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991.
992.
Identification and characterization of novel amphioxus microRNAs by Solexa sequencing 总被引:1,自引:0,他引:1
993.
Dan Su HongXin Deng Xia Zhao Xi Zhang LiJuan Chen XianCheng Chen ZhengYu Li Yu Bai YongSheng Wang Qian Zhong Tao Yi ZhiYong Qian YuQuan Wei 《Cytotherapy》2009,11(5):642-652
Background aimsCD24 is markedly overexpressed in ovarian cancer and plays a critical role in ovarian cancer survival and metastasis, rendering it an interesting target for anti-tumor therapy. Using short hairpin RNA (shRNA) targeting CD24, we aimed to investigate the anti-tumor efficacy of CD24 knockdown in ovarian cancer cells in vitro and in vivo.MethodsCD24 shRNA vector (CD24–shRNA) and empty plasmid vector (EP) were transfected into ovarian cancer SKOV3 cells and the knockdown efficacy assessed by Western blot analysis. The effects of CD24 knockdown in SKOV3 cells in vitro, including cell viability and apoptosis, were determined using methyl thiazolyl blue tetrazolium bromide (MTT), flow cytometry and propidium iodide (PI) staining assays. The effects in vivo of CD24 knockdown on angiogenesis, cell proliferation and apoptosis were assessed using immunohistochemistry against CD31, proliferating cell nuclear antigen (PCNA) and terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) assays.ResultsTransfection of CD24–shRNA effectively down-regulated CD24 expression in vitro and in vivo. Administration of CD24–shRNA into nude mice bearing ovarian cancer significantly suppressed tumor volume growth.ConclusionsKnockdown of CD24 expression by CD24–shRNA significantly inhibited cell viability and induced apoptosis of SKOV3 cells in vitro. Administration with CD24–shRNA in vivo suppressed tumor volume increase by microvessel density (MVD) decrease, cell proliferation inhibition and apoptosis induction. All the data suggested that knockdown of CD24 by shRNA might be a potential therapeutic approach against human ovarian cancer. 相似文献
994.
995.
Xi W M Robert N. Coulson Andrew G. Birt Shang Z B John D. Waldron Charles W. Lafon David M. Cairns Maria D. Tchakerian Kier D. Klepzig 《农业工程》2009,29(1):69-78
Forest landscape models simulate forest change through time using spatially referenced data across a broad spatial scale (i.e. landscape scale) generally larger than a single forest stand. Spatial interactions between forest stands are a key component of such models. These models can incorporate other spatio-temporal processes such as natural disturbances (e.g. wildfires, hurricanes, outbreaks of native and exotic invasive pests and diseases) and human influences (e.g. harvesting and commercial thinning, planting, fire suppression). The models are increasingly used as tools for studying forest management, ecological assessment, restoration planning, and climate change. In this paper, we define forest landscape models and discuss development, components, and types of the models. We also review commonly used methods and approaches of modeling forest landscapes, their application, and their strengths and weaknesses. New developments in computer sciences, geographic information systems (GIS), remote sensing technologies, decision-support systems, and geo-spatial statistics have provided opportunities for developing a new generation of forest landscape models that are increasingly valuable for ecological research, restoration planning and resource management. 相似文献
996.
Robin R. Craven Xi Gao Irving C. Allen Denis Gris Juliane Bubeck Wardenburg Erin McElvania-TeKippe Jenny P. Ting Joseph A. Duncan 《PloS one》2009,4(10)
Community Acquired Methicillin Resistant Staphylococcus aureus (CA-MRSA) causes severe necrotizing infections of the skin, soft tissues, and lungs. Staphylococcal α-hemolysin is an essential virulence factor in mouse models of CA-MRSA necrotizing pneumonia. S. aureus α-hemolysin has long been known to induce inflammatory signaling and cell death in host organisms, however the mechanism underlying these signaling events were not well understood. Using highly purified recombinant α-hemolysin, we now demonstrate that α-hemolysin activates the Nucleotide-binding domain and leucine-rich repeat containing gene family, pyrin domain containing 3 protein (NLRP3)-inflammasome, a host inflammatory signaling complex involved in responses to pathogens and endogenous danger signals. Non-cytolytic mutant α-hemolysin molecules fail to elicit NLRP3-inflammasome signaling, demonstrating that the responses are not due to non-specific activation of this innate immune signaling system by bacterially derived proteins. In monocyte-derived cells from humans and mice, inflammasome assembly in response to α-hemolysin results in activation of the cysteine proteinase, caspase-1. We also show that inflammasome activation by α-hemolysin works in conjunction with signaling by other CA-MRSA-derived Pathogen Associated Molecular Patterns (PAMPs) to induce secretion of pro-inflammatory cytokines IL-1β and IL-18. Additionally, α-hemolysin induces cell death in these cells through an NLRP3-dependent program of cellular necrosis, resulting in the release of endogenous pro-inflammatory molecules, like the chromatin-associated protein, High-mobility group box 1 (HMGB1). These studies link the activity of a major S. aureus virulence factor to a specific host signaling pathway. The cellular events linked to inflammasome activity have clear relevance to the disease processes associated with CA-MRSA including tissue necrosis and inflammation. 相似文献
997.
