ライフサイエンスコーパス: pulmonary surfactant

1 BCA3 may play a similar role in transporting pulmonary surfactant.

2 otal roles in the adsorption and function of pulmonary surfactant.

3 cal properties and physiological function of pulmonary surfactant.

4 line (DPPC), the most prevalent component of pulmonary surfactant.

5 including blood serum, nasal secretions, and pulmonary surfactant.

6 (AP) were originally isolated from an ovine pulmonary surfactant.

7 ycerols, which are major lipid components of pulmonary surfactant.

8 cal properties and physiological function of pulmonary surfactant.

9 crucial role in the effective functioning of pulmonary surfactant.

10 health by acting as stem cells and producing pulmonary surfactant.

11 eration of foamy AMs and the accumulation of pulmonary surfactant.

12 erosols on the biophysical properties of the pulmonary surfactant.

13 esponse to oxidative stress, and the loss of pulmonary surfactant.

14 arette aerosols on an animal-derived natural pulmonary surfactant.

15 II pneumocytes, which synthesize and secrete pulmonary surfactant.

16 ls and Clara cells, the primary producers of pulmonary surfactant.

17 pids, and proteins, a composition similar to pulmonary surfactants.

18 dones (PVPs) of various molecular weights to pulmonary surfactants.

19 filters due to the solubilization effect of pulmonary surfactants.

20 vely in the respiratory epithelium including pulmonary surfactant A, B, C and Clara cell secretory pr

21 e, it likely reacts with target molecules in pulmonary surfactant, a lipid-rich material that lines t

22 Pulmonary surfactant, a lipid/protein complex that lines

23 key regulator of neonatal lung inflation is pulmonary surfactant, a lipoprotein complex which increa

24 n A (SP-A) is the major protein component of pulmonary surfactant, a material secreted by the alveola

25 alveolar patency at end expiration requires pulmonary surfactant, a mixture of phospholipids and pro

26 Breathing depends on pulmonary surfactant, a mixture of phospholipids and pro

27 Pulmonary surfactant, a mixture of proteins and phosphol

28 Pulmonary surfactant, a thin lipid/protein film lining m

29 Long-chain acylcarnitines co-localize with pulmonary surfactant, a unique film of phospholipids and

30 cterized by myeloid dysfunction resulting in pulmonary surfactant accumulation and respiratory failur

31 erized by myeloid cell dysfunction, abnormal pulmonary surfactant accumulation, and innate immune def

32 hances the molecular-level interpretation of pulmonary surfactant action and facilitates the developm

33 estigate the mechanisms by which vesicles of pulmonary surfactant adsorb to an air-liquid interface,

34 To determine how different constituents of pulmonary surfactant affect its phase behavior, we measu

35 s a receptor to mediate bacterial binding to pulmonary surfactant and alveolar epithelial cells.

36 s impose new challenges such as crossing the pulmonary surfactant and evading mucus entrapment.

37 Pulmonary surfactant and its components are essential fo

38 helial cells through which the cell packages pulmonary surfactant and regulates its secretion.

39 ein B (SP-B) is essential to the function of pulmonary surfactant and to alveolar type 2 cell phenoty

40 ein B (SP-B) is essential to the function of pulmonary surfactant and to lamellar body genesis in alv

41 oline (DPPC), the most abundant component of pulmonary surfactant, and higher and less variable with

42 tidylinositol, which are minor components of pulmonary surfactant, and synthetic dimyristoylphosphati

43 ely the surface tension-lowering activity of pulmonary surfactants, and this effect may be important

44 se phospholipid polar heads abundant in host pulmonary surfactant as an alternative phosphate source.

45 directly inhibits the surface adsorption of pulmonary surfactant as well as its ability to reduce su

46 ed mice: fatty acid synthase, transketolase, pulmonary surfactant-associated protein C (SP-C), L-plas

47 , growth differentiation factor-15 (GDF-15), pulmonary surfactant-associated protein D (PSP-D) and Sp

48 arison of Q1 and Q4 of PVR identified PSP-D (pulmonary surfactant-associated protein D) as a marker o

49 ul platform capable of penetrating mucus and pulmonary surfactant barriers, enhancing lung distributi

50 (SP-A), one of four proteins associated with pulmonary surfactant, binds with high affinity to alveol

51 f hydrophobic vaping liquid chemicals on the pulmonary surfactant biophysical function.

52 for proper lung function due to its role in pulmonary surfactant biosynthesis.

53 t proteins and lipids that together form the pulmonary surfactant complex necessary for lung function

54 o minor anionic phospholipids present in the pulmonary surfactant complex, palmitoyl-oleoyl-phosphati

55 the exact mode of interaction between model pulmonary surfactant components.

