OBM Genetics is an international Open Access journal published quarterly online by LIDSEN Publishing Inc. It accepts papers addressing basic and medical aspects of genetics and epigenetics and also ethical, legal and social issues. Coverage includes clinical, developmental, diagnostic, evolutionary, genomic, mitochondrial, molecular, oncological, population and reproductive aspects. It publishes research articles, reviews, communications and technical notes, etc. There is no restriction on the length of the papers and we encourage scientists to publish their results in as much detail as possible.
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Rapid publication: manuscripts are undertaken in 15.0 days from acceptance to publication (median values for papers published in this journal in the second half of 2021, 1-2 days of FREE language polishing time is also included in this period).
Oxygen Transport Physiology and COVID at High Altitude
Submission Deadline: November 30, 2022 (Open) Submit Now
Prof. Dr. Gustavo Zubieta-Calleja, MD, F.P.V.R.I
Head of High Altitude Pulmonary and Pathology Institute (HAPPI-IPPA), La Paz, Bolivia
Research interests: hypoxia; chronic hypoxia; high altitude; space travel; bioengineering; Acute and Chronic Mountain Sickness and their treatment; pulmonary function; COVID-19, adaptation to high altitude; philosophy of science, tolerance to hypoxia; quantum mechanics in biology.
Dr. Natalia Zubieta-DeUrioste, MD
High Altitude Pulmonary and Pathology Institute (HAPPI-IPPA), La Paz, Bolivia
Research interests: Chronic, intermittent, and acute hypoxia, exercise physiology, stroke, COVID-19, high altitude physiology and medicine, nutrition, respiratory physiology, neuroscience
About the topic:
Oxygen is the fundamental critical element for life on planet Earth. Unavailability of inspired oxygen for more than 5 minutes can lead to death. Generalized hypoxemia can result from hypobaric hypoxia present at high altitude, but it can also result from pulmonary diseases. Localized tissue hypoxemia can arise from vascular obstruction of circulation. The COVID-19 pandemic has shown that extensive lung affectation can be associated with "silent hypoxemia". This condition is not entirely understood, although several papers have addressed the subject. Hypoxemia levels previously thought intolerable at sea level have changed the concepts of oxygen transport physiology. High altitude physiology includes “silent hypoxemia” as humans live under low levels of oxygen pressure known as chronic hypoxia. The Oxygen Transport Triad, described at high altitude, is based on three systems: the pneumo-dynamic pump (air vacuum ventilation of the lungs), the hemo-dynamic pump (blood compression through valve mechanism of the heart), and hemoglobin (oxygen transport molecule in red blood cells). These three pillars of oxygen transport in mammals respond with variations in acute and chronic hypobaric hypoxia. The extensive lung compromise in the COVID aggression, which we have defined as pneumolysis (lung destruction), gives rise to altered oxygen transport and resulting extreme hypoxemia that can be lethal. In COVID, studies are required to show the different hypoxic etiopathogenesis conditions, including shunts, uneven ventilation/ perfusion, diffusion alterations, and hypoventilation. This involves not only alveolar-capillary affectation but also respiratory center alterations. Furthermore, high altitude decreased COVID incidence, and lethality need further studies.
This special issue welcomes the submission of original research, short communications, and review manuscripts within oxygen transport physiology and COVID at high altitude, moving science towards new horizons.
COVID-19, lung, hypoxemia, chronic hypoxia, hypoxia, pneumolysis, pathophysiology, lung fibrosis, respiration, high altitude, chronic hypobaric hypoxia
Received: 18 July 2022; Published: 09 September 2022; doi: 10.21926/obm.genet.2203163
High-altitude pulmonary edema (HAPE) and COVID-19 pneumonia are different diseases, but HAPE-susceptible individuals (whose susceptibility often has a genetic basis) can also suffer from severe COVID-19. We hypothesized that certain pathogenic mechanisms might overlap if such a coincidence occurs, since these patients could react [...]
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