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Sports Medicine - Open Sep 2019There is abundant and mounting information related to the molecular and biological structure and function of the Aquaporin-1 (AQP1) gene and the AQP1-Aquaporin channel.... (Review)
Review
BACKGROUND
There is abundant and mounting information related to the molecular and biological structure and function of the Aquaporin-1 (AQP1) gene and the AQP1-Aquaporin channel. Regulation of water flow across cell membranes is essential for supporting inter- and intracellular fluid balance, which is critical for health and exercise performance. The transmembrane water channel AQP1 is important for cardiorespiratory endurance (CE) because it influences fluid transfers in erythrocytes, endothelial, and pulmonary cells and is vital for transport of ammonium, bicarbonate, carbon dioxide, glycerol, nitric oxide, potassium ion, water, and trans-epithelial and renal water. Very recent publications suggest the association between a DNA sequence variant, rs1049305 (C > G), in the 3'-untranslated region of the AQP1 gene and CE performance. Other reports indicate further significant associations between AQP1 channel and CE phenotypes. The purposes of this systematic review were to examine the extent of the associations between the AQP1 rs1049305 genotype and CE exercise performance and body fluid loss in long-distance runners and AQP1 channel associations with other CE phenotypes.
METHODS
Data sources: A comprehensive review was conducted using PubMed, EMBASE, CINAHL, and Cochrane electronic databases. The search ranged from January 1, 1988, to December 31, 2018. Studies reported in English, French, and Spanish were considered. Eligibility criteria: The criteria for inclusion in the review were (a) case-control study; (b) unequivocal definition of cases and controls; (c) CE was defined as performance in endurance events, laboratory tests, and/or maximal oxygen consumption; (d) exclusion criteria of known causes; (e) genotyping performed by PCR or sequencing; (f) genotype frequencies reported; and (g) no deviation of genotype frequencies from Hardy-Weinberg equilibrium in the control group. Study appraisal: The systematic review included studies examining the AQP1 gene and AQP1 channel structure and function, associations between the AQP1 gene sequence variant rs1049305 (C > G) and CE performance, body fluid loss in long-distance runners, and other studies reporting on the AQP1 gene and channel CE phenotype associations. Synthesis methods: For each selected study, the following data were extracted: authors, year of publication, sample size and number of cases and controls, CE definition, exclusion criteria, inclusion criteria for cases and controls, methods used for genotyping, genotype, allele frequencies and HWE for genotype frequencies in cases and control groups, and method of AQP1 gene and AQP1 channel analysis.
RESULTS
The initial databases search found 172 pertinent studies. Of those, 46 studies were utilized in the final synthesis of the systematic review. The most relevant findings were (a) the identification of an independent replication of the association between AQP1 gene sequence variant rs1049305 (C > G) and CE performance; (b) the association of the rs1049305 C-allele with faster CE running performance; (c) in knockout model, using a linear regression analysis of distance run as a function of Aqp1 status (Aqp1-null vs. wild-type mice) and conditions of hypoxia (ambient [O] = 16%), normoxia (21%), and hyperoxia (40%) indicated that the Aqp1 knockout ran less distance than the wild-type mice (p < 0.001); (d) in vitro, a reduced AQP1 expression was associated with the presence of the rs1049305 G-allele; (e) AQP1 null humans led normal lives and were entirely unaware of any physical limitations. However, they could not support fluid homeostasis when exposed to chronic fluid overload. The limited number of studies with "adequate sample sizes" in various racial and ethnic groups precluding to perform proper in-depth statistical analysis.
CONCLUSIONS
The AQP1 gene and AQP1 channel seems to support homeostatic mechanisms, yet to be totally understood, that are auxiliary in achieving an advantage during endurance exercise. AQP1 functions are vital during exercise and have a profound influence on endurance running performance. AQP1s are underappreciated structures that play vital roles in cellular homeostasis at rest and during CE endurance running exercise. The outcome of the present systematic review provide support to the statement of hypotheses and further research endeavors on the likely influence of AQP1 gene and AQP1 channel on CE performance. Registration: The protocol is not registered.
