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Basic Thermal Physics: Heat Exchange and Infrared Radiation
Published in Kurt Ammer, Francis Ring, The Thermal Human Body, 2019
The energy possessed and exchanged by living creatures is made up from dynamic(kinetic) and static forms (potential: mass-, chemical-, and force-related energies). Energy release in living tissues is based on the chemical oxidation-reduction reaction. The term oxidation conveys the impression of a reaction involving combination with oxygen:
Riboflavin
Published in Judy A. Driskell, Ira Wolinsky, Sports Nutrition, 2005
Assessment of riboflavin status should include direct and indirect biochemical measures, as well as dietary intake data (Table 4.1). While the degree of urinary riboflavin excretion is a direct reflection of tissue saturation, urinary excretion is not a sensitive marker of very low riboflavin intakes.16 More appropriately, riboflavin status is determined by an oxidation-reduction reaction in which oxidized glutathione is reduced by GSSH in an FAD-dependent glutathione reductase reaction.17,18 Specifically, riboflavin status is obtained by determining the erythrocyte riboflavin concentration measured by the urinary excretion of riboflavin. The erythrocyte glutathione reductase activity coefficient (EGRAC) can be calculated from the erythrocyte riboflavin concentration. EGRAC and the erythrocyte transketolase enzyme activity coefficient (ETKAC) are determined by dividing the stimulated enzyme activity (with added FAD) by the basal enzyme activity (without added FAD). Thus, a high EGRAC indicates impaired riboflavin status (low riboflavin excretion indicates deficiency). This technique of determining riboflavin status has been confirmed by human depletion studies.2Table 4.2 depicts frequently used cutoff values for EGRAC. The sensitivity of EGRAC, found to be useful in determining impaired riboflavin status, is the preferred method for assessing riboflavin status.19 In women, it is important to note that the phase of the menstrual cycle should be considered when assessing riboflavin status, due to some blood and urinary assessment indexes influenced by recent nutrient intakes. Martini et al. found that riboflavin intakes were significantly higher in the midluteal phase than in the midfollicular phase of menstruating women.20
Meal Patterns, Physical Activity, Sleep, and Circadian Rhythm
Published in Dale A. Schoeller, Margriet S. Westerterp-Plantenga, Advances in the Assessment of Dietary Intake, 2017
Margriet S. Westerterp-Plantenga, Marta Garaulet
In relation to the well-known glucostatic theory, discovered in the animal model (Mayer 1953, 1955), and applied in research in humans (Campfield et al. 1996; Melanson et al. 1999a, 1999b, 1999c), it was observed that transient, spontaneously resolving declines in blood glucose precede meal initiation. Glucose concentrations do not necessarily act in a simple depletion-repletion model; the patterns serve as signals for meal initiation (Campfield and Smith 1990; Melanson et al. 1999a, 1999b, 1999c). In time-blinded humans, it was shown that in ~88% of the transient declines, a meal request followed, and that after a meal glucose concentrations rose dramatically, followed by a dynamic decline (Melanson et al. 1999c). Therefore, glucose monitoring can be used as a biomarker for physiological meal initiation indicated by the transient decline, and for actual feeding, indicated by the rise and fall of blood glucose concentrations. In practice, noninvasive glucose monitoring is needed. Noninvasive glucose monitoring is conducted using a glucose sensor that does not lead to blood collection and which does not need piercing of the skin with a solid object (Tura et al. 2007). The GlucoWatch (Cygnus Inc, Redwood City, CA) fulfills these requirements. It is a commercial device that monitors glucose noninvasively and in real time. Cygnus received FDA clearance for the GlucoWatch in 2001, updated in 2002 (Howsmon and Bequette 2015). The measurement is based on iontophoresis, a process by which an electric current brings interstitial glucose to the surface of the skin and then measures the amount of glucose via an electrochemical sensor (Tamada et al. 1999; Potts et al. 2002). The device is mainly used in diabetic patients in order to indicate hypoglycemic and hyperglycemic conditions (Dos Santos et al. 2006). Another possibility is the use of continuous subcutaneous glucose monitors (CSGMs). CGMs use small enzymatic sensors inserted beneath the skin to measure interstitial glucose. Subsequently, an oxidation–reduction reaction gives a measurable current that is calibrated with a blood glucose measurement (Gandrud et al. 2004). The commercial CGM named MiniMed (Medtronic, Northridge, CA) was approved by the FDA in 1999. Further development then refined these devices.
