instruction:
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".
question:
Paragraph: Background: Mechanisms influencing severity of acute lower respiratory infection (ALRI) in children are not established. We aimed to assess the role of inflammatory markers and respiratory viruses in ALRI severity. Methods: Concentrations of interleukin(IL)-33, soluble suppression of tumorigenicity (sST)2, IL-1ß, tumor necrosis factor α, IL-4, IL-6 and IL-8 and types of respiratory viruses were evaluated in children at the first and fifth days after hospital admission. Disease severity was defined as need for mechanical ventilation. Results: Seventy-nine children < 5 years-old were included; 33(41.8%) received mechanical ventilation. No associations between virus type, viral load or co-detections and severity of disease were observed. Detection of IL-33 and sST2 in nasopharyngeal aspirates (NPA) on admission were associated with higher risk for mechanical ventilation (RR = 2.89 and RR = 4.57, respectively). IL-6 and IL-8 concentrations were higher on Day 5 in mechanically ventilated children. IL-6 NPA concentrations decreased from Day 1 to Day 5 in children who did not receive mechanical ventilation. Increase in sST2 NPA concentrations from Day 1 to Day 5 was associated with longer hospital length of stay (p < 0.01). Conclusions: An exacerbated local activation of the IL-33/ST2 axis and persistently high sST2 concentrations over time were associated with severity of viral ALRI in children. 
 Title: IL-33 and ST2 as predictors of disease severity in children with viral acute lower respiratory infection
answer:
False


question:
Paragraph: We aimed to test the hypothesis that gene silencing of tumor necrosis factor alpha converting enzyme (TACE) may attenuate lesion inflammation and positive vascular remodeling and enhance plaque stability in a rabbit model of atherosclerosis. Lentivirus-mediated TACE shRNA was injected into the abdominal aortic plaques of rabbits which effectively down-regulated TACE expression and activities from week 8 to week 16. TACE gene silencing reduced remodeling index and plaque burden, and diminished the content of macrophages and lipids while increased that of smooth muscle cells and collagen in the aortic plaques. In addition, TACE gene silencing attenuated the local expression of P65, iNOS, ICAM-1, VEGF and Flt-1 and activities of MMP9 and MMP2 while increased the local expression of TGF-β1 together with reduced number of neovessels in the aorta. TACE shRNA treatment resulted in down-regulated expression of TACE in macrophages and blunted ERK-P38 phosphorylation and tube formation of co-cultured mouse vascular smooth muscle cells or human umbilical vein endothelial cells. In conclusion, gene silencing of TACE enhanced plaque stability and improved vascular positive remodeling. The mechanisms may involve attenuated local inflammation, neovascularization and MMP activation, as well as enhanced collagen production probably via down-regulated ERK-NF-κB and upregulated TGF-β1 signaling pathways. Tumor necrosis factor alpha converting enzyme (TACE), also known as ADAM17 (A disintegrin and A metalloproteinase 17), was initially discovered as a protease that cleaves the 26-kDa precursor of TNF-α and sheds transmembrane TNF-α to generate a soluble form of TNF-α that can bind to TNF-α receptors to induce inflammatory response 1 . Recently it has been recognized that TACE is a type I transmembrane protein and a member of a superfamily of Zn dependent metalloproteases. The major physiological role of TACE is to regulate the proteolytic release of a number of growth factors, cytokines, adhesion molecules and cleavage enzymes from cellular membrane 2,3 . The major pro-inflammatory cytokine processed by TACE is TNF-α which is produced by macrophages, monocytes and T-cells, and acts as a major player in the pathogenesis of inflammation. It has been increasingly recognized that TACE-mediated shedding is involved in a variety of diseases such as ischemia, heart failure, arthritis, atherosclerosis, diabetes, cancer, neurological and immune diseases 3-5 . Ashley EA et al. provided functional evidence for TACE as a candidate gene of atherosclerosis susceptibility and found that polymorphisms of the TACE genes had relation to cardiovascular mortality in humans 6 . Canault M et al. found that TACE expression was associated with lesion formation in atherosclerosis-prone sites of apolipoprotein E-knockout (ApoE -/-) mice 7 . Oksala N demonstrated that TACE was upregulated in advanced human atherosclerotic lesions in samples from carotid, aortic, and femoral arteries compared to samples from internal thoracic artery free of atherosclerotic plaques 8 . In addition, Stoehr R et al. showed that loss of TIMP3, an endogenous inhibitor of TACE, exacerbated atherosclerosis 1 
 Title: Gene silencing of TACE enhances plaque stability and improves vascular remodeling in a rabbit model of atherosclerosis
answer:
False


question:
Paragraph: Porcine deltacoronavirus (PDCoV) is a newly discovered coronavirus, which belongs to the family Coronaviridae. It causes watery diarrhea, vomiting, and dehydration in newborn piglets. A sensitive RT-PCR method is urgently required to detect PDCoV infection. In this study, we developed and evaluated a conventional RT-PCR assay and a SYBR green-based real-time RT-PCR assay that targeted the PDCoV gene. Both assays are specific and have the same limit of detection at 2 × 10 1 copies of RNA molecules per reaction. Eighty-four clinical samples were subjected to both conventional RT-PCR and real-time RT-PCR, and the same positive rate (41.7%) was achieved, which was much higher than the positive rate (26.2%) using a previously described onestep RT-PCR technique. In summary, a conventional RT-PCR technique was successfully established for the detection of PDCoV with the same detection limit as a SYBR green-based real-time RT-PCR assay. 
 Title: Research Article
answer:

False