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".

[Q]: Paragraph: Daily oscillations of pulmonary function depend on the rhythmic activity of the circadian timing system. Environmental tobacco/cigarette smoke (CS) disrupts circadian clock leading to enhanced inflammatory responses. Infection with influenza A virus (IAV) increases hospitalization rates and death in susceptible individuals, including patients with Chronic Obstructive Pulmonary Disease (COPD). We hypothesized that molecular clock disruption is enhanced by IAV infection, altering cellular and lung function, leading to severity in airway disease phenotypes. C57BL/6J mice exposed to chronic CS, BMAL1 knockout (KO) mice and wild-type littermates were infected with IAV. Following infection, we measured diurnal rhythms of clock gene expression in the lung, locomotor activity, pulmonary function, inflammatory, pro-fibrotic and emphysematous responses. Chronic CS exposure combined with IAV infection altered the timing of clock gene expression and reduced locomotor activity in parallel with increased lung inflammation, disrupted rhythms of pulmonary function, and emphysema. BMAL1 KO mice infected with IAV showed pronounced detriments in behavior and survival, and increased lung inflammatory and pro-fibrotic responses. This suggests that remodeling of lung clock function following IAV infection alters clock-dependent gene expression and normal rhythms of lung function, enhanced emphysematous and injurious responses. This may have implications for the pathobiology of respiratory virus-induced airway disease severity and exacerbations. I nfluenza virus, rhinovirus, coronavirus, respiratory syncytial virus, parainfluenza, adenovirus and metapeumovirus are among the respiratory viruses known to cause exacerbations in Chronic Obstructive Pulmonary Disease (COPD) and asthma 1-4 . In fact, respiratory viral infections account for about 50-70% of acute exacerbations in patients with COPD 5 . COPD exacerbations are often followed by subsequent clinical pulmonary deterioration, including significant declines in forced expiratory volume at 1 second (FEV 1 ) and increased hospitalization or mortality 6 . This is associated with worsening of COPD phenotypes, such as cough, fever and mucus production; the timing of which depends on the activity of the biological clock. Circadian rhythms are biological oscillations that occur with a near-24-h period and are synchronized or entrained to environmental cues, such as the day-night cycle 7 . These rhythms are the manifestation of an autoregulatory molecular oscillator of interlocked positive and negative transcription factors collectively referred to as clock genes 8 . In mammals, the central pacemaker, localized to the suprachiasmatic nucleus (SCN) of the anterior hypothalamus, drives rhythms of physiology and behavior, and synchronizes internal timing with the external environment 7 . Apart from the central clock, peripheral tissues such as the liver, heart and the lung also contain autonomous circadian oscillators that coordinate tissue specific cellular functions and responses to environmental stimuli 7-12 . As an example, circadian rhythms in pulmonary function have been demonstrated in animal models and healthy individuals (highest at noon time and low during the early morning hours) [13] [14] [15] . The coordinated and synchronized activity of central and peripheral oscillators is referred to as the circadian timing system 9,12 . It has been shown that recruitment of leukocytes to tissues following infection is also regulated by the circadian timing system 16, 17 . For example, macrophages and mast cells exhibit robust rhythms of circadian clock and proinflammatory cytokine gene expression 18, 19 . The magnitude of immune and inflammatory parameters varies with time of day, and disruption of circadian rhythms (chronodisruption) has been implicated in cellular dysfunction, and in the pathogenesis of chronic metabolic disease, infection, and inflammatory diseases 20-22 . 
 Title: Influenza A virus-dependent remodeling of pulmonary clock function in a mouse model of COPD
[A]: False


[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
[A]: False


[Q]: Paragraph: In order to differentiate recent isolates of avian infectious bronchitis virus (IBV) in Taiwan, polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP), and direct sequencing methods were used to type 25 IBV Taiwan isolates. Two conserved sequences that flank the hypervariable region I (HVR I) in the N-terminus of S1 protein gene were chosen as primers. Sequences of 228-231 base pairs (bp) were amplified by PCR from 25 Taiwan isolates and 4 reference strains (H120, Conn, JMK, Holte). PCR products were digested with 5 restriction endonucleases, BsoFI, DdeI, MboII, AluI, RsaI, and different IBV isolates were grouped according to their RFLP patterns. The RFLP patterns of the 4 reference strains in this study matched the published sequences in GenBank. Except 1 vaccine strain, the other 24 Taiwan isolates were different from these 4 and 18 other IBV strains whose sequences were published. The data from PCR-RFLP and sequencing of IBV genomes showed that the 24 Taiwan isolates can be divided into 2 distinct groups, I and II. Seven RFLP patterns are identified in group I and only 1 in group II. 1678 C.-H. Wang and C.-T. Tsai antibodies that normally form the basis for comparison of IBV isolates are induced largely by the N-terminus of the S1 protein [7, 9, 11-]. In the present study, we used reverse transcription polymerase chain reaction (RT-PCR) coupled with restriction fragment length p o l y m o r p h i s m (RFLP) of the R T -P C R products to classify our isolates. Using these techniques, we present a convenient m e t h o d for identifying the R F L P patterns of IBV isolates in Taiwan which are different from those of k n o w n IBV strains. Materials and methods Twenty-five Taiwan isolates of IBV were used in this study. and V1397. Four sets of primers successfully used by other [1, 12, 13, 18] and one new set of primers were used in this study. The published primers included S1 [12], $2 [13], M-N [-1], and N primers [18] . For the new primers, the S1 sequence of the 22 published IBV were analyzed using the Clustal method to find conserved sequences. The new primers (C2U-C3L) were located in the N-terminus of the S1 gene which contains hypervariabte region I (HRV I, nucleotides, nt 142 320); this region is reponsible for induction of antibodies to the IBV that have been the basis for defining of different IBV serotypes [9, 11] . The sequences and locations of the new primers used for the PCR were C2U: TGGTT GGCAT TTACA CGGGG (114-133) and C3L: CAATG GGTAA CAAAC AC (341-325, as in Beaudette strain). Viral RNA was extracted as described [t2] with some modification. Briefly, guanidine thiocyanate (Sigma), and NaOAC were added to allantoic fluid, and extracted with phenolchloroform-isoamylalcohol. The RNA was further precipitated in isopropanol (Merck) and resuspended in alcohol and stored at -20 °C until it was used in RT-PCR. Genetic typing of infectious bronchitis virus in Taiwan 1679 All glassware and double distilled water (DDW) were treated with 0.1% diethyl-pyrocarbonate (Sigma) for removing RNase contamination. The RT-PCR was accomplished in one step. The mixture included 10 ~tl of pfu polymerase 10 x buffer (Stratagene, USA), 8 gl of 2.5 mM dNTP (Stragene), 0.4 gl of 40 U/gl RNasin (Promega), 0.3 gl RTase (AMV, Promega), 1 ~tl primers (20 ~tM), 0.8 gl of 2.5 U/gl pfu polymerase (Stragene), 60 gl DDW and 20 gl viral RNA. The RT-PCR was conducted in a FTS-960 thermal cycler (Corbett Research, Australia) where the RT was performed at 42 °C for 1 h. PCR was then performed during 35 cycles of denaturation at 94 °C for 30 sec, annealing at 45 °C for 1 rain, and polymerization at 72 °C for 1 rain. The final polymerization step was conducted at 72 °C for 7 rain. The PCR products were analyzed on a 2% gel containing ethidium bromide (0.5 gg/ml), and the amplified DNA was detected using an ultaviolet transilluminator. 
 Title: Genetic grouping for the isolates of avian infectious bronchitis virus in Taiwan
[A]:
False