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1 syndrome caused by prematurity of the type I pneumocyte.
2  under the control of doxycycline in type II pneumocytes.
3 l epithelium and appears in type II alveolar pneumocytes.
4 seen associated with the mycobacteria on the pneumocytes.
5 ocytes (19%) but not in endothelial cells or pneumocytes.
6 t in both rat lung and isolated rat granular pneumocytes.
7 en conidia and A549 cells, a line of type II pneumocytes.
8 rus replication occurring mainly in alveolar pneumocytes.
9  and is associated with apoptosis of type II pneumocytes.
10  factor (KGF) is a growth factor for type II pneumocytes.
11 thelial cells expressing markers of alveolar pneumocytes.
12 ells) and predominantly localized in type II pneumocytes.
13 tiation to alveolar type I- and type II-like pneumocytes.
14  ESAT6 causes cytolysis of type 1 and type 2 pneumocytes.
15 ng cells, middle ear cells, and A549 type II pneumocytes.
16 ific gene expression by fusing with diseased pneumocytes.
17 s, and accounted for 0% to 0.553% of type II pneumocytes.
18 evaluate for Y-chromosome-containing type II pneumocytes.
19 ferentiated, with some maturation of type II pneumocytes.
20 ure, bronchial epithelial cells, and type II pneumocytes.
21  is expressed in bronchial cells and type II pneumocytes.
22 on, did we detect any engraftment as type II pneumocytes.
23 C lines, as compared to normal human type-II pneumocytes.
24    Marked apoptosis of CD68-negative type II pneumocytes (30 to 80%) was detected in four of the seve
25 eltaRD1 mutants failed to cause cytolysis of pneumocytes, a phenotype that had been previously used t
26 l incorporates human lung epithelial type II pneumocyte (A549) (upper chamber) and endothelial cell (
27                     Following germination of pneumocyte-adherent conidia for 12 h, direct penetration
28  growth mechanics of fetal lungs and type II pneumocytes after tracheal ligation (TL).
29 ral RNA was detected in approximately 20% of pneumocytes and alveolar endothelial cells as determined
30 ining Langerhans' cells, hyperplastic type 2 pneumocytes and alveolar macrophages within and surround
31 munohistology revealed abundant PVM-positive pneumocytes and bronchial and bronchiolar epithelial cel
32 ly active in cell lines derived from type II pneumocytes and Clara cells (MLE-15 and mtCC1-2 mouse ce
33 ung cancer of sheep that arises from type II pneumocytes and Clara cells of the lung epithelium.
34 ng cancer of sheep, originating from type II pneumocytes and Clara cells.
35 y, mice without lung Klf2 lack mature type I pneumocytes and die shortly after birth, closely recapit
36 ry for cytokeratin and surfactant identified pneumocytes and epithelial syncytial cells as important
37               CXCR3 was expressed by type II pneumocytes and fibroblasts in fibrotic areas in close p
38 ive lipid deposition in both macrophages and pneumocytes and increased levels of surfactant.
39 mice, S. aureus alpha-toxin directly injures pneumocytes and increases mortality, whereas alpha-toxin
40     BAX expression was markedly increased in pneumocytes and interstitial cells in DAD compared with
41 in determining the susceptibility of type II pneumocytes and interstitial cells to apoptosis.
42        The percentage of positively staining pneumocytes and interstitial cells was estimated in each
43 NA-78 demonstrated that hyperplastic Type II pneumocytes and macrophages were the predominant cellula
44 used loss of the cytolytic phenotype in both pneumocytes and macrophages.
45 ective localization of the viral RNA in many pneumocytes and pulmonary endothelial cells using a high
46                               Virus-positive pneumocytes and renal tubular epithelial cells also were
47 ptidase 4 showed colocalization in scattered pneumocytes and syncytial cells.
48 fficient infection of human alveolar type II pneumocytes and thus more-severe lung damage.
49 apacity to productively replicate in type II pneumocytes and to cope with the induced cytokine respon
50 lity of self-renewal and differentiated into pneumocytes and tracheal epithelial cells.
51 mbers of bacteria attached to and within the pneumocytes and we determined by viable-cell counting th
52 asolateral laminin-expressing surface of the pneumocytes, and damage the cells and the basement membr
53 f CYP1A1 in airway epithelial cells, type II pneumocytes, and endothelial cells.
54 were defective for adherence to macrophages, pneumocytes, and hepatocytes.
55 irway smooth muscle cells, cardiac myocytes, pneumocytes, and infiltrated inflammatory cells, but was
56  mycobacterial DNA was found in endothelium, pneumocytes, and macrophages from the lung and in Bowman
57 us antigen was observed in airway epithelia, pneumocytes, and macrophages.
58                                      Type II pneumocyte apoptosis was confirmed by electron microscop
59 ift in polyamine metabolism may occur as new pneumocytes are produced.
60 nd life-threatening respiratory illness with pneumocytes as its main target.