PubMed: 31486928
DOI: 10.1186/s40798-019-0213-0 -
Free Radical Biology & Medicine Dec 2009Sepsis and multiple organ dysfunction syndrome (MODS) are major causes of morbidity and mortality in the intensive care unit. Recently mitochondrial dysfunction has been... (Review)
Review
Sepsis and multiple organ dysfunction syndrome (MODS) are major causes of morbidity and mortality in the intensive care unit. Recently mitochondrial dysfunction has been proposed as a key early cellular event in critical illness. A growing body of experimental evidence suggests that mitochondrial therapies are effective in sepsis and MODS. The aim of this article is to undertake a systematic review of the current experimental evidence for the use of therapies for mitochondrial dysfunction during sepsis and MODS and to classify these mitochondrial therapies. A search of the MEDLINE and PubMed databases (1950 to July 2009) and a manual review of reference lists were conducted to find experimental studies containing data on the efficacy of mitochondrial therapies in sepsis and sepsis-related MODS. Fifty-one studies were included in this review. Five categories of mitochondrial therapies were defined-substrate provision, cofactor provision, mitochondrial antioxidants, mitochondrial reactive oxygen species scavengers, and membrane stabilizers. Administration of mitochondrial therapies during sepsis was associated with improvements in mitochondrial electron transport system function, oxidative phosphorylation, and ATP production and a reduction in cellular markers of oxidative stress. Amelioration of proinflammatory cytokines, caspase activation, and prevention of the membrane permeability transition were reported. Restoration of mitochondrial bioenergetics was associated with improvements in hemodynamic parameters, organ function, and overall survival. A substantial body of evidence from experimental studies at both the cellular and the organ level suggests a beneficial role for the administration of mitochondrial therapies in sepsis and MODS. We expect that mitochondrial therapies will have an increasingly important role in the management of sepsis and MODS. Clinical trials are now required.
Topics: Animals; Antioxidants; Apoptosis; Cell Hypoxia; Coenzymes; Electron Transport; Free Radical Scavengers; Humans; Mitochondria; Mitochondrial Membranes; Multiple Organ Failure; Oxidative Stress; Recovery of Function; Sepsis
PubMed: 19715753
DOI: 10.1016/j.freeradbiomed.2009.08.019 -
International Journal of Sports... Apr 2018The aim of this study was to carry out a systematic review and meta-analysis of the effects of caffeine supplementation on physiological responses to submaximal... (Meta-Analysis)
Meta-Analysis Review
The aim of this study was to carry out a systematic review and meta-analysis of the effects of caffeine supplementation on physiological responses to submaximal exercise. A total of 26 studies met the inclusion criteria of adopting double-blind, randomized crossover designs that included a sustained (5-30 min) fixed-intensity bout of submaximal exercise (constrained to 60-85% maximal rate of oxygen consumption) using a standard caffeine dose of 3-6 mg·kg administered 30-90 min prior to exercise. Meta-analyses were completed using a random-effects model, and data are presented as raw mean difference (D) with associated 95% confidence limits (CLs). Relative to placebo, caffeine led to significant increases in submaximal measures of minute ventilation (D = 3.36 L·min; 95% CL, 1.63-5.08; P = .0001; n = 73), blood lactate (D = 0.69 mmol·L; 95% CL, 0.46-0.93; P < .00001; n = 208), and blood glucose (D = 0.42 mmol·L; 95% CL, 0.29-0.55; P < .00001; n = 129). In contrast, caffeine had a suppressive effect on ratings of perceived exertion (D = -0.8; 95% CL, -1.1 to -0.6; P < .00001; n = 147). Caffeine had no effect on measures of heart rate (P = .99; n = 207), respiratory exchange ratio (P = .18; n = 181), or oxygen consumption (P = .92; n = 203). The positive effects of caffeine supplementation on sustained high-intensity exercise performance are widely accepted, although the mechanisms to explain that response are currently unresolved. This meta-analysis has revealed clear effects of caffeine on various physiological responses during submaximal exercise, which may help explain its ergogenic action.
