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: The tertiary structures of the S1 and S2 domains of the spike protein of the coronavirus which is responsible of the severe acute respiratory syndrome (SARS) have been recently predicted. Here a molecular assembly of SARS coronavirus peplomer which accounts for the available functional data is suggested. The interaction between S1 and S2 appears to be stabilised by a large hydrophobic network of aromatic side chains present in both domains. This feature results to be common to all coronaviruses, suggesting potential targeting for drugs preventing coronavirus-related infections.
Title: Prediction of quaternary assembly of SARS coronavirus peplomer
Example Output: False

Example Input: Paragraph: A new disease, the severe acute respiratory distress syndrome (SARS), caused by the SARS coronavirus (SARS-CoV), emerged at the beginning of 2003 and rapidly spread throughout the world. Although the disease had disappeared in June 2003 its re-emergence cannot be excluded. The development of vaccines against SARS-CoV may take years. Therefore, the availability of effective antiviral drugs against SARS-CoV may be crucial for the control of future SARS outbreaks. In this review, experimental and clinical data about potential anti-SARS drugs is summarised and discussed. Animal model studies will be needed to help to determine which interventions warrant controlled clinical testing.
Title: Development of antiviral therapy for severe acute respiratory syndrome
Example Output: False

Example Input: Paragraph: Pulmonary edema (PE) may occur with enterovirus 71 (EV71) infection. We monitored arterial pressure (AP) and heart rate (HR) in patients with EV71 infection and analyzed the variability of AP and HR. Sympathetic activity, AP, and HR increased with respiratory stress. Thereafter, parasympathetic activity increased with decreases in AP and HR. The lungs showed edema with inducible nitric oxide synthase (iNOS) expression. Destruction of the medial, ventral, and caudal medulla may lead to sympathetic overactivation, causing blood to shift to the lungs. The pathogenesis of PE may also involve iNOS and nitric oxide. Epidemic or sporadic infection with enterovirus 71 (EV71) usually occurs during the summer months. Children infected with EV71 develop rashes on the hand, foot, and mouth. Most patients recover without complications. Some patients manifest signs such as headache, profuse sweating, lethargy, paraparesis, and weakness of the limbs. Several patients infected with EV71 have died of fulminant pulmonary edema (PE) soon after infection [1, 2] . The pathogenesis of PE is still unknown. Chang et al. [2] postulated that viral destruction of the CNS may be the cause of death. Central sympathetic activation resulting in systemic vasoconstriction and the shift of blood volume to the pulmonary region of the circulatory system, as demonstrated in earlier findings from our laboratory, was used to explain centrogenic PE [2, 3] . However, studies by Chang et al. [1, 2] did not provide pathological evidence of CNS lesions, nor did they assess autonomic activity. In the present study, we report CNS lesions in patients associated with PE due to enterovirus
Title: Mechanism of Fulminant Pulmonary Edema Caused by Enterovirus 71
Example Output:
False