TASK DEFINITION: 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".
PROBLEM: 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

SOLUTION: False

PROBLEM: 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

SOLUTION: True

PROBLEM: Paragraph: Low Clostridium leptum levels are a risk factor for the development of asthma. C. leptum deficiency exacerbates asthma; however, the impact of early-life C. leptum exposure on cesarean-delivered mice remains unclear. This study is to determine the effects of early-life C. leptum exposure on asthma development in infant mice. We exposed infant mice to C. leptum (fed-CL) and then induced asthma using the allergen ovalbumin (OVA). Fed-CL increased regulatory T (Treg) cells in cesarean-delivered mice compared with vaginally delivered mice. Compared with OVA-exposed mice, mice exposed to C. leptum + OVA did not develop the typical asthma phenotype, which includes airway hyper-responsiveness, cell infiltration, and T helper cell subset (Th1, Th2, Th9, Th17) inflammation. Early-life C. leptum exposure induced an immunosuppressive environment in the lung concurrent with increased Treg cells, resulting in the inhibition of Th1, Th2, Th9, and Th17 cell responses. These findings demonstrate a mechanism whereby C. leptum exposure modulates adaptive immunity and leads to failure to develop asthma upon OVA sensitization later in life. Fig 2. Schematic of a mouse model of early-life C. leptum OVA asthma. All analyses were carried out 48 h after the final protocol day. HE, hematoxylin-eosin; AL(OH) 3 , aluminum hydroxide.
Title: Early-Life Exposure to Clostridium leptum Causes Pulmonary Immunosuppression

SOLUTION:
True