带3蛋白(band3)、eALAS、整合素相关蛋白(CD47)、RhD血型抗原(RhD)、锚蛋白(ankyrin)、红细胞膜带4.2蛋白(EPB4.2)的mRNA水平为对照组的8.05、14.58、22.87、14.52、26.53、3.48、2.71、1.94倍,而bcr/ablmRNA水平为对照组的39%;红系膜蛋白CD47、band3、RhD水平明显增高(P<0.01),血型糖蛋白A(GPA)无明显差异。结论优化组合体外红系诱导分化法可使K562细胞稳定向红系分...     

白血病病人红细胞膜蛋白电泳观察

人红细胞膜的浆膜面装饰着一层浓密的蛋白网络,按Fairbank等报道膜蛋白凝胶电泳命名主要有收缩蛋白、锚蛋白、带3蛋白。4·1蛋白和肌动蛋白,它们在维持红细胞形态、变形及运动等方面起着重要作用。本研究结果表明:白血病病人红细胞膜收缩蛋白和肌动蛋白存在异常。     

人胚胎干细胞来源红系细胞膜蛋白表达的研究

目的探讨人胚胎干细胞(h ESCs)来源红系细胞在发育过程中其膜蛋白,包括膜表型分子、膜骨架蛋白和跨膜蛋白的表达情况。方法 h ESCs与小鼠主动脉-性腺-中肾(m AGM-S3)基质细胞共培养产生造血干祖细胞(CD34+CD45+)和GPA+细胞,挑取共培养12 d的细胞,同时磁珠分选人脐血中的CD34~+细胞,在多种特定细胞因子SCF、IL-6、IL-3、FLT3-L、TPO、EPO等诱导下,分别进行集落培养12-14 d产生红系爆发式集落形成单位(BFU-E),运用流式细胞术(FACs)、qRT-PCR和免疫荧光染色等方法检测并比较hESCs和人脐血CD34~+细胞2种来源的红系细胞膜蛋白的表达情况,并以后者作为对照组。结果 hESCs来源BFU-E的膜蛋白的表达趋势与对照组相近:其膜骨架蛋白和跨膜蛋白的基因,如SPTA、SPTB、ANK1、EPB41等基因转录水平都在逐渐增强,而一些膜蛋白如黏附分子CD49d、CD29、CD71等的表达逐渐降低,CD47基本不表达;带3蛋白(Band 3)表达量较高且与成体型血红蛋白β-globin的表达呈正相关。结论在hESCs向红系诱导生成过程中,一些膜表型分子表达在逐渐降低,而膜蛋白表达逐渐增强。     

一例隐性遗传性溶血性贫血的红细胞膜蛋白4.1和蛋白3异常

2例同胞姐弟患严重的隐性遗传性溶血性贫血。红细胞形态大小不一,有椭圆形,小球形,薄红细胞及裂红细胞等异常,其父母系近亲婚配。父母均有轻度的红细胞形态改变,但无明显临床症状。全家人的热溶血试验正常。作者对其中一例作了红细胞膜研究,红细胞膜蛋白4.1减少30%。蛋白3电泳带异常:较浓,较窄及轻度向正极移位,4.1/3比率减少,4.1/4.2比率减少。但即使在溶血状态,其4.1a/4.1b比率仍正常。患者的唾液酸糖蛋白分析和红细胞膜内蛋白分析未见异常。     

膜式氧合器中膜材料的研究进展

检索Pubmed数据库和万方数据库以及中国期刊全文数据库文献,分析膜式氧合器的特点.结果表明现在人工肺的应用主要是分离膜式,其形式已从最初的卷筒式、平板折叠式发展到今天广为采用的微孔中空纤维膜式.中空纤维膜氧合器使用中空纤维膜作为交换的主要场所,完成氧气和二氧化碳的交换,由于其在交换面积、氧合形态等方面具有优势,近年来已经成为人工肺研究的主要方向.用于制造中空纤维的材料主要为一些成纤性能良好的高分子材料,对膜材料的要求是具有良好的成膜性、热稳定性、化学稳定性、耐酸碱性、微生物侵蚀性和抗氧化性.当前的研究主要是为了提高气体交换能力和提高生物相容性,采用的方法主要有改进膜材料,优化设计以及对各种性能的实验评估和临床评价.     

