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: Objective: The aim of this study was to further clarify clinical characteristics and predict mortality risk among patients with viral pneumonia. Methods: A total of 528 patients with viral pneumonia at RuiJin hospital in Shanghai from May 2015 to May 2019 were recruited. Multiplex real-time RT-PCR was used to detect respiratory viruses. Demographic information, comorbidities, routine laboratory examinations, immunological indexes, etiological detections, radiological images and treatment were collected on admission. Results: 76 (14.4%) patients died within 90 days in hospital. A predictive MuLBSTA score was calculated on the basis of a multivariate logistic regression model in order to predict mortality with a weighted score that included multilobular infiltrates (OR = 5.20, 95% CI 1.41-12.52, p = 0.010; 5 points), lymphocyte 0.8 * 10 9 /L (OR = 4.53, 95% CI 2.55-8.05, p < 0.001; 4 points), bacterial coinfection (OR = 3.71, 95% CI 2.11-6.51, p < 0.001; 4 points), acute-smoker (OR = 3.19, 95% CI 1.34-6.26, p = 0.001; 3 points), quit-smoker (OR = 2.18, 95% CI 0.99-4.82, p = 0.054; 2 points), hypertension (OR = 2.39, 95% CI 1.55-4.26, p = 0.003; 2 points) and age 60 years (OR = 2.14, 95% CI 1.04-4.39, p = 0.038; 2 points). 12 points was used as a cut-off value for mortality risk stratification. This model showed sensitivity of 0.776, specificity of 0.778 and a better predictive ability than CURB-65 (AUROC = 0.773 vs. 0.717, p < 0.001). Conclusion: Here, we designed an easy-to-use clinically predictive tool for assessing 90-day mortality risk of viral pneumonia. It can accurately stratify hospitalized patients with viral pneumonia into relevant risk categories and could provide guidance to make further clinical decisions.
Title: Citation: Clinical Features Predicting Mortality Risk in Patients With Viral Pneumonia: The MuLBSTA Score
[A]: False

[Q]: 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
[A]: False

[Q]: Paragraph: Background: Human metapneumovirus (hMPV) infection can cause acute lower respiratory tract illness in infants, the immunocompromised, and the elderly. Currently there are no licensed preventative measures for hMPV infections. Using a variant of hMPV/NL/1/00 that does not require trypsin supplementation for growth in tissue culture, we deleted the M2-2 gene and evaluated the replication of rhMPV/M2-2 virus in vitro and in vivo. In vitro studies showed that the ablation of M2-2 increased the propensity for insertion of U nucleotides in poly-U tracts of the genomic RNA. In addition, viral transcription was up-regulated although the level of genomic RNA remained comparable to rhMPV. Thus, deletion of M2-2 alters the ratio between hMPV genome copies and transcripts. In vivo, rhMPV/M2-2 was attenuated compared to rhMPV in the lungs and nasal turbinates of hamsters. Hamsters immunized with one dose of rhMPV/M2-2 were protected from challenge with 10 6 PFU of wild type (wt) hMPV/NL/1/ 00. Our results suggest that hMPV M2-2 alters regulation of transcription and influences the fidelity of the polymerase complex during viral genome replication. In the hamster model, rhMPVM2-2 is attenuated and protective suggesting that deletion of M2-2 may result in a potential live vaccine candidate. A more thorough knowledge of the hMPV polymerase complex and the role of M2-2 during hMPV replication are being studied as we develop a potential live hMPV vaccine candidate that lacks M2-2 expression.
Title: Virology Journal Deletion of human metapneumovirus M2-2 increases mutation frequency and attenuates growth in hamsters
[A]:
True