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1  both distal air and vascular tubulogenesis (alveolarization).
2 ults in decreased inflammation and increased alveolarization.
3  no inflammatory response and undergo normal alveolarization.
4 ion, IL1beta and inflammation, and decreased alveolarization.
5 kely explanation for our finding is catch-up alveolarization.
6 gainst a model of lung expansion with no new alveolarization.
7 mice inhibits production of MMP14, impairing alveolarization.
8  ventricular hypertrophy, and decreased lung alveolarization.
9 lation-fixed for histopathologic analyses of alveolarization.
10 ronic lung disease characterized by arrested alveolarization.
11 cluding interstitial fibrosis and diminished alveolarization.
12 in antibodies reduce lung injury and promote alveolarization.
13 interstitial fibrosis but reduced defects in alveolarization.
14 st of lung development and interference with alveolarization.
15 a critical and dual role in angiogenesis and alveolarization.
16 asia, a disease characterized by compromised alveolarization.
17 helial-derived NO in the enhancement of lung alveolarization.
18 ions, causing vascular defects and impairing alveolarization.
19 tal areas, likely due to disrupted secondary alveolarization.
20 ice decreased neonatal lung angiogenesis and alveolarization.
21 nesis and corresponding decreases in primary alveolarization.
22 with time-dependent, progressive decrease in alveolarization.
23 at ASLD is a model to study NO-mediated lung alveolarization.
24  implicating NO plays a pivotal role in lung alveolarization.
25 f Asl (AslNeo/Neo) results in decreased lung alveolarization, accompanied with reduced level of S-nit
26 lecular defects were associated with blocked alveolarization and airway collapse in the lung.
27 hyperoxia-induced lung injury, with improved alveolarization and alveolar integrity compared with wil
28        Increased expression of TTF-1 altered alveolarization and caused chronic pulmonary inflammatio
29                 Lung inflammation interrupts alveolarization and causes bronchopulmonary dysplasia (B
30 SDF-1/CXCR4 axis significantly improved lung alveolarization and decreased pulmonary hypertension, ri
31 ing lung to profile mesenchymal cells during alveolarization and in the context of lung injury.
32 smooth muscle cells/myofibroblasts, impaired alveolarization and maturation defects of the microvascu
33                        FOXA2 is required for alveolarization and regulates airway epithelial cell dif
34 hyperoxia injury contributes to the impaired alveolarization and septal thickening observed in BPD.
35                Hyperoxia disrupted pulmonary alveolarization and vascularization at PND 21; however,
36                                    Pulmonary alveolarization and vascularization were analyzed at pos
37                                   Defects in alveolarization and vasculogenesis were observed in subs
38 olescent exposure (with impacts on secondary alveolarization), and iii) cumulative exposure across bo
39 unctions in mid-pulmonary patterning (during alveolarization), and is distinct from the Wnt canonical
40 everal time points to quantify inflammation, alveolarization, and vascularization.
41                     In particular, defective alveolarization appears to be a common and potentially a
42 rin Cre; Aslflox/flox) exhibit impaired lung alveolarization at 12 weeks old, supporting an essential
43 ological abnormalities: e.g., disrupted lung alveolarization, atrophy of intestinal villus and colon-
44 sed, and tissues were harvested to determine alveolarization by radial alveolar counts, pulmonary ves
45 reased lung volume, total lung capacity, and alveolarization compared to wild type controls following
46 2 in mouse leads to defective postnatal lung alveolarization, contributing to postnatal lethality.
47 die in respiratory distress, with diminished alveolarization, decreased Shh, Fgf9, Fgf10, and Bmp4 mR
48 es demonstrate that premature birth disrupts alveolarization, decreasing the gas exchange surface are
49 istent with this, Cic deficiency causes lung alveolarization defect.
50 lial cell adhesion and migration, as well as alveolarization defects and persistent macrophage-mediat
51 es using liposomal clodronate, we found that alveolarization defects were secondary to persistent alv
52 mpletion of airway branching, we showed that alveolarization defects, characterized by disrupted seco
53 ce have hydrocephalus, omphalocele, and lung alveolarization defects.
54                                       If new alveolarization does not occur, alveolar size should inc
55 M1 or FOXF1 stimulates lung angiogenesis and alveolarization during recovery from neonatal hyperoxic
56  regulate mesenchymal development as well as alveolarization during the saccular phase of lung morpho
57 proliferation and differentiation as well as alveolarization during the saccular stage of lung develo
58 number of alveoli, but rather from increased alveolarization early in life.
59 nt at birth with increasing diversity during alveolarization even while expressing a distinct transcr
60 In the PCLS model, Wnt5A inhibition improved alveolarization following hyperoxia exposure, and treatm
61 estational exposure (with impacts on primary alveolarization), ii) peri-adolescent exposure (with imp
62 all three NOS isoforms display impaired lung alveolarization, implicating NO plays a pivotal role in
63  to stimulate neonatal lung angiogenesis and alveolarization in ACDMPV mice.Conclusions: Cell-based t
64 ent with BMP9 restored lung angiogenesis and alveolarization in ACVRL1-deficient and Foxf1(WT/S52F) m
65                       Here, we assessed lung alveolarization in ASL-deficient mice.
66 stores total S-nitrosylation as well as lung alveolarization in AslNeo/Neo mice.
67  supplementation could partially rescue lung alveolarization in AslNeo/Neo mice.
68                  Second, bombesin diminished alveolarization in C57BL/6 (but not Swiss-Webster) mice.
69 d in lung development along with an impaired alveolarization in female prenatally stressed mice.
70 in vivo mouse hyperoxia model, with improved alveolarization in the PCLS model.Conclusions: Increased
71 ctomy (PNX) model that promotes regenerative alveolarization in the remaining intact lung.
72  The current hypothesis that human pulmonary alveolarization is complete by 3 years is contradicted b
73 nsgene in the postnatal period did not alter alveolarization, lung size, or histology.
74    However, there is new evidence that human alveolarization might continue throughout childhood and
75  novel research aimed at promoting postnatal alveolarization offers a unique opportunity to develop e
76    These findings correlated with changes in alveolarization on morphometric analysis.
77 fically corresponds to the primary septation/alveolarization phase of lung development.
78 tration promoted branching morphogenesis and alveolarization, rescued tissue homeostasis, and stimula
79 veloping lung during the period of postnatal alveolarization, resulting in markedly enlarged parenchy
80 GRP, but only part of the bombesin effect on alveolarization, suggesting that novel receptors may med
81 microvasculature through angiogenesis drives alveolarization, the final stage of lung development tha
82  demonstrate that a significant component of alveolarization, the final stage of lung development, oc
83  EPCs promote neonatal lung angiogenesis and alveolarization through FOXF1-mediated activation of BMP
84 y 3 years is contradicted by new evidence of alveolarization throughout adolescence in mammals.
85 vironmental exposures could adversely affect alveolarization throughout childhood.
86 quantification of lung inflammatory markers, alveolarization, vascularization, cell proliferation, an
87 in had multiple effects on Day 14 lung, when alveolarization was about half complete.
88 genesis early in lung development, postnatal alveolarization was not influenced by FGFR-HFc.
89 g morphology and physiology during postnatal alveolarization were assessed in transgenic mice express
90 ung mechanics, engraftment, lung growth, and alveolarization were evaluated 8 weeks after transplanta
91  compliance, non-parenchymal lung volume and alveolarization, were increased in both AAD and Control
92  when expressed from E16.5 but did not alter alveolarization when expressed after birth.
93 reased lung volume, total lung capacity, and alveolarization, while VEGF120 did not.