渗透胁迫对水稻幼苗膜脂过氧化及体内保护系统的影响

两个不同抗旱性的水稻品种对PEG6000渗透胁迫(-0.5MPa,-0.8MPa)的反应具有一定差异。渗透胁迫下SOD,POD和CAT活性及Vc,Car含量与膜脂过氧化水平及膜透性呈一定负相关性,表明这些指标可作为水稻抗旱育种的参考依据。     

渗透胁迫下稻苗中铁催化的膜脂过氧化作用

在－０．７ＭＰａ渗透胁迫下,水稻幼苗体内和Ｈ２Ｏ２大量产生,Ｆｅ２＋积累,膜脂过氧化作用加剧。水稻幼苗体内Ｆｅ２＋含量与膜脂过氧化产物ＭＤＡ含量呈极显著的正相关。外源Ｆｅ２＋、Ｆｅ３＋、Ｈ２Ｏ２、Ｆｅ２＋＋Ｈ２Ｏ２、ＤＤＴＣ均能刺激膜脂过氧化作用,而铁离子的螯合剂ＤＴＰＡ则有缓解作用。ＯＨ的清除剂苯甲酸钠和甘露醇能明显地抑制渗透胁迫下Ｆｅ２＋催化的膜脂过氧化作用。这都表明渗透胁迫下水稻幼苗体内铁诱导的膜脂过氧化作用主要是由于其催化Ｆｅｎｔｏｎ型Ｈａｂｅｒ－Ｗｅｉｓｓ反应形成ＯＨ所致。     

利用归一化互相关算法去除吸收强度涨落调制血管造影图像模糊

吸收强度涨落调制成像（AIFM）方法是基于血红细胞和背景组织对低相干光照明的吸收差异,通过在频域分离动态的血红细胞信号和静态的背景信号,实现对近透明活体生物样本全场无标记的光学血管造影成像. 但此成像方法需采集较长的原始图像序列,系统漂移或生物抖动会造成图像模糊,难以实现对某些特定区域的血管造影成像. 本文提出一种结合AIFM成像和归一化互相关算法的新方法来提升血管造影图像的质量：原始的图像序列被分成若干短时序列,每个短时序列先利用AIFM成像算法重构得到全场的血管造影图像;再利用归一化的互相关算法将所有的短时重构图像与第一帧重构图像相匹配,并融合得到最终的血管造影片. 我们以活体鸡蛋胚胎为样品,通过实验验证了利用短时归一化互相关AIFM成像方法,能够消除鸡胚胎心跳引起的图像模糊,从而获得高分辨率和信噪比的心血管造影片,对研究活体动物心脑血管疾病具有重要应用价值.     

脐带血造血干/祖细胞体外分化为不同阶段红系祖细胞的动力学观察

目的:探讨体外培养脐带血单个核细胞定向诱导分化为不同阶段红系祖细胞的动力学变化情况。方法:用0.5%甲基纤维素沉降脐带血红细胞及人淋巴细胞分离液密度梯度离心法得到单个核细胞,在含EPO、SCF、IGF-1等细胞因子的无血清培养体系中诱导其定向分化为红系祖细胞,观察细胞增殖、存活率、细胞集落形成情况,并检测不同阶段细胞红系特异性表面标志CD71和CD235a的表达。结果:随着培养时间的延长,细胞数逐渐增多,14 d细胞可扩增140倍左右,收集诱导后的细胞进行瑞氏吉姆萨染色,可见大量红系祖细胞,诱导后的细胞集落形成能力强,形成的克隆大部分为红系集落。诱导过程中,14 d前CD71、CD235a的表达逐渐增高。按细胞表面标志表达的不同可将诱导的细胞分为4群,分别对应红系祖细胞的不同阶段;随着诱导天数的增加,各时间点细胞对应的早期红系祖细胞群(P2、P3)比例逐渐下降,中晚期红系祖细胞群(P4、P5)的比例逐渐上升。结论:无血清培养基添加细胞因子组合的红系诱导培养体系可较好地诱导扩增红系祖细胞,流式分选可获得相对均一而处于不同分化阶段的红系祖细胞群体。获得了红系祖细胞体外分化的动力学数据,为今后进一步优化红系诱导分化体系获得均一的红系祖细胞奠定了基础,并对未来利用干细胞制备均一的红系祖细胞应用于临床治疗有一定的指导作用。     