61 ruginosa invasion of rat primary type I-like pneumocytes as well as a murine lung epithelial cell lin
62 edigrees differentiate to type I and type II pneumocytes as well as bronchiolar secretory cells follo
63 munoreactivity was present in normal type II pneumocytes as well as in a range of atypical lesions de
64 ean 0.95+/-1.18 Sp-C+ cells per 1000 type II pneumocytes by confocal microscopy).
65 binding of ESAT6 to laminin and the lysis of pneumocytes by free and bacterium-associated ESAT6 toget
66  to infected alveolar macrophages and type-1 pneumocytes by immunohistochemistry.
67  to monitor gene expression in the A549 lung pneumocyte cell line during exposure to P. aeruginosa.
68 UC1 is a powerful new marker for the type II pneumocyte cell lineage that allows us to follow the typ
69 ation of M. tuberculosis with human alveolar pneumocyte cells (2%) was less than that observed with f
70 erculosis replicated in association with the pneumocyte cells by more than 55-fold by day 7 postinfec
71 cytosed and degraded by cultured pre-type II pneumocyte cells, and both processes could be blocked by
72 , which are expressed exclusively in type II pneumocytes, cells that proliferate in ventilator associ
73 an and bovine lung tissue containing primary pneumocytes could be used as a more accurate and relevan
74              CXCL12 was expressed in type II pneumocytes covering LAM nodules and caused AML cell gro
75 ining differentiation of human fetal type II pneumocyte culture.
76 othelial cells, and primary alveolar type II pneumocytes, demonstrating a much broader tissue tropism
77 mediated PCR was performed in murine type II pneumocyte-derived MLE-15 cells infected with a chimeric
78 in mid-gestation HFL explants during type II pneumocyte differentiation in culture, we performed miRN
79      We show that TR and SMRT control type I pneumocyte differentiation through Klf2, which, in turn,
80 ved in lung development, specifically type I pneumocyte differentiation, and suggest a possible new t
81 ow significant distal airspace formation and pneumocyte differentiation.
82                       Cells expressing ET-1 (pneumocytes, endothelial cells, airway epithelial cells,
83 These model systems include a human alveolar pneumocyte epithelial cell line, a murine macrophage cel
84                                Both types of pneumocytes express membrane laminin, and ESAT6 exhibits
85 migatus conidia may be binding of conidia to pneumocytes, followed by hyphal penetration of the epith
86 GSH) is essential for adequate protection of pneumocytes from potential toxicity mediated by extracel
87  turn, seems to directly activate the type I pneumocyte gene program.
88 ssion of neuroendocrine genes and of type II pneumocyte genes, respectively.
89 fluent monolayers of alveolar type II (ATII) pneumocytes has been decreased by NO.
90                         Apoptosis of type II pneumocytes has been identified in diffuse alveolar dama
91                     Proliferation of type II pneumocytes has been linked to a repair process during t
92 myomatosis (LAM) and multifocal micronodular pneumocyte hyperplasia (MMPH) produce cystic and nodular
93       Histopathology showed abundant type II pneumocyte hyperplasia in the lungs of animals pretreate
94           KGF pretreatment and the resultant pneumocyte hyperplasia reduce fluid flux in models of lu
95 In conclusion, KGF, through type II alveolar pneumocyte hyperplasia with increased sodium-potassium-a
96                                      Type II pneumocyte hyperplasia, a common reaction to lung injury
97 his protection are likely related to type II pneumocyte hyperplasia, but remain to be specifically el
98 g growth factor that causes alveolar type II pneumocyte hyperplasia.
99 r septal thickening and intermittent type II pneumocyte hyperplasia.
100 iated with death on a ventilator and type II pneumocyte hyperplasia.
101                                              Pneumocyte II population kinetics were analyzed using a
102 ceptor inactivation also resulted in type II pneumocyte immaturity, which was apparent from their inc
103 istry studies localized MMP-1 to the Type II pneumocyte in patients with emphysema and not normal con
104 hat up-regulation of p53 and WAF1 in type II pneumocytes in DAD is associated with underlying DNA dam
105 ruses preferentially infect alveolar type II pneumocytes in human lung.
106 al pulmonary surfactant production by type 2 pneumocytes in lung.
107 l types, including distal type I and type II pneumocytes in the late term.
108     The authors investigated whether type II pneumocytes in the lungs of cross-gender lung transplant
109 ation of lipid-laden macrophages and type II pneumocytes in the lungs.
110 idence suggesting the involvement of type II pneumocytes in the replication of PRRSV.
111 role of the epithelium, particularly type II pneumocytes, in the initiation and perpetuation of fibro
112 lar bacterial CFU obtained from the infected pneumocytes increased by fourfold by day 7 after the add
113  lung injury, extensive apoptosis of type II pneumocytes is largely responsible for the disappearance
114  was observed in endothelial cells, alveolar pneumocytes, kidney glomeruli, mammary myoepithelial cel
115 lineage that allows us to follow the type II pneumocyte lineage during the process of lung carcinogen
116 s for the peripheral lung, i.e., the type II pneumocyte lineage markers MUC1 and surfactant protein-A
117 ic interstitial pneumonia, only rare type II pneumocytes (< 5%) exhibited apoptosis, and they showed
118 alized in ciliated cells, endothelial cells, pneumocytes, macrophages, and smooth muscle cells; fibro
119  of bone marrow cells can express the type I pneumocyte markers, T1alpha and aquaporin-5.