56 We observed that pulmonary surfactant containing SP-A1 reaches lower surf

57 Pulmonary surfactant contains homeostatic and antimicrob

58 Lipid-protein complexes are the basis of pulmonary surfactants covering the respiratory surface a

59 (COL5A2, COL6A3, and COL12A1), synthesis of pulmonary surfactant (CTSH, LPCAT1, and NAPSA), ribosoma

60 Pulmonary surfactant deposited in vitro on liquid layers

61 If pulmonary surfactant develops a dysfunction, its ability

62 lar epithelium, leads to alveolar oedema and pulmonary surfactant dysfunction.

63 es in lung mechanics were found to be due to pulmonary surfactant dysfunction.

64 Pulmonary surfactant enters the interface by a process a

65 Notably, pulmonary surfactant failed to reduce surface tension af

66 lecular dynamics simulation to study a model pulmonary surfactant film interacting with a carbonaceou

67 the formation and biophysical properties of pulmonary surfactant films at the air-water interface.

68 Pulmonary surfactant forms a lipid-rich monolayer that c

69 icroscopy to test the classical model of how pulmonary surfactant forms films that are metastable at

70 our knowledge, the biophysical properties of pulmonary surfactant from individual humanized transgeni

71 We conclude that SP-A protects pulmonary surfactant from inhibition by fibrinogen in vi

72 participate in cholesterol mobilization and pulmonary surfactant homeostasis at the alveolar interfa

73 s and IL-1a contribute to the maintenance of pulmonary surfactant homeostasis is not well understood.

74 d deleterious inflammation, AM also maintain pulmonary surfactant homeostasis, a vital lung function

75 rminal differentiation and immune functions, pulmonary surfactant homeostasis, and lung host defense.

76 hey play very important roles in maintaining pulmonary surfactant homeostasis.

77 investigating whether LPCAT1 is required for pulmonary surfactant homeostasis.

78 g, such as dipalmitoylphosphatidylcholine in pulmonary surfactant; however, many of the roles of spec

79 e of IgA autoantibodies and their effects on pulmonary surfactant in COVID-19 using the following met

80 nimal models and to probe the direct role of pulmonary surfactant in early infection.

81 factor in the disruption of the structure of pulmonary surfactant in neonates of ICP.

82 Films of pulmonary surfactant in the lung are metastable at surfa

83 Dysfunction of pulmonary surfactant in the lungs is associated with res

84 ovided fundamental insights into the role of pulmonary surfactant in the pathogenesis and treatment o

85 econium) that interfere with the activity of pulmonary surfactant in vitro may also be important in t

86 ng disruption of the biophysical function of pulmonary surfactants in the lung.

87 Many of these metabolites belonged to pulmonary surfactants, indicating IVI-induced aberration

88 Pulmonary surfactant is a complex mixture of lipids and

89 Pulmonary surfactant is a complex mixture of lipids and

90 Pulmonary surfactant is a complex of lipids and proteins

91 Pulmonary surfactant is a critical component of lung fun

92 Pulmonary surfactant is a lipid-protein complex that low

93 Pulmonary surfactant is a lipoprotein complex consisting

94 Pulmonary surfactant is a lipoprotein complex essential

95 Pulmonary surfactant is a lipoprotein complex that lower

96 Pulmonary surfactant is a lipoprotein complex that reduc

97 Pulmonary surfactant is a lipoprotein synthesized and se

98 Ovine pulmonary surfactant is bactericidal for Pasteurella hae

99 is of early-onset disease, particularly when pulmonary surfactant is deficient.

100 The pulmonary surfactant is modeled as a dipalmitoylphosphat

101 Pulmonary surfactant is primarily composed of phosphatid

102 e most critical and abundant phospholipid in pulmonary surfactant is saturated phosphatidylcholine (S

103 Pulmonary surfactant is secreted as a complex mixture of

104 Pulmonary surfactant isolated from gene-targeted surfact

105 Our findings indicate markedly impaired pulmonary surfactant levels in COVID-19 patients, justif

106 epithelial cells that synthesize and secrete pulmonary surfactant lipids and proteins, reducing the c

107 lectasis, hyaline membranes, and the lack of pulmonary surfactant lipids and proteins.

