905 research outputs found
THE INTELLECTUAL CAPITAL AND JOURNALISTS\u27 PERFORMANCE
In the age of knowledge-based economy, intellectual capital (IC) is of growing and substantial importance more so than the tangible assets such as land and financial capital. IC includes human capital, organizational capital and social capital. IC has become a driving force for an organization to stay competitive. Journalists are vital human capital in a news organization. They are the knowledge workers who need both independence (autonomy) and interdependence (teamwork) in order to accumulate and share knowledge. In addition to playing the role as \u27gate-keepers\u27 in the information delivery process, part of a journalist\u27s job is to develop relationships with news sources from outside of the organization. Therefore, journalists are also the social capital in their organization. A news organization loses both human and social capital whenever a journalist resigns or job-hops. The purpose of this research is to examine relationships between IC and journalists? performance in the media. We argue that journalists embody both human and social capitals which are mediated by job autonomy which journalists need in order to achieve high individual job performance. We also argue that organizational capital is mediated by team-level task interdependence which also leads to better individual job performance
CK2beta gene silencing increases cell susceptibility to influenza A virus infection resulting in accelerated virus entry and higher viral protein content
Background: Influenza A virus (IVA) exploits diverse cellular gene products to support its replication in the host. The significance of the regulatory (β) subunit of casein kinase 2 (CK2β) in various cellular mechanisms is well established, but less is known about its potential role in IVA replication. We studied the role of CK2β in IVA-infected A549 human epithelial lung cells. Results: Activation of CK2β was observed in A549 cells during virus binding and internalization but appeared to be constrained as replication began. We used small interfering RNAs (siRNAs) targeting CK2β mRNA to silence CK2β protein expression in A549 cells without affecting expression of the CK2α subunit. CK2β gene silencing led to increased virus titers, consistent with the inhibition of CK2β during IVA replication. Notably, virus titers increased significantly when CK2β siRNA-transfected cells were inoculated at a lower multiplicity of infection. Virus titers also increased in cells treated with a specific CK2 inhibitor but decreased in cells treated with a CK2β stimulator. CK2β absence did not impair nuclear export of viral ribonucleoprotein complexes (6 h and 8 h after inoculation) or viral polymerase activity (analyzed in a minigenome system). The enhancement of virus titers by CK2β siRNA reflects increased cell susceptibility to influenza virus infection resulting in accelerated virus entry and higher viral protein content. Conclusion: This study demonstrates the role of cellular CK2β protein in the viral biology. Our results are the first to demonstrate a functional link between siRNA-mediated inhibition of the CK2β protein and regulation of influenza A virus replication in infected cells. Overall, the data suggest that expression and activation of CK2β inhibits influenza virus replication by regulating the virus entry process and viral protein synthesis. © 2008 Marjuki et al; licensee BioMed Central Ltd.link_to_subscribed_fulltex
Cyber-victimization and perceived depression: Serial mediation of self-esteem and learned-helplessness
Literature suggests that the perception of being cyber-victimized is a stronger predictor of depression symptoms than the perception of being victimized offline, and that learned-helplessness can explain the prediction of perceived cyber-victimization on perceived depression. Nevertheless, other studies suggested that the link between perceived cyber-victimized and learned-helplessness is weakened by state self-esteem. This study investigates the double mediation effect of state self-esteem and learned-helplessness on the relationship between perceived cyber-victimized and perceived depression. 104 participants between 18 and 30 years of age (63 females, 41 males, 1 prefer not to say) have been recruited through haphazard sampling method to fill in the Cyberbullying Victimization Scale, State Self-Esteem Scale, Learned Helplessness Scale, and Beck’s Depression Inventory. Our findings suggest that the double mediation effect occurs. As a conclusion, our findings suggested that cyberbullied social media users will only fall into perceived depression when their state self-esteem is also negatively affected by their perception of being cyberbullied, up to the point where they learn that they are helpless. Further implication are discussed at the end of the paper
Higher polymerase activity of a human influenza virus enhances activation of the hemagglutinin-induced Raf/MEK/ERK signal cascade
