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.

Ex Input:
Background: Despite the seriousness of dengue-related disease, with an estimated 50-100 million cases of dengue fever and 250,000-500,000 cases of dengue hemorrhagic fever/dengue shock syndrome each year, a clear understanding of dengue pathogenesis remains elusive. Because of the lack of a disease model in animals and the complex immune interaction in dengue infection, the study of host response and immunopathogenesis is difficult. The development of genomics technology, microarray and high throughput quantitative PCR have allowed researchers to study gene expression changes on a much broader scale. We therefore used this approach to investigate the host response in dengue virusinfected cell lines and in patients developing dengue fever. Methodology/Principal Findings: Using microarray and high throughput quantitative PCR method to monitor the host response to dengue viral replication in cell line infection models and in dengue patient blood samples, we identified differentially expressed genes along three major pathways; NF-kB initiated immune responses, type I interferon (IFN) and the ubiquitin proteasome pathway. Among the most highly upregulated genes were the chemokines IP-10 and I-TAC, both ligands of the CXCR3 receptor. Increased expression of IP-10 and I-TAC in the peripheral blood of ten patients at the early onset of fever was confirmed by ELISA. A highly upregulated gene in the IFN pathway, viperin, was overexpressed in A549 cells resulting in a significant reduction in viral replication. The upregulation of genes in the ubiquitin-proteasome pathway prompted the testing of proteasome inhibitors MG-132 and ALLN, both of which reduced viral replication. Conclusion/Significance: Unbiased gene expression analysis has identified new host genes associated with dengue infection, which we have validated in functional studies. We showed that some parts of the host response can be used as potential biomarkers for the disease while others can be used to control dengue viral replication, thus representing viable targets for drug therapy.

Ex Output:
Host Gene Expression Profiling of Dengue Virus Infection in Cell Lines and Patients


Ex Input:
Bovine renal brush-border membrane vesicle aminopeptidase N at various stages of purity was treated with two bifunctional cross-linking agents. A pattern of emergence of higher molecular weight forms was observed. By using a cleavable cross-linker, aminopeptidase N was shown to cross-link both to itself and to its breakdown products as well as to dipeptidyl peptidase IV. Using this technique it was possible to identify three of the breakdown products as 45 kDa, 66 kDa and 95 kDa peptides. N-terminal amino acid sequence analysis was used to define the precise cleavage points for the bovine renal aminopeptidase N breakdown products. The short amino acid sequences obtained show strong sequence similarity with the human intestinal and rat kidney aminopeptidase N.

Ex Output:
The oligomeric structure of renal aminopeptidase N from bovine brush-border membrane vesicles


Ex Input:
This article summarizes the contributions of high throughput genomic, proteomic, metabolomic, and gene expression investigations to our understanding of inherited or acquired risk for acute respiratory distress syndrome (ARDS). While not yet widely applied to a complex trait like ARDS, these techniques are now routinely employed to study a variety of disease states. Omic applications hold great promise for identifying novel factors that may contribute to ARDS pathophysiology or may be appropriate for further development as biomarkers or surrogates in clinical studies. Opportunities and challenges of different techniques are discussed, and examples of successful applications in non-ARDS fields are used to illustrate the potential utility of each technique. As future GWAS are published, new candidates will undoubtedly emerge and meta-analysis will be possible to harness the power of multiple populations. At the same time, however, GWAS may prove more fruitful if the heterogeneity of ARDS is acknowledged a priori, and analyses are conducted within more homogenous subtypes. For instance, Tejera and Christiani demonstrated that the genetic risk factors for extrapulmonary ARDS and pulmonary ARDS were distinct, 54 a finding echoed by most reviews. 9,41 In addition to Meyer

Ex Output:

Beyond SNPs-genetics, genomics and other 'omic approaches to ARDS