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.

[Q]: with the pathological structure of BPD, as seen in the lungs of preterm infants who died and in animal models (3, 7). As the authors note, this study was limited in that the subjects with BPD were stable outpatients younger than 3 years who did not require oxygen therapy at the time of the study. Whether their findings hold true in infants with persistent severe BPD, including those with chronic ventilator-dependent hypoxemic respiratory failure, is not clear. In addition, BPD classification was based on clinical decision making, rather than a physiologic assessment such as the oxygen reduction test (11). In an earlier article, members of this group studied DL CO and its components, DM and Vc, in full-term infants without lung disease and showed that DL CO and Vc (but not DM) correlated with the level of proangiogenic circulating hematopoietic stem/progenitor cells (pCHSPCs) (12). However, this study did not include preterm infants with or without BPD. Both pCHSPCs, also referred to as circulating progenitor cells, as well as late-outgrowth endothelial colony-forming cells, are decreased in the cord blood of preterm infants who later develop moderate or severe BPD (13, 14) . Together, these findings suggest that early disruptions in the number and function of angiogenic progenitor cells, possibly by maternal complications of pregnancy known to be associated with BPD risk, may lead to impaired development of the pulmonary vasculature and sustained impaired gas exchange in preterm infants with BPD. This study shows how a physiologic assessment, such as infant pulmonary function testing, may be used in the clinical setting to provide an estimation of impaired gas exchange in preterm infants with varying degrees of lung injury. Combining functional assays such as this with measurement of pCHSPCs and other angiogenic biomarkers in the cord blood, as well as novel imaging techniques such as quantitative pulmonary magnetic resonance imaging (15), will lead to improved disease phenotyping of preterm infants at risk for BPD. Given the spectrum of disease severity among infants with severe BPD (as determined by the currently accepted diagnostic criteria), novel methods such as these will help identify preterm neonates more accurately, permit targeted therapies for the most severely affected infants, and provide quantitative evidence of the efficacy of these interventions in young children after preterm birth (16). n
[A]: Jobe AH, Bancalari E. Bronchopulmonary dysplasia


[Q]: Low cost, high throughput, easy quantitation, and rich descriptions have made gene expression profiling generated by DNA microarrays an optimal approach for describing host transcriptional responses (HTRs). However, efforts to characterize the landscape of HTRs to diverse pathogens are far from offering a comprehensive view. Here, we developed an HTR Connectivity Map based on systematic assessment of pairwise similarities of HTRs to 50 clinically important human pathogens using 1353 gene-expression profiles generated from >60 human cells/tissues. These 50 pathogens were further partitioned into eight robust "HTR communities" (i.e., groups with more consensus internal HTR similarities). These communities showed enrichment in specific infection attributes and differential gene expression patterns. Using query signatures of HTRs to external pathogens, we demonstrated four distinct modes of HTR associations among different pathogens types/class, and validated the reliability of the HTR community divisions for differentiating and categorizing pathogens from a host-oriented perspective. These findings provide a first-generation HTR Connectivity Map of 50 diverse pathogens, and demonstrate the potential for using annotated HTR community to detect functional associations among infectious pathogens.
[A]: Inferring Infection Patterns Based on a Connectivity Map of Host Transcriptional Responses


[Q]: Background: Hepatocellular carcinoma (HCC) is one of most common and aggressive human malignancies in the world, especially, in eastern Asia, and its mortality is very high at any phase. We want to investigate mechanism of niclosamide inducing cell apoptosis in HCC. Methods: Two hepatoma cell lines were used to evaluate activity of niclosamide inducing cell apoptosis and study its mechanism. Quantitative real-time PCR and western blotting were used in analysis of genes expression or protein active regulated by niclosamide. Results: Niclosamide remarkably induced cell apoptosis in hepatoma cells. Furthermore, our study revealed that RNA-dependent protein kinase-like kinase (PERK) is activated and its expression is up-regulated in HCC cells which are exposed to niclosamide. niclosamide also significantly increase activating transcription factor 3 (ATF3), activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-homologous protein (CHOP) expression in HCC cells. It's suggested that the function of niclosamide was abrogated by PERK inhibitor or absent ATF3. Expression of PERK and CHOP is correlated with ATF3 level in the cells. Conclusion: Taken together, our results indicate that ATF3 plays an integral role in ER stress activated and cell apoptosis induced by niclosamide in HCC cells. In this study, the new mechanism of niclosamide as anti-cancer we investigated, too.
[A]:
Niclosamide induced cell apoptosis via upregulation of ATF3 and activation of PERK in Hepatocellular carcinoma cells