为了充分利用实际高速公路路段交通拥堵信息,更合理地聚类交通拥堵的内在规律和特征变化,提出自适应确定聚类中心C和类别K值(adaptive center and K-means value,ACK-Means)的聚类算法,进行高速公路拥堵路段聚类。ACK-Means算法借助簇...为了充分利用实际高速公路路段交通拥堵信息,更合理地聚类交通拥堵的内在规律和特征变化,提出自适应确定聚类中心C和类别K值(adaptive center and K-means value,ACK-Means)的聚类算法,进行高速公路拥堵路段聚类。ACK-Means算法借助簇类密度、簇类间距以及簇类强度,同时又考虑到数据样本的偶然性,对离群点进行合理分配,ACK-Means算法可实现自适应确定聚类中心C和类别K值。基于实际交通拥堵信息构建数据集,Python编程实现高速公路拥堵路段ACK-Means聚类,巧妙解决了高速公路拥堵路段聚类数目K和聚类中心C设定问题。聚类结果表明,ACK-Means算法实现高速公路拥堵路段无监督聚类,聚类结果完全基于实际的高速公路交通拥堵信息,具有更高的实用性。展开更多
Over time, the world has transformed digitally and there is total dependence on the internet. Many more gadgets are continuously interconnected in the internet ecosystem. This fact has made the Internet a global infor...Over time, the world has transformed digitally and there is total dependence on the internet. Many more gadgets are continuously interconnected in the internet ecosystem. This fact has made the Internet a global information source for every being. Despite all this, attacker knowledge by cybercriminals has advanced and resulted in different attack methodologies on the internet and its data stores. This paper will discuss the origin and significance of Denial of Service (DoS) and Distributed Denial of Service (DDoS). These kinds of attacks remain the most effective methods used by the bad guys to cause substantial damage in terms of operational, reputational, and financial damage to organizations globally. These kinds of attacks have hindered network performance and availability. The victim’s network is flooded with massive illegal traffic hence, denying genuine traffic from passing through for authorized users. The paper will explore detection mechanisms, and mitigation techniques for this network threat.展开更多
目的:探讨ACK1(活化的CDC42结合激酶)对肝细胞肝癌(HCC)增殖影响的分子机制。方法:用q RTPCR法和Western blotting法检测细胞中ACK1 m RNA和蛋白的表达。用ACK1 sh RNA p RS质粒转染细胞法构建基因敲除模型。用免疫印迹法来检验肝癌细胞...目的:探讨ACK1(活化的CDC42结合激酶)对肝细胞肝癌(HCC)增殖影响的分子机制。方法:用q RTPCR法和Western blotting法检测细胞中ACK1 m RNA和蛋白的表达。用ACK1 sh RNA p RS质粒转染细胞法构建基因敲除模型。用免疫印迹法来检验肝癌细胞中ACK1对p-ACK1、AKT、p-AKT、MMP2和MMP9的调节效应。用流式细胞仪,凋亡蛋白酶3/7活力测定仪,Brd U渗入法,MTT法,检测肝癌细胞的凋亡、增殖能力。结果:肝癌细胞株SMMC-7721,Huh-7,Hep G2,BEL-7402和MHCC-97H细胞ACK1 m RNA和蛋白的表达明显比正常肝细胞LO2中要高,差异有统计学意义(P均<0.01)。肝癌细胞MHCC-97H中沉默ACK1可使活化态的AKT(p-AKT)明显减少,而非活化态的AKT量变化不大,差异有统计学意义(P<0.01)。在研究中,我们发现沉默ACK1可引起肝癌细胞MHCC-97H中作为AKT信号通路下游的MMP2和MMP9表达下调,差异有统计学意义(P<0.01)。此外,沉默ACK1可促进肝癌细胞MHCC-97H凋亡并抑制其增殖能力,差异有统计学意义(P<0.01)。结论:在肝细胞肝癌中,过表达ACK1通过激活AKT信号通路来促进肝癌细胞的增殖。展开更多
文摘为了充分利用实际高速公路路段交通拥堵信息,更合理地聚类交通拥堵的内在规律和特征变化,提出自适应确定聚类中心C和类别K值(adaptive center and K-means value,ACK-Means)的聚类算法,进行高速公路拥堵路段聚类。ACK-Means算法借助簇类密度、簇类间距以及簇类强度,同时又考虑到数据样本的偶然性,对离群点进行合理分配,ACK-Means算法可实现自适应确定聚类中心C和类别K值。基于实际交通拥堵信息构建数据集,Python编程实现高速公路拥堵路段ACK-Means聚类,巧妙解决了高速公路拥堵路段聚类数目K和聚类中心C设定问题。聚类结果表明,ACK-Means算法实现高速公路拥堵路段无监督聚类,聚类结果完全基于实际的高速公路交通拥堵信息,具有更高的实用性。
文摘Over time, the world has transformed digitally and there is total dependence on the internet. Many more gadgets are continuously interconnected in the internet ecosystem. This fact has made the Internet a global information source for every being. Despite all this, attacker knowledge by cybercriminals has advanced and resulted in different attack methodologies on the internet and its data stores. This paper will discuss the origin and significance of Denial of Service (DoS) and Distributed Denial of Service (DDoS). These kinds of attacks remain the most effective methods used by the bad guys to cause substantial damage in terms of operational, reputational, and financial damage to organizations globally. These kinds of attacks have hindered network performance and availability. The victim’s network is flooded with massive illegal traffic hence, denying genuine traffic from passing through for authorized users. The paper will explore detection mechanisms, and mitigation techniques for this network threat.
文摘目的:探讨ACK1(活化的CDC42结合激酶)对肝细胞肝癌(HCC)增殖影响的分子机制。方法:用q RTPCR法和Western blotting法检测细胞中ACK1 m RNA和蛋白的表达。用ACK1 sh RNA p RS质粒转染细胞法构建基因敲除模型。用免疫印迹法来检验肝癌细胞中ACK1对p-ACK1、AKT、p-AKT、MMP2和MMP9的调节效应。用流式细胞仪,凋亡蛋白酶3/7活力测定仪,Brd U渗入法,MTT法,检测肝癌细胞的凋亡、增殖能力。结果:肝癌细胞株SMMC-7721,Huh-7,Hep G2,BEL-7402和MHCC-97H细胞ACK1 m RNA和蛋白的表达明显比正常肝细胞LO2中要高,差异有统计学意义(P均<0.01)。肝癌细胞MHCC-97H中沉默ACK1可使活化态的AKT(p-AKT)明显减少,而非活化态的AKT量变化不大,差异有统计学意义(P<0.01)。在研究中,我们发现沉默ACK1可引起肝癌细胞MHCC-97H中作为AKT信号通路下游的MMP2和MMP9表达下调,差异有统计学意义(P<0.01)。此外,沉默ACK1可促进肝癌细胞MHCC-97H凋亡并抑制其增殖能力,差异有统计学意义(P<0.01)。结论:在肝细胞肝癌中,过表达ACK1通过激活AKT信号通路来促进肝癌细胞的增殖。