Anionic nanoparticle-lipid membrane interactions: the protonation of anionic ligands at the membrane surface reduces membrane disruption

Monolayer-protected gold nanoparticles (Au NPs) are promising biomedical tools with applications in diagnosis and therapy, thanks to their biocompatibility and versatility. Here we show how the NP surface functionalization can drive the mechanism of interaction with lipid membranes. In particular, we show that the spontaneous protonation of anionic carboxylic groups on the NP surface can make the NP-membrane interaction faster and less disruptive.

The interaction between anionic Au nanoparticles and model lipid membranes is facilitated by the spontaneous protonation of the NP ligand carboxylate groups, COO⁻˙ → COOH, in the lipid headgroup region.     

Placental membrane transport

Brush border (microvillous) plasma membranes (BBM) and the basal surfaces (BCM) from the syncytiotrophoblast of human term placenta were prepared by a method of sonication, dialysis and differential centrifugation in specific buffer systems. Such plasma membranes formed closed, osmotically active, right-side-out vesicles in which amino acid transport could be studied unidirectionally by a carefully designed membrane filtration assay under reduced pressure. In such vesicles,l-leucine (1 mM) was found to be transported in a time-dependent manner, peak accumulation being attained at 45 s in both BBM and BCM. The accumulation of leucine in the vesicles was dependent on an inward NaCl gradient, as replacing the Na⁺with K⁺, Li⁺and choline, or replacing the Cl^? with SO ₄ ^2? failed to influence the amino acid movement. Leucine transport in the vesicles also appeared to be dependent on the substrate concentration, indicating saturation at a higher concentration. The transport process showed a k_t (affinity constant) of 3.85 and 6.67 mM, while the values recorded for the J_max (maximum apparent initial velocity) were 270.27 and 384.62 nmol/mg protein^?1 per min in the BBM and BCM respectively. Leucine transport was inhibited by a number of amino acids, among which amino isobutyric acid (AIB) produced the maximum inhibition. The k_i (inhibition constant) for different amino acids has also been listed. Lysine showed the least k_i value, thus showing it to be the most inhibitory compound. These findings are discussed in relation to the mechanism and regulation of transplacental amino acid transfer.     

Extracorporeal membrane oxygenation

PURPOSE OF REVIEW: Extracorporeal membrane oxygenation (ECMO) has become a more or less accepted standard in the algorithm of advanced acute respiratory distress syndrome therapy in adult patients when all other treatment options have failed. This article reviews the current status of ECMO therapy with particular focus on new technical developments and their potential implications for performance and indications for ECMO therapy. RECENT FINDINGS: A recently published review on a single-center experience in 255 adult ECMO patients identified using multivariate logistic regression analysis age, sex, initial pH 7.10 or lower and PaO2/FiO2 ratio, and days of mechanical ventilation before ECMO as a significant predictors of survival. Additionally, a careful cost-effectiveness study for neonatal ECMO relating a 4-year base to the UK neonatal ECMO trial has clearly demonstrated cost-effectiveness. SUMMARY: Over the years, the technique for ECMO therapy underwent substantial changes in indications and the materials used. Impressive technical progress has been made in pumps, oxygenators, and coating of artificial surfaces, leading to a higher biocompatibility and to a lower rate of procedure-related complications. The potential of new inline pumps in combination with a decreasing rate of procedure-related complications might lead to a re-evaluation of the role of extracorporeal lung support in acute respiratory distress syndrome therapy. A very recent development is the use of spontaneous arteriovenous devices for carbon dioxide removal, allowing significant reduction of ventilator settings at decreased carbon dioxide partial pressures and at increased pH values. Ongoing studies are looking at the potential of this approach to reduce side effects of mechanical ventilation further.     

Association between the glycation of erythrocyte membrane proteins and membrane fluidity

Erythrocyte membrane ghosts prepared from normal individuals were incubated in vitro at different glucose concentrations for 72 h. Incubation with increasing concentrations of glucose resulted in increased glycation (nonenzymatic glycosylation) of membrane proteins and a decrease of erythrocyte membrane fluidity measured by the use of the fluorescent label pyrene. It would therefore seem likely that the changes in erythrocyte membrane fluidity previously reported in diabetic subjects (1-3) are related to in vivo glycation of membrane proteins as well as to changes in lipid composition, as was previously suggested (2).