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".

Example Input: Paragraph: Insults to the alveoli usually lead to inefficient gas exchange or even respiratory failure, which is difficult to model in animal studies. Over the past decade, stem cell-derived self-organizing three-dimensional organoids have emerged as a new avenue to recapitulate respiratory diseases in a dish. Alveolar organoids have improved our understanding of the mechanisms underlying tissue homeostasis and pathological alterations in alveoli. From this perspective, we review the state-of-the-art technology on establishing alveolar organoids from endogenous lung epithelial stem/progenitor cells or pluripotent stem cells, as well as the use of alveolar organoids for the study of respiratory diseases, including idiopathic pulmonary fibrosis, tuberculosis infection, and respiratory virus infection. We also discuss challenges that need to be overcome for future application of alveolar organoids in individualized medicine. 
 Title: Organoids as a Powerful Model for Respiratory Diseases
Example Output: True

Example Input: Paragraph: Introduction: Outbreaks of infectious diseases trigger an increase in scientific research and output. Early in outbreaks, evidence is scarce, but it accumulates rapidly. We are continuously facing new disease outbreaks, including the new coronavirus (SARS-nCoV-2) in December 2019.The objective of this study was to describe the accumulation of evidence during the 2013-2016 Zika virus (ZIKV) outbreak in the Pacific and the Americas related to aetiological causal questions about congenital abnormalities and Guillain-Barré syndrome. Methods: We hypothesised that the temporal sequence would follow a pre-specified order, according to study design. We assessed 1) how long it takes before findings from a specific study design appear, 2) how publication of preprints could reduce the time to publication and 3) how time to publication evolves over time. Results: We included 346 publications published between March 6, 2014 and January 1, 2019. In the 2013--2016 ZIKV outbreak, case reports, case series and basic research studies were published first. Case-control and cohort studies appeared between 400-700 days after ZIKV was first detected in the region of the study origin. Delay due to the publication process were lowest at the beginning of the outbreak. Only 4.6% of the publications was available as preprints. Discussion: The accumulation of evidence over time in new causal problems generally followed a hierarchy. Preprints reduced the delay to initial publication. Our methods can be applied to new emerging infectious diseases. 
 Title: Emergence of evidence during disease outbreaks: lessons learnt from the Zika virus outbreak
Example Output: False

Example Input: Paragraph: The Sabin I poliovirus live, attenuated vaccine strain encodes for four amino acid changes (i.e., D53N, Y73H, K250E, and T362I) in the RNA-dependent RNA polymerase (RdRp). We have previously shown that the T362I substitution leads to a lower fidelity RdRp, and viruses encoding this variant are attenuated in a mouse model of poliovirus. Given these results, it was surprising that the nucleotide incorporation rate and nucleobase fidelity of the Sabin I RdRp is similar to that of wild-type enzyme, although the Sabin I RdRp is less selective against nucleotides with modified sugar groups. We suggest that the other Sabin amino acid changes (i.e., D53N, Y73H, K250E) help to re-establish nucleotide incorporation rates and nucleotide discrimination near wild-type levels, which may be a requirement for the propagation of the virus and its efficacy as a vaccine strain. These results also suggest that the nucleobase fidelity of the Sabin I RdRp likely does not contribute to viral attenuation. Viruses 2015, 7, 5571-5586 viral virulence, likely because the T362I RdRp is a more error-prone polymerase than the "wild-type" (WT) enzyme [22] . These results are intriguing, and might suggest that the Sabin I RdRp also contributes to viral attenuation. Such findings would be intriguing in light of the suggestion that viruses encoding RdRp enzymes with altered fidelity might serve as live, attenuated vaccine candidates [23] . PV RdRp has a highly-conserved canonical cupped right-hand structure with palm, thumb, and finger subdomains (Figure 1) [24]. There are seven conserved structural motifs, five of which (A to E) are located in the palm subdomain [25, 26] . The T362I amino acid change occurs on structural motif D, which we have proposed is important in phosphodiester bond formation and nucleotide discrimination [27, 28] . More specifically, motif D contains a highly-conserved lysine residue (Lys359 in PV RdRp), which we have proposed acts as a general acid to protonate the β-phosphate of the incoming nucleotide to facilitate bond breakage between the αand β-phosphates and create a better pyrophosphate leaving group [28, 29] . We have suggested that the active-site loop containing Lys359 fluctuates between "closed" and "open" conformations in which Lys359 is positioned and out-of-position for catalysis, respectively. Our previous nuclear magnetic resonance (NMR) studies are consistent with this proposal [22, 29, 30] . We have shown that the Sabin-derived T362I amino acid substitution alters the motions of motif D, allowing the enzyme to fluctuate more readily into a closed conformation even in the presence of incorrect nucleotide, leading to a less faithful polymerase [22] . Other amino acid substitutions in the Sabin I RdRp may also change RdRp function. The Y73H substitution has been shown to interfere with the initiation of RNA synthesis [19] , which might help to explain why PV encoding the Y73H substitution is attenuated [17, 20] . The D53N, Y73H, and T362I substitutions also contribute to the temperature sensitivity of the Sabin I vaccine [15] [16] [17] 31] . The Sabin substitutions may also affect each other. Our previous molecular dynamics (MD) simulations suggest that the T362I amino acid substitution induces different nanosecond timescale motions in distant parts of the enzyme, including around Asp53 [22] . We have also previously noted anti-correlated motions between motif D and the α-helix containing Tyr73 [32] . It is also noted that the helices containing Tyr73 and Lys250 are packed closely together (Figure 1 ). Altogether, these results suggest that there are structural and dynamic connections between the various Sabin sites, which may contribute to the function of the Sabin I RdRp. 
 Title: Nucleobase but not Sugar Fidelity is Maintained in the Sabin I RNA-Dependent RNA Polymerase
Example Output:
True