Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

High-performance μ-thermoelectric device based on Bi2Te3/Sb2Te3 p-n junctions

A flexible and ultralight planar thermoelectric generator based on 15 thermocouples composed of n-type bismuth telluride (Bi2Te3) and p-type antimony telluride (Sb2Te3) legs (each with 400 nm thick) connected in series, on 25 μm thick Kapton substrate, was fabricated with impressive power factor values of 2.7 and 0.8 mW K-2 m-1 (at 298 K) for Bi2Te3 and Sb2Te3 films, respectively. The p-n junction thermoelectric device can generate a maximum open-circuit voltage and output power of 210 mV and 0.7 μW (3.3 mW cm-2), respectively, for a temperature difference of 35 K, which is higher than the one observed for a conventional thermoelectric device with metallic contacts for p-n junctions. The results were combined with numerical simulations, showing a good match between the experimental and the numerical results. The current density versus voltage (J-V) characteristics of the fabricated p-n junctions revealed a diode behavior with a turn-on voltage of ≈0.3 V and an impressive rectifying ratio (I+1V/I-1V) of ≈2 × 104.The present work is supported by Portuguese Foundation for Science and Technology (FCT) in the framework of the (1) reference project UID/EEA/04436/2019, by FEDER funds through the COMPETE 2020, Programa Operacional Competitividade e Internacionalização (POCI); (2) Strategic Funding Contract UID/FIS/04650/2019; (3) project PTDC/CTM - NAN/5414/2014 (POCI-01-0145-FEDER-016723), (4) co-financed by Programa Operacional Regional do Norte (NORTE2020), through Fundo Europeu de Desenvolvimento Regional (FEDER), Project NORTE-01-0145-FEDER-000032, NextSea; and (5) project PTDC/EEI-TEL/5250/2014, by FEDER funds through POCI-01-145-FEDER-16695

Interaction Between Vitamin E and Polyunsaturated Fatty Acids

Polyunsaturated fatty acids (PUFA) are nutritionally essential since they cannot be synthesized de novo from two-carbon fragments. As a result of their unsaturated double bonds, PUFA are susceptible to chemical reactions with reactive oxygen and nitrogen species (ROS and RNS, respectively). PUFA incorporated into phospholipids and present in biological membranes not only influence membrane fluidity, curvature, and the properties of membrane microdomains, but increase also the risk for chain reactions of lipid peroxidation leading to membrane destabilization and cellular dysfunction. Vitamin E, the main lipid-soluble antioxidant, stabilizes membranes by itself and protects PUFA by scavenging lipid peroxyl radicals. Thus, vitamin E and PUFA form an interdependent chemical pair in which vitamin E protects PUFA, whereas excess PUFA “consume” vitamin E, a high PUFA/vitamin E ratio being generally assumed as disadvantageous. In cells, both PUFA and vitamin E have their own redox-independent regulatory functions, mostly after being metabolized to active lipid mediators able to bind to specific enzymes and receptors involved in modulating specific signal transduction and gene expression pathways. Thus, the efficiency of uptake, transport, and metabolism of vitamin E and PUFA, their interaction, and their consequent relative levels in cells and tissues are important determinants for both physiological and pathophysiological cellular functions and therefore influence the risk for a number of diseases

Global urban environmental change drives adaptation in white clover

Urbanization transforms environments in ways that alter biological evolution. We examined whether urban environmental change drives parallel evolution by sampling 110,019 white clover plants from 6169 populations in 160 cities globally. Plants were assayed for a Mendelian antiherbivore defense that also affects tolerance to abiotic stressors. Urban-rural gradients were associated with the evolution of clines in defense in 47% of cities throughout the world. Variation in the strength of clines was explained by environmental changes in drought stress and vegetation cover that varied among cities. Sequencing 2074 genomes from 26 cities revealed that the evolution of urban-rural clines was best explained by adaptive evolution, but the degree of parallel adaptation varied among cities. Our results demonstrate that urbanization leads to adaptation at a global scale

Rationale and design of a randomized, double-blind, parallel-group study of terutroban 30 mg/day versus aspirin 100 mg/day in stroke patients: the prevention of cerebrovascular and cardiovascular events of ischemic origin with terutroban in patients with a history of ischemic stroke or transient ischemic attack (PERFORM) study.

BACKGROUND: Ischemic stroke is the leading cause of mortality worldwide and a major contributor to neurological disability and dementia. Terutroban is a specific TP receptor antagonist with antithrombotic, antivasoconstrictive, and antiatherosclerotic properties, which may be of interest for the secondary prevention of ischemic stroke. This article describes the rationale and design of the Prevention of cerebrovascular and cardiovascular Events of ischemic origin with teRutroban in patients with a history oF ischemic strOke or tRansient ischeMic Attack (PERFORM) Study, which aims to demonstrate the superiority of the efficacy of terutroban versus aspirin in secondary prevention of cerebrovascular and cardiovascular events. METHODS AND RESULTS: The PERFORM Study is a multicenter, randomized, double-blind, parallel-group study being carried out in 802 centers in 46 countries. The study population includes patients aged > or =55 years, having suffered an ischemic stroke (< or =3 months) or a transient ischemic attack (< or =8 days). Participants are randomly allocated to terutroban (30 mg/day) or aspirin (100 mg/day). The primary efficacy endpoint is a composite of ischemic stroke (fatal or nonfatal), myocardial infarction (fatal or nonfatal), or other vascular death (excluding hemorrhagic death of any origin). Safety is being evaluated by assessing hemorrhagic events. Follow-up is expected to last for 2-4 years. Assuming a relative risk reduction of 13%, the expected number of primary events is 2,340. To obtain statistical power of 90%, this requires inclusion of at least 18,000 patients in this event-driven trial. The first patient was randomized in February 2006. CONCLUSIONS: The PERFORM Study will explore the benefits and safety of terutroban in secondary cardiovascular prevention after a cerebral ischemic event.Journal ArticleMulticenter StudyRandomized Controlled TrialResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe