In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Input: Consider Input: Concepts are the most fundamental units of cognition in philosophy and how to learn concepts from various aspects in the real world is the main concern within the domain of conceptual knowledge presentation and processing. In order to improve efficiency and flexibility of concept learning, in this paper we discuss concept learning via granular computing from the point of view of cognitive computing. More precisely, cognitive mechanism of forming concepts is analyzed based on the principles from philosophy and cognitive psychology, including how to model concept-forming cognitive operators, define cognitive concepts and establish cognitive concept structure. Granular computing is then combined with the cognitive concept structure to improve efficiency of concept learning. Furthermore, we put forward a cognitive computing system which is the initial environment to learn composite concepts and can integrate past experiences into itself for enhancing flexibility of concept learning. Also, we investigate cognitive processes whose aims are to deal with the problem of learning one exact or two approximate cognitive concepts from a given object set, attribute set or pair of object and attribute sets.

Output: Concept learning via granular computing: A cognitive viewpoint


Input: Consider Input: Estimation of the fraction and contagiousness of undocumented novel coronavirus infections is critical for understanding the overall prevalence and pandemic potential of this disease. Many mild infections are typically not reported and, depending on their contagiousness, may support stealth transmission and the spread of documented infection. Here we use observations of reported infection and spread within China in conjunction with mobility data, a networked dynamic metapopulation model and Bayesian inference, to infer critical epidemiological characteristics associated with the emerging coronavirus, including the fraction of undocumented infections and their contagiousness. We estimate 86% of all infections were undocumented (95% CI: [82%-90%]) prior to the Wuhan travel shutdown (January 23, 2020). Per person, these undocumented . CC-BY 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. (which was not peer-reviewed) The copyright holder for this preprint .

Output: Substantial undocumented infection facilitates the rapid dissemination of novel coronavirus (COVID-19)


Input: Consider Input: Infection of mammalian cells with vesicular stomatitis virus (VSV) results in the inhibition of cellular translation while viral translation proceeds efficiently. VSV RNA synthesis occurs entirely within the cytoplasm, where during transcription the viral polymerase produces 5 mRNAs that are structurally indistinct to cellular mRNAs with respect to their 5 0 cap-structure and 3 0 -polyadenylate tail. Using the global approach of massively parallel sequencing of total cytoplasmic, monosome-and polysome-associated mRNA, we interrogate the impact of VSV infection of HeLa cells on translation. Analysis of sequence reads in the different fractions shows >60% of total cytoplasmic and polysome-associated reads map to the 5 viral genes by 6 hours post-infection, a time point at which robust host cell translational shutoff is observed. Consistent with an overwhelming abundance of viral mRNA in the polysome fraction, the reads mapping to cellular genes were reduced. The cellular mRNAs that remain most polysome-associated following infection had longer half-lives, were typically larger, and were more AU rich, features that are shared with the viral mRNAs. Several of those mRNAs encode proteins known to positively affect viral replication, and using chemical inhibition and siRNA depletion we confirm that the host chaperone heat shock protein 90 (hsp90) and eukaryotic translation initiation factor 3A (eIF3A)-encoded by 2 such mRNAs -support viral replication. Correspondingly, regulated in development and DNA damage 1 (Redd1) encoded by a host mRNA with reduced polysome association inhibits viral infection. These data underscore the importance of viral mRNA abundance in the shut-off of host translation in VSV infected cells and link the differential translatability of some cellular mRNAs with pro-or antiviral function. Viruses co-opt the host translational machinery and frequently suppress host cell protein synthesis. Many positive-strand RNA viruses manipulate initiation factors while bypassing their need for viral protein production using internal ribosome entry sites. Negativestrand RNA viruses and DNA viruses produce mRNAs that contain host-like 5 0 cap-structures and 3 0 polyadenylate tails. Those similarities necessitate a different mechanism for controlling viral versus host protein synthesis. We infected cells with vesicular stomatitis PLOS Pathogens | https://doi.virus and sequenced polysome-associated mRNAs at 2 and 6 hours post-infection providing 2 snapshots of how infection alters translation. We present evidence that the 5 viral mRNAs outcompete cellular mRNAs for ribosomes and demonstrate that individual host mRNAs vary in the extent to which their polysome association is altered by infection. Host mRNAs that are more abundant, have longer half-lives, greater than average length, and a similar AU content to the viral mRNAs were more likely to be enriched among polysome-associated cellular mRNAs. Several of the enriched mRNAs encode proteins that promote viral replication, whereas mRNAs that exhibit the largest decrease in polysome association include those that encode antiviral functions. Control of VSV protein synthesis PLOS Pathogens | https://doi.org/10.


Output: Global analysis of polysome-associated mRNA in vesicular stomatitis virus infected cells