instruction:
In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".
question:
Abstract: Uncontrolled proteolysis by neutrophil serine proteases (NSPs) in lung secretions is a hallmark of cystic fibrosis (CF). We have shown that the active neutrophil elastase, protease 3, and cathepsin G in CF sputum resist inhibition in part by exogenous protease inhibitors. This resistance may be due to their binding to neutrophil extracellular traps (NETs) secreted by the activated neutrophils in CF sputum and to genomic DNA released from senescent and dead neutrophils. Treating CF sputum with DNase dramatically increases its elastase activity, which can then be stoichiometrically inhibited by exogenous elastase inhibitors. However, DNase treatment does not increase the activities of protease 3 and cathepsin G, indicating their different distribution and/or binding in CF sputum. Purified blood neutrophils secrete NETs when stimulated by the opportunistic CF bacteria Pseudomonas aeruginosa and Staphylococcus aureus. The activities of the three proteases were unchanged in these conditions, but subsequent DNase treatment produced a dramatic increase in all three proteolytic activities. Neutrophils activated with a calcium ionophore did not secrete NETs but released huge amounts of active proteases whose activities were not modified by DNase. We conclude that NETs are reservoirs of active proteases that protect them from inhibition and maintain them in a rapidly mobilizable status. Combining the effects of protease inhibitors with that of DNA-degrading agents could counter the deleterious proteolytic effects of NSPs in CF lung secretions.. Title: Influence of DNA on the activities and inhibition of neutrophil serine proteases in cystic fibrosis sputum.
answer:
yes

question:
Abstract: Inhibition of VEGF signaling leads to a proinvasive phenotype in mouse models of glioblastoma multiforme (GBM) and in a subset of GBM patients treated with bevacizumab. Here, we demonstrate that vascular endothelial growth factor (VEGF) directly and negatively regulates tumor cell invasion through enhanced recruitment of the protein tyrosine phosphatase 1B (PTP1B) to a MET/VEGFR2 heterocomplex, thereby suppressing HGF-dependent MET phosphorylation and tumor cell migration. Consequently, VEGF blockade restores and increases MET activity in GBM cells in a hypoxia-independent manner, while inducing a program reminiscent of epithelial-to-mesenchymal transition highlighted by a T-cadherin to N-cadherin switch and enhanced mesenchymal features. Inhibition of MET in GBM mouse models blocks mesenchymal transition and invasion provoked by VEGF ablation, resulting in substantial survival benefit.. Title: VEGF inhibits tumor cell invasion and mesenchymal transition through a MET/VEGFR2 complex.
answer:
yes

question:
Abstract: Salmonellosis poses a health problem of large proportions in the United States. Annually, it accounts for more than 40,000 reported cases, 500 deaths, and financial costs well in excess of $50 million. Antimicrobial resistance is increasing in Salmonella strains, a finding that has important public health implications. Although the chain of transmission of the bacteria is often complex, combined epidemiologic and laboratory studies with the use of new methods in molecular biology make it possible to trace antimicrobial-resistant salmonellae to their primary source--foods of animal origin. These studies suggest that the antimicrobial drugs to which food animals are exposed provide selective pressure that leads to the appearance and persistence of resistant strains.. Title: Drug-resistant Salmonella in the United States: an epidemiologic perspective.
answer:
yes