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.

Example Input: Acute cough is a major symptom of viral respiratory tract infection and causes excessive morbidity in human populations across the world. A wide variety of viruses play a role in the development of cough after acute infection and all of these manifest a similar clinical picture across different age groups. Despite the large disease burden surprisingly little is known about the mechanism of acute cough following viral infection. Both in vitro and in vivo experiments show that increased production of neuropeptides and leukotrienes mediate cough after viral infection, along with altered expression of neural receptors. Increased airway mucus production is also likely to play a significant role. This work is reviewed in this article. Following the recent development of a mouse model for rhinovirus infection and the establishment of experimental models of rhinovirus challenge in human subjects with both asthma and COPD the field is expanding to translate in vitro research into clinical studies and hopefully eventually into clinical practice. Developing a clearer understanding of the mechanisms underlying virus induced cough may lead to more specific and effective therapies.
Example Output: Cough and viruses in airways disease: Mechanisms

Example Input: Ability of CD8 + T cells to act as cytolytic effectors and produce IFN-γ was shown to mediate resistance to Toxoplasma gondii in murine models due to recognition of peptides restricted by murine MHC Class I molecules. However, no T. gondii specific HLA-B07 restricted peptides were proven protective against T gondii. Recently, two T gondii-specific HLA-B*0702-restricted T cell epitopes, GRA7 20-28 (LPQFATAAT) and GRA3 27-35 (VPFVVFLVA), displayed highaffinity binding to HLA-B*0702, and elicited IFN-γ from PBMCs of seropositive HLA-B*0702 persons. Herein, these peptides were evaluated to determine whether they could elicit IFN-γ in splenocytes of HLA-B*0702 transgenic mice when administered with adjuvants and protect against subsequent challenge. Peptide-specific IFN-γ producing T cells were identified by ELISPOT and proliferation assays utilizing splenic T lymphocytes from HLA transgenic mice. When HLA-B*0702 mice were immunized with one of the epitopes identified, GRA7 20-28 in conjunction with a universal CD4 + T cell epitope (PADRE) and adjuvants (CD4 + T cell adjuvant, GLA-SE, and TLR2 stimulatory Pam 2 Cys for CD8 + T cells), this immunization induced CD8 + T cells to produce IFN-γ and protected mice against high parasite burden when challenged with T gondii. This work demonstrates feasibility of bioinformatics followed by an empirical approach based on HLA binding to test this biological activity for identifying protective HLA-B*0702 restricted T gondii peptides and adjuvants that elicit protective immune responses in HLA-B*0702 mice.
Example Output: Toxoplasma gondii HLA-B*0702 restricted GRA7 20-28 peptide with adjuvants and an universal helper T cell epitope elicits CD8 + T cells producing IFN-γ and reduces parasite burden in HLA- B*0702 mice 1 NIH Public Access

Example Input: Acute lung injury (ALI), and its more severe form, acute respiratory distress syndrome (ARDS), are syndromes of acute hypoxemic respiratory failure resulting from a variety of direct and indirect injuries to the gas exchange parenchyma of the lungs. The clinical syndrome is characterized by critical hypoxemia (partial pressure of oxygen in arterial blood/fraction of inspired oxygen <300 for ALI and <200 for ARDS), bilateral pulmonary infiltrates suggesting edema, no clinical or measured evidence of cardiac failure, and no other explanation for these findings. Pulmonary or nonpulmonary infections with sepsis are the most common causes of ALI and ARDS, although gastric aspiration, massive transfusions, trauma, and other factors contribute. 1 The diversity of causes and the stereotyped physiologic and pathologic responses have made modeling human ALI and ARDS difficult, but new themes are evolving from experimental studies, some of which are reviewed in this article. Most of what is known about the pathology of ALI and ARDS comes from the studies of patients who have died, although a limited number of patients have undergone open lung biopsy (Fig. 1) . The pathologic changes include an early phase of diffuse alveolar damage, with an increase in endothelial permeability, evidence of intravascular thrombi, severe epithelial injury with denudation of alveolar wall basement membranes, accumulation of protein and fibrin-rich alveolar infiltrates in the airspaces, and abundant alveolar neutrophilic infiltrates. If patients survive, these changes progress for days to a repair phase, characterized by hyaline membrane formation, transition from neutrophilic to mononuclear infiltrates, and the appearance of intra-alveolar and
Example Output:
Experimental Models and Emerging Hypotheses for Acute Lung Injury Lung injury Animal model Respiratory distress