China
Africa
Explore chapters and articles related to this topic
Envisioning Utilization of Super Grains for Healthcare
Published in Megh R. Goyal, Preeti Birwal, Santosh K. Mishra, Phytochemicals and Medicinal Plants in Food Design, 2022
The lipid content of millets varies from 1% to 5% with pearl, proso, and foxtail millets containing the highest (5%) and kodo and finger millet containing lowest amounts (1%). Since the germ contains higher content of lipids, pearl, and foxtail millets have higher levels due to larger germs. Approximately 88% of the total pearl millet fat is concentrated in the germ, which contains 32% of the lipid content [177]. The lipids contain neutral lipids (85%), phospholipids (12%), and glycolipids (3%). The unsaturated fatty acids constitute 78%–82% with high levels of LA followed by oleic acid. Linolenic acid and erucic acid are also present in trace amounts [7, 81]. Oleic acid is the chief fatty acid in finger millet, which itself contains lower amount of lipids content, thus accounting for the superior shelf stability [177]. Major phospholipids include lysophosphatidylcholine (42%), phos-phatidylcholine (24%), lysophosphatidylethanolamine (21%), and traceable amounts of phosphatidylserine, phosphatidic acid, phosphatidylinositol, and phosphatidylglycerol [81].
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The changes in protein synthesis and degradation associated with proteinase activity and protein synthesis may derive from alteration of the membrane permeability of the various organelles in the neurons from the damaged peripheral nerve.270 Proteinases contain proteolipids which may be responsible for their enzyme activity. Therefore, the primary modifications of the macromolecular organization of the neuronal structures and denaturation of lipoproteins occuring during early stages of neuron injury are associated with conformational changes of these complex molecules. Reduced enzyme activity may represent unmasking of the enzyme function. Later, increased enzyme activity may be related to changes in membrane permeability due to the injury or release of proteolipid from protein binding through the action of cytolytic substances, such as lysolecithin or lysophosphatidylethanolamine. These phospholipids are normally present in small amounts in the nervous system and exert a direct cytolytic or myelinolytic action on the cell, releasing enzymes from lysosomes of myelin. This step may be the initiator of the demyelinating process, indicating the participation of neural lysosomes in events of Wallerian degeneration. Lysosome-like particles are described in neuronal cells, axon, and glial cells and in the Schwann cell. It may be that lysosomal activity largely of axonal origin is responsible for the degradation and enzyme changes manifesting in the early stage of degeneration.
Lipids Of Cryptococcus Neoformans
Published in Rajendra Prasad, Mahmoud A. Ghannoum, Lipids of Pathogenic Fungi, 2017
A. S. Ibrahim, H. Sanati, M. A. Ghannoum
The major polar lipids of C. neoformans are phosphatidylcholines (PC), phosphatidylethanolamines (PE) and tentatively identified glycolipid fraction (GL) (based on spraying with α-naphthol reagent).14 Phosphatidylglycerols (PG), phosphatidylinositols (PI), ceramide monohexosides (CMH), steryl glycosides (SG), phosphatidylserines (PS), lysophosphatidylcholine (LPC), lysophosphatidylethanolamine (LPE), phosphatidic acid (PA), monogalactosyl diacylglycerols (MGD), and cardiolipins (CL) are also present in variable amounts among C. neoformans isolates (Table 1).
