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".

[EX Q]: Paragraph: Background: Mechanisms influencing severity of acute lower respiratory infection (ALRI) in children are not established. We aimed to assess the role of inflammatory markers and respiratory viruses in ALRI severity. Methods: Concentrations of interleukin(IL)-33, soluble suppression of tumorigenicity (sST)2, IL-1ß, tumor necrosis factor α, IL-4, IL-6 and IL-8 and types of respiratory viruses were evaluated in children at the first and fifth days after hospital admission. Disease severity was defined as need for mechanical ventilation. Results: Seventy-nine children < 5 years-old were included; 33(41.8%) received mechanical ventilation. No associations between virus type, viral load or co-detections and severity of disease were observed. Detection of IL-33 and sST2 in nasopharyngeal aspirates (NPA) on admission were associated with higher risk for mechanical ventilation (RR = 2.89 and RR = 4.57, respectively). IL-6 and IL-8 concentrations were higher on Day 5 in mechanically ventilated children. IL-6 NPA concentrations decreased from Day 1 to Day 5 in children who did not receive mechanical ventilation. Increase in sST2 NPA concentrations from Day 1 to Day 5 was associated with longer hospital length of stay (p < 0.01). Conclusions: An exacerbated local activation of the IL-33/ST2 axis and persistently high sST2 concentrations over time were associated with severity of viral ALRI in children. 
 Title: IL-33 and ST2 as predictors of disease severity in children with viral acute lower respiratory infection
[EX A]: False

[EX Q]: Paragraph: We describe the association of caspase-dependent and caspase-independent mechanisms in macrophage apoptosis induced by LpqH, a 19 kDa Mycobacterium tuberculosis lipoprotein. LpqH triggered TLR2 activation, with upregulation of death receptors and ligands, which was followed by a death receptor signaling cascade with activation of initiator caspase 8 and executioner caspase 3. In this caspase-mediated phase, mitochondrial factors were involved in loss of mitochondrial transmembrane potential (ΔΨm), release of cytochrome c, and caspase 9 activation. Interestingly, a caspase-independent pathway was also identified; by immunoblot, the mitochondrial apoptosis inducing factor (AIF) was demonstrated in nuclei and cytosol of LpqH-treated macrophages. Confocal microscopy revealed translocation of AIF to the nuclei of the majority of apoptotic cells. These findings emphasize the complex and redundant nature of the macrophage death response to mycobacteria. 
 Title: Mycobacterium tuberculosis Lipoprotein (LpqH) Induces Macrophage Apoptosis through Extrinsic and Intrinsic Pathways: A Role for the Mitochondrial Apoptosis-Inducing Factor
[EX A]: True

[EX Q]: Paragraph: In this paper, we propose and analyze a nonautonomous predator-prey model with disease in prey, and a discrete time delay for the incubation period in disease transmission. Employing the theory of differential inequalities, we find sufficient conditions for the permanence of the system. Further, we use Lyapunov's functional method to obtain sufficient conditions for global asymptotic stability of the system. We observe that the permanence of the system is unaffected due to presence of incubation delay. However, incubation delay affects the global stability of the positive periodic solution of the system. To reinforce the analytical results and to get more insight into the system's behavior, we perform some numerical simulations of the autonomous and nonautonomous systems with and without time delay. We observe that for the gradual increase in the magnitude of incubation delay, the autonomous system develops limit cycle oscillation through a Hopf-bifurcation while the corresponding nonautonomous system shows chaotic dynamics through quasiperiodic oscillations. We apply basic tools of non-linear dynamics such as Poincaré section and maximum Lyapunov exponent to confirm the chaotic behavior of the system. 
 Title: Chaos in a nonautonomous eco-epidemiological model with delay
[EX A]:
True