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The Chemistry and Biology of Lipooligosaccharides: The Endotoxins of Bacteria of the Respiratory and Genital Mucosae
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
J. McLeod Griffiss, Herman Schneider
The addition of Gal ²1→4 to the Hep-1-linked Glc that invariably initiates the α chain forms the disaccharide, lactose (Lac; Gal²1→4Glc), and creates an α chain that mimics lactosylceramide GSL. Neisserial lactosyl LOS were estimated to have a mass of 3.6 kDa by reference to the mass of rough mutant LPS of Salmonella with which they were co-electrophoresed (6,35), and this denominator remains current even though it overestimates their mass by a few hundred daltons (55). Lactosyl LOS are made by all Neisseria and many Haemophilus (56), although the latter genus also makes a diglucoside α chain (57).
Histiocytosis and Lipid Storage Diseases
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Salwa Shabbir Sheikh, David F. Garvin
The lipid storage diseases are hereditary disorders with lipid deposition in one or more tissues. The type of lipid and its distribution have a characteristic pattern for each of the different lipid disorders. The various sphingolipids are normally degraded within lysosomes of macrophages in the reticuloendothelial system, particularly in liver, spleen, and bone marrow. Figure 5 summarizes the pathways for catabolism of sphingolipids by lysosomal enzymes. Breakdown of these lipids in visceral organs begins with engulfment of red cell and white cell membranes rich in lactosylceramide (Cer-Glc-Gal) and hematoside (Cer-Glc-Gal-NANA). In the brain, most of the cerebroside-type lipids are gangliosides. There is extensive turnover of the gangliosides in the central nervous system of neonates.
Genosomes for Gene Delivery and Transfection
Published in Danilo D. Lasic, LIPOSOMES in GENE DELIVERY, 2019
As in the cell culture work, the beginning of a liposome-mediated transfection goes back to conventional liposomes. Rat insulin gene injected in egg yolk lecithimox brain phosphatidylserine to cholesterol (8:2:10) large liposomes prepared by reverse phase evaporation was expressed and lowered the blood glucose levels. Furthermore, liposomes could be targeted from Kupffer cells to hepatocytes by inclusion of lactosylceramide which is a ligand for hepatocyte asialoglycoprotein receptors (Nicolau and Cudd, 1989). Due to low efficiency and demanding preparation, such experiments were not continued until the field of liposomal gene delivery became revived after the introduction of high-surface-charge cationic liposomes and the mounting safety concerns of viral vectors.
Noninvasive biomarkers to guide intervention: toward personalized patient management in prostate cancer
Published in Expert Review of Precision Medicine and Drug Development, 2020
Maria Frantzi, Enrique Gomez-Gomez, Harald Mischak
To investigate the potential of lipids as biomarkers in urinary exosomes, a pilot lipidomics study was performed using high-throughput mass spectrometry to analyze urinary exosomes [76]. The 36 most abundant lipid molecules in urinary exosomes were quantified in 15 PCa patients and 13 healthy individuals. The highest significance was shown for phosphatidylserine (PS) 18:1/18:1 and lactosylceramide (LacSer) (d18:1/16:0). The combination of PS and LacSer distinguished the two groups with 93% sensitivity and 100% specificity. Although this was the first time that lipidomics markers were reported as promising candidates, this was a small pilot study and further validation studies must be performed before drawing any conclusions [76]. Additionally, urinary metabolomic profiling using 1H nuclear magnetic resonance (1H-NMR) was performed in 64 PCa and 51 BPH patients. 108 metabolic features were assessed and integrated using orthogonal partial least squares discriminant analysis (OPLS-DA). Subsequently, a model consisting of 40 metabolic variables was developed to discriminate PCa patients from individuals with BPH. The model included among others increased concentrations of branched-chain amino acids (BCAA), glutamate and pseudouridine, and decreased concentrations of glycine, dimethylglycine, fumarate, 4-imidazole-acetate, and one unknown metabolite (U1) associated with PCa (p ≤ 0.01; permutation test of 100 repeats) [77]. Yet, validation in an independent cohort to demonstrate potential value should be performed.
An exploration of aptamer internalization mechanisms and their applications in drug delivery
Published in Expert Opinion on Drug Delivery, 2019
Lin-Yan Wan, Wen-Fang Yuan, Wen-Bing Ai, Yao-Wei Ai, Jiao-Jiao Wang, Liang-Yin Chu, Yan-Qiong Zhang, Jiang-Feng Wu
Different rates and mechanisms of endocytosis have been observed in different cells for the same aptamer, except for AS1411. AS1411, transferrin and lactosylceramide had higher rates of endocytosis in breast cancer stem (BCS) cells than in the differentiated breast cancer cells and baby hamster kidney (BHK) cells. Mechanistically, in BCS cells, the aptamers may undergo clathrin-independent and caveolin-independent endocytosis, because neither caveolin-dependent endocytosis inhibitors (such as Genistein [GEN] or methyl-β-cyclodextrin) nor clathrin-dependent endocytosis inhibitors (such as sucrose or monodansylcadaverine) inhibited aptamer internalization. However, both kinds of inhibitors blocked aptamer internalization in the differentiated breast cancer cells [55].
Sudden onset of nephrotic syndrome in an asymptomatic Fabry patient: a case report
Published in Renal Failure, 2020
Ruixiao Zhang, Zeqing Chen, Yanhua Lang, Shihong Shao, Yan Cai, Qingqing You, Yan Sun, Sai Wang, Xiaomeng Shi, Zhiying Liu, Wencong Guo, Yue Han, Leping Shao
FD was first described independently by two dermatologists, Johannes Fabry and William Anderson in 1898, was also named Andeson–Fabry Disease [12,13]. It is the second most common lysosomal storage disorder after Gaucher disease [14]. FD is caused by the deficient activity of α-Gal A, resulting from inherited or de novo pathogenic variants in the GLA gene [15]. α-Gal A is a dimeric glycoprotein that catalyzes the removal of terminal nonreducing α-D-galactose residues in ceramide trihexoside [3,15]. Impairment of α-Gal A activity may result in obstacle of the glycolipid conversion from globotriosylceramide (GL-3) to lactosylceramide (GL-2), leading to widespread intralysosomal accumulation of glycolipid in different tissue and organs [16].