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1 tion analysis showed that baseline values of surfactant protein D (46.6 ng/mL vs 34.6 ng/mL, p=0.0018
4 monstrate that reduced pulmonary edema fluid surfactant protein D and elevated plasma surfactant prot
5 olar lavage and various serum markers (e.g., surfactant protein D and KL-6) each may provide useful i
6 In a subset, we compared plasma levels of surfactant protein-D and von Willebrand factor antigen b
7 on molecules in the collectin family, namely surfactant proteins D and A (Sp-D and Sp-A, respectively
8 ptor for advanced glycation end products and surfactant protein D) and endothelial injury (angiopoiet
10 r inhibitor-1 (PAI-1), surfactant protein-A, surfactant protein-D, and intracellular adhesion molecul
11 n molecule-1, von Willebrand factor antigen, surfactant protein-D, and soluble tumor necrosis factor
12 eceptor for advanced glycation end products, surfactant protein D, angiopoietin-2, interleukin-6, int
13 soluble multitrimers of BAFF and APRIL using surfactant protein D as a scaffold, and we vaccinated mi
15 a levels of fibrinogen, chemokine ligand 18, surfactant protein D, C-reactive protein, Clara cell sec
16 surfactant protein A-deficient (SP-A-/-) or surfactant protein D-deficient (SP-D-/-) BALF, or a mixt
18 in, which evolved through duplication of the surfactant protein D gene in ruminants, prefers mannose
19 oluble tumor necrosis factor receptor-1, and surfactant protein-D) had nearly equivalent prognostic v
20 ding of three innate immune lectins, namely, surfactant protein D, human galectin-8, and Siglec-14, t
21 nt of peritoneal Mos with the lung collectin surfactant protein D inhibited AC uptake, and fluticason
24 ated proteins such as endogenous eotaxin and surfactant protein D levels, which were both increased f
26 alysis, we identified four serum biomarkers (surfactant protein D, matrix metalloproteinase 7, CA19-9
27 + carbohydrate recognition domains of human surfactant protein D (NCRD) with CL-43 (RCL-43-NCRD) and
28 re generally not inhibited by the collectins surfactant protein D or mannose binding lectin because o
29 ct of leukoreduced blood on plasma levels of surfactant protein-D or von Willebrand factor antigen wa
31 es, including von Willebrand factor antigen, surfactant protein D, protein C, plasminogen activator i
32 RATIONALE: Recombinant fragment of human surfactant protein D (rfhSP-D) has been shown to suppres
35 nary and activation-regulated chemokine, and surfactant protein D significantly increased the areas u
36 nary and activation-regulated chemokine, and surfactant protein D significantly strengthens this asso
38 tudies reveal that substantial quantities of surfactant protein D (SP-D) accumulate in the airspaces
50 m mannose-binding lectin (MBL) and pulmonary surfactant protein D (SP-D) have distinctive monosacchar
61 he recognition of influenza A virus (IAV) by surfactant protein D (SP-D) is mediated by interactions
77 previous studies documenting that pulmonary surfactant protein D (SP-D) protects C. neoformans cells
78 recognition domains (CRDs) of lung collectin surfactant protein D (SP-D) recognize sugar patterns on
85 ins, Clara cell secretory protein (CC16) and surfactant protein D (SP-D), and five systemic inflammat
87 emonstrated direct interactions of HNPs with surfactant protein D (SP-D), another important effector
88 f a collagenous C-type lectin, rat pulmonary surfactant protein D (SP-D), are sufficient to drive the
103 d, a tripartite fusion protein was made from surfactant protein D (SPD), HIV-1 Gag as a test antigen,
104 e was no detectable compensatory increase in surfactant protein D, the other known pulmonary collecti
105 infection, and, when combined with pulmonary surfactant protein D, their antiviral effects were addit
107 e 2-trimer form, and fusion with the body of surfactant protein D was used to produce the 4-trimer fo
110 ombinant homotrimeric fragment of human lung surfactant protein D with a series of bound ligands have
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