Thus assembling real data poses additional difficulties; in that regard, our simulations represent an upper limit of what can be achieved with a given average sequencing coverage. With increasing efforts to assemble genome sequences de novo by utilizing high-throughput sequencing technologies, there is a great interest in generating tools and strategies for the assembly task. Many assembly tools have been devised and found to be highly useful in the context of specific assembly tasks. However, choosing the best tool to use with a given sequencing and assembly strategy for a novel organism has received less attention. In the above, we presented a protocol for evaluating the chosen assembly strategy on a related model organism and applied it to several publicly available algorithms. By varying sequencing coverage, error rates and sequence composition of the target genome in a controlled setting, we estimated the extent and nature of errors that one ought to expect in a real-world setting. In addition, by pinpointing when reasonable assemblies are no longer achieved, we were able to establish limits on the read coverage, read lengths, and sequencing errors that a given assembler can tolerate. Generally speaking, short bacterial genomes and otherwise simple sequences can be assembled accurately with many of the available assembly tools, in the presence of few sequencing errors and a high LDN-193189 coverage of the target genomic sequence. When focusing on genomes that are architecturally more complex, such as those containing repeats or other internal structures, the assembly process becomes a less straight-forward proposition, even in the case of short genomes such as the HIV1. Additionally, in the presence of sequencing errors affecting as few as 1% of the read positions, the assembly statistics can deteriorate notably. The evaluated tools can leave up to 20% of the reference sequence uncovered when working with reads of 50 nts at 506coverage. It is important to stress that the assembly quality and performance issues that we observed manifest themselves even when working with short genomes. In view of all these observations, it is apparent that attempting to assemble large and complex genomes is a substantially more challenging proposition. Chronic obstructive pulmonary disease is an important pulmonary inflammatory disease whose prevalence and associated mortality rates have been increasing. In this disease, T cells and Th1 cells), neutrophils and macrophages are activated in the lungs, producing proteases such as neutrophil elastase and matrix metalloproteinase -9, resulting in alveolar wall destruction and mucus hypersecretion. COPD patients also show increased concentrations of MMP-1 and MMP-9 in bronchial lavage fluid, and higher expression of these enzymes in lung macrophages. In addition, various cytokines, growth factors, and chemokines may be involved in the development of pulmonary inflammation, emphysema, and fibrosis around small airways in COPD. Furthermore, Th17 cells can also activate neutrophils, and are thought to contribute to the development of COPD. The proinflammatory cytokines IL-1, IL-18, and IL-33 belongs to the IL-1 family.