Campylobacter jejuni permeabilizes the host cell membrane by short chain lysophosphatidylethanolamines
Published in Gut Microbes, 2022
Xuefeng Cao, Chris H.A. van de Lest, Liane Z.X. Huang, Jos P.M. van Putten, Marc M.S.M. Wösten
Lysophospholipids (LPLs) are bioactive signaling molecules containing a single fatty acid tail. In eukaryotic cells, LPLs exhibit diverse biological properties, such as promoting cell growth, acting as potent lipid mediators, or reducing bacterial infections.1,2 LPLs are generated as metabolic intermediates in phospholipid synthesis or during membrane degradation.3 The formation of LPLs from phospholipids is due to activation of phospholipase A1 or A2. Phospholipase A1 (PldA1) and phospholipase A2 (PldA2), hydrolyzing the stereospecific numbering (Sn)-1 and −2 acyl chain, respectively.4 (Sn)-1 LPLs possess more shorter, saturated acyl chains than (Sn)-2 LPLs while (Sn)-2 LPLs possess more unsaturated acyl chains.5 (Sn)-1 LPLs and (Sn)-2 LPLs might have different biological functions as only (Sn)-1 LPLs can act as mediators of antimicrobial activity toward Gram-positive bacteria.6 Lysophosphatidic acid (lysoPA) is important in controlling and signaling cancer;7 lysophosphatidylcholine (lysoPC) evokes cellular injury by oxidative events that involve formation of low-density lipoprotein. Both lysoPA and lysoPC of the host trigger the release of the proinflammatory flagellin from Salmonella thereby enhancing the innate and inflammatory responses toward this bacterium.8 The role of other LPLs like lysophosphatidylethanolamine (lysoPE) has not been elucidated to such a high degree.
The cardiovascular aspect of COVID-19
Published in Annals of Medicine, 2021
Joseph Adu-Amankwaah, Richard Mprah, Adebayo Oluwafemi Adekunle, Marie Louise Ndzie Noah, Gabriel Komla Adzika, Jeremiah Ong’achwa Machuki, Hong Sun
SARS-CoV infections tend to downregulate ACE2, which might contribute to myocardial dysfunction hence affecting the CVS at large [46]. However, whether SARS-CoV-2 directly affects the CVS by targeting ACE2-expressing cells remains to be clarified [47]. Another theory may involve an indirect effect of the immune response to SARS-CoV-2 on the heart along with the blood vessels [47] (see Figure 1). A 12- year follow-up study of 25 patients who recuperated from SARS-CoV infection revealed that 68% developed hyperlipidaemia, 44% developed CVS disorders, and 60% experienced abnormalities of glucose metabolism [48,49]. Additionally, metabolomics analysis reported that the deregulation of lipid metabolism occurred in patients having a history of SARS-CoV infection. In these patients, the serum levels of lysophosphatidylcholine, free fatty acids, phosphatidylglycerol, and lysophosphatidylethanolamine were significantly elevated compared with those without a history of SARS-CoV infection [48,49]. Nevertheless, the underlying processes by which SARS-CoV infection causes lipid and glucose metabolic disorders remains unclear. In a study of 75 hospitalised SARS patients, acute myocardial infarction (AMI) was the cause of mortality in 2 out of 5 severe cases [50]. Given that COVID-19 has a comparable structure and pathogeneses of SARS-CoV, then this novel virus can also cause chronic damage to the cardiovascular system; hence cardiovascular protection during treatment for COVID-19 should not be disregarded [49].
Microparticles and cardiovascular diseases
Published in Annals of Medicine, 2019
Christos Voukalis, Eduard Shantsila, Gregory Y. H. Lip
Microparticles contain a wide variety of biological molecules as part of their phospholipid membrane or within the cytosol that they enclose (Figure 3). These molecules are proteins (signal proteins, receptors and effector proteins), lipids and nucleic acids [38–40]. Various techniques have been tried in order to characterize the components of the microparticles [41,42]. Irrespective of the origin of microparticles, the plasma membrane is negatively charged due to translocation of phospholipids such as phosphatidylserine and phosphatidylcholine from internal to external surface [43,44]. Other phospholipids of the membrane include lysophosphatidylcholine, sphingomyelin, lysophosphatidylethanolamine, phosphatidylethanolamine, lysophosphatidylserine and phosphatidylinositol [45]. It appears that the bi-lipid layer of the microparticles affects the attached protein activities and the general properties of the vesicles [46].