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1.
Daily washing in vivo of the lung with 0.15 M saline did not deplete the Beagle dog lung of surfactant lipids, but rather increased the quantity of surfactant lipid in the tissue. Replacement time for the lung lipids removed by the lavage was approximately 5 hours. This rate is one indication of the time required for movement of surfactant lipid from storage areas to the surface of the alveoli. The increase in tissue surfactant lipid following multiple lavage suggests that the rate of surfactant lipid synthesis is controlled in part by the level of surfactant lipid in the alveoli.  相似文献   
2.
Using the imidate procedure, 2,3,4,6-tetra-O-benzyl-1-O-(N-methylacetimidoyl)-β-d-galactopyranose was condensed with various monosaccharides to provide, in good yield and with high stereoselectivity, α-linked disaccharides.  相似文献   
3.
To assess the effects of perturbing the surface of low density lipoprotein (LDL) on the conformation of apoB-100, LDL (d 1.030-1.050 g/ml) isolated from normal subjects were treated with phospholipase A2 (PL-A2) for 0.5 to 15 min. The resulting P-LDL and concurrent control LDL (C-LDL) incubated without PL-A2 were isolated by gel permeation chromatography. Approximately 50% of LDL-phosphatidylcholine was hydrolyzed in 2 min and approximately 85% in 5 min. Lysophosphatidylcholine compounds (LPC) and free fatty acids (FFA) accumulated during lipolysis but most of the LPC and all of FFA could be removed by adding FFA-free albumin to the lipolysis mixtures. Immunoreactivities of P-LDL and C-LDL were evaluated in competitive radioimmunoassays, using a library of anti-human LDL monoclonal antibodies directed against the major regions of apoB-100 (the T4, T3, and T2 thrombin fragments). One epitope defined by monoclonal antibody 465B6C3 and localized near the carboxyl end of the apoB-100 molecule became less immunoreactive (ED 50s increased); three other epitopes on the T2 fragment near the LDL receptor recognition site and four epitopes localized towards the middle (T3) and amino terminal (T4) regions did not change. Altered immunoreactivities were not related to LPC and FFA contents. Thus, the conformation of apoB-100 was selectively altered by phospholipolysis. The interactions of P-LDL with cultured fibroblasts were grossly altered: P-LDL were bound nonspecifically to fibroblasts of both normal and homozygous familial hypercholesterolemic subjects and P-LDL were not degraded. LPC and FFA retained in LDL did not explain these alterations, nor did changes of epitope expression near the LDL receptor recognition site. It is likely that the apoB-100 aberrant cell interaction is due to loss of surface phospholipids and "uncovering" of core lipids that react nonspecifically with cell surface components.  相似文献   
4.
The temperature-sensitive mutation cc1 blocks a number of cell cycle processes in Paramecium including macronuclear DNA synthesis, oral morphogenesis, and the later stages of micronuclear mitosis. Oral morphogenesis and micronuclear mitosis also occur in the sexual pathway. This study shows that cc1 cells can proceed through conjugation or autogamy under restrictive conditions; neither stomatogenesis nor micronuclear mitosis is blocked. Fertilization and macronuclear determination occur normally, but DNA synthesis in macronuclear anlagen is blocked. Therefore, this mutation discriminates between oral replacement during meiosis and vegetative prefission stomatogenesis, and between mitotic spindle elongation during the pregamic and postzygotic divisions and spindle elongation during the vegetative cell cycle. These results point to a fundamental regulatory difference between morphogenesis in the vegetative and sexual pathways. © 1994 Wiley-Liss, Inc.  相似文献   
5.
The synthesis of two series of glycopeptides, part of the N-terminal region of human glycophorin A, was accomplished starting from derivatives ofO--d-galactopyranosyl-(1–3)-O-(2-acetamido-2-deoxy--d-galactopyranosyl)-l-serine and-l-threonine.  相似文献   
6.
The electron impact mass spectra of 19 trimethyl silylated flavonol mono-, di- and -triglycosides are reported for the first time. All spectra show wel  相似文献   
7.
8.
In this study, we extracted the essential oils of the stem, leaf, and flower of Achillea filipendulina, analyzed them, and studied their antibacterial properties. Of 16, 53, and 35 compounds identified in the stem, leaf, and flowers, respectively, only five are present in all three segments of the plant. The essential oil of the stem was mainly composed of neryl acetate, spathulenol, carvacrol, santolina alcohol, and trans‐caryophyllene oxide. However, the main identified components of leaf were 1,8‐cineole, camphor, ascaridole, trans‐isoascaridole, and piperitone oxide and the main components of the flower oil were ascaridole, trans‐isoascaridole, 1,8‐cineole, p‐cymene, and camphor. The extracted oil from different segments demonstrated varying antibacterial properties against both Gram‐positive and Gram‐negative bacteria, demonstrated by disk, minimum inhibitory concentration, and minimum bactericidal concentration methods. These suggest that the application of all segments of aerial parts of A. filipendulina may have a better therapeutic effect in fighting pathogenic systems.  相似文献   
9.
Splicing is catalyzed by the spliceosome, a compositionally dynamic complex assembled stepwise on pre-mRNA. We reveal links between splicing machinery components and the intrinsically disordered ciliopathy protein SANS. Pathogenic mutations in SANS/USH1G lead to Usher syndrome—the most common cause of deaf-blindness. Previously, SANS was shown to function only in the cytosol and primary cilia. Here, we have uncovered molecular links between SANS and pre-mRNA splicing catalyzed by the spliceosome in the nucleus. We show that SANS is found in Cajal bodies and nuclear speckles, where it interacts with components of spliceosomal sub-complexes such as SF3B1 and the large splicing cofactor SON but also with PRPFs and snRNAs related to the tri-snRNP complex. SANS is required for the transfer of tri-snRNPs between Cajal bodies and nuclear speckles for spliceosome assembly and may also participate in snRNP recycling back to Cajal bodies. SANS depletion alters the kinetics of spliceosome assembly, leading to accumulation of complex A. SANS deficiency and USH1G pathogenic mutations affects splicing of genes related to cell proliferation and human Usher syndrome. Thus, we provide the first evidence that splicing dysregulation may participate in the pathophysiology of Usher syndrome.  相似文献   
10.
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