In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

Paragraph: Rapid diagnosis of adenoviral respiratory infections is required in order to decide optimal treatment strategies. The adenovirus antigen immunochromatography Adeno Respiratory Card Letitest (Leti diagnostics, Barcelona, Spain), was evaluated versus the shell-vial culture and multiplex PCR (Clart Pneumovir Version 3.0, Genomica, Madrid, Spain), in nasopharyngeal washes and oropharyngeal swabs specimens from subjects with respiratory tract infections. Between April 2011 and November 2012, 224 patients were included. The IC Adeno Respiratory Card Letitest was positive for 77.9% (74 of 95) of patients diagnosed at bedside. Using multiplex-PCR as the reference standard, the overall sensitivity was 77.9% and the specificity was 73.6%. Taking shell-viral culture as the reference method, the Adeno Respiratory Card Letitest (Leti diagnostics, Barcelona, Spain) sensitivity and specificity values were 80.0% and 60.9%, respectively. Using RT-PCR (Clart Pneumovir Version 3.0, Genomica, Madrid, Spain) as the reference standard, the viral culture sensitivity was 53.2% and the specificity was 100%. The Adeno Respiratory Card Letitest (Leti diagnostics, Barcelona, Spain) assay could be a simple and rapid method for antigenic detection of adenovirus in pediatric respiratory samples although it would be necessary to improve the specificity and sensitivity of the test. 
 Title: Immunochromatographic test for detection of adenovirus from respiratory samples: Is it a real solution for pediatric emergency department?
True

Paragraph: Background: Hirschsprung's disease (HSCR) is a type of megacolon induced by defi ciency or dysfunction of ganglion cells in the distal intestine and is associated with developmental disorders of the enteric nervous system. To explore the mechanisms of HSCR, we analyzed the RNAsequencing data of the expansion and the narrow segments of colon tissues separated from children with HSCR. Methods: RNA-sequencing of the expansion segments and the narrow segments of colon tissues isolated from children with HSCR was performed. After differentially expressed genes (DEGs) were identified using the edgeR package in R, functional and pathway enrichment analyses of DEGs were carried out using DAVID software. To further screen the key genes, protein-protein interaction (PPI) network and module analyses were conducted separately using Cytoscape software. Results: A total of 117 DEGs were identified in the expansion segment samples, including 47 up-regulated and 70 down-regulated genes. Functional enrichment analysis suggested that FOS and DUSP1 were implicated in response to endogenous stimulus. In the PPI network analysis, FOS (degree=20), EGR1 (degree=16), ATF3 (degree=9), NOS1 (degree=8), CCL5 (degree=8), DUSP1 (degree=7), CXCL3 (degree=6), VIP (degree=6), FOSB (degree=5), and NOS2 (degree=4) had higher degrees, which could interact with other genes. In addition, two significant modules (module 1 and module 2) were identifi ed from the PPI network. Conclusion: Several genes (including FOS, EGR1, ATF3, NOS1, CCL5, DUSP1, CXCL3, VIP, FOSB, and NOS2) might be involved in the development of HSCR through their effect on the nervous system. World J Pediatr 2017;13(3):267-273 
 Title: Genes involved in HSCR Identifying key genes associated with Hirschsprung's disease based on bioinformatics analysis of RNA-sequencing data
False

Paragraph: Coronavirus (CoV) infection is usually detected by cellular sensors, which trigger the activation of the innate immune system. Nevertheless, CoVs have evolved viral proteins that target different signaling pathways to counteract innate immune responses. Some CoV proteins act as antagonists of interferon (IFN) by inhibiting IFN production or signaling, aspects that are briefly addressed in this review. After CoV infection, potent cytokines relevant in controlling virus infections and priming adaptive immune responses are also generated. However, an uncontrolled induction of these proinflammatory cytokines can lead to pathogenesis and disease severity as described for SARS-CoV and MERS-CoV. The cellular pathways mediated by interferon regulatory factor (IRF)-3 and 7, activating transcription factor (ATF)-2/jun, activator protein (AP)-1, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and nuclear factor of activated T cells (NF-AT), are the main drivers of the inflammatory response triggered after viral infections, with NF-κB pathway the most frequently activated. Key CoV proteins involved in the regulation of these pathways and the proinflammatory immune response are revisited in this manuscript. It has been shown that the envelope (E) protein plays a variable role in CoV morphogenesis, depending on the CoV genus, being absolutely essential in some cases (genus α CoVs such as TGEV, and genus β CoVs such as MERS-CoV), but not in others (genus β CoVs such as MHV or SARS-CoV). A comprehensive accumulation of data has shown that the relatively small E protein elicits a strong influence on the interaction of SARS-CoV with the host. In fact, after infection with viruses in which this protein has been deleted, increased cellular stress and unfolded protein responses, apoptosis, and augmented host immune responses were observed. In contrast, the presence of E protein activated a pathogenic inflammatory response that may cause death in animal models and in humans. The modification or deletion of different motifs within E protein, including the transmembrane domain that harbors an ion channel activity, small sequences within the middle region of the carboxy-terminus of E protein, and its most carboxy-terminal end, which contains a PDZ domainbinding motif (PBM) is sufficient to attenuate the virus. Interestingly, a comprehensive collection of SARS-CoVs in which these motifs have been modified elicited full and long-term protection even in old mice, making those deletion mutants promising vaccine candidates. These data indicate that despite its small size, E protein drastically influences the replication of CoVs and their pathogenicity. Although E protein is not essential for CoV genome replication or subgenomic mRNA synthesis, it affects virus morphogenesis, budding, assembly, intracellular trafficking, and virulence. In fact, E protein is responsible in a significant proportion of the inflammasome activation and the associated inflammation elicited by SARS-CoV in the lung parenchyma. This exacerbated inflammation causes edema accumulation leading to acute respiratory distress syndrome (ARDS) and, frequently, to the death of infected animal models or human patients. 
 Title: CORONAVIRUS VIRULENCE GENES WITH MAIN FOCUS ON SARS-CoV ENVELOPE GENE NIH Public Access NIH-PA Author Manuscript

True