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".

[EX Q]: Paragraph: Background: Human papillomavirus 16 (HPV16) is a high-risk DNA tumour virus, which is a major causative agent of cervical cancer. Cellular transformation is associated with deregulated expression of the E6 and E7 oncogenes. E7 has been shown to bind a number of cellular proteins, including the cell cycle control protein pRb. In this study, RNA aptamers (small, singlestranded oligonucleotides selected for high-affinity binding) to HPV16 E7 were employed as molecular tools to further investigate these protein-protein interactions. This study is focused on one aptamer (termed A2). Transfection of this molecule into HPV16-transformed cells resulted in inhibition of cell proliferation (shown using real-time cell electronic sensing and MTT assays) due to the induction of apoptosis (as demonstrated by Annexin V/propidium iodide staining). GST-pull down and bead binding assays were used to demonstrate that the binding of A2 required N-terminal residues of E7 known to be involved in interaction with the cell cycle control protein, pRb. Using a similar approach, A2 was shown to disrupt the interaction between E7 and pRb in vitro. Furthermore, transfection of HPV16-transformed cells with A2 appeared to result in the loss of E7 and rise in pRb levels, as observed by immunoblotting. Conclusions/Significance: This paper includes the first characterisation of the effects of an E7 RNA aptamer in a cell line derived from a cervical carcinoma. Transfection of cells with A2 was correlated with the loss of E7 and the induction of apoptosis. Aptamers specific for a number of cellular and viral proteins have been documented previously; one aptamer (Macugen) is approved for clinical use and several others are in clinical trials. In addition to its role as a molecular tool, A2 could have further applications in the future. 
 Title: An RNA Aptamer Provides a Novel Approach for the Induction of Apoptosis by Targeting the HPV16 E7 Oncoprotein
[EX A]: True

[EX Q]: 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
[EX A]: False

[EX Q]: Paragraph: The aim of this review is to examine the causes, pathophysiology and experimental models of noninfectious pharyngitis (sore throat). Introduction The causes of sore throat can be infectious (viruses, bacteria, and fungi) or non-infectious, although the relative proportion of each is not well documented. Methods A PubMed database search was performed for studies of non-infectious sore throat. Results and conclusions Non-infectious causes of sore throat include: physico-chemical factors, such as smoking, snoring, shouting, tracheal intubation, medications, or concomitant illness; and environmental factors including indoor and outdoor air pollutants, temperature and humidity, and hazardous or occupational irritants. The pathophysiology underlying non-infectious sore throat is largely uncharacterised, although neurogenic inflammation looks to be a promising candidate. It is likely that there will be individual disposition factors or the coincidence of more than one irritant with possible-up to now unknown-interactions between them. Therefore, experimental models with defined conditions and objective endpoints are needed. A new model using cold dry air to directly induce pharyngeal irritation in humans, with pharyngeal lavage to measure biomarkers, may provide a useful tool for the study of mechanisms and treatment of non-infectious sore throat. 
 Title: Environmental and non-infectious factors in the aetiology of pharyngitis (sore throat)
[EX A]:
True