Catalogue Search | MBRL
Search Results Heading
Explore the vast range of titles available.
MBRLSearchResults
-
DisciplineDiscipline
-
Is Peer ReviewedIs Peer Reviewed
-
Series TitleSeries Title
-
Reading LevelReading Level
-
YearFrom:-To:
-
More FiltersMore FiltersContent TypeItem TypeIs Full-Text AvailableSubjectCountry Of PublicationPublisherSourceTarget AudienceDonorLanguagePlace of PublicationContributorsLocation
Done
Filters
Reset
233,030
result(s) for
"oxidation"
Sort by:
Advanced oxidation technologies : sustainable solutions for environmental treatments
by
Litter, Marta I., editor
,
Candal, Roberto J., editor
,
Meichtry, J. Martín (Jorge Martín), editor
in
Sewage Purification Oxidation.
,
Oxidation Environmental aspects.
,
Environmental chemistry.
2017
Providing a state-of-the-art overview on environmental applications of Advanced Oxidation Technologies (AOTs) as sustainable, low-cost and low-energy consuming treatments of water, air, and soil. It includes information on innovative research and development on TiO2 photocatalytic redox processes, Fenton, Photo-Fenton processes, zerovalent iron technology, etc highlighting possible applications of ATOs in developing and industrialized countries around the world in the framework of 'A crosscutting and comprehensive look at environmental problems'.
A metabolic switch of fate
by
Strzyz Paulina
in
Oxidation
2018
Fatty acid oxidation and increased acetyl-CoA levels act to suppress endothelial–mesenchymal transition.
Journal Article
Understanding the factors that effect maximal fat oxidation
by
Dokladny, Karol
,
Purdom, Troy
,
Kravitz, Len
in
adipose tissue
,
Adipose tissues
,
beta oxidation
2018
Lipids as a fuel source for energy supply during submaximal exercise originate from subcutaneous adipose tissue derived fatty acids (FA), intramuscular triacylglycerides (IMTG), cholesterol and dietary fat. These sources of fat contribute to fatty acid oxidation (FAox) in various ways. The regulation and utilization of FAs in a maximal capacity occur primarily at exercise intensities between 45 and 65% VO
2max
, is known as maximal fat oxidation (MFO), and is measured in g/min. Fatty acid oxidation occurs during submaximal exercise intensities, but is also complimentary to carbohydrate oxidation (CHOox). Due to limitations within FA transport across the cell and mitochondrial membranes, FAox is limited at higher exercise intensities. The point at which FAox reaches maximum and begins to decline is referred to as the crossover point. Exercise intensities that exceed the crossover point (~65% VO
2max
) utilize CHO as the predominant fuel source for energy supply. Training status, exercise intensity, exercise duration, sex differences, and nutrition have all been shown to affect cellular expression responsible for FAox rate. Each stimulus affects the process of FAox differently, resulting in specific adaptions that influence endurance exercise performance. Endurance training, specifically long duration (>2 h) facilitate adaptations that alter both the origin of FAs and FAox rate. Additionally, the influence of sex and nutrition on FAox are discussed. Finally, the role of FAox in the improvement of performance during endurance training is discussed.
Journal Article
Methods for nitrogen activation by reduction and oxidation
in
Oxidation
2021
This PrimeView describes a strategic workflow for studying N2 activation methods, emphasizing the importance of verifying genuine product formation.
Journal Article
Beyond the Calorie Paradigm: Taking into Account in Practice the Balance of Fat and Carbohydrate Oxidation during Exercise?
by
Mercier, Jacques
,
Varlet-Marie, Emmanuelle
,
Brun, Jean-Frédéric
in
Adipose Tissue - metabolism
,
Blood Glucose - metabolism
,
Carbohydrates
2022
Recent literature shows that exercise is not simply a way to generate a calorie deficit as an add-on to restrictive diets but exerts powerful additional biological effects via its impact on mitochondrial function, the release of chemical messengers induced by muscular activity, and its ability to reverse epigenetic alterations. This review aims to summarize the current literature dealing with the hypothesis that some of these effects of exercise unexplained by an energy deficit are related to the balance of substrates used as fuel by the exercising muscle. This balance of substrates can be measured with reliable techniques, which provide information about metabolic disturbances associated with sedentarity and obesity, as well as adaptations of fuel metabolism in trained individuals. The exercise intensity that elicits maximal oxidation of lipids, termed LIPOXmax, FATOXmax, or FATmax, provides a marker of the mitochondrial ability to oxidize fatty acids and predicts how much fat will be oxidized over 45–60 min of low- to moderate-intensity training performed at the corresponding intensity. LIPOXmax is a reproducible parameter that can be modified by many physiological and lifestyle influences (exercise, diet, gender, age, hormones such as catecholamines, and the growth hormone-Insulin-like growth factor I axis). Individuals told to select an exercise intensity to maintain for 45 min or more spontaneously select a level close to this intensity. There is increasing evidence that training targeted at this level is efficient for reducing fat mass, sparing muscle mass, increasing the ability to oxidize lipids during exercise, lowering blood pressure and low-grade inflammation, improving insulin secretion and insulin sensitivity, reducing blood glucose and HbA1c in type 2 diabetes, and decreasing the circulating cholesterol level. Training protocols based on this concept are easy to implement and accept in very sedentary patients and have shown an unexpected efficacy over the long term. They also represent a useful add-on to bariatric surgery in order to maintain and improve its weight-lowering effect. Additional studies are required to confirm and more precisely analyze the determinants of LIPOXmax and the long-term effects of training at this level on body composition, metabolism, and health.