Skin Autofluorescence Is Associated with Endothelial Dysfunction in Uremic Subjects on Hemodialysis

Background

Elevated levels of advanced glycation end products (AGEs) within tissues may contribute to endothelial dysfunction, an early indicator of atherosclerosis. We aimed to investigate whether levels of skin AGEs could be a useful marker to predict endothelial dysfunction in uremic subjects on hemodialysis.

Methods and Results

One hundred and nineteen uremic patients on hemodialysis and 57 control subjects with moderate-to-high cardiovascular risk factors and without chronic kidney disease (CKD) were enrolled. We used ultrasound to measure flow-mediated vasodilation (FMD). An AGE reader measured skin autoflurorescence (AF). We then compared differences in FMD and skin AF values between the two groups. The uremic subjects had significantly higher levels of skin AF (3.47±0.76 AU vs. 2.21±0.45 arbitrary units; P<0.01) and significantly lower levels of FMD (4.79%±1.88% vs. 7.19%±2.17%; P<0.01) than the non-CKD subjects. After adjusting for all potential covariates, we found that skin AF level independently predicted FMD in both the hemodialysis and the non-CKD groups. In the hemodialysis group, skin AF ≥ 3.05 arbitrary units predicted abnormal FMD at a sensitivity of 87.9% and a specificity of 78.6% (P<0.01).

Conclusions

Skin AF could be a useful marker to predict endothelial dysfunction in uremic subjects on hemodialysis.     

高动态光学血管造影成像

我们提出一种高动态光学血管造影成像(HDOA)方法来实现活体生物样本血管造影成像.该方法通过设置高动态范围曝光时间,依据动态积分效应和吸收效应以实现高动态积分时间调制.通过该方法,不仅能够同时获得各级血管清晰的造影图像,还能消除样品厚度不均、吸收系数不同对成像造成的影响.论文以仿体和活体金鱼为样品,通过实验验证了HDOA方法根据动态积分调制效应和吸收效应,能有效实现各级血管同时成像.     

Reactive thrombocytosis alone does not affect the patency of microvascular anastomosis in the splenectomy rat

Vascular thrombosis is a harbinger of failure in microsurgery. However, there is still controversy regarding the correlation of the complications of thrombocytosis and thrombosis. Some evidence indicates that patients with elevated platelet counts tend to have a higher flap failure rate, and surgeons usually hesitate to operate on patients with thrombocytosis. Nevertheless, the authors have experienced successful free tissue transfer in seven patients with thrombocytosis resulting from traumatic splenectomy or multiple trauma. On the basis of clinical observation, the authors investigated whether reactive thrombocytosis contributes to the patency of a microvascular anastomosis. In a rodent splenectomy-induced thrombocytosis model (n = 40), stable reactive thrombocytosis occurred after postoperative days 5 to 10, with the peak on postoperative day 7. Femoral artery division and reanastomosis was performed in rats with or without splenectomy-induced thrombocytosis, and vascular patency was assessed. Platelet counts and platelet activation were studied in correlation to microvascular patency. Platelet activation as demonstrated by CD62P expression on platelets was not significantly different between rats with and without thrombocytosis (6.41 +/- 0.95 percent versus 4.51 +/- 0.55 percent, respectively; p = 0.089). As immature platelets were not increased (2.86 +/- 0.33 percent versus 1.99 +/- 0.32 percent, p = 0.074), it seems that the splenectomy-induced thrombocytosis is the result of redistribution of platelets instead of an increase in bone marrow production. There were no significant differences in the patency rates or perfusion units of femoral artery after arterial anastomosis between rats with and without thrombocytosis (90 percent and 95 percent, respectively; p = 0.561). In conclusion, this study demonstrates that microvascular anastomosis can be performed safely in patients with reactive thrombocytosis without platelet activation.     

