In an effort to probe the origin of surface brightness profile (SBP) breaks widely observed in nearby disk galaxies, we carry out a comparative study of stellar population profiles of 635 disk galaxies selected from the Mapping Nearby Galaxies at Apache Point Observatory spectroscopic survey. We classify our galaxies into single exponential (Ti), down-bending (Tii), and up-bending (Tiii) SBP types and derive their spin parameters and radial profiles of age/metallicity-sensitive spectral features. Most Tii (Tiii) galaxies have down-bending (up-bending) star formation rate (SFR) radial profiles, implying that abrupt radial changes of SFR intensities contribute to the formation of both Tii and Tiii breaks. Nevertheless, a comparison between our galaxies and simulations suggests that stellar migration plays a significant role in weakening down-bending Σ⋆ profile breaks. While there is a correlation between the break strengths of SBPs and age/metallicity-sensitive spectral features for Tii galaxies, no such correlation is found for Tiii galaxies, indicating that stellar migration may not play a major role in shaping Tiii breaks, as is also evidenced by a good correspondence between the break strengths of Σ⋆ and SBPs of Tiii galaxies. We do not find evidence for galaxy spin being a relevant parameter for forming different SBP types, nor do we find significant differences between the asymmetries of galaxies with different SBP types, suggesting that environmental disturbances or satellite accretion in the recent past do not significantly influence the break formation. By dividing our sample into early and late morphological types, we find that galaxies with different SBP types follow nearly the same tight stellar mass– relation, which makes the hypothesis that stellar migration alone can transform SBP types from Tii to Ti and then to Tiii highly unlikely.

Asthma is a common inflammatory pulmonary disorder involving a diverse array of immune cells such as proinflammatory T helper 2 (Th2) cells. We recently reported that intraperitoneal injection of ␣-galactosylceramide (␣-GalCer) can stimulate the lung invariant natural killer T (iNKT) cells and does not lead to airway inflammation in WT mice. Other studies indicate that iNKT cells play an important role in inducing regulatory T cells (Treg cells) and peripheral tolerance. Using iNKT cellknockout mice, functional inactivation of Treg cells, and co-culture experiments in murine asthma models, we investigated the immunoregulatory effects of ␣-GalCer treatment before allergen sensitization on Th2 cell responses. We also studied whether ␣-GalCer's effects require lung Treg cells induced by activated iNKT cells. Our results disclosed that intraperitoneal administration of ␣-GalCer before allergen sensitization could promote the expansion and suppressive activity of lung CD4 ؉ FoxP3 ؉ Treg cells. These effects were accompanied by down-regulated Th2 cell responses and decreased immunogenic maturation of lung dendritic cells in WT mice. However, these changes were absent in CD1d ؊/؊ mice immunized and challenged with ovalbumin or house dust mites, indicating that the effects of ␣-GalCer on Treg cells mainly require iNKT cells. Moreover, functional inactivation of Treg cells could reverse the inhibitory ability of this ␣-GalCer therapy on Th2 cell responses in a murine asthma model. Our findings indicate that intraperitoneal administration of ␣-GalCer before the development of asthma symptoms induces the generation of lung Treg cells via iNKT cells and may provide a potential therapeutic strategy to prevent allergic asthma.

Our previous study showed that intraperitoneal injection of α‐galactosylceramide (α‐GalCer) has the ability to activate lung iNKT cells, but α‐GalCer‐activated iNKT cells do not result in airway inflammation in wild‐type (WT) mice. Many studies showed that iNKT cells had the capacity to induce Treg cells, which gave rise to peripheral tolerance. Therefore, we examined the influence of intraperitoneal administration of α‐GalCer on the expansion and suppressive activity of lung Treg cells using iNKT cell‐knockout mice and co‐culture experiments in vitro. We also compared airway inflammation and airway hyperresponsiveness (AHR) after α‐GalCer administration in specific anti‐CD25 mAb‐treated mice. Our data showed that intraperitoneal injection of α‐GalCer could promote the expansion of lung Treg cells in WT mice, but not in iNKT cell‐knockout mice. However, α‐GalCer administration could not boost suppressive activity of Treg cells in WT mice and iNKT cell‐knockout mice. Interestingly, functional inactivation of Treg cells could induce airway inflammation and AHR in WT mice treated with α‐GalCer. Furthermore, α‐GalCer administration could enhance iNKT cells to secrete IL‐2, and neutralization of IL‐2 reduced the expansion of Treg cells in vivo and in vitro. Thus, intraperitoneal administration of α‐GalCer can induce the generation of lung Treg cells in mice through the release of IL‐2 by the activated iNKT cells.

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IntroductionAcute exacerbation of COPD (AECOPD) and left heart failure (LHF) commonly exist together in clinical practice. However, the identification of AECOPD concurrent with LHF is currently challenging. Our study aimed to investigate the role of plasma N-terminal brain natriuretic pro-peptide (NT-proBNP) in diagnosing elderly patients with AECOPD associated with LHF.Methods and resultsLHF was diagnosed in patients with AECOPD according to echocardiographic criteria, and the levels of NT-proBNP in plasma were measured by quantitative electrochemiluminescence assay. Among the 655 patients with AECOPD, 158 (24.1%) had comorbid LHF, whether systolic (n=108, 68.4%) or diastolic (n=50, 31.6%). The plasma concentrations of NT-proBNP in elderly patients with AECOPD associated with LHF were markedly elevated, compared with those with only AECOPD (4,542.5 and 763.0 ng/L, respectively, P<0.01). The receiver operating characteristic curve indicated a diagnostic cutoff value of 1,677.5 ng/L of NT-proBNP in plasma for ascertaining the presence of LHF in AECOPD, with a sensitivity of 87.9%, a specificity of 88.5%, and an accuracy of 88.4%.ConclusionThe plasma level of NT-proBNP may be a useful indicator in diagnosing AECOPD associated with LHF.

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