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.

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
Jobe AH, Bancalari E. Bronchopulmonary dysplasia

Here we describe a novel endonuclease IV (Endo IV) based assay utilizing a substrate that mimics the abasic lesions that normally occur in doublestranded DNA. The three component substrate is characterized by single-stranded DNA target, an oligonucleotide probe, separated from a helper oligonucleotide by a one base gap. The oligonucleotide probe contains a non-fluorescent quencher at the 5 0 end and fluorophore attached to the 3 0 end through a special rigid linker. Fluorescence of the oligonucleotide probe is efficiently quenched by the interaction of terminal dye and quencher when not hybridized. Upon hybridization of the oligonucleotide probe and helper probe to their complementary target, the phosphodiester linkage between the rigid linker and the 3 0 end of the probe is efficiently cleaved, generating a fluorescent signal. In this study, the use of the Endo IV assay as a post-PCR amplification detection system is demonstrated. High sensitivity and specificity are illustrated using single nucleotide polymorphism detection.
A novel endonuclease IV post-PCR genotyping system

3C-like protease (3CL pro ) plays pivotal roles in the life cycle of severe acute respiratory syndrome coronavirus (SARS-CoV) and only the dimeric protease is proposed as the functional form. Guided by the crystal structure and molecular dynamics simulations, we performed systematic mutation analyses to identify residues critical for 3CL pro dimerization and activity in this study. Seven residues on the dimer interface were selected for evaluating their contributions to dimer stability and catalytic activity by biophysical and biochemical methods. These residues are involved in dimerization through hydrogen bonding and broadly located in the N-terminal finger, the a-helix A 0 of domain I, and the oxyanion loop near the S1 substrate-binding subsite in domain II. We revealed that all seven single mutated proteases still have the dimeric species but the monomer-dimer equilibria of these mutants vary from each other, implying that these residues might contribute differently to the dimer stability. Such a conclusion could be further verified by the results that the proteolytic activities of these mutants also decrease to varying degrees. The present study would help us better understand the dimerizationactivity relationship of SARS-CoV 3CL pro and afford potential information for designing anti-viral compounds targeting the dimer interface of the protease.

Residues on the Dimer Interface of SARS Coronavirus 3C-like Protease: Dimer Stability Characterization and Enzyme Catalytic Activity Analysis