The mechanisms for progressive fibrosis and exacerbation by steatosis in patients with chronic hepatitis C (HCV) are still unknown. We hypothesized that proliferative blockade in HCV-infected and steatotic hepatocytes...The mechanisms for progressive fibrosis and exacerbation by steatosis in patients with chronic hepatitis C (HCV) are still unknown. We hypothesized that proliferative blockade in HCV-infected and steatotic hepatocytes results in the default activation of hepatic progenitor cells (HPC), capable of differentiating into both biliary and hepatocyte lineages, and that the resultant ductular reaction promotes portal fibrosis. To study this concept, 115 liver biopsy specimens from subjects with HCV were scored for steatosis, inflammation, and fibrosis. Biliary epithelium and HPC were decorated by cytokeratin 7 immunoperoxidase, and the replicative state of hepatocytes was assessed by p21 and Ki-67 immunohistochemistry. A ductular reaction at the portal interface was common. There was a highly significant correlation between the area of ductular reaction and fibrosis stage (r = 0.453, P < .0001), which remained independently associated after multivariate analysis. HPC numbers also correlated with fibrosis (r = 0.544, P < .0001) and the ductular area (r = 0.624, P < .0001). Moreover, steatosis correlated with greater HPC proliferation (r = 0.372, P = .0004) and ductular reaction (r = 0.374, P < .0001) but was not an obligate feature. Impaired hepatocyte replication by p21 expression was independently associated with HPC expansion (P =.002) and increased with the body mass index (P < .001) and lobular inflammation (P = .005). In conclusion, the strong correlation between portal fibrosis and a periportal ductular reaction with HPC expansion, the exacerbation by steatosis, and the associations with impaired hepatocyte replication suggest that an altered regeneration pathway drives the ductular reaction. We believe this triggers fibrosis at the portal tract interface. This may be a stereotyped response of importance in other chronic liver diseases.展开更多
单位有多台Hyper-V主机，每台Hyper-V主机上运行着多个虚拟机，那么如果有一台Hyper-V主机出现物理故障宕机后，将导致所有虚拟机停止对外提供服务，或者有一台虚拟饥突然出现宕机，怎样快速恢复正常对外提供服务呢？我们可以使用Window...单位有多台Hyper-V主机，每台Hyper-V主机上运行着多个虚拟机，那么如果有一台Hyper-V主机出现物理故障宕机后，将导致所有虚拟机停止对外提供服务，或者有一台虚拟饥突然出现宕机，怎样快速恢复正常对外提供服务呢？我们可以使用Windows Server 2012或者2012R2的HypeV新功能HyperV复制来实现虚拟机的副本，这样当一台Hyper-V主机或者虚机出现故障后，另外一台Hyper-V主机上因为有这些重要虚拟机的副本，我们启用副本就可以对外继续提供服务。展开更多
文摘基于不可复制功能(PUF)的射频识别(RFID)认证协议是近年来的研究热点。2011年,Bassil等在ITST国际会议上提出了一种新的基于PUF的RFID认证协议(BASSIL R,EL-BEAINO W,KAYSSI A,et al.A PUF-basedultra-lightweight mutual-authentication RFID protocol[C]//2011 International Conference on Internet Technology andSecured Transactions.Piscataway:IEEE,2011:495-499)。分析了该认证协议的安全性,通过假设敌手参与协议,指出其不能抵抗密钥泄露攻击、跟踪攻击,也不能抵抗阅读器冒充攻击以及同步破坏攻击;同时描述了这些攻击的细节,并给出了它们的成功概率和计算复杂度。
文摘The mechanisms for progressive fibrosis and exacerbation by steatosis in patients with chronic hepatitis C (HCV) are still unknown. We hypothesized that proliferative blockade in HCV-infected and steatotic hepatocytes results in the default activation of hepatic progenitor cells (HPC), capable of differentiating into both biliary and hepatocyte lineages, and that the resultant ductular reaction promotes portal fibrosis. To study this concept, 115 liver biopsy specimens from subjects with HCV were scored for steatosis, inflammation, and fibrosis. Biliary epithelium and HPC were decorated by cytokeratin 7 immunoperoxidase, and the replicative state of hepatocytes was assessed by p21 and Ki-67 immunohistochemistry. A ductular reaction at the portal interface was common. There was a highly significant correlation between the area of ductular reaction and fibrosis stage (r = 0.453, P < .0001), which remained independently associated after multivariate analysis. HPC numbers also correlated with fibrosis (r = 0.544, P < .0001) and the ductular area (r = 0.624, P < .0001). Moreover, steatosis correlated with greater HPC proliferation (r = 0.372, P = .0004) and ductular reaction (r = 0.374, P < .0001) but was not an obligate feature. Impaired hepatocyte replication by p21 expression was independently associated with HPC expansion (P =.002) and increased with the body mass index (P < .001) and lobular inflammation (P = .005). In conclusion, the strong correlation between portal fibrosis and a periportal ductular reaction with HPC expansion, the exacerbation by steatosis, and the associations with impaired hepatocyte replication suggest that an altered regeneration pathway drives the ductular reaction. We believe this triggers fibrosis at the portal tract interface. This may be a stereotyped response of importance in other chronic liver diseases.
文摘单位有多台Hyper-V主机，每台Hyper-V主机上运行着多个虚拟机，那么如果有一台Hyper-V主机出现物理故障宕机后，将导致所有虚拟机停止对外提供服务，或者有一台虚拟饥突然出现宕机，怎样快速恢复正常对外提供服务呢？我们可以使用Windows Server 2012或者2012R2的HypeV新功能HyperV复制来实现虚拟机的副本，这样当一台Hyper-V主机或者虚机出现故障后，另外一台Hyper-V主机上因为有这些重要虚拟机的副本，我们启用副本就可以对外继续提供服务。
