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The pear (Pyrus spp.) is well known for diverse flavors, textures, and global horticultural importance. However, the genetic diversity responsible for its extensive phenotypic variations remains largely unexplored. Here, we de novo assembled and annotated the genomes of the maternal (PsbM) and paternal (PsbF) lines of the hybrid 'Yuluxiang' pear and constructed the pear pangenome of 1.15 Gb by combining these two genomes with five previously published pear genomes representing cultivated and wild germplasm. Using the constructed pangenome, we identified 21 224 gene PAVs (Presence-absence variation) and 1 158 812 SNPs (Single Nucleotide Polymorphism) in the non-reference genome that were absent in the PsbM reference genome. Compared with SNP markers, PAV-based analysis provides additional insights into the pear population structure. In addition, some genes associated with pear fruit quality traits have differential occurrence frequencies and differential gene expression between Asian and European populations. Moreover, our analysis of the pear pangenome revealed a mutated SNP and an insertion in the promoter region of the gene PsbMGH3.1 potentially enhance sepal shedding in 'Xuehuali' which is vital for pear quality. PsbMGH3.1 may play a role in the IAA pathway, contributing to a distinct low-auxin phenotype observed in plants by heterologously overexpressing this gene. This research helps capture the genetic diversity of pear populations and provides genomic resources for accelerating breeding. [ABSTRACT FROM AUTHOR]

The electrocardiographic (ECG) inverse problem offers more sophisticated approaches for assessing the electrical condition of the heart than the standard 12-lead ECG. Because of the ill-posted nature of the ECG inverse problem, regularization must be used to obtain clinically meaningful estimates of heart-surface potentials. We compared optimal inverse solutions using L1 regularization with those found using zero-order Tikhonov (ZOT) regularization in two heart-torso models with known heart-surface potentials, but different spatial detail. In the model based on the Visible Human Male with an epicardial-shell heart-model, there was no difference in relative error (RE) and correlation coefficient (CC) during activation and recovery of the ventricles (QT interval) between L1 and ZOT inferred heart-surface potentials. In the heart-torso model based on the ECGSIM package with a ventricular heart model there were significant differences in RE and CC throughout the QT interval. At the peak of the R wave, RE was reduced from 0.841 (ZOT) to 0.358 (L1). L1 regularization reduced RE compared to ZOT except during the downstroke of the R wave. These results suggest that improvement with L1 regularization is dependent on heart model complexity, not its sampling density. [ABSTRACT FROM AUTHOR]

Background: A sizeable body of data demonstrates that membrane ICAM-1 (mICAM-1) plays a significant role in host defense in a site-specific fashion. On the pulmonary vascular endothelium, mICAM-1 is necessary for normal leukocyte recruitment during acute inflammation. On alveolar epithelial cells (AECs), we have shown previously that the presence of normal mICAM-1 is essential for optimal alveolar macrophage (AM) function. We have also shown that ICAM-1 is present in the alveolar space as a soluble protein that is likely produced through cleavage of mICAM-1. Soluble intercellular adhesion molecule-1 (sICAM-1) is abundantly present in the alveolar lining fluid of the normal lung and could be generated by proteolytic cleavage of mICAM-1, which is highly expressed on type I AECs. Although a growing body of data suggesting that intravascular sICAM-1 has functional effects, little is known about sICAM-1 in the alveolus. We hypothesized that sICAM-1 in the alveolar space modulates the innate immune response and alters the response to pulmonary infection. Methods: Using the surfactant protein C (SPC) promoter, we developed a transgenic mouse (SPC-sICAM-1) that constitutively overexpresses sICAM-1 in the distal lung, and compared the responses of wild-type and SPC-sICAM-1 mice following intranasal inoculation with K. pneumoniae. Results: SPC-sICAM-1 mice demonstrated increased mortality and increased systemic dissemination of organisms compared with wild-type mice. We also found that inflammatory responses were significantly increased in SPCsICAM- 1 mice compared with wild-type mice but there were no difference in lung CFU between groups. Conclusions: We conclude that alveolar sICAM-1 modulates pulmonary inflammation. Manipulating ICAM-1 interactions therapeutically may modulate the host response to Gram negative pulmonary infections. [ABSTRACT FROM AUTHOR]