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".

Q: 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

A: False
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Q: Paragraph: Bovine viral diarrhea virus (BVDV) is a pestivirus member of the Flaviviridae family, closely related to, and used as a surrogate model for the hepatitis C virus. Its envelope contains the E1 and E2 glycoproteins, disulfide linked into homo-and heterodimers. In this study, we investigate the role of disulfide bond formation in the folding, assembly, and stability of BVDV glycoproteins. We provide molecular evidence that intact disulfide bonds are critical for the acquirement of a stable conformation of E2 monomers. Forcing the E2 glycoproteins to adopt a reduced conformation either co-or post-translationally before assembly into dimers, determines their misfolding and degradation by proteasome. In contrast, dimerization of E2 glycoproteins results in a conformation resistant to reducing agents and degradation. Furthermore, inhibition of the ER-a-mannosidase activity leads to impairment of misfolded E2 degradation, demonstrating the involvement of this enzyme in targeting viral proteins towards proteasomal degradation. Ó 
 Title: Role of disulfide bond formation in the folding and assembly of the envelope glycoproteins of a pestivirus

A: False
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Q: Paragraph: Background: Chronic Obstructive Pulmonary Disease (COPD) exacerbations are associated with viral infections. We wished to determine if respiratory viral infection of children in the community was associated with hospital admissions of patients with exacerbations of COPD. Methods: We collected data over a 45-month period from the Northern Ireland Regional Virus Laboratory and from a general hospital in the same locality. We studied the relationship between upper respiratory infections in children and COPD admissions. We also examined the role of school holidays. Results: Correlations were seen between the frequency of all viral infections in children and the number of adult COPD hospitalizations ðPo0:005Þ. Subgroup analysis showed distinct relationships with epidemics of; influenza A ðPo0:001Þ, influenza B ðPo0:05Þ, adenovirus ðP ¼ 0:05Þ, respiratory syncytial virus ðPo0:005Þ and hospital admissions of patients with COPD. There were significantly fewer COPD admissions in the week after the start of a school holiday period ðPo0:05Þ. Conclusions: When children are hospitalized with viral respiratory infection there is an associated rise in adult COPD admissions. This suggests exacerbations of COPD are associated with epidemics of respiratory viruses. When children are on school holidays there is a reduction in COPD admissions in the community. This provides further support for respiratory viruses in the pathogenesis of COPD exacerbations. 
 Title: Childhood respiratory infections and hospital admissions for COPD ARTICLE IN PRESS

A:
True
****