Topics: Adult; Blood Glucose; Caffeine; Exercise; Heart Rate; Humans; Lactic Acid; Oxygen Consumption; Perception; Physical Exertion; Pulmonary Gas Exchange
PubMed: 28872376
DOI: 10.1123/ijspp.2017-0312 -
Environmental Research Jan 2023Volatile organic compound (VOC) emissions have attracted wide attention due to their impacts on atmospheric quality and public health. However, most studies reviewed... (Review)
Review
Volatile organic compound (VOC) emissions have attracted wide attention due to their impacts on atmospheric quality and public health. However, most studies reviewed certain aspects of natural VOCs (NVOCs) or anthropogenic VOCs (AVOCs) rather than comprehensively quantifying the hotspots and evolution trends of AVOCs and NVOCs. We combined the bibliometric method with the evolution tree and Markov chain to identify research focus and uncover the trends in VOC emission sources. This study found that research mainly focused on VOC emission characteristics, effects on air quality and health, and VOC emissions under climate change. More studies concerned on AVOCs than on NVOCs, and AVOC emissions have shifted with a decreasing proportion of transport emissions and an increasing share of solvent utilization in countries with high emissions and publications (China and the USA). Research on AVOCs is imperative to develop efficient and economical abatement techniques specific to solvent sources or BTEX species to mitigate the detrimental effects. Research on NVOCs originating from human sources risen due to their application in medicine, while studies on sources sensitive to climate change grew slowly, including plants, biomass burning, microbes, soil and oceans. Research on the long-term responses of NVOCs derived from various sources to climate warming is warranted to explore the evolution of emissions and the feedback on global climate. It is worthwhile to establish an emission inventory with all kinds of sources, accurate estimation, high spatial and temporal resolution to capture the emission trends in the synergy of industrialization and climate change as well as to simulate the effects on air quality. We review VOC emissions from both anthropogenic and natural sources under climate change and their effects on atmospheric quality and health to point out the research directions for the comprehensive control of global VOCs and mitigation of O pollution.
Topics: Humans; Volatile Organic Compounds; Air Pollutants; Ozone; Air Pollution; Solvents; China; Environmental Monitoring
PubMed: 36162470
DOI: 10.1016/j.envres.2022.114386 -
Frontiers in Physiology 2017The European Space Agency has recently announced to progress from low Earth orbit missions on the International Space Station to other mission scenarios such as... (Review)
Review
The European Space Agency has recently announced to progress from low Earth orbit missions on the International Space Station to other mission scenarios such as exploration of the Moon or Mars. Therefore, the Moon is considered to be the next likely target for European human space explorations. Compared to microgravity (μg), only very little is known about the physiological effects of exposure to partial gravity (μg < partial gravity <1 g). However, previous research studies and experiences made during the Apollo missions comprise a valuable source of information that should be taken into account when planning human space explorations to reduced gravity environments. This systematic review summarizes the different effects of partial gravity (0.1-0.4 g) on the human musculoskeletal, cardiovascular and respiratory systems using data collected during the Apollo missions as well as outcomes from terrestrial models of reduced gravity with either 1 g or microgravity as a control. The evidence-based findings seek to facilitate decision making concerning the best medical and exercise support to maintain astronauts' health during future missions in partial gravity. The initial search generated 1,323 publication hits. Out of these 1,323 publications, 43 studies were included into the present analysis and relevant data were extracted. None of the 43 included studies investigated long-term effects. Studies investigating the immediate effects of partial gravity exposure reveal that cardiopulmonary parameters such as heart rate, oxygen consumption, metabolic rate, and cost of transport are reduced compared to 1 g, whereas stroke volume seems to increase with decreasing gravity levels. Biomechanical studies reveal that ground reaction forces, mechanical work, stance phase duration, stride frequency, duty factor and preferred walk-to-run transition speed are reduced compared to 1 g. Partial gravity exposure below 0.4 g seems to be insufficient to maintain musculoskeletal and cardiopulmonary properties in the long-term. To compensate for the anticipated lack of mechanical and metabolic stimuli some form of exercise countermeasure appears to be necessary in order to maintain reasonable astronauts' health, and thus ensure both sufficient work performance and mission safety.
PubMed: 28860998
DOI: 10.3389/fphys.2017.00583 -
Journal of Applied Physiology... Feb 2022Pulmonary gas exchange during diving or in a dry hyperbaric environment is affected by increased breathing gas density and possibly water immersion. During free diving,... (Review)
Review
Pulmonary gas exchange during diving or in a dry hyperbaric environment is affected by increased breathing gas density and possibly water immersion. During free diving, there is also the effect of apnea. Few studies have published blood gas data in underwater or hyperbaric environments: this review summarizes the available literature and was used to test the hypothesis that arterial Po under hyperbaric conditions can be predicted from blood gas measurement at 1 atmosphere assuming a constant arterial/alveolar Po ratio (a:A). A systematic search was performed on traditional sources including arterial blood gases obtained on humans in hyperbaric or underwater environments. The a:A was calculated at 1 atmosphere absolute (ATA). For each condition, predicted arterial partial pressure of oxygen ([Formula: see text]) at pressure was calculated using the 1 ATA a:A, and the measured [Formula: see text] was plotted against the predicted value with Spearman correlation coefficients. Of 3,640 records reviewed, 30 studies were included: 25 were reports describing values obtained in hyperbaric chambers, and the remaining were collected while underwater. Increased inspired O at pressure resulted in increased [Formula: see text], although underlying lung disease in patients treated with hyperbaric oxygen attenuated the rise. [Formula: see text] generally increased only slightly. In breath-hold divers, hyperoxemia generally occurred at maximum depth, with hypoxemia after surfacing. The a:A adequately predicted the [Formula: see text] under various conditions: dry ( = 0.993, < 0.0001), rest versus exercise ( = 0.999, < 0.0001), and breathing mixtures ( = 0.995, < 0.0001). In conclusion, pulmonary oxygenation under hyperbaric conditions can be reliably and accurately predicted from 1 ATA a:A measurements.
