References: Lecithin
Gynecol Obstet Invest. 1989;27(4):173-8.
Amniotic fluid isoamylase activity in uneventful pregnancies.
Goepel E, Ulmer HU, Pahnke VG, Schlotfeldt TC, Bode F.
Department of Gynecology and Obstetrics, University Hospital, Hamburg-Eppendorf, FRG.
A kinetic test (Phadebas) was used to determine the isoamylase activity in 50 serum specimens and 159 samples of amniotic fluid. A highly significant difference between the isoamylase patterns of serum and amniotic fluid was ascertained which strongly supports the view that amylase activity in amniotic fluid is not of maternal origin. During the whole course of gestation the activity of pancreatic isoamylase was constantly low whereas there was an increase of nonpancreatic activity (S-type amylase) from 44 +/- 10 U/l in the 18th week of gestation to 445 +/- 170 U/l in week 39/40. A comparison between the dispersion of the ascertained values and the lecithin-sphingomyelin (L/S) ratio showed a clear overlapping. There was a correlation coefficient of r = 0.645 for 115 amniotic fluid specimens examined in our investigation. The findings show that the estimation of nonpancreatic isoamylase (S-type amylase) activity in amniotic fluid is a valuable indirect parameter for determining fetal maturity and fetal lung maturity. The easy and quick determination method will provide even those hospitals with an index of fetal maturity which are presently not in a position to estimate the L/S ratio, thus being of great assistance in the field of premature deliveries.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2744618&dopt=Abstract lecithin
unito.it
Deformable liposomes were prepared to investigate the effectiveness of dermal administration of methotrexate (MTX). The phospholipids used to prepare the liposomes were soybean lecithin (PC) or hydrogenated lecithin (HPC) and dipotassium glycyrrhizinate (KG) as surfactant. The lipid/KG ratio (w/w) was 2:1 and 4:1. Liposomes size, entrapment efficiency and MTX release through dialysis membrane were determined and the interaction between MTX and liposomes was investigated using differential scanning calorimetry. The MTX amount permeated through pig skin were three- to four-fold higher using liposomes containing KG compared to those from water solution or normal liposomes. No significant differences were observed between PC-KG liposomes and HPC-KG liposomes. At the end of the skin permeation assay using deformable liposomes, up to 50% of the administered dose was found in the skin. This capability depends on the self-regulating carrier deformability. These results suggest that liposomes containing KG may be of value for the topical administration of MTX in the treatment of psoriasis.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14726128&dopt=Abstract lecithin [PubMed - in process]
Biochim Biophys Acta. 2003 Dec 30;1635(2-3):127-41.
Interaction of apolipoprotein A-I with lecithin-cholesterol vesicles in the presence of phospholipase C.
Gudheti MV, Gonzalez YI, Lee SP, Wrenn SP.
Department of Chemical Engineering, College of Engineering, Drexel University, Philadelphia, PA 19104, USA.
Here we study the anti-nucleating mechanism of apolipoprotein A-I (apo A-I) on model biliary vesicles in the presence of phospholipase C (PLC) utilizing dynamic light scattering (DLS), steady-state fluorescence spectroscopy, cryogenic transmission electron microscopy (cryo-TEM), and UV/Vis spectroscopy. PLC induces aggregation of cholesterol-free lecithin vesicles from an initial, average size of 100 nm to a maximal size of 600 nm. The presence of apo A-I likely inhibits vesicle aggregation by shielding the PLC-generated hydrophobic moieties, which results in vesicles of an average size of 200 nm. A similar phenomenon is observed in cholesterol-enriched lecithin vesicles. Whereas PLC alone produces aggregates of 300 nm, no aggregation is observed when apo A-I is present along with PLC. However, the ability of apo A-I to inhibit aggregation is temporary, and after 8 h, a broad particle size distribution with sizes as high as 800 nm is observed. Apo A-I possibly induces the formation of small apo A-I/lecithin/cholesterol complexes of about 5-20 nm similar to the discoidal pre-HDL complexes found in blood when it can no longer effectively shield all the DAG molecules. Concomitant with formation of complexes, DAG molecules coalesce into large oil droplets, which account for the large particles observed by light scattering. Thus, apo A-I acts as an anti-nucleating agent by two mechanisms, anti-aggregation and microstructural transition. The mode of protection is dependent on the cholesterol content and the relative amounts of DAG and apo A-I present. This study supports the possibility of apo A-I solubilizing lipids in bile in a similar fashion as it does in blood and also delineates the mechanism of form
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