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51.
匍匐茎草本植物形态可塑性、整合作用与觅食行为研究进展   总被引:25,自引:1,他引:25  
综述了匍匐茎型克隆植物在形态可塑性、整合作用及觅食行为方面的研究进展。资源斑块性分布是生境异质性的特征之一,适应于异质性生境,匍匐茎植物对环境资源表现了一系列可塑性反应。本文着重从匍匐茎植物对光、水、肥的可塑性反应及其整合作用以及觅食行为等方面的研究进行总结分析,以期对匍匐茎型克隆植物进行更广泛深入的研究。  相似文献   
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采用细胞外记录的方法,在单独刺激经典感受野(classical receptive field,CRF)或同时刺激CRF和感受野外区域(extra-receptive field,ERF)的情况下,测量了猫初级视觉皮层细胞的对比度响应函数。当刺激所用的中心和外周运动光栅的参数一致时,与仅刺激CRF相比,强的ERF抑制使对比度响应函数动态区增加,响应增益和对比度增益降低。当中心和外周光栅的方位相差90度时,与方位参数一致的情况相比,大部分细胞的ERF抑制减弱,对比度响应函数的动态区减小,对比度增益和响应增益增加;少数细胞的ERF对CRF的作用从抑制变为易化,其对比度响应函数的动态区与只刺激CRF相比还要小,而对比度增益和响应增益还要大。揭示了初级视觉皮层细胞的抑制型整合野在CRF和ERF图像的方位及对比度差异检测中的作用机制。  相似文献   
54.
Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death worldwide. In China, the situation is even worse as cancer incidence and mortality continue to increase rapidly. Although tremendous progress has been made toward HCC treatments, the benefits for liver cancer patients are still limited. Therefore, it is necessary to identify and develop novel therapeutic methods. Neuronally expressed developmentally downregulated 4 (NEDD4), an E3 ubiquitin ligase, plays a critical role in the development and progression of various types of human cancers. In our study, NEDD4 acts as an oncoprotein in both QGY7703 and SMMC7721 liver cancer cell lines. We found that depletion of NEDD4 by siRNA transfection led to inhibition of cell growth, invasion and migration, and promotion of apoptosis. In contrast, overexpression of NEDD4 via plasmid transfection resulted in facilitated cell proliferation, invasion and migration, and decreased apoptosis. Importantly, we observed that tumor suppressor LATS1, also a core component of Hippo pathway, was negatively regulated by NEDD4 in liver cancer cells. Our findings suggested that NEDD4 may be involved in the HCC progression via regulating LATS1 associated signaling pathway. Therefore, targeting NEDD4-LATS1 signaling could be a potential therapeutic option for HCC treatment.  相似文献   
55.
The purpose of this study was to use functional near-infrared spectroscopy (fNIRS) to examine patterns of both activation and deactivation that occur in the frontal lobe in response to noxious stimuli. The frontal lobe was selected because it has been shown to be activated by noxious stimuli in functional magnetic resonance imaging studies. The brain region is located behind the forehead which is devoid of hair, providing a relative ease of placement for fNIRS probes on this area of the head. Based on functional magnetic resonance imaging studies showing blood-oxygenation-level dependent changes in the frontal lobes, we evaluated functional near-infrared spectroscopy measures in response to two levels of electrical pain in awake, healthy human subjects (n = 10; male = 10). Each subject underwent two recording sessions separated by a 30-minute resting period. Data collected from 7 subjects were analyzed, containing a total of 38/36 low/high intensity pain stimuli for the first recording session and 27/31 pain stimuli for the second session. Our results show that there is a robust and significant deactivation in sections of the frontal cortices. Further development and definition of the specificity and sensitivity of the approach may provide an objective measure of nociceptive activity in the brain that can be easily applied in the surgical setting.  相似文献   
56.
Cysteine oxidation induced by reactive oxygen species (ROS) on redox-sensitive targets such as zinc finger proteins plays a critical role in redox signaling and subsequent biological outcomes. We found that arsenic exposure led to oxidation of certain zinc finger proteins based on arsenic interaction with zinc finger motifs. Analysis of zinc finger proteins isolated from arsenic-exposed cells and zinc finger peptides by mass spectrometry demonstrated preferential oxidation of C3H1 and C4 zinc finger configurations. C2H2 zinc finger proteins that do not bind arsenic were not oxidized by arsenic-generated ROS in the cellular environment. The findings suggest that selectivity in arsenic binding to zinc fingers with three or more cysteines defines the target proteins for oxidation by ROS. This represents a novel mechanism of selective protein oxidation and demonstrates how an environmental factor may sensitize certain target proteins for oxidation, thus altering the oxidation profile and redox regulation.  相似文献   
57.
RNA干扰(RNA interference,RNA i)是由双链RNA(doub le-stranded RNA,dsRNA)引发的转录后基因沉默(posttran-scridptional gene silenc ing,PTGS)。dsRNA经D icer酶降解成21-23nt的siRNA,并以其为模板,特定位点、特定间隔降解与之序列相应的mRNA。随着RNA i机制的深入研究与广泛应用,目前该技术已经普遍应用于细胞周期研究中,在阐明各种调控机制的同时也为基因治疗提供了新靶点。  相似文献   
58.
