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: Acute respiratory distress syndrome (ARDS) is common among mechanically ventilated children and accompanies up to 30% of all pediatric intensive care unit deaths. Though ARDS diagnosis is based on clinical criteria, biological markers of acute lung damage have been extensively studied in adults and children. Biomarkers of inflammation, alveolar epithelial and capillary endothelial disruption, disordered coagulation, and associated derangements measured in the circulation and other body fluids, such as bronchoalveolar lavage, have improved our understanding of pathobiology of ARDS. The biochemical signature of ARDS has been increasingly well described in adult populations, and this has led to the identification of molecular phenotypes to augment clinical classifications. However, there is a paucity of data from pediatric ARDS (pARDS) patients. Biomarkers and molecular phenotypes have the potential to identify patients at high risk of poor outcomes, and perhaps inform the development of targeted therapies for specific groups of patients. Additionally, because of the lower incidence of and mortality from ARDS in pediatric patients relative to adults and lack of robust clinical predictors of outcome, there is an ongoing interest in biological markers as surrogate outcome measures. The recent definition of pARDS provides additional impetus for the measurement of established and novel biomarkers in future pediatric studies in order to further characterize this disease process. This chapter will review the currently available literature and discuss potential future directions for investigation into biomarkers in ARDS among children.

A: Biomarkers in Pediatric ARDS: Future Directions
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Q: All coronaviruses (CoVs), including the causative agent of severe acute respiratory syndrome (SARS), encode a nucleocapsid (N) protein that harbors two independent RNA binding domains of known structure, but poorly characterized RNA binding properties. We show here that the Nterminal domain (NTD) of N protein from mouse hepatitis virus (MHV), a virus most closely related to SARS-CoV, employs aromatic amino acidnucleobase stacking interactions with a triple adenosine motif to mediate high-affinity binding to single-stranded RNAs containing the transcriptional regulatory sequence (TRS) or its complement (cTRS). Stoichiometric NTD fully unwinds a TRS-cTRS duplex that mimics a transiently formed transcription intermediate in viral subgenomic RNA synthesis. Mutation of the solvent-exposed Y127, positioned on the -platform surface of our 1.75 A structure, binds the TRS far less tightly and is severely crippled in its RNA unwinding activity. In contrast, the C-terminal domain (CTD) exhibits no RNA unwinding activity. Viruses harboring Y127A N mutation are strongly selected against and Y127A N does not support an accessory function in MHV replication. We propose that the helix melting activity of the coronavirus N protein NTD plays a critical accessory role in subgenomic RNA synthesis and other processes requiring RNA remodeling.

A: Coronavirus N Protein N-Terminal Domain (NTD) Specifically Binds the Transcriptional Regulatory Sequence (TRS) and Melts TRS-cTRS RNA Duplexes
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Q: The role of host genetic variation in pneumonia development and outcome is poorly understood. We studied common polymorphisms in the genes of proinflammatory cytokines (IL6 rs1800795, IL8 rs4073, IL1B rs16944), anti-inflammatory cytokines (IL10 rs1800896, IL4 rs2243250, IL13 rs20541) and toll-like receptors (TLR2 rs5743708 and rs4696480, TLR4 rs4986791, TLR9 rs352139, rs5743836 and rs187084) in patients with community-acquired pneumonia (CAP) (390 cases, 203 controls) and nosocomial pneumonia (355 cases, 216 controls). Experimental data were included in a series of 11 meta-analyses and eight subset analyses related to pneumonia susceptibility and outcome. TLR2 rs5743708 minor genotype appeared to be associated with CAP/Legionnaires' disease/pneumococcal disease. In CAP patients, the IL6 rs1800795-C allele was associated with severe sepsis/septic shock/severe systemic inflammatory response, while the IL10 rs1800896-A allele protected against the development of these critical conditions. To contribute to deciphering of the above results, we performed an in silico analysis and a qualitative synthesis of literature data addressing basal and stimulated genotype-specific expression level. This data together with database information on transcription factors' affinity changes caused by SNPs in putative promoter regions, the results of linkage disequilibrium analysis along with SNPs functional annotations supported assumptions about the complexity underlying the revealed associations. Pneumonia, one of the most common infectious diseases, is associated with high morbidity and mortality worldwide. Pneumonia is classified according to the site of acquisition as community-acquired (CAP) and hospital-acquired (or nosocomial) pneumonia (HAP or NP), which includes healthcare-associated pneumonia (HCAP) and ventilator-associated pneumonia (VAP). HAP tends to be a more serious problem than CAP since HAP patients have an increased risk of infection caused by antibiotic-resistant organisms, besides they are often older and burdened by comorbidities. Pneumonia is considered to be the the most prevalent cause of sepsis associated with the highest mortality rates 1 . In infection, host genetic background may be of even more importance than in cancer and cardiovascular diseases which are known to have a high hereditary component 2 . Most infectious phenotypes result from a complex interplay between multiple genetic factors related to host and pathogen genetics and a variety of non-genetic factors. Since infectious diseases are related to immune-mediated disorders, genetic susceptibility loci for immune traits can be considered as good candidates in genetic association studies of pneumonia and its complications 3 . The first line of defence of the innate immune system is represented by pattern-recognition receptors that sense bacterial, viral or fungal molecular structures and induce systemic inflammation. The most studied class of pattern-recognition receptors is that of the toll-like receptors (TLRs). Once inflammation has been launched a crosstalk between pro-and anti-inflammatory branches of the immune response should provide a balanced immune reaction crucial for a favorable resolution of infection. Genetic studies of pneumonia are not numerous while investigations assessing the role of host genetics in sepsis due to pneumonia are even more unfrequent. Furthermore, to date there are no GWAS reported for pneumonia. Meta-analyses of genetic susceptibility to pneumonia provided very limited coverage of common genetic 1 V. A. Negovsky Research Institute of General Reanimatology, Russian Academy of Sciences, 25 Petrovka str., build.2,

A:
Genetic dissection of host immune response in pneumonia development and progression OPEN
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