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".
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Question: Paragraph: Next year will mark the 100th anniversary of the Michaelis-Menten equation [1], one of the most important and well known models in enzymology. Remarkable progress in enzymology over the past hundred years has not only provided deep insight into biological processes, but also has dramatically changed our lives. However, because of limitations in available techniques, enzymologists primarily investigate the in vitro properties and catalytic mechanisms of individual enzymes. Thus, they often fail to address a fundamental scientific question: how are biological processes, most of which are chemical reactions catalyzed by enzymes, coordinated in space and time to produce a living organism [2]? Fortunately, applications of new techniques and, in particular, wide acceptance of the idea of systems have enabled enzymologists to begin studying enzymes in the context of dynamic, complicated biological systems in recent years. Many excellent reviews and research articles on enzymology have been published in the past few years. These articles highlight the latest developments in enzymology, and should prove helpful for understanding how to best integrate the idea of systems into enzymology research. In living organisms, protein post-translational modification (PTM) pathways are large and interconnected networks. Via reversible or irreversible covalent modifications, allo-steric regulations of PTM enzymes and cross-talk of PTM pathways, PTM networks enable organisms to respond to stimuli faster than is possible through gene transcription regulation. Therefore, PTM enzymes, as key nodes of biological networks, are a recent focus of attention.
Title: SCIENCE CHINA A glimpse of enzymology within the idea of systems

Answer: False

Question: Paragraph: During viral entry, enveloped viruses require the fusion of their lipid envelope with host cell membranes. For coronaviruses, this critical step is governed by the virally-encoded spike (S) protein, a class I viral fusion protein that has several unique features. Coronavirus entry is unusual in that it is often biphasic in nature, and can occur at or near the cell surface or in late endosomes. Recent advances in structural, biochemical and molecular biology of the coronavirus S protein has shed light on the intricacies of coronavirus entry, in particular the molecular triggers of coronavirus S-mediated membrane fusion. Furthermore, characterization of the coronavirus fusion peptide (FP), the segment of the fusion protein that inserts to a target lipid bilayer during membrane fusion, has revealed its particular attributes which imparts some of the unusual properties of the S protein, such as Ca 2+ -dependency. These unusual characteristics can explain at least in part the biphasic nature of coronavirus entry. In this review, using severe acute respiratory syndrome coronavirus (SARS-CoV) as model virus, we give an overview of advances in research on the coronavirus fusion peptide with an emphasis on its role and properties within the biological context of host cell entry.
Title: Physiological and molecular triggers for SARS-CoV membrane fusion and entry into host cells

Answer: True

Question: Paragraph: Background Pseudomonas aeruginosa (PA) is the most important opportunistic pathogen in causing nosocomial infections and, furthermore, poses a permanent threat for severe chronic infections in patients with cystic fibrosis or COPD. The transmembrane protein CD26 with dipeptidyl peptidase-4 (DPP4) activity shows an increased expression in inflamed tissue. We tested whether CD26/DPP4 deficiency leads to reduced inflammation and decreased structural damage when infected with PA. Methods CD26/DPP4 + and CD26/DPP4 rats were instilled intratracheally with NaCl (controls) or with PA. Six hours later, bacterial distribution was detected with the in vivo imaging system 200 (IVIS). Lungs were then processed for molecular biology, light and electron microscopy and analyzed qualitatively, quantitatively and stereologically. Bacterial numbers were determined in homogenized lungs. Results Compared to saline treated controls, in both infected groups (1) the acinar airspace was significantly increased, (2) the volume density of the alveolar epithelium was significantly decreased, (3) the septal thickness was significantly reduced, (4) more than 40% of the alveolar epithelial surface was damaged, and up to 36% of the epithelial surface was covered with edema. In infected CD26 rats, the increase in lung weight was significantly less pronounced, the portion of edematous alveolar airspace was significantly lower and the part of edema interspersed with PA was decreased significantly. Conclusions CD26/DPP4 deficiency resulted in reduced pulmonary edema under sublethal PA infection, implicating a role for CD26 in infection progression. The partly pronounced structural damage may mask further possible influences of CD26 on the inflammatory response. Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Title: Lung infection caused by Pseudomonas aeruginosa in a CD26/DPP4 deficient F344 rat model

Answer:
False