Topics: Blood Gas Analysis; Diving; Humans; Hyperbaric Oxygenation; Oxygen; Partial Pressure; Pulmonary Gas Exchange
PubMed: 34941439
DOI: 10.1152/japplphysiol.00569.2021 -
Pharmaceuticals (Basel, Switzerland) May 2020Epilepsy is a serious neurological disorder affecting around 70 million people globally and is characterized by spontaneous recurrent seizures. Recent evidence indicates... (Review)
Review
Epilepsy is a serious neurological disorder affecting around 70 million people globally and is characterized by spontaneous recurrent seizures. Recent evidence indicates that dysfunction in metabolic processes can lead to the alteration of neuronal and network excitability, thereby contributing to epileptogenesis. Developing a suitable animal model that can recapitulate all the clinical phenotypes of human metabolic epilepsy (ME) is crucial yet challenging. The specific environment of many symptoms as well as the primary state of the applicable neurobiology, genetics, and lack of valid biomarkers/diagnostic tests are the key factors that hinder the process of developing a suitable animal model. The present systematic review summarizes the current state of available animal models of metabolic dysfunction associated with epileptic disorders. A systematic search was performed by using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) model. A range of electronic databases, including google scholar, Springer, PubMed, ScienceDirect, and Scopus, were scanned between January 2000 and April 2020. Based on the selection criteria, 23 eligible articles were chosen and are discussed in the current review. Critical analysis of the selected literature delineated several available approaches that have been modeled into metabolic epilepsy and pointed out several drawbacks associated with the currently available models. The result describes available models of metabolic dysfunction associated with epileptic disorder, such as mitochondrial respiration deficits, Lafora disease (LD) model-altered glycogen metabolism, causing epilepsy, glucose transporter 1 (GLUT1) deficiency, adiponectin responsive seizures, phospholipid dysfunction, glutaric aciduria, mitochondrial disorders, pyruvate dehydrogenase (PDH) α-subunit gene (PDHA1), pyridoxine dependent epilepsy (PDE), BCL2-associated agonist of cell death (BAD), Kcna1 knock out (KO), and long noncoding RNAs (lncRNA) cancer susceptibility candidate 2 (lncRNA CASC2). Finally, the review highlights certain focus areas that may increase the possibilities of developing more suitable animal models and underscores the importance of the rationalization of animal models and evaluation methods for studying ME. The review also suggests the pressing need of developing precise robust animal models and evaluation methods for investigating ME.
PubMed: 32466498
DOI: 10.3390/ph13060106 -
Medicine Apr 2016Iron is required for most forms of organisms, and it is the most essential element for the functions of many iron-containing proteins involved in oxygen transport,... (Review)
Review
Iron is required for most forms of organisms, and it is the most essential element for the functions of many iron-containing proteins involved in oxygen transport, cellular respiration, DNA replication, and so on. Disorders of iron metabolism are associated with diverse diseases, including anemias (e.g., iron-deficiency anemia and anemia of chronic diseases) and iron overload diseases, such as hereditary hemochromatosis and β-thalassemia. Hepcidin (encoded by Hamp gene) is a peptide hormone synthesized by hepatocytes, and it plays an important role in regulating the systematic iron homeostasis. As the systemic iron regulator, hepcidin, not only controls dietary iron absorption and iron egress out of iron storage cells, but also induces iron redistribution in various organs. Deregulated hepcidin is often seen in a variety of iron-related diseases including anemias and iron overload disorders. In the case of iron overload disorders (e.g., hereditary hemochromatosis and β-thalassemia), hepatic hepcidin concentration is significantly reduced.Since hepcidin deregulation is responsible for iron disorder-associated diseases, the purpose of this review is to summarize the recent findings on therapeutics targeting hepcidin.Continuous efforts have been made to search for hepcidin mimics and chemical compounds that could be used to increase hepcidin level. Here, a literature search was conducted in PubMed, and research papers relevant to hepcidin regulation or hepcidin-centered therapeutic work were reviewed. On the basis of literature search, we recapitulated recent findings on therapeutic studies targeting hepcidin, including agonists and antagonists to modulate hepcidin expression or its downstream signaling. We also discussed the molecular mechanisms by which hepcidin level and iron metabolism are modulated.Elevating hepcidin concentration is an optimal strategy to ameliorate iron overload diseases, and also to relieve β-thalassemia phenotypes by improving ineffective erythropoiesis. Relative to the current conventional therapies, such as phlebotomy and blood transfusion, therapeutics targeting hepcidin would open a new avenue for treatment of iron-related diseases.
