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Diagnosis and Treatment of Inhalation Injury in Burn Patients
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Khan Z. Shirani, Joseph A. Moylan, Basil A. Pruitt
The most abundant gas generated in fires, carbon monoxide, on the other hand, has no direct cytotoxic properties but causes injury through the production of systemic hypoxemia. Carbon monoxide causes a leftward shift in the oxygen dissociation curve, which accentuates tissue hypoxia and leads to cell injury. Both hypoxia and hypothermia cause a suppression of membrane-based adenosine triphosphate synthesis rate that is unmatched by a reciprocal reduction in the intracellular metabolic processes. Such imbalance in the supply and demand of energy results in uncoupling of the metabolic and membrane cell functions, increased membrane permeability, and irreversible cell damage (Hochachka, 1986).
Aberrant Conduction Patterns in and Around an Ischemic Zone by a Finite Element Model
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
I would like to make a remark regarding the inhomogeneity of the tissue and the different models of arrhythmia generation and reentry. It is very important to distinguish between the acute, reversible phase of ischemia, where certainly no uncoupling occurs, and the more chronic ischemia. I do not entirely agree with the statement that one needs an inhomogeneity in terms of local changes at the membrane. We have many arguments to say that the membrane properties may be perfectly homogeneous and still there will always be some inhomogeneity in propagation. One may postulate, for instance, that the margin of safety for propagation is becoming low and then there exists an impedance mismatch at the fibers’ branching sites microscopically and this will suffice to produce circuits. In chronic ischemia, uncoupling does exist and transmission times in low-coupled cells may reach 20 to 30 ms between two cells. There are, therefore, different types of pathophysiological mechanisms leading to slow conduction, and it’s important to state what physiological model is referred to.
Ultrastructure of The Myometrium and The role of Gap Junctions in Myometrial Function
Published in Gabor Huszar, The Physiology and Biochemistry of the Uterus in Pregnancy and Labor, 2020
Arie Verhoeff, Robert E. Garfield
Recently it has become apparent that cells connected by gap junctions may not necessarily show a free exchange of dyes, isotopes, and current.41,42,44,46,50 Electrophysiologic studies show that gap junctions can rapidly switch from a low to a high resistance.44,46 It is now recognized that the channels or pores created by the gap junction may not always be in the open state.44,46,51,52 There may be times when the channels are open and times when they are closed. This uncoupling mechanism may be a safety device to uncouple injured cells44 or to uncouple cells when metabolically or electrically desirable. Closing the channels or uncoupling has been achieved by changes in internal and external Ca++ and pH.41,44,46,50-52
A comprehensive insight into the potential roles of VDR gene polymorphism in obesity: a systematic review
Published in Archives of Physiology and Biochemistry, 2022
Amir Hossein Faghfouri, Elnaz Faghfuri, Vahid Maleki, Laleh Payahoo, Adam Balmoral, Yaser Khaje Bishak
The role of vitamin D in obesity has not fully been understood. A piece of crucial evidence in this area is the result of a study on the transgenic mice, which revealed that the expression of the human vitamin D receptor gene in adipose tissues reduced energy consumption. This effect might be due to the upregulation of uncoupling proteins (UCPs) and activation of enzymes involved in β-oxidation and lipolysis (Wong et al.2011). Another in vivo study proposed the role of VDR in decreasing hormone-sensitive lipase and adipose triglyceride lipase gene expression in rats via increasing intracellular calcium and decreasing the intracellular cAMP level (He et al.2011). Also, it has been found that VDR is expressed in human adipocytes and, thereby, vitamin D suppresses adipogenesis and regulates the differentiation of adipocytes through the inhibition of transcription factors (Ding et al.2012).
Uncoupling proteins: are they involved in vitamin D3 protective effect against high-fat diet-induced cardiac apoptosis in rats?
Published in Archives of Physiology and Biochemistry, 2022
Zienab Alrefaie, Hossam Awad, Khadeejah Alsolami, Enas A. Hamed
Uncoupling refers to a state in which nutrient fuels are oxidised but the energy is not linked to ATP synthesis but dissipated as heat. Uncoupling is mediated by (UCPs 1–4) located on the inner mitochondrial membrane, although the presence of other proteins has been argued. Emerging functions of UCP2 and UCP3 are broadly different and findings are conflicting depending on the specific uncoupling protein (UCP) and site of expression; upregulation of UCP2 in pancreatic islets may develop insulin insufficiency in type 2 diabetes mellitus, while increased expression of UCP3 in skeletal muscle prevents development of insulin resistance (Chan and Harper 2006). UCPs are pivotal regulators of cellular energy metabolism and mitochondrial dynamics, they mediate a beneficial defence process to decrease reactive species production so guard against cardiomyocyte apoptosis and the same time ensure ATP production for normal cardiomyocyte function. Measuring cardiac UCPs links the mitochondrial function to oxidative status to apoptosis. The implication of UCPs in cardiac apoptosis was not much investigated. So, further evidence concerning UCPs expression in various models and tissues is extremely needed.
Current and emerging gluconeogenesis inhibitors for the treatment of Type 2 diabetes
Published in Expert Opinion on Pharmacotherapy, 2021
The many transcription factors involved in gluconeogenesis identified by the use of gene knockout and gene knockdown in mouse models has opened a host of potential targets for drug development. However, transcription factors are not limited in their actions to gluconeogenesis alone. These molecules function in many different processes including tumor development in some cases. Therefore, assurance of the unique action and the safety of potential therapeutic agents is a significant challenge. It is ironic that metformin, the primary drug treatment for Type 2 diabetes, is a very small simple molecule with a large margin of safety [153]. Metformin targets the mitochondrion, and perhaps the greatest opportunities to influence the combined pathways of gluconeogenesis and lipolysis exist in molecules that have mitochondrial effects. The mitochondrion has its own mechanisms including possessing DNA separate from the nucleus. Thus modifications at the mitochondrial pathways may have less detrimental effects than those affecting the cell nucleus. The uncoupling proteins, in particular, have great popular interest due to the thought that they may permit metabolic caloric dissipation rather than adipose accumulation.