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: Graphical Abstract Highlights d DENV NS4B induces mitochondria elongation during viral infection d Elongated mitochondria and virus-induced convoluted membranes are physically linked d NS4B inhibits activation of the mitochondrial fission factor DRP1 d Mitochondria elongation alleviates DENV-induced RIG-Idependent innate immunity SUMMARY With no antiviral drugs or widely available vaccines, Dengue virus (DENV) constitutes a public health concern. DENV replicates at ER-derived cytoplasmic structures that include substructures called convoluted membranes (CMs); however, the purpose of these membrane alterations remains unclear. We determine that DENV nonstructural protein (NS)4B, a promising drug target with unknown function, associates with mitochondrial proteins and alters mitochondria morphology to promote infection. During infection, NS4B induces elongation of mitochondria, which physically contact CMs. This restructuring compromises the integrity of mitochondria-associated membranes, sites of ER-mitochondria interface critical for innate immune signaling. The spatio-temporal parameters of CM biogenesis and mitochondria elongation are linked to loss of activation of the fission factor Dynamin-Related Protein-1. Mitochondria elongation promotes DENV replication and alleviates RIG-I-dependent activation of interferon responses. As Zika virus infection induces similar mitochondria elongation, this perturbation may protect DENV and related viruses from innate immunity and create a favorable replicative environment. 
 Title: Dengue Virus Perturbs Mitochondrial Morphodynamics to Dampen Innate Immune Responses Article Dengue Virus Perturbs Mitochondrial Morphodynamics to Dampen Innate Immune Responses

A: True
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Q: Paragraph: In this paper, we propose and discuss a stochastic SIRS epidemic model with non-monotone incidence rate under regime-switching. First of all, we show that there is a unique positive solution, which is a prerequisite for analyzing the long-term behavior of the stochastic model. Then, a threshold dynamic determined by the basic reproduction number R s 0 is established: the disease can be eradicated almost surely if R s 0 < 1 and under mild extra conditions, whereas if R s 0 > 1 , the densities of the distributions of the solution can converge in L 1 to an invariant density by using the Markov semigroups theory. Finally, based on realistic parameters obtained from previous literatures, numerical simulations have been performed to verify our analytical results. 
 Title: A stochastic SIRS epidemic model with non-monotone incidence rate under regime-switching

A: True
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Q: Paragraph: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a progressive upper and lower motor neuron degeneration. One of the peculiar clinical characteristics of ALS is the wide distribution in age of onset, which is probably caused by different combinations of intrinsic and exogenous factors. We investigated whether these modifying factors are converging into common pathogenic pathways leading either to an early or a late disease onset. This would imply the identification of phenotypic biomarkers, that can distinguish the two populations of ALS patients, and of relevant pathways to consider in a therapeutic intervention. Toward this aim a differential proteomic analysis was performed in peripheral blood mononuclear cells (PBMC) from a group of 16 ALS patients with an age of onset ≤55 years and a group of 16 ALS patients with an age of onset ≥75 years, and matched healthy controls. We identified 43 differentially expressed proteins in the two groups of patients. Gene ontology analysis revealed that there was a significant enrichment in annotations associated with protein folding and response to stress. We next validated a selected number of proteins belonging to this functional group in 85 patients and 83 age-and sex-matched healthy controls using immunoassays. The results of the validation study confirmed that there was a decreased level of peptidyl-prolyl cis-trans isomerase A (also known as cyclophilin A), heat shock protein HSP 90-alpha, 78 kDa glucose-regulated protein (also known as BiP) and protein deglycase DJ-1 in PBMC of ALS patients with an early onset. Similar results were obtained in PBMC and spinal cord from two SOD1 G93A mouse models with an early and late disease onset. This study suggests that a different ability to upregulate proteins involved in proteostasis, such as foldase and chaperone proteins, may be at the basis of a different susceptibility to ALS, putting forward the development of therapeutic approaches aiming at boosting the protein quality control system. 
 Title: Decreased Levels of Foldase and Chaperone Proteins Are Associated with an Early-Onset Amyotrophic Lateral Sclerosis

A:
False
****