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.

[Q]: Background: Influenza is a zoonotic disease that infects millions of people each year resulting in hundreds of thousands of deaths, and in turn devastating pandemics. Influenza is caused by influenza viruses, including influenza A virus (IAV). There are many subtypes of IAV but only a few seem to be able to adapt to humans and to cause disease. In 2013, an H7N9 IAV subtype emerged in China that does not cause clinical symptoms in its chicken host but leads to severe infections when transmitted into humans. Since 2013, there have been six epidemic waves of H7N9 with 1567 laboratory-confirmed human infections and 615 deaths. Pathogenicity of IAV is complex, but a crucial feature contributing to virulence is the activation of the hemagglutinin (HA) fusion protein by host proteases that triggers membrane fusion and leads to subsequent virus propagation. : 293T, VERO, and MDCK cells were used to conduct Western blot analysis, immunofluorescence assays, and pseudoparticle and live virus infections, and to evaluate H7N9 HA cleavage-activation. Results/Conclusions: We show that human matriptase/ST 14 is able to cleave H7N9 HA. Cleavage of H7N9 HA expressed in cell culture results in fusogenic HA and syncytia formation. In infection studies with viral pseudoparticles carrying matriptase/ ST 14-activated H7N9 HA, we observed a high infectivity of cells. Finally, human matriptase/ST 14 also activated H7N9 live virus which resulted in high infectivity. Our data demonstrate that human matriptase/ST 14 is a likely candidate protease to promote H7N9 infections in humans.
[A]: Human matriptase/ST 14 proteolytically cleaves H7N9 hemagglutinin and facilitates the activation of influenza A/Shanghai/2/2013 virus in cell culture


[Q]: 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.
[A]: Concept learning via granular computing: A cognitive viewpoint


[Q]: TABLE 40.1 Proposed Mechanisms of Virus-Induced CNS Demyelination CNS infection Infection of oligodendrocytes Direct destruction Pathogenic immune response to viral antigens on cell membranes Introduction of cell membranes into systematic circulation Infection of other CNS cells Release of cytokines or viral proteins toxic to myelin supporting cells or myelin membranes Extraneural infection Molecular mimicry (virus proteins and myelin proteins) Disruption of immune responses 954 40. INFECTIOUS DEMYELINATING DISEASES Definition ADEM is an acute, inXammatory, demyelinating disease of the brain and spinal cord. In most patients it has an abrupt onset days to several weeks after a viral exanthem or viruslike illness. But the disease is not speciWc to viruses and has been reported after several bacterial illnesses, immunizations, and drug and serum administration. The nosology is confusing, since the disease has been described under a remarkable variety of names. Post-infectious, parainfectious, post-exanthematous, post-vaccinal, postmeasles, and post-inXuenzal encephalomyelitis have been applied to describe the clinical settings. Acute disseminated encephalomyelitis, perivascular myelinoclasis, perivenous encephalitis, and acute demyelinating encephalomyelitis have been coined to describe the pathological features. Allergic encephalomyelitis, immune-mediated encephalomyelitis, hyperergic encephalomyelitis, and disseminated vasculomyelinopathy imply knowledge of pathogenetic mechanisms . Since the essential features for diagnosis are the neuropathological changes, ADEM will be used here except in speciWc cases such as post-measles and post-vaccinal encephalomyelitis. Acute hemorrhagic necrotizing leukoencephalits is generally regarded as a more intense, ''hyperacute'' form of ADEM. However, this rare acute demyelinating disease has distinct clinical and pathological features and is associated with a diVerent spectrum of antecedent infections. ADEM was a common disease in the mid-20th century, representing about one-third of all cases of encephalitis. The most common cause of ADEM was measles, which, along with ADEM cases following rubella and mumps, has been largely eliminated in regions of the world that have adequately protected children with the measles-mumps-rubella (MMR) vaccine. The second major cause of ADEM was a vaccine, vaccinia virus, which was discontinued after the worldwide eradication of natural smallpox in 1977. More recently, the varicella vaccine has further reduced the risk of ADEM. Now in countries with active childhood vaccination programs, ADEM makes up less than 10% of the cases of encephalitis, and the most common antecedent illnesses are nonspeciWc respiratory infections (Johnson, 1998) . The incidence of ADEM after clinically distinctive virus illnesses is highly variable (Tab. 40.2); the incidence after Epstein-Barr (EB) virus, Mycoplasma pneumoniae, inXuenza, and nonspeciWc upper respiratory infections are uncertain. The clinical Wndings after speciWc infections show some distinctive features, and the mortality and morbidity rates are quite diVerent. Despite the common pathology, the pathogenesis may vary. Most data on pathogenesis relate to post-measles encephalomyelitis. In acute fatal cases the brain may be congested and swollen. On gross sections, vessels are prominent in white matter with discoloration along the veins.
[A]:
Infectious Demyelinating Diseases