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Uptake Mechanisms of 99mTc-Labeled Perfusion Imaging Agents in Detection of Breast Cancers
Published in Raymond Taillefer, Iraj Khalkhali, Alan D. Waxman, Hans J. Biersack, Radionuclide Imaging of the Breast, 2021
These observations apparently support the statement that the mechanism of cellular accumulation of 99mTc-sestamibi is through passive diffusion [5] since no ATP is directly consumed during this process. However, in living organisms, the transmembrane chemical and electrical gradients represent stores of energy. They are the end results of the metabolic activity and are generated mostly through the consumption of ATP. Consequently, since a part of this energy is dissipated in order to accumulate 99mTc-sestamibi, its mechanism of accumulation corresponds more appropriately, in our opinion, to the so-called secondary active transport [6].
The endocrine system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Hyperthyroidism is also known as thyrotoxicosis. The symptoms and signs of hyperthyroidism are related to an increase in metabolic activity due to an increase in thyroid hormone secretion. The commonest cause of hyperthyroidism is Graves’ disease (Box 18.3).
Exposure Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
More recently, the disappearance from the body of water doubly labeled with isotopes has been used to measure inhalation rates for periods up to three weeks. In this method, water is labeled with the stable isotopes 2H and 18O (deuterium and heavy oxygen). These isotopes can be measured in urine, saliva, or blood. The disappearance of 2H is a measure of water output, and the disappearance of 18O reflects water output plus CO2 production. CO2 production, as a measure of metabolic activity, is then calculated by subtraction. Daily energy expenditures can then be determined from CO2 production.7,244–247
GSPE pre-treatment protects against long-term cafeteria diet-induced mitochondrial and inflammatory affectations in the hippocampus of rats
Published in Nutritional Neuroscience, 2022
Oriol Busquets, Marina Carrasco, Triana Espinosa-Jiménez, Miren Ettcheto, Ester Verdaguer, Carme Auladell, Mònica Bullò, Antoni Camins, Montserrat Pinent, Esther Rodríguez-Gallego, Jaume Folch
In our study, we started by analyzing components linked to energetic balances and the maintenance of physiological metabolic activity. As we described above, we observed changes in GSK3β and IDE after a long-term feeding with cafeteria diet as a consequence. In the context of neurodegeneration, deregulations GSK3β have been linked with pathological processes such as the increase in Tau hyperphosphorylation, increased amyloid-β production and mitochondrial dysfunction [33]. Furthermore, several studies have linked changes in IDE expression with changes in insulin signaling and increased accumulation of amyloid-β [34,35]. These results are in agreement with the appearance of an early state of insulin resistance induced by the cafeteria diet previously reported in the periphery by Ginés I et al. [8]. In the hippocampus, affectations in the normal energetic metabolism and the impairment of neuronal survival may lead to the development of small alterations that, over time, can build up into more severe consequences like the appearance of deregulations in cognitive capacity [11,15]. Some researchers have linked these deregulations with neurodegenerative diseases like sporadic forms of AD under a theory known as the metabolic-cognitive syndrome or type III diabetes [12–14,16,17]. Interestingly, the pre-treatment with GSPE protected the animals from showing these alterations and, in fact, showed a very significant increase in the phosphorylation rate of AKT. This response has already been described by our research group in the periphery [36].
Implication of metabolomics and transporter modulation based strategies to minimize multidrug resistance and enhance site-specific bioavailability: a needful consideration toward modern anticancer drug discovery
Published in Drug Metabolism Reviews, 2022
Megha Rachmale, Niraj Rajput, Tarang Jadav, Amit Kumar Sahu, Rakesh K. Tekade, Pinaki Sengupta
When the administered drug (say drug A) itself is a potent activator of PXR as well as a substrate of p-gp, it may up-regulate the expression of DMET proteins (auto-induction) by altering their regulation through the PXR receptor. This process may lead to a decrease in intestinal uptake and accumulation of drug ‘A’ at target tissue (tumor cells) due to increased efflux of the drug. This simultaneously increases the metabolic activity of enzymes resulting in an increase in drug metabolism and clearance. This whole sequential process subsequently ends up with drug resistance due to the unavailability of drug ‘A’ at the target site. An opposite scenario is also possible if drug ‘A’ is a potent inhibitor of the PXR receptor. In such case, it may decrease its own metabolism and efflux (auto-inhibition) which can lead to toxicity and unwanted adverse effect due to increased accumulation of Drug ‘A’ at the target site (Hendrikx et al. 2013). Paclitaxel is a potent PXR agonist as well as a substrate of DMET which causes induction of DMET. As a result, increased metabolic, as well as transporter activity causes failure in attaining an optimum concentration of drug in target tissues leading to the resistance (Synold et al. 2001; Nallani et al. 2003; Masuyama et al. 2005).
Translational activity is uncoupled from nucleic acid content in bacterial cells of the human gut microbiota
Published in Gut Microbes, 2021
Mariia Taguer, B. Jesse Shapiro, Corinne F. Maurice
As this bimodal distribution of HNA and LNA has already been identified in the gut,10 we set out to determine if HNA and LNA components of the microbiota differ in their metabolic activity. To do so, a broad yet clearly defined measurement of single-cell levels of activity was required to compare and contrast with relative nucleic acid content determination. In this paper, we focus on protein translation as an important aspect of metabolic activity. We optimize bioorthogonal non-canonical amino acid tagging (BONCAT), a recent application of click chemistry, to identify the translationally active bacteria in the gut microbiota.30 BONCAT allows for the unbiased detection of proteins produced in situ under biologically relevant conditions, without the need for radioactivity, isotopes, antibodies, long incubations, or altering conditions. A methionine analogue, L-homopropargylglycine (HPG), is added to a short in vitro incubation of the gut microbiota, and is then “clicked” to an azide-modified fluorophore. HPG has been shown to be taken up by all bacteria under all physiological states tested, and due to the promiscuity of methionyl-tRNA synthetase, is incorporated into nascent proteins.30 The alkyne-azide groups quickly undergo a cycloaddition to form a stable triazole conjugate at biologically relevant conditions. Azide and alkyne modifications are considered biologically inert: they do not interfere with biological processes and do not naturally exist in most biological systems, including bacteria.30–32