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本文主要就激光在国外兽医领域的激光内窥镜外科、肿瘤外科、眼外科、小动物外科以及激光动力学治疗等方面的应用及基础理论方面的研究进展进行综述。 相似文献
123.
为了确定从噬菌体抗体文库中筛选出的抗体的属性和方便目的基因的表达及其产物的纯化,对两株具有“1F7”独特型的抗HIV-1gp160抗体基因进行了序列分析并构建了可溶性表达载体.发现3B株含有完整的Fab段,1D株只有重链Fd段.序列测定表明两株克隆的Fd段基因完全相同,其可变区VH属于VHⅠ亚群,而3B株的“轻链”序列与已知的人的κ和λ轻链无同源性.用从另外的Fab抗体文库中筛选出来的3株抗乙肝表面抗原抗体的轻链与3B的重链重组,并选择一个HIV-1gp160特异性较好的重组抗体株,命名为3Bs.构建了1D株与3Bs株的可溶性表达载体,免疫印迹实验证实了具有“1F7”独特型的抗gp160独特型阳性抗体的表达. 相似文献
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Yun Sook Kim Dae-Sung Lee Seong-Yun Jeong Woe Jae Lee Myung-Suk Lee 《Journal of microbiology (Seoul, Korea)》2009,47(1):9-18
A bacterial strain named AB-4 showing algicidal activity against Chattonella marina was isolated from coastal water of ULjin, Republic of Korea. The isolated strain was identified as Bacillus sp. by culture morphology, biochemical reactions, and homology research based on 16S rDNA. The bacterial culture led to the
lysis of algal cells, suggesting that the isolated strain produced a latent algal-lytic compound. Amongst changes in algicidal
activity by different culture filtrate volumes, the 10% (100 μl/ml) concentration showed the biggest change in algicidal activity;
there, estimated algicidal activity was 95%. The swimming movements of Chattonella marina cells were inhibited because of treatment of the bacterial culture; subsequently, Chattonella marina cells became swollen and rounded. With longer exposure time, algal cells were disrupted and cellular components lost their
integrity and decomposed. The released algicide(s) were heat-tolerant and stable in pH variations, except pH 3, 4, and 5.
Culture filtrate of Bacillus sp. AB-4 was toxic against harmful algae bloom (HAB) species and nontoxic against livefood organisms. Bacillus sp. AB-4 showed comparatively strong activity against Akashiwo sanguinea, Fibriocapsa japonica, Heterosigma akashiwo, and Scrippsiella trochoidea. These results suggest that the algicidal activity of Bacillus sp. AB-4 is potentially useful for controlling outbreaks of Chattonella marina. 相似文献
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The cytopathic effects induced during parvovirus infection have been widely documented. Parvovirus infection-induced cell death is often directly associated with disease outcomes (e.g., anemia resulting from loss of erythroid progenitors during parvovirus B19 infection). Apoptosis is the major form of cell death induced by parvovirus infection. However, nonapoptotic cell death, namely necrosis, has also been reported during infection of the minute virus of mice, parvovirus H-1 and bovine parvovirus. Recent studies have revealed multiple mechanisms underlying the cell death during parvovirus infection. These mechanisms vary in different parvoviruses, although the large nonstructural protein (NS)1 and the small NS proteins (e.g., the 11 kDa of parvovirus B19), as well as replication of the viral genome, are responsible for causing infection-induced cell death. Cell cycle arrest is also common, and contributes to the cytopathic effects induced during parvovirus infection. While viral NS proteins have been indicated to induce cell cycle arrest, increasing evidence suggests that a cellular DNA damage response triggered by an invading single-stranded parvoviral genome is the major inducer of cell cycle arrest in parvovirus-infected cells. Apparently, in response to infection, cell death and cell cycle arrest of parvovirus-infected cells are beneficial to the viral cell lifecycle (e.g., viral DNA replication and virus egress). In this article, we will discuss recent advances in the understanding of the mechanisms underlying parvovirus infection-induced cell death and cell cycle arrest. 相似文献
129.
Type II collagen is a major protein that maintains biological and mechanical characteristics in articular cartilage. Focal adhesion kinase (FAK) is known to play a central role in integrin signaling of cell–extracellular matrix (ECM) interactions, and chondrocyte–type II collagen interactions are very important for cartilage homeostasis. In this study, we focused on phosphorylation of FAK and MAP kinase in chondrocyte–type II collagen interaction and dedifferentiation, and the effects of FAK knockdown on chondrocyte‐specific gene expression and cell proliferation were determined. The addition of exogenous type II collagen to chondrocytes increased levels of tyrosine phosphorylation, p‐FAKY397, and p‐ERK1/2. In contrast, expression levels of p‐FAKY397 and p‐ERK1/2, but not p‐Smad2/3, were decreased in dedifferentiated chondrocytes with loss of type II collagen expression. Type II collagen expression was significantly increased when dedifferentiated chondrocytes were transferred to alginate beads with TGF‐β1 or type II collagen, but transfected cells with small interfering RNA for FAK (FAK‐siRNA) inhibited mRNA expression of type II collagen and SOX‐6 compared to the control. These FAK‐siRNA‐transfected cells could not recover type II collagen even in the presence of TGF‐β1 or type II collagen in alginate beads culture. We also found that FAK‐siRNA‐transfected cells decreased cell proliferation rate, but there was no effect on glycosaminoglycans (GAGs) secretion. We suggest that FAK is essentially required in chondrocyte communication with type II collagen by regulating type II collagen expression and cell proliferation. J. Cell. Physiol. 218: 623–630, 2009. © 2008 Wiley‐Liss, Inc. 相似文献
130.
Xi Lu Xinyi Yang Xue Li Yun Lu Zhitao Ren Longyin Zhao Xinxin Hu Jiandong Jiang Xuefu You 《PloS one》2013,8(7)