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: Protease-activated receptor 2 (PAR-2) is activated by proteases involved in allergy and triggers airway epithelial secretion and inflammation. PAR-2 is normally expressed basolaterally in differentiated nasal ciliated cells. Objective: We tested if epithelial remodeling during diseases characterized by loss of cilia and squamous metaplasia may alter PAR-2 polarization. Methods: Endogenous PAR-2 responses were measured by live cell calcium and cilia imaging, measurement of fluid secretion, and quantification of cytokines. We utilized airway squamous cell lines, primary differentiated air-liquid interface cultures, and tissue explants. Cells were exposed to disease-related modifiers that alter epithelial morphology, including IL-13, cigarette smoke condensate, and retinoic acid deficiency. We used concentrations and exposure times that altered epithelial morphology without causing breakdown of the epithelial barrier, likely reflecting early disease states.

Ex Output:
Altered polarization of PAR-2 signaling during airway epithelial remodeling


Ex Input:
The indirect immunoperoxidase (IIP) assay was compared with the reverse transcription-polymerase chain reaction (RT-PCR) for detection of 793/B serotype of infectious bronchitis virus in tissues samples collected from experimentally infected chickens. This technique was optimized in specific pathogen-free (SPF)-embryonated chicken eggs and broiler chickens inoculated with the Iranian IR/773/2001 strain of 793/B serotype The trachea, lung, kidney, and cecal tonsil tissue samples from experimentally infected chicken embryos and chickens were collected in order to prepare tissue sections in IIP assay and to detect in RT-PCR. The sensitivity and specificity values of IIP assay were, respectively, 83 and 84 %, and the positive and negative prediction values were 71 and 91 % when compared with RT-PCR.

Ex Output:
Detection of 793/B serotype of infectious bronchitis virus in tissue sample by indirect immunoperoxidase assay


Ex Input:
Introduction-A dysregulated immune response leading to sepsis is the most frequent cause of late post-traumatic deaths. We have found a novel anti-inflammatory pathway that is initiated by the acute phase protein, C-reactive protein (CRP), interacting with Fcγ receptor (FcγR) on monocytes. This pathway is protective in animal models of endotoxin shock. We hypothesized that genetic polymorphisms in the FcγR might contribute to monocyte responses and susceptibility to infectious complications after severe trauma. Methods-We conducted an observational study on a prospectively identified cohort of adult patients with convenience enrollment admitted after severe trauma. We enrolled 66 patients and collected blood samples at enrollment and again at 48 and 72 hrs. Patients were followed through their hospital stay and any septic events before 14 days were recorded. Cytokine and CRP levels were determined in the plasma from all three blood draws. Additionally, DNA was extracted from blood and analyzed for the 131 H/R FcγRIIa polymorphism that strongly affects the binding of IgG and CRP to this receptor. Results-Elevated levels of IL-8, IL-6, IL-10 MCP-1 as well as CRP were associated with reduced time to post-traumatic sepsis in Cox regression analysis. Expression of monocyte HLA-DR below 45% on patient monocytes was also associated with sepsis (HR = 3.15, 95% CI 1.45-6.93). Genetic analysis found that individuals with the polymorphism of the FcγRIIa receptor that binds CRP poorly were also more likely to have decreased monocyte HLA-DR and posttraumatic sepsis. In vitro studies showed that CRP could attenuate monocyte deactivation in volunteers with the polymorphism of the FcγRIIa receptor that binds CRP. Conclusions-Our findings suggest that a common genetic variation in the FcγRIIa receptor may contribute to infectious susceptibility in trauma patients. In vitro experiments suggest that this association is related to the inability of CRP to bind to this FcγRIIa receptor variant. Keywords post-traumatic sepsis; monocyte deactivation; C reactive protein; FcγRIIa receptor We and others have found a correlation between post-traumatic sepsis in individuals with significant monocyte deactivation following their traumatic injury (7-9). Monocyte deactivation in these patients is characterized by 1) a lack of tumor necrosis factor (TNF)-α West et al.

Ex Output:

An FcγRIIa Polymorphism with Decreased C-Reactive Protein Binding is Associated with Sepsis and Decreased Monocyte HLA-DR Expression in Trauma Patients