目的:观察低浓度一氧化碳(CO)吸入和腹腔给予对脂多糖(LPS)诱导大鼠小肠损伤的作用及作用过程中丝裂原活化蛋白激酶p38(p38 MAPK)磷酸化水平的变化。方法:6组SD大鼠静脉注入5mg/kg体质量IPS或等容量生理盐水;1h后,对照及LPS注入组吸入室内空气,CO吸入及LPS注入+CO吸入组吸入体积分数为2.5×10^-4CO.CO腹腔及LPS注入+CO腹腔组腹腔通入体积分数为2.5×10^-4CO。观察1、3、6h后放血处死,取回盲部上小肠,酶联免疫吸附法测定血小板活化因子(PAV)及细胞间黏附分子-1(ICAM-1)水平;光镜观察组织形态学变化;蛋白印迹法测定p38 MAPK磷酸化水平。结果:LPS注入组PAF、ICAM-1及p38 MAPK磷酸化水平显著高于相应时间点的对照、CO吸入及CO腹腔组(P均〈0.01);组内各时间点比较,差异无统计学意义。与相应时间点的LPS注入组比较,LPS注入+CO吸入及LPS注入+CP腹腔组的PAF和ICAM-1明显降低(P均〈0.05),但p38 MAPK磷酸化水平进一步增高(P均〈0.05);此两组间及两组内各时间点比较,差异无统计学意义。结论:低浓度CO吸入和腹腔给予以非时间依赖方式下调LPS诱导的大鼠小肠PAF、ICAM-1表达而起相似的保护作用;p38 MAPK信号转导通路可能参与了这一过程。  相似文献   
59.
赵帅  周娜  赵振勇  张科  田长彦 《微生物学报》2016,56(6):1000-1008
【目的】探讨盐角草根部内生细菌群落多样性特征,揭示内生细菌群落结构在宿主关键发育期动态变化规律。【方法】通过罗氏454高通量测序获得内生细菌16S r RNA片段,然后进行生物信息分析。【结果】共获得20363条16S r RNA基因序列。各样品中可操作分类单元(operational taxonomic units,OTUs)在552–941之间。根部内生细菌群落主要包括4个门,其中Proteobacteri门占主导地位,其余依次是Firmicutes,Actinobacteria,Bacteroidetes。在Proteobacteria门中,Gammaproteobacteria是第一大纲,其后是Betaproteobacteria纲。宿主5个发育时期共同拥有7个细菌属,包括Azomonas,Serratia,Pantoea,Serpens,Pseudomonas,Halomonas,Kushneria。整体上看,Gammaproteobacteria纲在宿主5个发育时期呈现增长趋势。优势菌属在5个发育期存在差异,分别为Delftia,Kushneria,Serratia,Pantoea,Erwinia。所有文库总共含2108个特异OTUs,共同拥有5个相同OTUs。花期OTUs数量最多,结种期内生细菌多样性降低。在宿主的5个发育时期中,土壤p H、月均温和土壤盐含量这3个环境因子组成的集合对其内生细菌群落变化具有显著影响。【结论】盐角草内生细菌群落多样性丰富,宿主发育期决定了内生细菌群落结构。  相似文献   
60.
Su K  Tian Y  Wang J  Shi W  Luo D  Liu J  Tong Z  Wu J  Zhang J  Wei L 《DNA and cell biology》2012,31(6):1078-1087
Metastasis is the leading cause of death in breast cancer patients. Recent evidence suggests that inflammation-related cytokine tumor necrosis factor-alpha (TNF-α) is implicated in tumor invasion and metastasis, but the mechanism of its involvement remains elusive. In this study, we employed MCF-7 breast cancer cells as an experimental model to demonstrate that TNF-α inhibits breast cancer cell adhesion and cell proliferation through hypoxia inducible factor-1alpha (HIF-1α) mediated suppression of vasodilator-stimulated phosphoprotein (VASP). We observed that TNF-α treatment attenuated the adhesion and proliferation of MCF-7 cells it also dramatically increased HIF-1α expression and decreased VASP expression. Through a variety of approaches, including promoter assay, electrophoretic mobility shift assay (EMSA), and chromatin immunoprecipitation (ChIP), we identified VASP as a direct target gene of HIF-1α. In addition, we confirmed that HIF-1α mediated the repression of VASP expression by TNF-α in MCF-7 cells. We also demonstrated that exogenous VASP expression or knockdown of HIF-1α relieved TNF-α induced inhibition of cell adhesion and proliferation. We identified a novel TNF-α/HIF-1α/VASP axis in which HIF-1α acts downstream of TNF-α to inhibit VASP expression and modulate the adhesion and proliferation of breast cancer cells. These data provide new insight into the potential anti-tumor effects of TNF-α.  相似文献   
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