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.

Ex Input:
The complete nonstructural NS5 gene of Japanese encephalitis virus (JEV) was amplified and cloned into an expression vector. The NS5 protein was expressed in Escherichia coli and purified by His-tag based affinity chromatography. This recombinant NS5 protein exhibited RNA-dependent RNA polymerase (RdRp) activity in vitro in the absence of other viral or cellular factors. The RNA polymerase activity was dependent on divalent cations, and Mn 2þ was found to be 20 times more effective than Mg 2þ in coordinating the catalytic reaction of RdRp, while Ca 2þ inhibited enzyme activity. The optimal reaction conditions for the in vitro RdRp reaction were established. Characterization of the RdRp reaction products demonstrated that the JEV NS5 protein can initiate RNA synthesis through a de novo initiation mechanism in our in vitro reaction system. Comparing the efficiency of different RNA templates, we found that JEV NS5 protein was more efficient in using negative-strand RNA templates, indicating that the JEV NS5 protein is in-volved in regulating the ratio of positive-to negativestrand RNA. Four amino acid sequence motifs crucial for RdRp activity were also identified using site-directed mutagenesis analysis. All substitutions of the conserved residues within these motifs led to a complete inactivation or severe loss of enzyme activity.

Ex Output:
Identification and characterization of RNA-dependent RNA polymerase activity in recombinant Japanese encephalitis virus NS5 protein


Ex Input:
The red-crowned crane is one of the rarest crane species, and its population is decreasing due to loss of habitat, poisoning, and infections. Using a viral metagenomics approach, we analyzed the virome of feces from wild and captive red-crowned cranes, which were pooled separately. Vertebrate viruses belonging to the families Picornaviridae, Parvoviridae, Circoviridae, and Caliciviridae were detected. Among the members of the family Picornaviridae, we found three that appear to represent new genera. Six nearly complete genomes from members of the family Parvoviridae were also obtained, including four new members of the proposed genus "Chapparvovirus", and two members of the genus Aveparvovirus. Six small circular DNA genomes were also characterized. One nearly complete genome showing a low level of sequence identity to caliciviruses was also characterized. Numerous viruses believed to infect insects, plants, and crustaceans were also identified, which were probably derived from the diet of red-crowned cranes. This study increases our understanding of the enteric virome of red-crowned cranes and provides a baseline for comparison to those of other birds or following disease outbreaks.

Ex Output:
The fecal virome of red-crowned cranes


Ex Input:
To determine the role of CD13 as an adhesion molecule in trafficking of inflammatory cells to the site of injury in vivo and its function in wound healing following myocardial infarction induced by permanent coronary artery occlusion. Seven days post-permanent ligation, hearts from CD13 knockout (CD13 KO ) mice showed significant reductions in cardiac function, suggesting impaired healing in the absence of CD13. Mechanistically, CD13 KO infarcts showed an increase in small, endothelial-lined luminal structures, but no increase in perfusion, arguing against an angiogenic defect in the absence of CD13. Cardiac myocytes of CD13 KO mice showed normal basal contractile function, eliminating myocyte dysfunction as a mechanism of adverse remodelling. Conversely, immunohistochemical and flow cytometric analysis of CD13 KO infarcts demonstrated a dramatic 65% reduction in infiltrating haematopoietic cells, including monocytes, macrophages, dendritic, and T cells, suggesting a critical role for CD13 adhesion in inflammatory trafficking. Accordingly, CD13 KO infarcts also contained fewer myofibroblasts, consistent with attenuation of fibroblast differentiation resulting from the reduced inflammation, leading to adverse remodelling. In the ischaemic heart, while compensatory mechanisms apparently relieve potential angiogenic defects, CD13 is essential for proper trafficking of the inflammatory cells necessary to prime and sustain the reparative response, thus promoting optimal post-infarction healing. ---

Ex Output:

CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice