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: The bone marrow contains heterogeneous population of cells that are involved in the regeneration and repair of diseased organs, including the lungs. In this study, we isolated and characterized progenitor epithelial cells from the bone marrow of 4-to 5-week old germ-free pigs. Microscopically, the cultured cells showed epithelial-like morphology. Phenotypically, these cells expressed the stem cell markers octamer-binding transcription factor (Oct4) and stage-specific embryonic antigen-1 (SSEA-1), the alveolar stem cell marker Clara cell secretory protein (Ccsp), and the epithelial cell markers pan-cytokeratin (Pan-K), cytokeratin-18 (K-18), and occludin. When cultured in epithelial cell growth medium, the progenitor epithelial cells expressed type I and type II pneumocyte markers. Next, we examined the susceptibility of these cells to influenza virus. Progenitor epithelial cells expressed sialic acid receptors utilized by avian and mammalian influenza viruses and were targets for influenza virus replication. Additionally, differentiated type II but not type I pneumocytes supported the replication of influenza virus. Our data indicate that we have identified a unique population of progenitor epithelial cells in the bone marrow that might have airway reconstitution potential and may be a useful model for cell-based therapies for infectious and non-infectious lung diseases.
Example Output: Epithelial Cells Derived from Swine Bone Marrow Express Stem Cell Markers and Support Influenza Virus Replication In Vitro

Example Input: This experiment was conducted to evaluate whether pretreatment with fenofibrate could mitigate acute lung injury (ALI) in a mice model of intestinal ischemia/reperfusion (I/R). Male C57BL/6 mice were randomly assigned into three groups (n = 6): sham, intestinal I/R + vehicle, and intestinal I/R + fenofibrate. Intestinal I/R was achieved by clamping the superior mesenteric artery. Fenofibrate (100 mg/kg) or equal volume of vehicle was injected intraperitoneally 60 minutes before the ischemia. At the end of experiment, measurement of pathohistological score, inflammatory mediators and other markers were performed. In addition, a 24-hour survival experiment was conducted in intestinal I/R mice treated with fenofibrate or vehicle. The chief results were as anticipated. Pathohistological evaluation indicated that fenofibrate ameliorated the local intestine damage and distant lung injury. Pretreatment with fenofibrate significantly decreased inflammatory factors in both the intestine and the lung. Consistently, renal creatine levels and hepatic ALT levels were significantly decreased in the fenofibrate group. Moreover, serum systemic inflammatory response indicators were significantly alleviated in the fenofibrate group. In addition, fenofibrate administration significantly improved the survival rate. Collectively, our data indicated that pretreatment with fenofibrate prior to ischemia attenuated intestinal I/R injury and ALI. Acute lung injury (ALI) is a critically severe, life-threatening condition in ICU, characterized by high mortality of approximately 40% 1 . ALI, along with its more severe form, acute respiratory distress syndrome, often results from a massive insult to the lung, whether be the direct alveolar infiltration or the indirect effects of systemic inflammatory response syndrome or multiple organ dysfunction syndromes 2 . An effective treatment of this life-threatening disorder calls for a better understanding of the molecular pathophysiology of ALI. The intestine is recognized to be one of the largest immune barrier systems and to be the source of bacteria and endotoxins in the body 3 . Previous reports indicate that the intestinal organ plays a crucial role in the development of ALI 4 . Mesenteric artery ischemia, a commonly seen critical state during small bowel transplantation or trauma, may lead to intestinal ischemia/reperfusion (I/R) injury. During the process of intestinal I/R injury, local bacteria overgrow and translocate, gastrointestinal mobility decreases, and mucosal permeability increases, all of which subsequently lead to the local intestine damage or distant lung injuries through the activation of systemic inflammatory response syndrome or multiple organ dysfunction syndromes 5,6 . Intestinal I/R is, therefore, a useful model for the investigation of pathophysiological mechanism of indirect ALI. Fenofibrate is known as an agonist of the peroxisome proliferator-activated receptor -α (PPARα ), the nuclear receptor superfamily member 7 . As a nuclear receptor activator, fenofibrate up-regulates or down-regulates genes that are involved in many pathophysiological processes, such as oxidative stress, inflammation, and leukocyte endothelium interactions 8, 9 . Recent studies have demonstrated an anti-oxidant, anti-inflammatory, and anti-ischemic role of fenofibrate to attenuate I/R injury in kidney 10,11 , liver 12 , brain 13,14 and heart 15 . But to date there are no literatures reporting the protective effects of fenofibrate in I/R injury in the organ of intestine. Moreover, the functional significance of fenofibrate in the intestinal I/R-induced ALI remains unclear. Therefore, this experiment is aimed to investigate whether fenofibrate administration would ameliorate the lung injury and inflammation in the model of intestinal I/R injury. Animals. The male C57BL/6 mice (8-10-wk-old; 20 ± 2 g) were purchased from Charles River (Beijing, China). Mice were kept in a temperature (21 ± 2 °C) and humidity (60 ± 5%) controlled room on a 12-hour light/dark cycle. They were fed a standard mice chow and water ad liblitum. All experiments were performed in accordance with the Declaration of Helsinki and were approved by the Institutional Animal Ethical Committee of the Peking Union Medical College Hospital.
Example Output: Protective effects of fenofibrate against acute lung injury induced by intestinal ischemia/reperfusion in mice OPEN

Example Input: Highly pathogenic H5N1 avian influenza viruses pose a debilitating pandemic threat. Thus, understanding mechanisms of antibody-mediated viral inhibition and neutralization escape is critical. Here, a robust yeast display system for fine epitope mapping of viral surface hemagglutinin (HA)-specific antibodies is demonstrated. The full-length H5 subtype HA (HA0) was expressed on the yeast surface in a correctly folded conformation, determined by binding of a panel of extensively characterized neutralizing human monoclonal antibodies (mAbs). These mAbs target conformationally-dependent epitopes of influenza A HA, which are highly conserved across H5 clades and group 1 serotypes. By separately displaying HA1 and HA2 subunits on yeast, domain mapping of two anti-H5 mAbs, NR2728 and H5-2A, localized their epitopes to HA1. These anti-H5 mAb epitopes were further fine mapped by using a library of yeast-displayed HA1 mutants and selecting for loss of binding without prior knowledge of potential contact residues. By overlaying key mutant residues that impacted binding onto a crystal structure of HA, the NR2728 mAb was found to interact with a fully surface-exposed contiguous patch of residues at the receptor binding site (RBS), giving insight into the mechanism underlying its potent inhibition of virus binding. The non-neutralizing H5-2A mAb was similarly mapped to a highly conserved H5 strain-specific but poorly accessible location on a loop at the trimer HA interface. These data further augment our toolchest for studying HA antigenicity, epitope diversity and accessibility in response to natural and experimental influenza infection and vaccines.
Example Output:
Fine epitope mapping of monoclonal antibodies against hemagglutinin of a highly pathogenic H5N1 influenza virus using yeast surface display NIH Public Access Author Manuscript