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: Co-infections by multiple pathogens have important implications in many aspects of health, epidemiology and evolution. However, how to disentangle the non-linear dynamics of the immune response when two infections take place at the same time is largely unexplored. Using data sets of the immune response during influenza-pneumococcal coinfection in mice, we employ here topological data analysis to simplify and visualise high dimensional data sets. We identified persistent shapes of the simplicial complexes of the data in the three infection scenarios: single viral infection, single bacterial infection, and co-infection. The immune response was found to be distinct for each of the infection scenarios and we uncovered that the immune response during the co-infection has three phases and two transition points. During the first phase, its dynamics is inherited from its response to the primary (viral) infection. The immune response has an early shift (few hours post coinfection) and then modulates its response to react against the secondary (bacterial) infection. Between 18 and 26 h post co-infection the nature of the immune response changes again and does no longer resembles either of the single infection scenarios. 
 Title: Topological data analysis to model the shape of immune responses during co-infections
[A]: True


[Q]: Paragraph: A novel binding site for angiotensins II and III that is unmasked by parachloromercuribenzoate has been reported in rat, mouse and human brains. Initial studies of this binding site indicate that it is not expressed in the adrenal, liver or kidney of the rat and mouse. To determine if this binding site occurs in other mouse tissues, 8 tissues were assayed for expression of this binding site by radioligand binding assay and compared with the expression of this binding site in the forebrain. Particulate fractions of homogenates of testis, epididymis, seminal vesicles, heart, spleen, pancreas, lung, skeletal muscle, and forebrain were incubated with 125 I-sarcosine 1 , isoleucine 8 angiotensin II in the presence or absence of 0.3 mM parachloromercuribenzoate plus 10 µM losartan and 10 µM PD123319 (to saturate AT 1 and AT 2 receptors). Specific (3 µM angiotensin II displaceable) high affinity binding occurred in the testis N forebrainN epididymisN spleen N pancreas N lung when parachloromercuribenzoate was present. Binding could not be reliably observed in heart, skeletal muscle and seminal vesicles. High affinity binding of 125 I-sarcosine 1 , isoleucine 8 angiotensin II was observed in the absence of parachloromercuribenzoate in the pancreas on occasion. This suggests that this novel angiotensin binding site may have a functional role in these tissues. 
 Title: Distribution of a novel binding site for angiotensins II and III in mouse tissues
[A]: False


[Q]: Paragraph: A mong the infl ammatory processes triggering COPD exacerbations, respiratory tract viral infections are prime suspects. Although fi rst localized in the upper-respiratory tract (URT), these infections could trigger a cascade of infl ammatory events 1,2 that lead to clinically signifi cant exacerbations. Current guidelines recommend the administration of antibiotics based mainly on clinical criteria, 1 leading inevitably to an overuse of antibiotics, which is estimated to occur in approximately 55% of all acute exacerbations of COPD (AECOPD). 3 The participation of viral infections in AECOPD has been confi rmed in many studies. 4-7 The most recent reports using polymerase chain reaction (PCR)-based methods led to a positive detection of viral nucleic acids in 30% to 60% of AECOPD cases. 5,8-12 However, the role of recently identifi ed viruses, such as coronavirus NL63 and HKU1 and human bocavirus as well as the new human rhinoviruses C, which are reported as the most frequent ones circulating in the community, 13, 14 has not yet been fully established. Biomarkers such as procalcitonin (PCT), when elevated, have been proposed as surrogate markers of bacterial disease and, when within normal values, often are considered in clinical practice as the signature of a viral infection. Although PCT has been studied Background: Respiratory viruses frequently are recovered in the upper-respiratory tract during acute exacerbations of COPD (AECOPD), but their role as contributing pathogens remains unclear. The usefulness of procalcitonin and C-reactive protein as indicators of the presence or absence of viral infection in this setting also needs to be evaluated. Methods: The study was of a prospective cohort of patients with COPD admitted to the ED for AECOPD. Reverse transcriptase-polymerase chain reaction (RT-PCR) for 14 respiratory viruses was performed on nasopharyngeal swabs collected at admission and after recovery in stable condition. Conclusions: Prevalence of upper-respiratory viral infection, as detected from nasopharyngeal swab by RT-PCR, is high in AECOPD and low after clinical recovery, suggesting that AECOPD frequently are triggered by viral infections initiated in the upper-respiratory tract. In our study, serum procalcitonin and C-reactive protein did not discriminate virus-associated exacerbations from others. Trial registration: clinicaltrials.gov; Identifi er: NCT00448604. Abbreviations: AECOPD 5 acute exacerbations of COPD; CRP 5 C-reactive protein; OR 5 odds ratio; PCR 5 polymerase chain reaction; PCT 5 procalcitonin; PEF 5 peak expiratory fl ow; RSV 5 respiratory syncytial virus; RT-PCR 5 reverse transcriptase-polymerase chain reaction; URT 5 upper-respiratory tract 
 Title: Upper-Respiratory Viral Infection, Biomarkers, and COPD Exacerbations
[A]:
True