In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[Q]: Among RNA viruses, the order Nidovirales stands out for including viruses with the largest RNA genomes currently known. Nidoviruses employ a complex RNAsynthesizing machinery comprising a variety of non-structural proteins (nsps). One of the postulated drivers of the expansion of nidovirus genomes is the presence of a proofreading 3 -to-5 exoribonuclease (ExoN) belonging to the DEDDh family. ExoN may enhance the fidelity of RNA synthesis by correcting nucleotide incorporation errors made by the RNA-dependent RNA polymerase. Here, we review our current understanding of ExoN evolution, structure, and function. Most experimental data are derived from studies of the ExoN domain of coronaviruses (CoVs), which were triggered by the bioinformatics-based identification of ExoN in the genome of severe acute respiratory syndrome coronavirus (SARS-CoV) and its relatives in 2003. Although convincing data supporting the proofreading hypothesis have been obtained, from biochemical assays and studies with CoV mutants lacking ExoN functionality, the features of ExoN from most other nidovirus families remain to be characterized. Remarkably, viable ExoN knockout mutants were obtained only for two CoVs, mouse hepatitis virus (MHV) and SARS-CoV, whose RNA synthesis and replication kinetics were mildly affected by the lack of ExoN function. In several other CoV species, ExoN inactivation was not tolerated, and knockout mutants could not be rescued when launched using a reverse genetics system. This suggests that ExoN is also critical for primary viral RNA synthesis, a property that poorly matches the profile of an enzyme that would merely boost longterm replication fidelity. In CoVs, ExoN resides in a bifunctional replicase subunit (nsp14) whose C-terminal part has (N7-guanine)-methyltransferase activity. The crystal structure of SARS-CoV nsp14 has shed light on the interplay between these two domains, and on nsp14's interactions with nsp10, a co-factor that strongly enhances ExoN activity in vitro assays. Further elucidation of the structure-function relationships of ExoN and its interactions with other (viral and/or host) members of the CoV replication machinery will be key to understanding the enzyme's role in viral RNA synthesis and pathogenesis, and may contribute to the design of new approaches to combat emerging nidoviruses.
[A]: The Curious Case of the Nidovirus Exoribonuclease: Its Role in RNA Synthesis and Replication Fidelity


[Q]: Business integration is an important determinant of business value and firm performance which enables a firm to respond to pressing competitive forces. Given its significant role, business integration in general has been an enduring research topic over the years. However, due to its complex nature, the ways to achieve this important organisational capability in firms are still not clearly understood. Hence, the present study is an attempt to 'open this black box' and examine the relevant issues through a case study of M.com, one of the largest e-commerce firms in China. The findings of this case study emphasise that the ability to coordinate organisational interdependencies and asset orchestration according to the needs of business processes is challenging but necessary in order to achieve business integration in e-commerce firms. It is found that asset orchestration in a firm is contingent on the organisational interdependencies such that different interdependence types demand different coordination methods at the very least. It also shows the significant role of IT in asset orchestration and the coordination of organisational interdependencies during business integration. With these capabilities, firms can experience growth and improve the quality of conformance to customer needs.
[A]: The role of organisational interdependencies and asset orchestration in business integration: A case study of M.com


[Q]: Chronic obstructive pulmonary disease (COPD) is a progressive chronic disease characterized by airflow limitation that is frequently progressive and associated with respiratory impairment. As the fourth leading cause of death in the United States and Europe, COPD results in a substantial and ever increasing economic and social burden [1] . Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are frequently encountered in the intensive care unit (ICU). Although there is no standardized definition, AECOPD are characterized by a significant change in patient symptoms from baseline accompanied by overall increased airway resistance [2] . These exacerbations carry a significant risk to patients, with 10 % in-hospital mortality and 1-year and 2-year all-cause mortality rates of 43 % and 49 %, respectively, in patients with hypercapnic exacerbations [3] . Other studies note in-hospital mortality rates as high as 30 % with worse outcomes associated with older age, severity of respiratory and non-respiratory organ dysfunction, and hospital length of stay [4] . Given that patients transferred to the ICU with AECOPD are at high risk for complications and adverse outcomes, early diagnosis and management are critical to improve patient outcomes and survival in this population. AECOPD are the result of increased airway resistance as a consequence of inflammation and/or increased airway secretions. Data suggests that 50-70 % of AECOPD are due to respiratory infections, with greater than 50 % being due to bacterial pathogens. The most commonly isolated organisms include Haemophilus influenza, Streptococcus pneumonia, Moraxella catarrhalis, and Pseudomonas aeruginosa. Gram-negative rods are isolated less frequently but are more common in patients with advanced disease and more severe exacerbations as well as those with diabetes. Patients may be chronically colonized with bacteria in the respiratory tract, but it is unclear whether asymptomatic colonization leads to exacerbations caused by the same bacterial strains or predisposes to new bacterial growth. Atypical bacteria such as Mycoplasma pneumonia may be responsible for up to 14 % of exacerbations [2, 5] . Viral infections are estimated to cause 20-40 % of exacerbations. However, many patients with documented bacterial infections report a viral prodrome, making the true prevalence of viral illness difficult to estimate. Estimates indicate that rhinovirus (17-25 %), influenza (5-28 %), parainfluenza (5-10 %), and respiratory syncytial virus (5-10 %) are among the most common viral pathogens in AECOPD. Adenovirus, human metapneumovirus, and coronavirus are also potential but less common culprits. In many cases the exact precipitant of an exacerbation may never be identified [2, 5-7]. Acute exacerbations are typically defined by worsening dyspnea, cough with or without increased sputum production, wheezing, and a subjective sense of chest tightness and may be accompanied by pain [1, 7] . It is important to appreciate the severity of underlying airflow limitation, comorbid conditions, duration of worsened symptoms, current outpatient treatment regimen, and previous exacerbations including any 13 S.M. Kassutto, MD Pulmonary, Allergy and Critical Care,
[A]:
Care of the Surgical ICU Patient with Chronic Obstructive Pulmonary Disease and Pulmonary Hypertension Chronic Obstructive Pulmonary Disease Overview and Epidemiology