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".

Q: Paragraph: Although coronavirus tropism is most often ascribed to receptor availability, increasing evidence suggests that for the neurotropic strains of the murine coronavirus mouse hepatitis virus (MHV), spike-receptor interactions cannot fully explain neurovirulence. The canonical MHV receptor CEACAM1a and its spike-binding site have been extensively characterized. However, CEACAM1a is poorly expressed in neurons, and the extremely neurotropic MHV strain JHM.SD infects ceacam1a S/S mice and spreads among ceacam1a S/S neurons. Two proposed alternative MHV receptors, CEACAM2 and PSG16, also fail to account for neuronal spread of JHM.SD in the absence of CEACAM1a. It has been reported that JHM.SD has an unusually labile spike protein, enabling it to perform receptor-independent spread (RIS), but it is not clear if the ability to perform RIS is fully responsible for the extremely neurovirulent phenotype. We propose that the extreme neurovirulence of JHM.SD is multifactorial and might include as yet unidentified neuron-specific spread mechanisms. 
 Title: Pathogenesis of neurotropic murine coronavirus is multifactorial

A: True
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Q: Paragraph: Fast simulation tools for the prediction of transient particle transport are critical in designing the air distribution indoors to reduce the exposure to indoor particles and associated health risks. This investigation proposed a combined fast fluid dynamics (FFD) and Markov chain model for fast predicting transient particle transport indoors. The solver for FFD-Markov-chain model was programmed in OpenFOAM, an open-source CFD toolbox. This study used two cases from the literature to validate the developed model and found well agreement between the transient particle concentrations predicted by the FFD-Markov-chain model and the experimental data. This investigation further compared the FFD-Markov-chain model with the CFD-Eulerian model and CFD-Lagrangian model in terms of accuracy and efficiency. The accuracy of the FFD-Markov-chain model was similar to that of the other two models. For the two studied cases, the FFD-Markovchain model was 4.7 and 6.8 times faster, respectively, than the CFD-Eulerian model, and it was 137.4 and 53.3 times faster than the CFD-Lagrangian model in predicting the steady-state airflow and transient particle transport. Therefore, the FFD-Markov-chain model is able to greatly reduce the computing cost for predicting transient particle transport in indoor environments. computational fluid dynamics, indoor environment, Eulerian model, Lagrangian model, particle dispersion, aerosol dynamics Article History 
 Title: Modeling transient particle transport by fast fluid dynamics with the Markov chain method

A: True
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Q: Paragraph: Background: Fibrotic remodeling of airway and lung parenchymal compartments is attributed to pulmonary dysfunction with an involvement of reactive oxygen species (ROS) in chronic lung diseases such as idiopathic pulmonary fibrosis and asthma. Methods: The in vitro study elucidated inhibitory effects of astragalin, kaempferol-3-O-glucoside from leaves of persimmon and green tea seeds, on oxidative stress-induced airway fibrosis. The in vivo study explored the demoting effects of astragalin on epithelial to mesenchymal transition in BALB/c mice sensitized with ovalbumin (OVA). Results: The exposure of 20 μM H 2 O 2 for 72 h accelerated E-cadherin loss and vimentin induction in airway epithelial BEAS-2B cells, which was reversed by non-toxic astragalin at 1-20 μM. Astragalin allayed the airway tissue levels of ROS and vimentin enhanced by OVA challenge. Collagen type 1 production increased in H 2 O 2 -exposed epithelial cells and collagen fiber deposition was observed in OVA-challenged mouse airways. This study further investigated that the oxidative stress-triggered autophagic regulation was responsible for inducing airway fibrosis. H 2 O 2 highly enhanced the expression induction of the autophagy-related beclin-1 and light chains 3A/B (LC3A/B) within 4 h and astragalin blocked such induction by H 2 O 2 . This compound deterred the ROS-promoted autophagosome formation in BEAS-2B cells. Consistently, in OVA-sensitized mice the expression of beclin-1 and LC3A/B was highly induced, and oral administration of astragalin suppressed the autophagosome formation with inhibiting the induction of these proteins in OVA-challenged airway subepithelium. Induction of autophagy by spermidine influenced the epithelial induction of E-cadherin and vimentin that was blocked by treating astragalin. Conclusion: These results demonstrate that astragalin can be effective in allaying ROS-promoted bronchial fibrosis through inhibiting autophagosome formation in airways. 
 Title: Astragalin inhibits autophagy-associated airway epithelial fibrosis

A:
False
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