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1 otal roles in the adsorption and function of pulmonary surfactant.
2 cal properties and physiological function of pulmonary surfactant.
3 line (DPPC), the most prevalent component of pulmonary surfactant.
4 (AP) were originally isolated from an ovine pulmonary surfactant.
5 cal properties and physiological function of pulmonary surfactant.
6 crucial role in the effective functioning of pulmonary surfactant.
7 including blood serum, nasal secretions, and pulmonary surfactant.
8 II pneumocytes, which synthesize and secrete pulmonary surfactant.
9 ycerols, which are major lipid components of pulmonary surfactant.
10 ls and Clara cells, the primary producers of pulmonary surfactant.
11 BCA3 may play a similar role in transporting pulmonary surfactant.
12 pids, and proteins, a composition similar to pulmonary surfactants.
13 dones (PVPs) of various molecular weights to pulmonary surfactants.
14 vely in the respiratory epithelium including pulmonary surfactant A, B, C and Clara cell secretory pr
15 e, it likely reacts with target molecules in pulmonary surfactant, a lipid-rich material that lines t
17 key regulator of neonatal lung inflation is pulmonary surfactant, a lipoprotein complex which increa
18 n A (SP-A) is the major protein component of pulmonary surfactant, a material secreted by the alveola
19 alveolar patency at end expiration requires pulmonary surfactant, a mixture of phospholipids and pro
22 Long-chain acylcarnitines co-localize with pulmonary surfactant, a unique film of phospholipids and
23 cterized by myeloid dysfunction resulting in pulmonary surfactant accumulation and respiratory failur
24 hances the molecular-level interpretation of pulmonary surfactant action and facilitates the developm
25 estigate the mechanisms by which vesicles of pulmonary surfactant adsorb to an air-liquid interface,
29 ein B (SP-B) is essential to the function of pulmonary surfactant and to alveolar type 2 cell phenoty
30 ein B (SP-B) is essential to the function of pulmonary surfactant and to lamellar body genesis in alv
31 oline (DPPC), the most abundant component of pulmonary surfactant, and higher and less variable with
32 tidylinositol, which are minor components of pulmonary surfactant, and synthetic dimyristoylphosphati
33 ely the surface tension-lowering activity of pulmonary surfactants, and this effect may be important
34 directly inhibits the surface adsorption of pulmonary surfactant as well as its ability to reduce su
35 ed mice: fatty acid synthase, transketolase, pulmonary surfactant-associated protein C (SP-C), L-plas
36 (SP-A), one of four proteins associated with pulmonary surfactant, binds with high affinity to alveol
37 t proteins and lipids that together form the pulmonary surfactant complex necessary for lung function
46 lecular dynamics simulation to study a model pulmonary surfactant film interacting with a carbonaceou
47 the formation and biophysical properties of pulmonary surfactant films at the air-water interface.
49 icroscopy to test the classical model of how pulmonary surfactant forms films that are metastable at
50 our knowledge, the biophysical properties of pulmonary surfactant from individual humanized transgeni
52 participate in cholesterol mobilization and pulmonary surfactant homeostasis at the alveolar interfa
53 rminal differentiation and immune functions, pulmonary surfactant homeostasis, and lung host defense.
