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Elimination Reactions
Published in Michael B. Smith, A Q&A Approach to Organic Chemistry, 2020
The Cope elimination is the reaction of trialkylamine N-oxide, which is heated, and syn elimination leads to the less substituted alkene and a hydroxylamine. What is the structure of trimethylamineN-oxide?
“Omics”
Published in Kirk A. Phillips, Dirk P. Yamamoto, LeeAnn Racz, Total Exposure Health, 2020
Recently, we have begun to recognize that the host microbiome may influence and modulate exposure risk, for example, by biotransforming chemicals and drugs (Klaassen and Cui 2015, Koppel et al. 2017, Vazquez-Baeza et al. 2018). Microbial composition and interaction with diet strongly influences many metabolic diseases like obesity and diabetes (Palau-Rodriguez et al. 2015). The promotion of arthrosclerosis by meat has been traced to microbes metabolizing dietary choline and carnithine to the proatherogenic metabolite Trimethylamine-N-Oxide (TMAO) in concert with host enzymes (Tang and Hazen 2017). Evidence for this comes from mice rendered free of microbes through antibiotic treatment or raised under germ-free conditions who fail to synthesize TMAO from choline/carnithine-rich diets (Koeth et al. 2013). Interestingly, an omnivore which was fed a steak (~180 mg carnithine) or isotopically labeled carnithine responds with an increase in TMAO. However, a vegetarian/vegan fed the same steak/isotopically labeled carnithine fails to produce TMAO since the resident gut microflora between carnivores and long-term vegans/vegetarians have different compositions. This observation vividly illustrates the interplay of exposure, host and microbiome (Koeth et al. 2013).
N-Heterocycles
Published in Navjeet Kaur, Metals and Non-Metals, 2020
Commercial trimethylamine N-oxide produces an un-stabilized azomethine ylide which undergoes 1,3-dipolar cycloaddition with unpolarized and electron rich olefins to produce good yields of 3,4-disubstituted pyrrolidines. A wide range of substituents can be tolerated on alkenes provided they are compatible with excess lithium diisopropylamide (Scheme 65) [190].
Basic pathogenic mechanisms of atherosclerosis
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hamad Abdulsalam Hamad Alfarisi, Zenab B. Hamad Mohamed, Muhammad Bin Ibrahim
Diet and dietary habits are major driving forces for development and modification of atherosclerotic diseases. Diet and intestinal bacteria (microbiome) are implicated in the pathogenesis of atherosclerosis. This approach was introduced after discovery of the role of metabolic factors other than dietary cholesterol [60]. Phosphatidylcholine found in egg yolk and in red meat carnitine is processed by intestinal bacteria to trimethylamine (TMA) this in turn oxidized in the liver to trimethylamine N-oxide (TMAO) which has been described in animal models and clinical trials as metabolite causing atherosclerosis and elevating risk of CHD [61,62]. Trimethylamine N-oxide found to promote formation of foamy macrophages (hallmark of fatty streak) [16]. Dietary choline or TMAO supplementation increases the expression of the SR on macrophages and reduces reverse cholesterol transport, promoting foam cell formation. Precursors of TMAO, choline or L-carnitine elicit alterations in cholesterol and sterol metabolic pathways in the vascular wall [63]. People such as vegans lacking intestinal bacteria that can produce trimethylamine; hence, they may be protected against atherosclerosis. Level of TMAO can be influenced by the type of diet, variations in expression of flavin monooxygenases (enzymes that convert TMA to TMAO) and perhaps the composition of gut flora [16]. This principle has raised a new approach for treatment of atherosclerosis through eradication of pathogenic bacteria with antibiotics and recolonization via stool transplantation with beneficial bacteria, but this novel work still under investigation [64].
Using chemical chaperones to increase recombinant human erythropoietin secretion in CHO cell line
Published in Preparative Biochemistry and Biotechnology, 2019
Mehri Mortazavi, Mohammad Ali Shokrgozar, Soroush Sardari, Kayhan Azadmanesh, Reza Mahdian, Hooman Kaghazian, Seyed Nezamedin Hosseini, Mohammad Hossein Hedayati
Chemical chaperones are small molecules that assist molecular chaperones to fold a protein in endoplasmic reticulum also integrate into the protein structure to protect its folding in the secretory pathway. Molecular chaperones and chemical chaperones collaborate with each other to reduce misfolded protein response and enhance protein secretion.[5,15] Such collaboration happens as a result of the increased activity of molecular chaperones after treatment of the cells by chemical chaperone. Also chemical chaperones cooperate with molecular chaperones by adjust their activity.[16] Chemical chaperones are from different groups of components, including polyols such as glycerol, methylamines such as trimethylamine N-oxide (TMAO), sugar, and amino acid derivatives. It is worth mentioning that media optimization is currently the most important plan in recombinant protein production using CHO cell line. The existing challenges in bioprocessing tasks such as low yield and aggregation can be studied and resolved to improve protein production using chemical chaperones through handling molecular chaperones.[3]
Non-targeted metabolomics in sport and exercise science
Published in Journal of Sports Sciences, 2019
Liam M. Heaney, Kevin Deighton, Toru Suzuki
A further study comparing distinct categorised groups of low and high fitness demonstrated that the low fitness group had lower levels of phosphatidylcholine and increased free choline (approximately 1.5-fold, P = 0.017, Bye et al., 2012). Circulating free choline has recently been implicated in cardiovascular disease (Wang et al., 2014) and is known to be metabolised by the gut microbiome to form an intermediary in the production of trimethylamine N-oxide (Wang et al., 2011), a small molecule metabolite associated with reduced survival in conditions such as heart failure and myocardial infarction (Suzuki, Heaney, Bhandari, Jones, & Ng, 2016; Suzuki, Heaney, Jones, & Ng, 2016; Tang et al., 2014). Bye and colleagues (2012) have provided a basis to further explore exercise training to reduce levels of metabolites such as free choline through improving cardiovascular fitness, with the intention of reducing the risk of later life development of cardiometabolic disorders.