instruction:
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".
question:
Paragraph: Mechanistic hypotheses about airborne infectious disease transmission have traditionally emphasized the role of coughing and sneezing, which are dramatic expiratory events that yield both easily visible droplets and large quantities of particles too small to see by eye. Nonetheless, it has long been known that normal speech also yields large quantities of particles that are too small to see by eye, but are large enough to carry a variety of communicable respiratory pathogens. Here we show that the rate of particle emission during normal human speech is positively correlated with the loudness (amplitude) of vocalization, ranging from approximately 1 to 50 particles per second (0.06 to 3 particles per cm 3 ) for low to high amplitudes, regardless of the language spoken (english, spanish, Mandarin, or Arabic). Furthermore, a small fraction of individuals behaves as "speech superemitters," consistently releasing an order of magnitude more particles than their peers. our data demonstrate that the phenomenon of speech superemission cannot be fully explained either by the phonic structures or the amplitude of the speech. these results suggest that other unknown physiological factors, varying dramatically among individuals, could affect the probability of respiratory infectious disease transmission, and also help explain the existence of superspreaders who are disproportionately responsible for outbreaks of airborne infectious disease. It has long been recognized that particles expelled during human expiratory events, such as sneezing, coughing, talking, and breathing, serve as vehicles for respiratory pathogen transmission 1-6 . The relative contribution of each expiratory activity in transmitting infectious microorganisms, however, remains unclear 4 . Much previous research has focused on coughing 7-12 and sneezing 11,13,14 activities that yield relatively large droplets (approximately 50 μm or larger) easily visible to the naked eye. Less noticeable, but arguably more infectious for some diseases, are the smaller particles emitted during sneezing and coughing as well as during breathing 15-17 and talking 16, 18, 19 . These small particles are believed to be generated during breathing and talking from the mucosal layers coating the respiratory tract via a combination of a "fluid-film burst" mechanism within the bronchioles and from vocal folds adduction and vibration within the larynx 6,20,21 . The particles emitted during breathing and typical speech predominantly average only 1 μm in diameter 15-17 and are thus too small to see without specialized equipment; most people outside of the community of bioaerosol researchers are less aware of them. Despite their small size, however, these micron-scale particles are sufficiently large to carry a variety of respiratory pathogens such as measles virus (50-500 nm) 22 , influenza virus (100 nm-1 µm) 23 , and Mycobacterium tuberculosis (1-3 µm) 24 . Indeed, recent work by Yan et al. has confirmed that significant amounts of influenza viral RNA are present in small particles (<5 μm) emitted by influenza-infected individuals during natural breathing, without coughing or sneezing 25 . These small particles are potentially more infectious than larger sneeze-or 
 Title: Aerosol emission and superemission during human speech increase with voice loudness
answer:
False


question:
Paragraph: During the replication cycle of Sindbis virus minus-strand synthesis stops normally at the time that plus-strand synthesis reaches a maximum rate. We have isolated and characterized revertants of ts24, a member of the A complementation group of Sindbis HR mutants, that we had demonstrated previously to have a temperature-sensitive defect in the regulation of minus-strand synthesis. These revertants of t&4 replicated efficiently at 40' but nevertheless retained the temperature sensitive defect in the regulation of minus-strand synthesis: they continued to synthesize minus strands late in the replication cycle at 40" but not at 30" and in the presence or absence of protein synthesis. Although failure to regulate the synthesis of minus strands resulted in continuous minus-strand synthesis and in the accumulation of minus strands, the rate of plus-strand synthesis was not increased concertedly. Minus strands synthesized after the rate of plus-strand synthesis had become constant were demonstrated to be utilized as templates for 26 S mRNA synthesis. Thus, the change from an increasing to a constant rate of plus-strand synthesis during the alphavirus replication cycle cannot be governed solely by the number of minus strands that accumulate in infected cells. We present a model for the preferential utilization of minus strands as a mechanism for the cessation of minus-strand synthesis that occurs normally during alphavirus replication. 
 Title: The Effect of Loss of Regulation of Minus-Strand RNA Synthesis on Sindbis Virus Replication
answer:
True


question:
Paragraph: Chronic obstructive pulmonary disease (COPD) exacerbations are an important cause of the considerable morbidity and mortality found in COPD. COPD exacerbations increase with increasing severity of COPD, and some patients are prone to frequent exacerbations leading to hospital admission and readmission. These frequent exacerbations may have considerable impact on quality of life and activities of daily living. Factors that increase the risk for COPD exacerbations are associated with increased airway inflammation caused by common pollutants and bacterial and/or viral infections. These inflammatory responses cause mucus hypersecretion and, thereby, airway obstruction and associated exacerbations. While chronic mucus hypersecretion is a significant risk factor for frequent and severe exacerbations, patients with chronic mucus hypersecretion have a lower rate of relapse after initial treatment for acute exacerbation. The benefit of antibiotics for treatment of COPD exacerbations is small but significant. While the mechanisms of actions are not clear, mucolytic agents reduce the number of days of disability in subjects with exacerbations. Reducing mucous cell numbers in small airways could be a useful way to reduce chronic mucus hypersecretion. Our studies suggest that programmed cell death is crucial in the resolution of metaplastic mucous cells, and understanding these mechanisms may provide novel therapies to reduce the risk of COPD exacerbations. 
 Title: Exacerbations of chronic obstructive pulmonary disease and chronic mucus hypersecretion
answer:

False