56 g, such as dipalmitoylphosphatidylcholine in pulmonary surfactant; however, many of the roles of spec
60 ovided fundamental insights into the role of pulmonary surfactant in the pathogenesis and treatment o
61 econium) that interfere with the activity of pulmonary surfactant in vitro may also be important in t
72 e most critical and abundant phospholipid in pulmonary surfactant is saturated phosphatidylcholine (S
75 epithelial cells that synthesize and secrete pulmonary surfactant lipids and proteins, reducing the c
78 iratory distress syndrome is associated with pulmonary surfactant loss that alters alveolar mechanics
79 bloodstream infections but is inactivated by pulmonary surfactant, making it of no use in the therapy
81 to tune ionic and lipidic flows through the pulmonary surfactant membrane network at the alveolar su
82 6 (Prdx6), a host factor that contributes to pulmonary surfactant metabolism and lung defense against
83 surfactant proteins affect the stability of pulmonary surfactant monolayers at an air/water interfac
84 shown previously that lateral compression of pulmonary surfactant monolayers initially induces separa
85 cture and dynamics of membrane arrays in the pulmonary surfactant network that covers the respiratory
86 methodology may guide further development of pulmonary surfactant pharmaceuticals that better mimic t
90 ly, several investigators have reported that pulmonary surfactant phospholipids and SP-A are present
91 Instead, one of the major and most important pulmonary surfactant phospholipids, dipalmitoylphosphati
92 arkers were all chlorohydrins of unsaturated pulmonary surfactant phospholipids; phosphatidylglycerol
93 ins (termed collectins) present in blood and pulmonary surfactant play a role in initial host defense
96 lar cells, there was no evidence of abnormal pulmonary surfactant production by type 2 pneumocytes in
97 surfactant requirement is met by the leptin pulmonary surfactant production pathway which normally a
101 We have also engineered MASP binding into a pulmonary surfactant protein (SP-A), which has the same
108 the collectin family of proteins, including pulmonary surfactant protein A (SP-A), we hypothesized t
110 otein C1q, mannose-binding lectin (MBL), and pulmonary surfactant protein A (SPA) are structurally si
113 e location and depth of each residue of lung pulmonary surfactant protein B (SP-B(1-25)) in a phospho
114 For identification of structural changes of pulmonary surfactant protein B (SP-B) due to the heterog
117 along with a peptide model for collagen and pulmonary surfactant protein C have been simulated very
118 human serum mannose-binding lectin (MBL) and pulmonary surfactant protein D (SP-D) have distinctive m
119 sed on our previous studies documenting that pulmonary surfactant protein D (SP-D) protects C. neofor
122 domains of a collagenous C-type lectin, rat pulmonary surfactant protein D (SP-D), are sufficient to
124 of viral infection, and, when combined with pulmonary surfactant protein D, their antiviral effects
126 been suggested to mimic some aspects of the pulmonary surfactant protein SP-B and has been tested cl
127 5), which is a truncated version of the full pulmonary surfactant protein SP-B, with dipalmitoylphosp
128 rfactant protein A (SP-A), the most abundant pulmonary surfactant protein, is implicated in multiple
132 We hypothesized that collectins, such as pulmonary surfactant proteins (SPs) SP-A and SP-D and se
134 the conformational organization of the lung pulmonary surfactant proteins in the environment that mi
135 n spectroscopy to in-situ IR spectroscopy of pulmonary surfactant proteins SP-B and SP-C in lipid-pro
137 nd ozone (O(3)) can cause dysfunction of the pulmonary surfactant (PS) layer in the human lung, resul
138 re syndrome characterized by accumulation of pulmonary surfactant, respiratory insufficiency, and inc
139 ptomycin was shown to interact in vitro with pulmonary surfactant, resulting in inhibition of antibac
143 l cells at E18.5, concomitant with decreased pulmonary surfactant, suggesting a delay or an arrest in
145 s, indicating IVI-induced aberrations of the pulmonary surfactant system might play an important role
147 t protein A (SP-A) is an abundant protein in pulmonary surfactant that has been shown to alter severa
148 cells lining the peripheral lung synthesize pulmonary surfactant that reduces surface tension at the
150 emature infants are known to be deficient in pulmonary surfactant, there is limited information regar
151 e conclude that the presence of SP-A1 allows pulmonary surfactant to adopt a particularly favorable s
152 ns SP-B and SP-C promote rapid adsorption of pulmonary surfactant to an air/water interface by an unk
155 lted in an inflammatory reaction that caused pulmonary surfactant to lose some of its ability to main
157 HA) on the structure and surface behavior of pulmonary surfactant to understand the mechanism for HA-
159 atidylcholine (DPPC), the major component of pulmonary surfactant, was investigated as a function of
160 ich has been shown to degrade and inactivate pulmonary surfactant, was significantly increased in LCA
161 lateral phase separation occurs in films of pulmonary surfactant, we used epifluorescence microscopy
163 peptide (AP) originally isolated from ovine pulmonary surfactant, were prepared and used to assess t
165 understanding the structure and function of pulmonary surfactant, which has informed understanding o
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