Topics: Hepcidins; Homeostasis; Humans; Iron; Iron Metabolism Disorders
PubMed: 27057839
DOI: 10.1097/MD.0000000000003150 -
Current Problems in Cardiology Feb 2023Transient receptor potential (TRP) family play critical roles in cardiovascular system. TRPM family as largest TRP subfamily is non-voltage Ca2+-activated selective... (Review)
Review
Transient receptor potential (TRP) family play critical roles in cardiovascular system. TRPM family as largest TRP subfamily is non-voltage Ca2+-activated selective channels which has 8 members. This study aimed to discuss the role of TRPM family in cardiovascular system and diseases. Systematic search was performed covering PubMed, ISI Web of Science, and Google Scholar from inception until June 2021 using related keywords and Mesh terms for English studies with human, animal and in-vitro subjects. Finally 10 studies were selected for data extraction. Reviewing the articles showed that TRPM2, TRPM4, TRPM5, TRPM6 and TRPM7 play important roles in cardiovascular system and diseases. TRPM2 could be activated by reactive oxygen species (ROS) and effects on cardiac injury and cardiac fibrosis. TRPM7 and TRPM6 also have been reported to be associated with cardiac fibrosis and atrial fibrosis development respectively. TRPM4 channels contributed to resting membrane potential of cerebral artery smooth muscle cells and atrial contraction. TRPM5 channels are bitter taste sensors and prevent high salt intake and consequently high blood pressure due to the high salt intake. In conclusion based on the proof of the effectiveness of some members of TRPM family in the cardiovascular system, research on other members of this channel group seems to be useful and necessary to find their possible connection to the cardiovascular system.
Topics: Animals; Humans; TRPM Cation Channels; Sodium Chloride, Dietary; Membrane Potentials; Clusterin; Cardiovascular System; Protein Serine-Threonine Kinases
PubMed: 34644560
DOI: 10.1016/j.cpcardiol.2021.101012 -
The Journal of Prosthetic Dentistry Jun 2023Titanium dental implants produced by additive manufacturing have pores that, depending on their size and quantity, may improve osteogenic cell adhesion without impairing... (Review)
Review
STATEMENT OF PROBLEM
Titanium dental implants produced by additive manufacturing have pores that, depending on their size and quantity, may improve osteogenic cell adhesion without impairing mechanical properties. A systematic review of in vitro studies on this topic is lacking.
PURPOSE
The purpose of this systematic review was to answer the question "What is the influence of pores on osteogenic cell adhesion on titanium surfaces produced by additive manufacturing?".
MATERIAL AND METHODS
The study was designed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) 2020 standards and registered in the Open Science Framework (OSF) (osf.io/baw59). A manual search of published articles without language or time restrictions was conducted in November 2022 in the electronic databases PubMed, Scopus, ScienceDirect, Embase, and in the nonpeer-reviewed literature via Google Scholar.
RESULTS
A total of 1338 initial results were found, and after removing duplicates and applying eligibility criteria, 13 articles were included in this review that, according to the Joanna Briggs Institute (JBI) tool, presented a low risk of bias. Pores with larger diameters provide greater a surface area that favors cell filopodia adhesion and has interconnection that optimizes the transport of nutrients and oxygen and bone cell activity.
CONCLUSIONS
The presence of pores on the surface of titanium produced by additive manufacturing increases the adhesion, migration, proliferation, and viability of osteogenic cells.
PubMed: 37353409
DOI: 10.1016/j.prosdent.2023.05.010