Influenza viruses replicate within the nucleus of infected cells. Viral genomic RNA, three polymerase subunits (PB2, PB1, and PA), and the nucleoprotein (NP) form ribonucleoprotein complexes (RNPs) that are exported from the nucleus late during the infectious cycle. The virus-induced Raf/MEK/ERK (MAPK) signal cascade is crucial for efficient virus replication. Blockade of this pathway retards RNP export and reduces virus titers. Hemagglutinin (HA) accumulation and its tight association with lipid rafts activate ERK and enhance localization of cytoplasmic RNPs. We studied the induction of MAPK signal cascade by two seasonal human influenza A viruses A/HK/218449/06 (H3N2) and A/HK/218847/06 (H1N1) that differed substantially in their replication efficiency in tissue culture. Infection with H3N2 virus, which replicates efficiently, resulted in higher HA expression and its accumulation on the cell membrane, leading to substantially increased activation of MAPK signaling compared to that caused by H1N1 subtype. More H3N2-HAs were expressed and accumulated on the cell membrane than did H1N1-HAs. Viral polymerase genes, particularly H3N2-PB1 and H3N2-PB2, were observed to contribute to increased viral polymerase activity. Applying plasmid-based reverse genetics to analyze the role of PB1 protein in activating HA-induced MAPK cascade showed that recombinant H1N1 virus possessing the H3N2-PB1 (rgH1N1/H3N2-PB1) induced greater ERK activation, resulting in increased nuclear export of the viral genome and higr virus titers. We conclude that enhanced viral polymerase activity promotes the replication and transcription of viral RNA leading to increased accumulation of HA on the cell surface and thereby resulting in an upregulation of the MAPK cascade and more efficient nuclear RNP-export as well as virus production
Isolation of Highly Pathogenic Avian Influenza H5N1 Virus from Saker Falcons ( Falco cherrug
There is accumulating evidence that birds of prey are susceptible to fatal infection with highly pathogenic avian influenza (HPAI) virus. We studied the antigenic, molecular, phylogenetic, and pathogenic properties of 2 HPAI H5N1 viruses isolated from dead falcons in Saudi Arabia and Kuwait in 2005 and 2007, respectively. Phylogenetic and antigenic analyses grouped both isolates in clade 2.2 (Qinghai-like viruses). However, the viruses appeared to have spread westward via different flyways. It remains unknown how these viruses spread so rapidly from Qinghai after the 2005 outbreak and how they were introduced into falcons in these two countries. The H5N1 outbreaks in the Middle East are believed by some to be mediated by wild migratory birds. However, sporting falcons may be at additional risk from the illegal import of live quail to feed them
Antibody-Dependent Enhancement (ADE) of infection and its possible role in the pathogenesis of influenza
In-depth analysis of music structure as a self-organized network
Words in a natural language not only transmit information but also evolve
with the development of civilization and human migration. The same is true for
music. To understand the complex structure behind the music, we introduced an
algorithm called the Essential Element Network (EEN) to encode the audio into
text. The network is obtained by calculating the correlations between scales,
time, and volume. Optimizing EEN to generate Zipfs law for the frequency and
rank of the clustering coefficient enables us to generate and regard the
semantic relationships as words. We map these encoded words into the
scale-temporal space, which helps us organize systematically the syntax in the
deep structure of music. Our algorithm provides precise descriptions of the
complex network behind the music, as opposed to the black-box nature of other
deep learning approaches. As a result, the experience and properties
accumulated through these processes can offer not only a new approach to the
applications of Natural Language Processing (NLP) but also an easier and more
objective way to analyze the evolution and development of music.Comment: 5 page
Autophagy Inhibition Enhances Apoptosis Induced by Dioscin in Huh7 Cells
Extensive research results support the application of herbal medicine or natural food as an augment during therapy for various cancers. However, the effect of dioscin on tumor cells autophagy has not been clearly clarified. In this study, the unique effects of dioscin on autophagy of hepatoma cells were investigated. Results found that dioscin induced caspase-3- and -9-dependent cell apoptosis in a dose-dependent manner. Moreover, inhibition of ERK1/2 phosphorylation significantly abolished the dioscin-induced apoptosis. In addition, dioscin triggered cell autophagy in early stages. With autophagy inhibitors to hinder the autophagy process, dioscin-induced cell apoptosis was significantly enhanced. An inhibition of caspase activation did not affect the dioscin-induced LC3-II protein expression. Based on the results, we believed that while apoptosis was blocked, dioscin-induced autophagy process also diminished in Huh7 cells. In conclusion, this study indicates that dioscin causes autophagy in Huh7 cells and suggests that dioscin has a cytoprotective effect
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