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".

Example Input: Paragraph: Background: Newcastle Disease virus (NDV) causes severe and economically significant disease in almost all birds. However, factors that affect NDV replication in host cells are poorly understood. NDV generates long double-stranded RNA (dsRNA) molecules during transcription of single-stranded genomic RNA. Protein kinase R (PKR) is activated by dsRNA. The aim of this study was to elucidate the role of PKR in NDV infection. Results: NDV infection led to the activation of dsRNA-dependent PKR and phosphorylation of its substrate, translation initiation factor eIF2, in a dose-dependent manner by either the lentogenic strain LaSota or a velogenic strain Herts/33. PKR activation coincided with the accumulation of dsRNA induced by NDV infection. PKR knockdown remarkably decreased eIF2 phosphorylation as well as IFN- mRNA levels, leading to the augmentation of extracellular virus titer. Furthermore, siRNA knockdown or phosphorylation of eIF2 or okadaic acid treatment significantly impaired NDV replication, indicating the critical role of the PKR/eIF2 signaling cascade in NDV infection. Conclusion: PKR is activated by dsRNA generated by NDV infection and inhibits NDV replication by eIF2 phosphorylation. This study provides insight into NDV-host interactions for the development of candidate antiviral strategies.
Title: Activation of the PKR/eIF2 signaling cascade inhibits replication of Newcastle disease virus
Example Output: False

Example Input: Paragraph: Background. Recent trials suggest procalcitonin-based guidelines can reduce antibiotic use for respiratory infections. However, the accuracy of procalcitonin to discriminate between viral and bacterial pneumonia requires further dissection. Methods. We evaluated the association between serum procalcitonin concentration at hospital admission with pathogens detected in a multicenter prospective surveillance study of adults hospitalized with community-acquired pneumonia. Systematic pathogen testing included cultures, serology, urine antigen tests, and molecular detection. Accuracy of procalcitonin to discriminate between viral and bacterial pathogens was calculated. Results. Among 1735 patients, pathogens were identified in 645 (37%), including 169 (10%) with typical bacteria, 67 (4%) with atypical bacteria, and 409 (24%) with viruses only. Median procalcitonin concentration was lower with viral pathogens (0.09 ng/ mL; interquartile range [IQR], <0.05-0.54 ng/mL) than atypical bacteria (0.20 ng/mL; IQR, <0.05-0.87 ng/mL; P = .05), and typical bacteria (2.5 ng/mL; IQR, 0.29-12.2 ng/mL; P < .01). Procalcitonin discriminated bacterial pathogens, including typical and atypical bacteria, from viral pathogens with an area under the receiver operating characteristic (ROC) curve of 0.73 (95% confidence interval [CI], .69-.77). A procalcitonin threshold of 0.1 ng/mL resulted in 80.9% (95% CI, 75.3%-85.7%) sensitivity and 51.6% (95% CI, 46.6%-56.5%) specificity for identification of any bacterial pathogen. Procalcitonin discriminated between typical bacteria and the combined group of viruses and atypical bacteria with an area under the ROC curve of 0.79 (95% CI, .75-.82). Conclusions. No procalcitonin threshold perfectly discriminated between viral and bacterial pathogens, but higher procalcitonin strongly correlated with increased probability of bacterial pathogens, particularly typical bacteria.
Title: Clinical Infectious Diseases Clinical Infectious Diseases ®️ 2017;65(2):183-90 Procalcitonin as a Marker of Etiology in Adults Hospitalized With Community-Acquired Pneumonia
Example Output: True

Example Input: Paragraph: publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. The Microbiology of Respiratory System Infections. http://dx. The variant 1 of the human bocavirus (HBoV-1) that causes respiratory infections in primates and humans belongs to the family of Parvoviridae, subfamily Parvovirinae, genus Bocaparvovirus, was discovered originally in 2005 by Tobias Allander 1 and his team and represents together with the strains HBoV-3 and the gorilla bocavirus the species Primate bocaparvovirus 1. 2 The discovery of HBoV-1 was one among a series of virus discoveries in the first decade of our millennium that was based on novel virus discovery systems developed in order to reduce the considerable number of cases in which a clinical diagnosis of a respiratory infection could not be confirmed by detection of a pathogen. Following the initial description of the virus, a huge number of clinical studies and case reports have been published which were supplemented by some basic research reports. Unfortunately, HBoV research still relies on clinical studies and case reports with accompanying cell culture studies as the major source of information on HBoV biology, as so far no animal model has been identified.
Title: RESPIRATORY INFECTIONS OF THE HUMAN BOCAVIRUS
Example Output:
True