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RAT α 2 -Macroglobulin and Related α-Macroglobulins in the Acute Phase Response
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
Rat α1-I3 electrophoretic mobility on nondenaturing polyacrylamide gels slows upon treatment with trypsin, but does not change after methylamine treatment. These differences are considered to be more related to the lower native molecular weight of this inhibitor and therefore less molecular sieving. Methylamine treatment abolishes its inhibiting activity.
Synthesis of Trichloro-(Methylamino)-Bis-(Methylamine) Tin(IV) Methylamine Hydrochloride*
Published in Nate F. Cardarelli, Tin as a Vital Nutrient:, 2019
Figure 2 shows the three products resulting from this synthesis. Using methylamine in excess, a methylamine-rich product is produced (Figure 2, Panel 3). This reaction requires 2 hr. Reaction products.
Creatine
Published in Linda M. Castell, Samantha J. Stear (Nottingham), Louise M. Burke, Nutritional Supplements in Sport, Exercise and Health, 2015
Jacques R. Poortmans, Eric S. Rawson
For instance, despite allegations of detrimental effects of oral creatine supplementation on liver metabolism, studies on humans have not shown any significant increase in plasma urea, nor liver enzyme activity, during five years of creatine supplementation (Poortmans and Francaux, 2008). No reports have observed a modification of the glomerular filtration rate, nor the presence of microalbuminuria (Portmans and Francaux, 2000, 2008). All values remained within the normal range adapted for the age range. Experimentally, an excess conversion of creatine to sarcosine may result in cytotoxic agents such as methylamine. However, in humans taking up to 20g creatine per day for two weeks (Poortmans et al., 2005; Sale et al., 2009), urine methylamine excretion remains largely under the upper limit for healthy individuals.
CDR-H3 loop ensemble in solution – conformational selection upon antibody binding
Published in mAbs, 2019
Monica L. Fernández-Quintero, Johannes Kraml, Guy Georges, Klaus R. Liedl
We deleted the co-crystallized antigen in all complex crystal structures, and refer to these structures as “AGed” structures, also sometimes described as holo structures. For every structure, the constant domains (CH1, CL) were removed. We followed a protocol that we developed in a previous study.44 All starting structures for simulations were prepared in MOE (Molecular Operating Environment, Chemical Computing Group, version 2018.01) using the Protonate3D tool.49,50 The C-termini of the antibodies were capped with N-methylamine (NME). To neutralize the charges, we used the uniform background charge.51-53 Using the tleap tool of the AmberTools1651,52 package, the crystal structures were soaked with cubic water boxes of TIP3P water molecules with a minimum wall distance of 10 Å to the protein (Table 1).54 The box size in MD simulations can influence the resulting dynamics if sampling is insufficient.55,56 For all crystal structures parameters of the AMBER force field 14SB were used.57 The antibodies were carefully equilibrated using a multistep equilibration protocol.58
HPLC–UV assay for the evaluation of inhibitors of plasma amine oxidase using crude bovine plasma
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Kira Mergemeier, Florian Galster, Matthias Lehr
For the determination of activity of PAO and for screening of inhibitors of the enzyme, a variety of methods have been reported. Mostly benzylamine is used as substrate and the formation of the enzyme product benzaldehyde is measured directly by UV-spectroscopy at 250 nm12–17 or by HPLC with UV-detection after derivatisation with dinitrophenylhydrazine18. Alternatively, 14C-benzaldehyde produced from 14C-benzylamine is quantified radiometrically19,20. Furthermore, hydrogen peroxide formed during benzylamine transformation is determined in enzyme-coupled colorimetric21–26 or fluorometric assays27–31. Besides, a direct fluorimetric method using a (naphthalene-2-yl)methylamine substrate was published32. A disadvantage of the methods using benzylamine as substrate is that this substrate only weakly binds to the enzyme. This property could lead to an overestimation of the inhibitory potency of inhibitors when the assay is performed under competitive conditions33. We have recently developed an HPLC/UV-method for evaluation of PAO inhibitors, which uses the new tightly binding substrate 6-(5-phenyl-2H-tetrazol-2-yl)hexan-1-amine33. Although the physiological substrates of PAO are not clearly defined presently, it can be assumed that inhibition data are more meaningful applying tightly instead of weakly binding substrates.
Enalapril decreases rat plasma concentration of TMAO, a gut bacteria-derived cardiovascular marker
Published in Biomarkers, 2018
Marek Konop, Marek Radkowski, Marta Grochowska, Karol Perlejewski, Emilia Samborowska, Marcin Ufnal
Blood TMAO mostly originates from gut bacteria metabolism. Mammalian gut flora, including Clostridium, Collinsella, Desulfovibrio, Lactobacillus and Proteus produce several methylamines, including TMA, dimethylamine and monomethylamine from dietary choline and lecithin (Craciun and Balskus 2012, Romano et al.2015). Some of these methylamines are absorbed into the bloodstream and eventually excreted with urine, sweat or exhaled air in unchanged or oxidized forms such as TMAO. Therefore, plasma TMAO level depends on numerous factors including a diet, microbiota composition, the gut–blood barrier permeability to TMA and TMAO, liver oxidation of TMA and the excretion of the methylamines (Zeisel et al.1989, Jaworska et al.2017, Nowinski and Ufnal 2018).