Lingyun Zhu Guoxun Sun Hongjie Zhang Yan Zhang Xi Chen Xiaohong Jiang Xueyuan Jiang Stefan Krauss Junfeng Zhang Yang Xiang Chen-Yu Zhang 《PloS one》2009,4(1)
Background
Atherosclerosis is a complex pathological condition caused by a number of mechanisms including the accelerated proliferation of vascular smooth muscle cells (VSMCs). Diabetes is likely to be an important risk factor for atherosclerosis, as hyperglycemia induces vascular smooth muscle cell (VSMC) proliferation and migration and may thus contribute to the formation of atherosclerotic lesions. This study was performed to investigate whether PGC-1α, a PPARγ coactivator and metabolic master regulator, plays a role in regulating VSMC proliferation and migration induced by high glucose.Methodology/Principal Findings
PGC-1α mRNA levels are decreased in blood vessel media of STZ-treated diabetic rats. In cultured rat VSMCs, high glucose dose-dependently inhibits PGC-1α mRNA expression. Overexpression of PGC-1α either by infection with adenovirus, or by stimulation with palmitic acid, significantly reduces high glucose-induced VSMC proliferation and migration. In contrast, suppression of PGC-1α by siRNA mimics the effects of glucose on VSMCs. Finally, mechanistic studies suggest that PGC-1α-mediated inhibition of VSMC proliferation and migration is regulated through preventing ERK1/2 phosphorylation.Conclusions/Significance
These results indicate that PGC-1α is a key regulator of high glucose-induced proliferation and migration in VSMCs, and suggest that elevation of PGC-1α in VSMC could be a useful strategy in preventing the development of diabetic atherosclerosis. 相似文献998.
Bo Bai Wengang Song Yewei Ji Xi Liu Lei Tian Chao Wang Dongwei Chen Xiaoning Zhang Minghui Zhang 《PloS one》2009,4(11)
The central nervous system (CNS) is generally regarded as a site of immune privilege, whether the antigen presenting cells (APCs) are involved in the immune homeostasis of the CNS is largely unknown. Microglia and DCs are major APCs in physiological and pathological conditions, respectively. In this work, primary microglia and microglia-like cells obtained by co-culturing mature dendritic cells with CNS endothelial cells in vitro were functional evaluated. We found that microglia not only cannot prime CD4 T cells but also inhibit mature DCs (maDCs) initiated CD4 T cells proliferation. More importantly, endothelia from the CNS can differentiate maDCs into microglia-like cells (MLCs), which possess similar phenotype and immune inhibitory function as microglia. Soluble factors including NO lie behind the suppression of CD4 T cell proliferation induced by both microglia and MLCs. All the data indicate that under physiological conditions, microglia play important roles in maintaining immune homeostasis of the CNS, whereas in a pathological situation, the infiltrated DCs can be educated by the local microenvironment and differentiate into MLCs with inhibitory function. 相似文献
999.
Ya Wang Yaoji Xuan Ping Zhang Xi Jiang Zhenhua Ni Linjiang Tong Xiangshan Zhou Liping Lin Jian Ding & Yuanxing Zhang 《FEMS yeast research》2009,9(5):732-741
The kinase insert domain receptor (KDR), also known as vascular endothelial growth factor receptor-2 (VEGFR2), is an important therapeutic target for the treatment of cancer because of its crucial role in angiogenesis, which is fundamental to the malignancy of tumors. Here, we expressed the catalytic domain of KDR in Pichia pastoris under the control of the AOX1 promoter. In order to facilitate its purification and detection, His-tag and green fluorescent protein (GFP) were fused to the N-terminus of KDR. At the same time, a peroxisomal targeting signal 1 (SKL) was fused to the C-terminus to avoid the potential negative effect on the host cell. The highly expressing clone K1 was selected by GFP fluorescence intensity analysis using flow cytometry (FCM). Furthermore, the GFP-KDR-SKL fusion protein was proved to be correctly targeted to the peroxisomes of P. pastoris by colocation with blue fluorescent protein-SKL. The expression of GFP-KDR-SKL led to extensive phosphorylation of endogenous proteins and significantly inhibited cell growth. However, the expression was not lethal to the cells. Both in vitro biological activity assay and inhibition rate assay demonstrated that the purified GFP-KDR-SKL fusion protein exhibited high kinase catalytic activity and could be used as a target for anticancer drug screening. 相似文献
1000.
Sandra L. Diaz Vered Padler-Karavani Darius Ghaderi Nancy Hurtado-Ziola Hai Yu Xi Chen Els C. M. Brinkman-Van der Linden Ajit Varki Nissi M. Varki 《PloS one》2009,4(1)