108 Pulmonary surfactant lipoproteins lower the surface tens

109 iratory distress syndrome is associated with pulmonary surfactant loss that alters alveolar mechanics

110 bloodstream infections but is inactivated by pulmonary surfactant, making it of no use in the therapy

111 h MitoQ during late gestation promoted fetal pulmonary surfactant maturation and an increase in the e

112 Fetal pulmonary surfactant matures more slowly in white than i

113 to tune ionic and lipidic flows through the pulmonary surfactant membrane network at the alveolar su

114 6 (Prdx6), a host factor that contributes to pulmonary surfactant metabolism and lung defense against

115 surfactant proteins affect the stability of pulmonary surfactant monolayers at an air/water interfac

116 shown previously that lateral compression of pulmonary surfactant monolayers initially induces separa

117 cture and dynamics of membrane arrays in the pulmonary surfactant network that covers the respiratory

118 ith human serum, albumin, polysorbate-80, or pulmonary surfactant) or assay parameters (inoculum dens

119 methodology may guide further development of pulmonary surfactant pharmaceuticals that better mimic t

120 Thus LPLA2 may be a major enzyme of pulmonary surfactant phospholipid degradation by alveola

121 The minor pulmonary surfactant phospholipid, palmitoyl-oleoyl-phos

122 Recently, we determined that the minor pulmonary surfactant phospholipid, palmitoyl-oleoyl-phos

123 ly, several investigators have reported that pulmonary surfactant phospholipids and SP-A are present

124 Instead, one of the major and most important pulmonary surfactant phospholipids, dipalmitoylphosphati

125 Two minor components of pulmonary surfactant phospholipids, phosphatidylglycerol

126 arkers were all chlorohydrins of unsaturated pulmonary surfactant phospholipids; phosphatidylglycerol

127 ins (termed collectins) present in blood and pulmonary surfactant play a role in initial host defense

128 The pulmonary surfactant prevents alveolar collapse and is r

129 es regulating the production and function of pulmonary surfactant prior to and after birth.

130 lar cells, there was no evidence of abnormal pulmonary surfactant production by type 2 pneumocytes in

131 surfactant requirement is met by the leptin pulmonary surfactant production pathway which normally a

132 Although many studies have shown that pulmonary surfactant protein (SP)-A functions in innate

133 Pulmonary surfactant protein (SP)-A is an endogenously p

134 Pulmonary surfactant protein (SP)-B plays a vital role i

135 We have also engineered MASP binding into a pulmonary surfactant protein (SP-A), which has the same

136 Expression of the rabbit pulmonary surfactant protein A (SP-A) gene is lung-speci

137 Pulmonary surfactant protein A (SP-A) is involved in inn

138 Pulmonary surfactant protein A (SP-A) plays a key role i

139 Nitrated pulmonary surfactant protein A (SP-A) was also detected

140 Pulmonary surfactant protein A (SP-A), a member of the c

141 Pulmonary surfactant protein A (SP-A), an alveolar glyco

142 the collectin family of proteins, including pulmonary surfactant protein A (SP-A), we hypothesized t

143 iates resistance to antibacterial effects of pulmonary surfactant protein A (SP-A).

144 otein C1q, mannose-binding lectin (MBL), and pulmonary surfactant protein A (SPA) are structurally si

145 C1q, mannose-binding lectin (MBL), and pulmonary surfactant protein A (SPA) interact with human

146 Rat pulmonary surfactant protein A is an oligomer of 18 poly

147 e location and depth of each residue of lung pulmonary surfactant protein B (SP-B(1-25)) in a phospho

148 For identification of structural changes of pulmonary surfactant protein B (SP-B) due to the heterog

149 Pulmonary surfactant protein B (SP-B) is an essential pr

150 Differences in selected proteins, namely pulmonary surfactant protein B, osteopontin, kallikrein

151 Bovine pulmonary surfactant protein C (SP-C) is a hydrophobic,

152 along with a peptide model for collagen and pulmonary surfactant protein C have been simulated very

153 human serum mannose-binding lectin (MBL) and pulmonary surfactant protein D (SP-D) have distinctive m

154 sed on our previous studies documenting that pulmonary surfactant protein D (SP-D) protects C. neofor

155 Pulmonary surfactant protein D (SP-D), a lung host defen

156 Pulmonary surfactant protein D (SP-D), a member of the c

157 domains of a collagenous C-type lectin, rat pulmonary surfactant protein D (SP-D), are sufficient to

158 ram-negative and gram-positive bacteria than pulmonary surfactant protein D (SP-D).

159 lation sites can be removed from the lung by pulmonary surfactant protein D (SP-D).

160 of viral infection, and, when combined with pulmonary surfactant protein D, their antiviral effects

161 ell differentiation marked by the absence of pulmonary surfactant protein gene expression.

