TASK DEFINITION: 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".
PROBLEM: 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

SOLUTION: False

PROBLEM: Paragraph: Background: Pseudomonas aeruginosa (PA) is an opportunistic Gram-negative bacterium that causes serious life threatening and nosocomial infections including pneumonia. PA has the ability to alter host genome to facilitate its invasion, thus increasing the virulence of the organism. Sphingosine-1-phosphate (S1P), a bioactive lipid, is known to play a key role in facilitating infection. Sphingosine kinases (SPHK) 1&2 phosphorylate sphingosine to generate S1P in mammalian cells. We reported earlier that Sphk2 −/− mice offered significant protection against lung inflammation, compared to wild type (WT) animals. Therefore, we profiled the differential expression of genes between the protected group of Sphk2 −/− and the wild type controls to better understand the underlying protective mechanisms related to the Sphk2 deletion in lung inflammatory injury. Whole transcriptome shotgun sequencing (RNA-Seq) was performed on mouse lung tissue using NextSeq 500 sequencing system. Results: Two-way analysis of variance (ANOVA) analysis was performed and differentially expressed genes following PA infection were identified using whole transcriptome of Sphk2 −/− mice and their WT counterparts. Pathway (PW) enrichment analyses of the RNA seq data identified several signaling pathways that are likely to play a crucial role in pneumonia caused by PA such as those involved in: 1. Immune response to PA infection and NF-κB signal transduction; 2. PKC signal transduction; 3. Impact on epigenetic regulation; 4. Epithelial sodium channel pathway; 5. Mucin expression; and 6. Bacterial infection related pathways. Our genomic data suggests a potential role for SPHK2 in PA-induced pneumonia through elevated expression of inflammatory genes in lung tissue. Further, validation by RT-PCR on 10 differentially expressed genes showed 100% concordance in terms of vectoral changes as well as significant fold change. (Continued on next page) 
 Title: Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung

SOLUTION: False

PROBLEM: Paragraph: Nipah virus (NiV) and Hendra virus (HeV) are closely related, recently emerged paramyxoviruses that are capable of causing considerable morbidity and mortality in several mammalian species, including humans. Henipavirus-specific vaccines are still commercially unavailable, and development of novel antiviral strategies to prevent lethal infections due to henipaviruses is highly desirable. Here we describe the development of adeno-associated virus (AAV) vaccines expressing the NiV G protein. Characterization of these vaccines in mice demonstrated that a single intramuscular AAV injection was sufficient to induce a potent and longlasting antibody response. Translational studies in hamsters further demonstrated that all vaccinated animals were protected against lethal challenge with NiV. In addition, this vaccine induced a cross-protective immune response that was able to protect 50% of the animals against a challenge by HeV. This study presents a new efficient vaccination strategy against henipaviruses and opens novel perspectives on the use of AAV vectors as vaccines against emergent diseases. 
 Title: Protection Against Henipavirus Infection by Use of Recombinant Adeno-Associated Virus-Vector Vaccines

SOLUTION:
True