Journal Article
Progression in the Oxidation Stability of MXenes
2023
HighlightsThe progression of MXene's oxidation stability, the techniques available to monitor the phenomenon as well as the variables that contribute to its oxidation rate are discussed.Comprehensive aspects of the oxidation process in various storage settings and the debated oxidation mechanism along with the most effective antioxidation strategies are addressed in conjunction with current challenges to the air stability of MXenes.MXenes are under the spotlight due to their versatile physicochemical characteristics. Since their discovery in 2011, significant advancements have been achieved in their synthesis and application sectors. However, the spontaneous oxidation of MXenes, which is critical to its processing and product lifespan, has gotten less attention due to its chemical complexity and poorly understood oxidation mechanism. This perspective focuses on the oxidation stability of MXenes and addresses the most recent advancements in understanding and the possible countermeasures to limit the spontaneous oxidation of MXenes. A section is dedicated to the presently accessible methods for monitoring oxidation, with a discussion on the debatable oxidation mechanism and coherently operating factors that contribute to the complexity of MXenes oxidation. The current potential solutions for mitigating MXenes oxidation and the existing challenges are also discussed with prospects to prolong MXene’s shelf-life storage and expand their application scope.
Journal Article
Electrochemical advanced oxidation processes: today and tomorrow. A review
by
Sirés, Ignasi
,
Brillas, Enric
,
Panizza, Marco
in
Aquatic Pollution
,
Atmospheric Protection/Air Quality Control/Air Pollution
,
Carbon
2014
In recent years, new advanced oxidation processes based on the electrochemical technology, the so-called electrochemical advanced oxidation processes (EAOPs), have been developed for the prevention and remediation of environmental pollution, especially focusing on water streams. These methods are based on the electrochemical generation of a very powerful oxidizing agent, such as the hydroxyl radical (•OH) in solution, which is then able to destroy organics up to their mineralization. EAOPs include heterogeneous processes like anodic oxidation and photoelectrocatalysis methods, in which •OH are generated at the anode surface either electrochemically or photochemically, and homogeneous processes like electro-Fenton, photoelectro-Fenton, and sonoelectrolysis, in which •OH are produced in the bulk solution. This paper presents a general overview of the application of EAOPs on the removal of aqueous organic pollutants, first reviewing the most recent works and then looking to the future. A global perspective on the fundamentals and experimental setups is offered, and laboratory-scale and pilot-scale experiments are examined and discussed.
Journal Article
Hydroxyoctadecadienoic Acids Regulate Apoptosis in Human THP-1 Cells in a PPARgamma-Dependent Manner
2014
Macrophage apoptosis, a key process in atherogenesis, is regulated by oxidation products, including hydroxyoctadecadienoic acids (HODEs). These stable oxidation products of linoleic acid (LA) are abundant in atherosclerotic plaque and activate PPARγ and GPR132. We investigated the mechanisms through which HODEs regulate apoptosis. The effect of HODEs on THP-1 monocytes and adherent THP-1 cells were compared with other C18 fatty acids, LA and [alpha]-linolenic acid (ALA). The number of cells was reduced within 24 hours following treatment with 9-HODE (p < 0.01, 30 [mu]M) and 13 HODE (p < 0.01, 30 [mu]M), and the equivalent cell viability was also decreased (p < 0.001). Both 9-HODE and 13-HODE (but not LA or ALA) markedly increased caspase-3/7 activity (p < 0.001) in both monocytes and adherent THP-1 cells, with 9-HODE the more potent. In addition, 9-HODE and 13-HODE both increased Annexin-V labelling of cells (p < 0.001). There was no effect of LA, ALA, or the PPARγ agonist rosiglitazone (1[mu]M), but the effect of HODEs was replicated with apoptosis-inducer camptothecin (10[mu]M). Only 9-HODE increased DNA fragmentation. The pro-apoptotic effect of HODEs was blocked by the caspase inhibitor DEVD-CHO. The PPARγ antagonist T0070907 further increased apoptosis, suggestive of the PPARγ-regulated apoptotic effects induced by 9-HODE. The use of siRNA for GPR132 showed no evidence that the effect of HODEs was mediated through this receptor. 9-HODE and 13-HODE are potent--and specific--regulators of apoptosis in THP-1 cells. Their action is PPARγ-dependent and independent of GPR132. Further studies to identify the signalling pathways through which HODEs increase apoptosis in macrophages may reveal novel therapeutic targets for atherosclerosis.[PUBLICATION ABSTRACT]
Journal Article