162 been suggested to mimic some aspects of the pulmonary surfactant protein SP-B and has been tested cl

163 5), which is a truncated version of the full pulmonary surfactant protein SP-B, with dipalmitoylphosp

164 rfactant protein A (SP-A), the most abundant pulmonary surfactant protein, is implicated in multiple

165 TGF-beta represses transcription of pulmonary surfactant protein-B gene in lung epithelial c

166 virus is, in significant part, dependent on pulmonary Surfactant Protein-B, which plays an unanticip

167 Pulmonary surfactant protein-D (SP-D) is a member of the

168 Pulmonary surfactant proteins (SP-) A and D are innate i

169 We hypothesized that collectins, such as pulmonary surfactant proteins (SPs) SP-A and SP-D and se

170 Pulmonary surfactant proteins and lipids are required fo

171 e COVID-19 harbor IgA autoantibodies against pulmonary surfactant proteins B and C and that these aut

172 d Main Results: IgA autoantibodies targeting pulmonary surfactant proteins B and C were elevated in p

173 the conformational organization of the lung pulmonary surfactant proteins in the environment that mi

174 n spectroscopy to in-situ IR spectroscopy of pulmonary surfactant proteins SP-B and SP-C in lipid-pro

175 work explores the potential for strategizing pulmonary surfactant (PS) for drug delivery over the res

176 Pulmonary surfactant (PS) is a lipid-protein complex tha

177 Pulmonary surfactant (PS) is an essential complex of lip

178 nd ozone (O(3)) can cause dysfunction of the pulmonary surfactant (PS) layer in the human lung, resul

179 We synthesized pulmonary surfactant (PS)-biomimetic liposomes encapsula

180 Pulmonary surfactants reduce the work of breathing, enha

181 ces in hydrophobicity of plasma membrane and pulmonary surfactant require different chemistries of ge

182 re syndrome characterized by accumulation of pulmonary surfactant, respiratory insufficiency, and inc

183 ptomycin was shown to interact in vitro with pulmonary surfactant, resulting in inhibition of antibac

184 and misaligned pulmonary veins, and reduced pulmonary surfactant secretion.

185 Pulmonary surfactant spreads on the thin ( approximately

186 ve elevated pulmonary bile acids and altered pulmonary surfactant structure.

187 l cells at E18.5, concomitant with decreased pulmonary surfactant, suggesting a delay or an arrest in

188 This review considers the pulmonary surfactant system and the genetic causes of ac

189 s, indicating IVI-induced aberrations of the pulmonary surfactant system might play an important role

190 The pulmonary surfactant system of the lung is a lipid and p

191 r epithelium by resident constituents of the pulmonary surfactant system suggests that POPG and PI fu

192 airment, at least in part, by disrupting the pulmonary surfactant system.

193 t protein A (SP-A) is an abundant protein in pulmonary surfactant that has been shown to alter severa

194 actant protein-A2 (hSP-A2) is a component of pulmonary surfactant that plays an important role in the

195 cells lining the peripheral lung synthesize pulmonary surfactant that reduces surface tension at the

196 With advent of the availability of pulmonary surfactants, the prevalence of wheezing at age

197 emature infants are known to be deficient in pulmonary surfactant, there is limited information regar

198 e conclude that the presence of SP-A1 allows pulmonary surfactant to adopt a particularly favorable s

199 ns SP-B and SP-C promote rapid adsorption of pulmonary surfactant to an air/water interface by an unk

200 ns SP-B and SP-C promote rapid adsorption of pulmonary surfactant to an air/water interface.

201 hase transitions that precede compression of pulmonary surfactant to high surface pressure.

202 lted in an inflammatory reaction that caused pulmonary surfactant to lose some of its ability to main

203 ory cells, which could reduce the ability of pulmonary surfactant to lower surface tension in asthmat

204 been considered essential for the ability of pulmonary surfactant to sustain low surface tensions.

205 rmodynamic barriers that limit adsorption of pulmonary surfactant to the air-water interface.

206 HA) on the structure and surface behavior of pulmonary surfactant to understand the mechanism for HA-

207 erved dose-dependent interaction of Psa with pulmonary surfactant was blocked by ChoP.

208 atidylcholine (DPPC), the major component of pulmonary surfactant, was investigated as a function of

209 ich has been shown to degrade and inactivate pulmonary surfactant, was significantly increased in LCA

210 lateral phase separation occurs in films of pulmonary surfactant, we used epifluorescence microscopy

211 Samples of pulmonary surfactant were obtained from the lungs of 18

212 peptide (AP) originally isolated from ovine pulmonary surfactant, were prepared and used to assess t

213 Psa also bound to pulmonary surfactant, which covers the alveolar surface

214 understanding the structure and function of pulmonary surfactant, which has informed understanding o