120 pithelial cells expressed type I and type II pneumocyte markers.
121 ression of these marker genes during type II pneumocyte maturation.
122 gand have long been known to promote type II pneumocyte maturation; prenatal administration of glucoc
123 in Mycobacterium tuberculosis replicating in pneumocytes may utilize surface ESAT6 to anchor onto the
124    We conclude that proliferation of type II pneumocytes occurs during the early phase of acute lung
125                        The number of type II pneumocytes of male karyotype showed a statistically sig
126 phological and molecular phenotype of type I pneumocytes of the alveolar epithelium.
127  TGF-beta1 within either hyperplastic type 2 pneumocytes or alveolar macrophages.
128                   SPARKY exhibited a Type II pneumocyte phenotype characterized by surfactant and thy
129   In chronic interstitial pneumonia, type II pneumocytes proliferate continuously, although to a much
130  has been shown to play an important role in pneumocyte proliferation and lung development.
131 ng a protective role for KGF-induced type II pneumocyte proliferation in lung injury.
132 se cells contribute minimally to the type II pneumocyte proliferation that is often present in these
133  enhanced bronchiolar epithelial and type II pneumocyte proliferation.
134 nute discrete foci of cytologically atypical pneumocyte proliferations designated as atypical adenoma
135 , BAX was identified on an average of 10% of pneumocytes (range 0 to 20%) but not in interstitial cel
136  identified on an average of 80% of alveolar pneumocytes (range 30 to 100%) and 70% of interstitial c
137  transplant recipients develop low levels of pneumocyte repopulation by bone marrow-derived stem cell
138                                      Type II pneumocytes respond to influenza A infection by activati
139     The decreased number of type II alveolar pneumocytes results in absent or reduced surfactant prod
140 s altered in emphysema such that the Type II pneumocyte secretes MMP-1 and suggests that MMP-1 may be
141 the setting of post-transplant inflammation, pneumocyte-specific reprogramming of transplanted BMDCs
142 n of a proteolytic enzyme within the Type II pneumocyte suggests that the cells within the lung itsel
143 Gene expression analysis of isolated type II pneumocytes suggests potential explanations for the obse
144 nally, differentiated type II but not type I pneumocytes supported the replication of influenza virus
145 ble conidia subsequently became clustered on pneumocyte surfaces.
146 g carcinoma (BAC), a neoplasm of the Type II pneumocyte that affects humans, sheep, and small animals
147 imilar reduction in DNMT activity in type II pneumocytes that give rise to the tumors.
148  pathway controlling the formation of type I pneumocytes, the cells that mediate gas exchange, is poo
149 esat6 transcripts in bacteria replicating in pneumocytes, the specific association of ESAT6 with the
150     Notably, the H5N1 virus targeted type II pneumocytes throughout the 7-day infection, and induced
151        Because this time frame is similar to pneumocyte turnover time, the shift in polyamine metabol
152 s and KS tumor cells, as well as epithelioid pneumocytes (two of two).
153 eural cellular accumulation, macrophage, and pneumocyte type 2 hypertrophy, massive lipid deposition
154 We found that it was the macrophage, and not pneumocyte type II cells or other nonhematopoietic cells
155        Studies with A-549 cells, a model for pneumocytes type 2, demonstrate that overexpression of A
156 or the L858R mutant (EGFR(L858R)) in type II pneumocytes under the control of doxycycline.
157  we showed that P. aeruginosa invades type I pneumocytes via a lipid raft-mediated mechanism.
158 ase of acute lung injury, PCNA positivity in pneumocytes was extremely rare.
159 a marker of terminally differentiated type I pneumocytes, was also induced.
160 ear epithelial cells (HMEE), as well as A549 pneumocytes, was measured.
161              Y-chromosome-containing type II pneumocytes were found in 9 of 25 biopsy specimens from
162                                  Rat type II pneumocytes were incubated with [3H]choline, purified gp
163                  Alveolar epithelial type II pneumocytes were isolated and purified from adult rat lu
164 way epithelium, and only occasional alveolar pneumocytes were labeled.
165 al proliferative lesions of alveolar type II pneumocytes were observed as early as seven days after i
166 acute/proliferative phase, apoptotic type II pneumocytes were rare whereas PCNA expression was quite
167 r lining cells, including type I and type II pneumocytes, were the primary infected cells.
168 y concentrated at the basolateral surface of pneumocytes where they rest on the basement membrane, wh
169 helium, airway submucosal glands, and type 1 pneumocytes, where it can participate in respiratory tra
170 fic proteins synthesized in alveolar type II pneumocytes, where it is assembled and stored intracellu
171 uman lung tissue, including alveolar type II pneumocytes, which express avian-type receptors.
172 calization of LCAD to human alveolar type II pneumocytes, which synthesize and secrete pulmonary surf
173  were detected almost exclusively in type II pneumocytes, with a minor involvement of alveolar macrop

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