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 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.
[EX A]: Biomarkers in Pediatric ARDS: Future Directions

[EX Q]: The present study describes the development of SYBR Green based real-time polymerase chain reaction (real-time PCR) for detection and quantitation of canine parvovirus type 2 (CPV 2) in faecal samples of dogs. In this assay, the primers were designed and custom-synthesized based on nucleotide sequence of VP2 gene of CPV 2. A standard curve was plotted using 10-fold serial dilution of standard plasmid DNA and Ct value. The standard curve was found to be linear over a 10 −7 dilution. The real-time PCR results were expressed as the number of DNA copies of CPV 2 per mg of faecal samples and showed range of 1.0 × 10 3 to 7.0 × 10 9 copies of viral DNA per mg of stool samples. The analytical sensitivity of the SYBR Green based real-time PCR was shown to be equivalent to 10 copies. Faecal samples (47) from dogs suspected of CPV 2 infection were analyzed by real-time PCR, haemagglutination (HA) assay and by a conventional PCR and 24, 20 and 22 samples were found positive for CPV 2, respectively. Comparison between the results of three different assays revealed that real-time PCR is more sensitive than HA and conventional PCR and allow the detection of low titers of CPV 2 in infected dogs.
[EX A]: Development of a SYBR Green based real-time PCR assay for detection and quantitation of canine parvovirus in faecal samples

[EX Q]: The ribosome is a molecular machine that converts genetic information in the form of RNA, into protein. Recent structural studies reveal a complex set of interactions between the ribosome and its ligands, mRNA and tRNA, that indicate ways in which the ribosome could avoid costly translational errors. Ribosomes must decode each successive codon accurately, and structural data provide a clear indication of how ribosomes limit recruitment of the wrong tRNA (sense errors). In a triplet-based genetic code there are three potential forward reading frames, only one of which encodes the correct protein. Errors in which the ribosome reads a codon out of the normal reading frame (frameshift errors) occur less frequently than sense errors, although it is not clear from structural data how these errors are avoided. Some mRNA sequences, termed programmed-frameshift sites, cause the ribosome to change reading frame. Based on recent work on these sites, this article proposes that the ribosome uses the structure of the codon-anticodon complex formed by the peptidyl-tRNA, especially its wobble interaction, to constrain the incoming aminoacyl-tRNA to the correct reading frame.
[EX A]:
Ribosome structure: revisiting the connection between translational accuracy and unconventional decoding