An approach to assessing the contribution of the high LET effect in strategies for Auger endoradiotherapy
Published in International Journal of Radiation Biology, 2023
Pavel Lobachevsky, Colin Skene, Laura Munforte, Andrea Smith, Jonathan White, Roger F. Martin
In order to understand the impact of RBE on the extent of radioprotection by methylproamine and analogs, it is important to consider the proposed mechanism of radioprotection, starting from an ionization event on DNA, such as extraction of an electron to form, for example, a guanine radical cation. This is a transient lesion that is a precursor to permanent DNA damage. Next, consider a minor groove binding radioprotector nearby to this lesion. The transient DNA lesion species is an oxidizing agent, whereas the ligand is a reductant. An oxidation-reduction reaction takes place, mediated by charge transfer within the DNA molecule. It is known from pulse radiolysis experiments (Martin and Anderson 1998) that the range of this charge transfer is of the order of 30 base pairs. The overall outcome is that the initial lesion is repaired and the ligand is oxidized. The mechanism is analogous to the so-called sacrificial anode, whereby a Zn electrode is attached, with an electrical connection, to steel. The Zn is preferentially oxidized, and the Fe is protected.
In vitro fertilization-frozen embryo transfer in a patient with cytochrome P450 oxidoreductase deficiency: a case report
Published in Gynecological Endocrinology, 2018
Tianran Song, Bin Wang, Huan Chen, Jingjing Zhu, Haixiang Sun
PORD, a rare autosomal recessive disease that affects both males and females, was first described in 1985; however, it was not until 2004 that researchers found this disease to be caused by POR mutations [10]. POR mutations affect the functions of CYP enzymes, which are involved in the metabolism and transformation of a variety of physiological substances and toxicants, and approximately 90% of drugs, as well as in the synthesis of steroid hormones [11]. The membranes of liver microsomes are rich in phospholipids and CYP enzymes, such as POR, which serves as an electron donor for all CYP enzymes [12]. After a CYP enzyme binds to its substrate, POR donates an electron to the enzyme and then an oxidation-reduction reaction occurs between the enzyme and substrate [13].
Ferroptosis inhibition shields house ear institute-organ of corti 1 cells from free fatty acids-induced inflammatory injuries
Published in Acta Oto-Laryngologica, 2023
Xuemin Chen, Yiding Yu, Ning Yu, Weiwei Guo, Qingqing Jiang, Shiming Yang
Ferroptosis is mainly caused by the imbalance between the production and degradation of lipid ROS in the cell. Critical to the homeostasis of lipid oxidation-reduction reaction are system Xc- and GPX4 pathway. System Xc- is a heterodimer comprising of a light chain subunit SLC7A11 and a heavy chain subunit SLC3A2 [16]. SLC7A11 functions as a cystine/glutamate antiporter to transport extracellular cystine into the cytosol for GSH biosynthesis and antioxidant defense, which serves as a promising therapeutic target in multiple cancer therapy [17]. GPX4 belongs to the family of GPxs. It can utilize GSH as the reductant to directly eliminate toxic lipid hydroperoxides into lipid alcohols. The inhibition of GPX4 have been proposed to trigger ferroptosis in multiple diseases, including acute renal failure, osteoarthritis, gastric cancer and stroke. In this study, PA treatment decreased GPX4 and SLC7A11 expression at both mRNA and protein level, while ferroptosis inhibitors Fer-1 restored PA-blocked GPX4 and SLC7A11 expression, suggesting that loss of GPX4/SLC7A11-mediated antioxidant defense is implicated in PA-induced ferroptosis in HEI-OC1 cells. Besides, ACSL4 is a central enzyme ligating coenzyme A to polyunsaturated fatty acids (PUFA) to trigger phospholipids synthesis [18]. PTGS2 encodes COX-2, which is the rate-limiting enzyme for the conversion of arachidonic acid (AA) to prostaglandins (PGs), and responsible for amplifying inflammation through recruitment of macrophages [2]. Immune cell-mediated inflammation induced by NOX1 elicited the release of ROS, which is also regarded as ferroptosis-related molecules. Our results showed that these ferroptosis-related factors also participate in PA-induced ferroptosis, and upregulation of ACSL4 and PTGS2 mRNA were markedly prevented by Fer-1 treatment.