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 Input:
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

Ex Output:
False


Ex Input:
Paragraph: To date, an effective therapeutic treatment that confers strong attenuation toward coronaviruses (CoVs) remains elusive. Of all the potential drug targets, the helicase of CoVs is considered to be one of the most important. Here, we first present the structure of the full-length Nsp13 helicase of SARS-CoV (SARS-Nsp13) and investigate the structural coordination of its five domains and how these contribute to its translocation and unwinding activity. A translocation model is proposed for the Upf1like helicase members according to three different structural conditions in solution characterized through H/D exchange assay, including substrate state (SARS-Nsp13-dsDNA bound with AMPPNP), transition state (bound with ADP-AlF 4 − ) and product state (bound with ADP). We observed that the ␤19-␤20 loop on the 1A domain is involved in unwinding process directly. Furthermore, we have shown that the RNA dependent RNA polymerase (RdRp), SARS-Nsp12, can enhance the helicase activity of SARS-Nsp13 through interacting with it directly. The interacting regions were identified and can be considered common across CoVs, which provides new insights into the Replication and Transcription Complex (RTC) of CoVs. 
 Title: Delicate structural coordination of the Severe Acute Respiratory Syndrome coronavirus Nsp13 upon ATP hydrolysis

Ex Output:
True


Ex Input:
Paragraph: Reports indicate that myeloid and plasmacytoid dendritic cells (mDCs and pDCs), which are key effector cells in host innate immune responses, can be infected with HIV-1 and are reduced in number and function during the chronic phase of HIV disease. Furthermore, it was recently demonstrated that a sustained loss of mDCs and pDCs occurs in SIV-infected macaques. Since loss of functional DC populations might impair innate immune responses to opportunistic microorganisms and neoplastic cells, we explored whether inoculation of naive and SIV-or SHIV-infected pigtailed macaques with the hematopoietic cytokine FLT3-ligand (FLT3-L) would expand the number of mDCs and pDCs in vivo. After the macaques received supraphysiologic doses of FLT3-L, mDCs, pDCs, and monocytes increased up to 45-fold in blood, lymph nodes, and bone marrow (BM), with DC expansion in the BM preceding mobilization in blood and lymphoid tissues. FLT3-L also increased serum levels of IL-12, at least transiently, and elicited higher surface expression of HLA-DR and the activation markers CD25 and CD69 on NK and T cells. During and after treatment of infected animals, APCs increased in number and were activated; however, CD4 þ T cell numbers, virion RNA, and anti-SIV=SHIV antibody titers remained relatively stable, suggesting that FLT3-L might be a safe modality to expand DC populations and provide therapeutic benefit during chronic lentivirus infections. 
 Title: Systemic Dendritic Cell Mobilization Associated with Administration of FLT3 Ligand to SIV- and SHIV-Infected Macaques

Ex Output:

True