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: The analysis of 26 longevity curves of different populations of inbred (Fischer 344) and outbred (Sprague-Dawley) rats highlighted a remarkable betweenpopulations variability in survival parameters. This variability is independent of the breeding characteristics of the strain. The two strains differed in the slope of the survival curves, with Fischer 344 rats showing a higher survival over the second year of life as well as a lower interindividual variability. A model-free approach based on principal component analysis allowed us to quantify these differences and to highlight some limitations of the classical Gompertzian approach.
Title: WITHIN-AND BETWEEN-STRAIN VARIABILITY IN LONGEVITY OF INBRED AND OUTBRED RATS UNDER THE SAME ENVIRONMENTAL CONDITIONS

Output: False

Input: Consider Input: Paragraph: There is increasing evidence that atypical respiratory pathogens such as Chlamydophila pneumoniae and Mycoplasma pneumoniae may contribute to the pathogenesis of both stable asthma and asthma exacerbations. It is postulated that these organisms may contribute to inflammation in the airways possibly by activating inflammatory mechanisms in the respiratory tract. The macrolide class of antibiotics may have a part to play in the management of asthma by exerting anti-inflammatory effects on the chronically inflamed airways in addition to their anti-infective action. The ketolide antibiotics may also have similar properties. This paper discusses the role of these antibiotics in the management of asthma.
Title: The role of antibiotics in asthma

Output: False

Input: Consider Input: Paragraph: Infection by viruses having lipid-bilayer envelopes proceeds through fusion of the viral membrane with a membrane of the target cell. Viral 'fusion proteins' facilitate this process. They vary greatly in structure, but all seem to have a common mechanism of action, in which a ligand-triggered, large-scale conformational change in the fusion protein is coupled to apposition and merger of the two bilayers. We describe three examples-the influenza virus hemagglutinin, the flavivirus E protein and the vesicular stomatitis virus G protein-in some detail, to illustrate the ways in which different structures have evolved to implement this common mechanism. Fusion inhibitors can be effective antiviral agents. 'Enveloped' viruses-those with lipid bilayers as integral parts of their structure-enter the cells they infect by fusion of viral and host-cell membranes. One or more viral membrane proteins facilitate the various fusion steps. Several such fusion proteins have now been studied in great detail, with crystal structures determined for both the form of the protein present on the viral surface before interaction with the cell ('pre-fusion' conformation) and the form of the protein after fusion is complete ('post-fusion' conformation). The proteins show a variety of molecular architectures, but what we can infer from the various structures and from experiments both in solution and with cells suggests that all of them catalyze fusion in essentially the same way. We can even draw a rough analogy to serine proteases, which can have very different polypeptide chain folds but identical active-site mechanisms.
Title: Viral membrane fusion
Output: False