Comparisons of microcarrier cell culture processes in one hundred mini-liter spinner flask and fifteen-liter bioreactor cultures

Microcarrier cell culture process can be used to culture anchorange-dependent cells in large bioreactor vessels. The process performance in large bioreactors is usually less prominent than that in spinner flask vessels and bench scale reactors. In this study we investigated the microcarrier cell culture processes in 100?ml spinner flask and 15-liter bioreactor cultures, including the kinetics for cell attachment, cell growth and the production of Japanese encephaltilis vaccine strain (Beijing-1) virus. Under a fixed concentration of microcarrier and cell density used in inoculations, the attachment kinetics of Vero cells on Cytodex 1 microcarrier in a 15-liter bioreactor vessel was 2 folds slower than with 100?ml spinner flask culture. Virus replication in 15-liter bioreactor culture also revealed an approximately one day lag-time compared to 100?ml spinner flask culture. Findings presented herein provide valuable information for designing and operating microcarrier cell culture processes in large bioreactor vessels.     

Mitochondrial mechanisms in amyloid beta peptide-induced cerebrovascular degeneration

Prevailing evidence suggests that amyloid beta peptide (Aβ), a key mediator in age-dependent neuronal and cerebrovascular degeneration, activates death signaling processes leading to neuronal as well as non-neuronal cell death in the central nervous system. A major cellular event in Aβ-induced death of non-neuronal cells, including cerebral endothelial cells, astrocytes and oligodendrocytes, is mitochondrial dysfunction. The death signaling cascade upstream of mitochondria entails Aβ activation of neutral sphingomyelinase, resulting in the release of ceramide from membrane sphingomyelin. Ceramide then activates protein phosphatase 2A (PP2A), a member in the ceramide-activated protein phosphatase (CAPP) family. PP2A dephosphorylation of Akt and FKHRL1 plays a pivotal role in Aβ-induced Bad translocation to mitochondria and transactivation of Bim. Bad and Bim are pro-apoptotic proteins that cause mitochondrial dysfunction characterized by excessive ROS formation, mitochnondrial DNA (mtDNA) damage, and release of mitochondrial apoptotic proteins including cytochrome c, apoptosis inducing factor (AIF), endonuclease G and Smac. The cellular events activated by Aβ to induce death of non-neuronal cells are complex. Understanding these death signaling processes will aid in the development of more effective strategies to slow down age-dependent cerebrovascular degeneration caused by progressive cerebrovascular Aβ deposition.     

Impact of taxol on dermal papilla cells--a proteomics and bioinformatics analysis

Dermal papilla (DP) cells play a regulatory role in hair growth, and also play a role in alopecia (hair loss). However, effects of taxol, which is a widely used chemotherapy drug, on DP cells remain unclear, despite that theoretically taxol can impact on DP cells to contribute to taxol-induced alopecia. To better understand pathophysiology of taxol-induced damage in DP cells, morphological and biochemical analyses were performed to check whether taxol can cause apoptosis in cultured DP cells or not. If it can, proteomics and bioinformatics analyses were then performed to investigate the protein networks which are impacted by the taxol treatment. Our data showed that taxol can cause apoptotic damage in DP cells in a concentration-dependant manner, as demonstrated by various apoptotic markers. Proteomic analysis on DP cells treated with the lowest apoptosis-inducible concentration of taxol revealed that taxol can affect expression of proteins involved in Ca2+-regulated biological processes, vesicles transport, protein folding, reductive detoxification, and biomolecules metabolism. Furthermore, bioinformatics analysis indicated that taxol can impact on multiple biological networks. Taken together, this biochemical, proteomics, and bioinformatics data may give an insight into pathophysiology of taxol-induced damage in DP cells and shed light on mechanisms underlying taxol-induced alopecia.