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1               SCLC is thought to derive from pulmonary neuroendocrine cells.
2 erentiation but had no effect on ciliated or pulmonary neuroendocrine cells.
3 sal cells, and activated UCHL1, a marker for pulmonary neuroendocrine cells.
4 olar septation and altered morphology of the pulmonary neuroendocrine cells.
5 elated peptide in embryonic and adult murine pulmonary neuroendocrine cells.
6 sruption of the ASH1 gene have no detectable pulmonary neuroendocrine cells.
7 s consistent with autonomic and C fibers and pulmonary neuroendocrine cells.
8 om basal cells, giving rise predominantly to pulmonary neuroendocrine cells and a subset of multicili
9 ved with a lower incidence of hyperplasia of pulmonary neuroendocrine cells and aggressive liver, bil
10 like cells are the likely progenitor of both pulmonary neuroendocrine cells and CFTR-rich ionocytes.
11                                              Pulmonary neuroendocrine cells and clusters of these cel
12  is critically required for the formation of pulmonary neuroendocrine cells and is a marker for human
13 atlas improves the description of ionocytes, pulmonary neuroendocrine cells, and brush cells and iden
14 itrosamine-treated hamsters also demonstrate pulmonary neuroendocrine cell apoptosis in situ during t
15 H1) is selectively expressed in normal fetal pulmonary neuroendocrine cells, as well as in the divers
16                                    Increased pulmonary neuroendocrine cells containing bombesin-like
17                         Increased numbers of pulmonary neuroendocrine cells containing bombesin-like
18 rucial role in hematopoietic, inner ear, and pulmonary neuroendocrine cell development and governs ce
19 ises a condition known as diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) as a
20                                    Transient pulmonary neuroendocrine cell hyperplasia and non-neuroe
21 nomatous hyperplasia, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia.
22 8(+) macrophages 4 weeks after radiation and pulmonary neuroendocrine cells hyperplasia 6 weeks after
23            Idiopathic diffuse hyperplasia of pulmonary neuroendocrine cells (IDHPNC) is a clinicopath
24 in-releasing peptide (GRP) is synthesized by pulmonary neuroendocrine cells in inflammatory lung dise
25 lial bodies but a reduced number of solitary pulmonary neuroendocrine cells in the neonatal lung.
26 tion in GFI1 display abnormal development of pulmonary neuroendocrine cells, indicating that GFI1 is
27 on factor required for proper development of pulmonary neuroendocrine cells, is essential for the sur
28      Clara cells, together with ciliated and pulmonary neuroendocrine cells, make up the epithelium o
29 Gastrin-releasing peptide (GRP), secreted by pulmonary neuroendocrine cells, mediates oxidant-induced
30 ntiation in many organs, but its function in pulmonary neuroendocrine cell (PNEC) differentiation has
31  We initiated a transgenic model for primary pulmonary neuroendocrine cell (PNEC) hyperplasia/neoplas
32                                              Pulmonary neuroendocrine cells (PNEC) are rare airway ep
33 ype II cells, free alveolar macrophages, and pulmonary neuroendocrine cells (PNEC).
34 r the distribution and abundance of solitary pulmonary neuroendocrine cells (PNECs) and neuroepitheli
35                                              Pulmonary neuroendocrine cells (PNECs) are proposed to b
36                                              Pulmonary neuroendocrine cells (PNECs) are rare airway c
37                                              Pulmonary neuroendocrine cells (PNECs) are rare airway e
38                                              Pulmonary neuroendocrine cells (PNECs) are sensory epith
39                                              Pulmonary neuroendocrine cells (PNECs) are the only inne
40 lls (hESCs) that were differentiated to form pulmonary neuroendocrine cells (PNECs), a putative cell
41 about receptor (Robo) genes are expressed in pulmonary neuroendocrine cells (PNECs), a rare, innervat
42  infancy, a pediatric disease with increased pulmonary neuroendocrine cells (PNECs), excess PNEC-deri
43 s up to 10% of lung progenitor cells to form pulmonary neuroendocrine cells (PNECs), putative precurs
44 y reflexes - carotid body glomus cells, and 'pulmonary neuroendocrine cells' (PNECs) - are obscure.
45                       Lesions resulting from pulmonary neuroendocrine cell proliferation range from b
46 ion requires augmented neural stimulation of pulmonary neuroendocrine cell secretion.
47                                              Pulmonary neuroendocrine cells, which constitute a small