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".

Input: Consider Input: Paragraph: CD13/Aminopeptidase N (CD13) is known to play an important role in tumour cell invasion. We examined whether basic fibroblast growth factor (bFGF) is involved in the regulation of CD13 expression in human melanoma cells. 1F6 human melanoma cells were stably transfected with constructs encoding either the 18 kDa (18kD) or all (ALL) bFGF isoform proteins. We observed highly increased CD13 mRNA and protein expression in the 1F6 clones regardless of the overexpression of either the 18kD or all isoform proteins. Neutral aminopeptidase activity was increased five-fold and could be inhibited by bestatin and the CD13-neutralising antibody WM15. The enhanced invasion through Matrigel, but not migration in a wound assay, was efficiently abrogated by both bestatin and WM15. Upregulation of CD13 expression was the result of increased epithelial and myeloid promoter activity up to 4.5fold in 1F6-18kD and 1F6-ALL clones. Interestingly, in a panel of human melanoma cell lines, a significant correlation (r 2 0.883, Po0.05) between bFGF and CD13 mRNA and protein expression was detected. High bFGF and CD13 expression were clearly related with an aggressive phenotype. Taken together, our data indicate that high bFGF expression upregulates CD13 expression in human melanoma cells by activating both the myeloid and the epithelial CD13 promoter. In addition, we show that high bFGF and CD13 expression results in enhanced invasive capacity and metastatic behaviour of human melanoma cells.
Title: CD13/Aminopeptidase N overexpression by basic fibroblast growth factor mediates enhanced invasiveness of 1F6 human melanoma cells

Output: False

Input: Consider Input: Paragraph: was first discovered in 2012. MERS-CoV can infect multiple host species and cause severe diseases in human. We conducted a series of phylogenetic and bioinformatic analyses to study the evolution dynamics of MERS-CoV among different host species with genomic data. Our analyses show: 1) 28 potential recombinant sequences were detected and they can be classified into seven potential recombinant types; 2) The spike (S) protein of MERS-CoV was under strong positive selection when Middle East Respiratory Syndrome coronavirus (MERS-CoV) is a novel beta-coronavirus with high pathogenicity, which imposes a serious threat to human health 1 . Substantial evidence has showed that MERS-CoVs have existed in central and east Africa for decades 2,3 , and have many natural hosts including two species of bats (Neoromicia capensis and Vespertilio superans), dromedary camel (Camelus dromedarius), and European hedgehog (Erinaceus europaeus) 4-7 . Yet it seemed that human MERS-CoV first isolated in Saudi Arabian in 2012, and then spread among humans worldwide 8 . Studies of prototype human MERS-CoV also suggested that the tMRCA (the time of most recent common ancestor) of human MERS-CoV can be traced back to about 2011 9 . Because the genome sequence of bat MERS-CoV is highly identical to that of human MERS-CoV, it has been indicated that human MERS-CoV might have a bat origin 10 , while there is also some evidence of camel-to-human MERS-CoV transmission 11,12 . Together, these studies proposed that zoonotic event may play a nontrivial part in MERS-CoV evolution and transmission. Previous studies showed that recombination was common among the members of beta-coronavirus 13,14 . By joining the previously unlinked DNA, recombination event can create new viral strains which may be capable of infecting new hosts and evading host's immuno-responses. The phylogenetic analysis showed that there were two main MERS-CoV clades-clade A and B, and clade B can be further divided into five phylogenetic groups 15 . There is evidence that recombination event had happened between group III and group V 15 . However, whether there was potential recombination event happened between the other groups or among multiple phylogenetic groups remains unclear. The genome of MERS-CoV is over 30,000 nucleotides (nt) in length, which contains seven predicted open reading frames (ORFs) and four structural genes-spike (S), envelope (E), membrane (M), and nucleocapsid (N) 16 (supplementary Fig. 1c ). The surface located spike (S) protein of beta-coronaviruses is one of the major determinants in their cross-species transmission because it mediates the virus-receptor recognition and thereby activates viral infection process 17 . Additionally, the receptor binding domain (RBD) on S protein's N-terminal is the key element for beta-coronavirus entering into host cells and the mutations in coronavirus's RBD affects its infection and cross-species capability 18, 19 . For example, the study of the spike protein from severe acute respiratory syndrome coronavirus (SARS-CoV), another beta-coronavirus with high pathogenicity, revealed four amino
Title: Evolutionary Dynamics of MERS- CoV: Potential Recombination, Positive Selection and Transmission OPEN

Output: False

Input: Consider Input: Paragraph: Increasing evidence points to an important role for neutrophils in participating in the pathogenesis of the human demyelinating disease MS and the animal model EAE. Therefore, a better understanding of the signals controlling migration of neutrophils as well as evaluating the role of these cells in demyelination is important to define cellular components that contribute to disease in MS patients. In this study, we examined the functional role of the chemokine CXCL1 in contributing to neuroinflammation and demyelination in EAE. Using transgenic mice in which expression of CXCL1 is under the control of a tetracycline-inducible promoter active within glial fibrillary acidic protein-positive cells, we have shown that sustained CXCL1 expression within the CNS increased the severity of clinical and histologic disease that was independent of an increase in the frequency of encephalitogenic Th1 and Th17 cells. Rather, disease was associated with enhanced recruitment of CD11b + Ly6G + neutrophils into the spinal cord. Targeting neutrophils resulted in a reduction in demyelination arguing for a role for these cells in myelin damage. Collectively, these findings emphasize that CXCL1-mediated attraction of neutrophils into the CNS augments demyelination suggesting that this signaling pathway may offer new targets for therapeutic intervention.
Title: Basic Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment
Output: True