Explore chapters and articles related to this topic
Integrated Omics Technology for Basic and Clinical Research
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Kuldeep Giri, Vinod Singh Bisht, Sudipa Maity, Kiran Ambatipudi
Metabolomics along with genomics and proteomics can diagnose and prognoses cancer (Prostate, breast and ovarian cancer) depending on host metabolic system and analyzes altered metabolites (Zhang et al., 2013; Turkoglu et al., 2016; Hadi et al., 2017). Tan et al. (2013) identified 39 differential serum metabolites in healthy subjects and 40 metabolites (e.g., gut flora, urea cycle, nucleotide synthesis, TCA cycle, fatty acid, phenylalanine, amino acid, and carbohydrate metabolism) in colorectal cancer patients. Cardiovascular diseases (e.g., hypertension, myocardial ischemia, acute coronary syndrome, and heart failure) are silent killers; their risk assessment is still a complex puzzle in clinical studies (Wang et al., 2017). Gao et al. (2017) identified 42 biomarkers to capture the physiological changes during the early stage of Coronary Atherosclerosis patients versus healthy controls. Of 42 biomarkers, lysophosphatidylcholine, elaidic acid, L-fucose, monoglyceride, diglyceride, indoxylsulfuric acid, prasterone sulfate, and phosphatidylglycerol were uniquely identified in the early stage of coronary atherosclerosis patients. These results indicate a significant role of metabolic markers in the prediction of early onset and diagnosis of coronary atherosclerosis, cardiovascular diseases, and many cancers.
Nanomedicine Therapeutic Approaches to Overcome Hypertension
Published in Sarwar Beg, Mahfoozur Rahman, Md. Abul Barkat, Farhan J. Ahmad, Nanomedicine for the Treatment of Disease, 2019
Md. Rizwanullah, Sadaf Jamal Gilani, Mohd Aqil, Syed Sarim Imam
Invasomes are flexible, neutrally charged, phospholipid-based vesicular system containing a mixture of soy phosphatidylcholine, lysophosphatidylcholine, terpenes, and ethanol. It has shown to improve skin penetration of hydrophilic and lipophilic drugs (Imam and Aqil, 2016; Dragicevic-Curic et al., 2009). Flexibility of the bilayer membrane is mainly due to the lysophosphatidylcholine acting as an edge activator. Ethanol is a good penetration enhancer while terpenes have also shown potential to increase the penetration of many drugs by disrupting the tight lipid packing of the SC (Qadri et al., 2017). Kamran et al. developed and evaluated the transdermal potential of nanoinvasomes, containing anti-hypertensive drug olmesartan (Kamran et al., 2016). The developed nanoinvasomes formulation showed vesicles size of 83.35 ± 3.25nm, entrapment efficiency of 65.21 ± 2.25% and transdermal flux of 32.78 ± 0.703 μg/cm2/h. CLSM of rat skin showed that the developed formulation was eventually distributed and permeated deep into the skin. Pharmacokinetic study in Wistar rats showed that transdermal treatment of nanoinvasomes formulation exhibited 1.15-fold higher bioavailability compared to olmesartan oral suspension.
Thin-Layer Chromatography of the Skin Secretions of Vertebrates
Published in Bernard Fried, Joseph Sherma, Practical Thin-Layer Chromatography, 2017
Phosphatides, including phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine, and lysophosphatidylcholine, from the skin secretions of reptiles, birds, and mammals generally have been separated on silica gel H plates. Chloroform–methanol (2:1) extracts of various keratinized tissues of vertebrates, including the hair, hooves, and horns of mammals; the feathers and epidermal scales of birds; and the shed skins of snakes, were separated on plates developed first with diethyl ether–acetic acid (100:1) and then chloroform–methanol–water (40:10:1).1 Bands consistent with phosphatidylcholine and phosphatidylethanolamine were visualized after plates were sprayed with sulfuric acid. Evidence of these and other phosphatides also has been observed in chromatograms of the epidermis or skin gland secretions of reptiles on silica gel H plates developed with chloroform–methanol–water (60:10:1 or 65:35:5)2,17,26,72,73,88 or chloro-form-2-propanol–triethylamine–methanol–0.25% KCl (30:20:18:9:6),16 or on silica gel HR plates developed first with acetone–hexane (1:1) and then with chloroform–methanol–acetic acid–water (25:15:4:2 89 or 50:25:7:3 15).
Longitudinal metabolic alterations in plasma of rats exposed to low doses of high linear energy transfer radiation
Published in Journal of Environmental Science and Health, Part C, 2021
Tixieanna Dissmore, Andrew G DeMarco, Meth Jayatilake, Michael Girgis, Shivani Bansal, Yaoxiang Li, Khyati Mehta, Vijayalakshmi Sridharan, Kirandeep Gill, Sunil Bansal, John B Tyburski, Amrita K Cheema
Complex cellular responses triggered by exposure to non-lethal doses of ionizing radiation may lead to changes in metabolomic profiles depending on radiation type and dose.18–22 In this study, we report the results from a rat model aimed at delineating longitudinal alterations in the plasma metabolome after exposure to 0.5 Gy of 1H (250 MeV) or 16O (600 MeV/n) radiation. The dysregulated metabolites included certain classes of lipids such as phosphatidylethanolamine (PE), ceramide, sphingomyelin (SM) and lysophosphatidic acid (LPA). Pro-inflammatory cytokines and oxidative stress may stimulate the generation of SMs, from the ceramide response to sphingomyelin synthase in the Golgi apparatus.23 Dysregulation observed in SM(24:1) at the 3-month time point may indicate some degree of neuronal damage.24 Additionally, we found a significant increase in eicosapentaenoyl PAF C-16 after exposure to 0.5 Gy of 1H at 12 the month time point, which may be because of ionizing radiation-mediated oxidation of phospholipids. Radiation-induced peroxidation of fatty acids may indicate cellular damage at various levels.25,26 Lastly, we observed decreased levels of LPA(18:0) after exposure to 1H and 16O at 12 months. Previously it has been reported that inflammatory prostaglandins Phosphatidylcholine (PC) generates lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA) through the actions of Pla2) and phospholipase D (Pld) that is further converted to Phosphatidic acid (PA). Decreased levels of LPA may suggest increased levels of PA that can directly stimulate G protein-coupled receptor activation of mTor through resulting in increased cell proliferation.27