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
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Q: Paragraph: Background 3 In silico bacterial, viral, and human truth datasets were generated to evaluate available metagenomics 4 algorithms. Sequenced datasets include background organisms, creating ambiguity in the true 5 source organism for each read. Bacterial and viral datasets were created with even and staggered 6 coverage to evaluate organism identification, read mapping, and gene identification capabilities of 7 available algorithms. These truth datasets are provided as a resource for the development and 8 refinement of metagenomic algorithms. Algorithm performance on these truth datasets can inform 9 decision makers on strengths and weaknesses of available algorithms and how the results may be best 10 leveraged for bacterial and viral organism identification and characterization. 11 12 Source organisms were selected to mirror communities described in the Human Microbiome Project as 13 well as the emerging pathogens listed by the National Institute of Allergy and Infectious Diseases. The 14 six in silico datasets were used to evaluate the performance of six leading metagenomics algorithms: 15 MetaScope, Kraken, LMAT, MetaPhlAn, MetaCV, and MetaPhyler. 16 Results Algorithms were evaluated on runtime, true positive organisms identified to the genus and species 19 levels, false positive organisms identified to genus and species level, read mapping, relative abundance 20 estimation, and gene calling. No algorithm out performed the others in all categories, and the 21 algorithm or algorithms of choice strongly depends on analysis goals. MetaPhlAn excels for bacteria 22 and LMAT for viruses. The algorithms were ranked by overall performance using a normalized 23 weighted sum of the above metrics, and MetaScope emerged as the overall winner, followed by Kraken 24 and LMAT. 25 Conclusions 27 Simulated FASTQ datasets with well--characterized truth data about microbial community composition 28 reveal numerous insights about the relative strengths and weaknesses of the metagenomics algorithms 29 evaluated. The simulated datasets are available to download from the Sequence Read Archive 30 (SRP062063). 31 32 
 Title: Evaluating performance of metagenomic characterization algorithms using in silico datasets generated with FASTQSim

A: False
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Q: Paragraph: the virus [9], highlighting the rapid responses of the scientific community to this previously unknown global pathogen. Advancements in synthetic organic chemistry, molecular biology, and informatics have made possible the in vitro and in vivo [10-13]. The term "chemical genetics" has been coined to signify the use of chemicals to per-1 Department of Microbiology 2 Department of Biochemistry turb systematically, and thus determine, the function of proteins in the same way that mutations are used in classical genetics [14-16]. We decided to dissect the pathogenic pathways of the SARS-CoV using chemical Pokfulam, Hong Kong SAR China genetics. We hypothesized that by using forward chemical genetics [15, 16], in which small molecules that in-4 The Aaron Diamond AIDS Research Center 455 First Avenue duce altered phenotypes in cells or organisms are identified and their cellular targets will then be determined New York, New York 10016 subsequently, we will be able to isolate novel small-molecule compounds perturbing the biological pathways that are essential for the pathogenesis of SARS-CoV. Summary The severe acute respiratory syndrome-associated tion with ACE2 [9]. After being internalized into the target coronavirus (SARS-CoV) infected more than 8,000 cells, SARS-CoV undergoes a very rapid replication cypeople across 29 countries and caused more than 900 cle through a series of concerted transcriptional, translafatalities. Based on the concept of chemical genetics, tional, posttranslational, and proteolytic processing we screened 50,240 structurally diverse small moleevents, leading to maturation and release of infective cules from which we identified 104 compounds with viral particles into the culture supernatant [17-19]. We anti-SARS-CoV activity. Of these 104 compounds, 2 speculated that the various biological pathways intarget the SARS-CoV main protease (M pro ), 7 target volved in viral pathogenesis could be perturbed by small helicase (Hel), and 18 target spike (S) protein-angiomolecules using chemical genetic approaches. To extensin-converting enzyme 2 (ACE2)-mediated viral enamine the feasibility of employing chemical genetic try. The EC 50 of the majority of the 104 compounds approaches in SARS-CoV research, we acquired a determined by SARS-CoV plaque reduction assay chemical library (ChemBridge Corporation) of 50,240 were found to be at low micromolar range. Three sestructurally diverse small-molecule compounds that lected compounds, MP576, HE602, and VE607, valivary in functional groups and charges. As the SARSdated to be inhibitors of SARS-CoV M pro , Hel, and viral CoV replicates effectively in Vero cells (African green entry, respectively, exhibited potent antiviral activity monkey kidney cell line) and full cytopathic effects (CPE) (EC 50 Ͻ 10 M) and comparable inhibitory activities in of the infected cells can be observed within 96 hr postintarget-specific in vitro assays. fection, Vero cell CPE was used as a phenotypic indicator of successful viral infection in a cell-based assay to 
 Title: Identification of Novel Small-Molecule Inhibitors of Severe Acute Respiratory Syndrome-Associated Coronavirus by Chemical Genetics use of large collections of small molecules (chemical libraries) to investigate protein/chemical interactions

A:
False
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