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.

O. is a 37-year-old male with no significant past medical history who presented to the Emergency Department with a one week history of worsening dysphagia and odynophagia. He reported he was usually in good health until the current symptoms began. Scott said that he had been unable to swallow solid foods over the past week, largely due to increasing pain on swallowing, and was now unable to swallow liquids as well. Although he stated that his appetite was unchanged, he estimated a fivepound weight loss over the last week due to poor oral intake. He otherwise denied fever, respiratory or gastrointestinal symptoms, or any other complaints. He takes no medications at home except for rare acetaminophen. He is married, has a twoyear-old son, and works as an attorney. He denied use of tobacco, alcohol, or illicit drugs. Family history was noncontributory. On physical exam, he was afebrile and his vital signs were within normal limits. Cardiovascular, respiratory, abdominal, extremity, and neurologic exam were unremarkable. There was some mild oropharyngeal thrush, palpable bilateral inguinal lymphadenopathy, and a 1 cm painless ulceration on the penile shaft. Laboratory evaluation was unremarkable.
When a Diagnosis Is Reportable The Patient

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.
Host Gene Expression Profiling of Dengue Virus Infection in Cell Lines and Patients

ForceÀdistance measurements have been used to examine differences in the interaction of the dendritic cell glycan-binding receptor DC-SIGN and the closely related endothelial cell receptor DC-SIGNR (L-SIGN) with membranes bearing glycan ligands. The results demonstrate that upon binding to membraneanchored ligand, DC-SIGNR undergoes a conformational change similar to that previously observed for DC-SIGN. The results also validate a model for the extracellular domain of DC-SIGNR derived from crystallographic studies. Force measurements were performed with DC-SIGNR variants that differ in the length of the neck that result from genetic polymorphisms, which encode different numbers of the 23-amino acid repeat sequences that constitute the neck. The findings are consistent with an elongated, relatively rigid structure of the neck repeat observed in crystals. In addition, differences in the lengths of DC-SIGN and DC-SIGNR extracellular domains with equivalent numbers of neck repeats support a model in which the different dispositions of the carbohydrate-recognition domains in DC-SIGN and DC-SIGNR result from variations in the sequences of the necks.

Geometry and Adhesion of Extracellular Domains of DC-SIGNR Neck Length Variants Analyzed by ForceÀDistance Measurements