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: Ebola virus (EboV) belongs to the Filoviridae family of viruses that causes severe and fatal hemhorragic fever. Infection by EboV involves fusion between the virus and host cell membranes mediated by the envelope glycoprotein GP2 of the virus. Similar to the envelope glycoproteins of other viruses, the central feature of the GP2 ectodomain postfusion structure is a six-helix bundle formed by the protein's N-and C-heptad repeat regions (NHR and CHR, respectively). Folding of this six-helix bundle provides the energetic driving force for membrane fusion; in other viruses, designed agents that disrupt formation of the six-helix bundle act as potent fusion inhibitors. To interrogate determinants of EboV GP2-mediated membrane fusion, we designed model proteins that consist of the NHR and CHR segments linked by short protein linkers. Circular dichroism and gel filtration studies indicate that these proteins adopt stable ahelical folds consistent with design. Thermal denaturation indicated that the GP2 six-helix bundle is highly stable at pH 5.3 (melting temperature, T m , of 86.8 6 2.0°C and van't Hoff enthalpy, DH vH , of 228.2 6 1.0 kcal/mol) and comparable in stability to other viral membrane fusion six-helix bundles. We found that the stability of our designed a-helical bundle proteins was dependent on buffering conditions with increasing stability at lower pH. Small pH differences (5.3-6.1) had dramatic effects (DT m 5 37°C) suggesting a mechanism for conformational control that is dependent on environmental pH. These results suggest a role for low pH in stabilizing six-helix bundle formation during the process of GP2-mediated viral membrane fusion.

Output: Designed protein mimics of the Ebola virus glycoprotein GP2 a-helical bundle: Stability and pH effects


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: Heightened surveillance of acute febrile illness in China since 2004 led to the identification of a severe fever with thrombocytopenia syndrome (SFTS) with unknown etiology. Sporadic patients hospitalized with SFTS in 2009 and 2010 were identified and serum samples were collected. Sequence from a novel species of phlebovirus was identified by sequence independent single primer amplification (SISPA) from the serum of a patient with SFTS. The virus was isolated in Vero cell culture and its complete genome sequence was determined, only distantly related to other known phleboviruses. Electron microscopic analysis revealed a virion morphologically characteristic of phleboviruses. The virus was named as SFTS virus. The viral RNA and/or specific antibodies were detected from the blood of patients with SFTS. Serological assays demonstrated a virus-specific immune response in pairs of sera collected from patients at acute and convalescent phases. The pathogenic mechanisms of thrombocytopenia in human SFTS disease was resembled in a mouse model. The results had been collected to demonstrate that SFTS virus was etiologically associated with an acute and novel infectious disease, SFTS in humans.


Output: The Discovery Process of SFTS in China