ABSTRACT High-altitude platforms (HAPs) are aircraft, usually unmanned airships or airplanes positioned above 20 km, in the stratosphere, in order to compose a telecommunications network or perform ...remote sensing. In the 1990 and 2000 decades, several projects were launched, but very few had continued. In 2014, 2 major Internet companies (Google and Facebook) announced investments in new HAP projects to provide Internet access in regions without communication infrastructure (terrestrial or satellite), bringing back attention to the development of HAP. This article aims to survey the history of HAPs, the current state-of-the-art (April 2016), technology trends and challenges. The main focus of this review will be on technologies directly related to the aerial platform, inserted in the aeronautical engineering field of knowledge, not detailing aspects of the telecommunications area.
After ascent to high altitude (≥2500 m), the inability of the human body to adapt to the hypobaric and hypoxia environment can induce tissue hypoxia, then a series of high altitude illnesses ...including acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), and high altitude cerebral edema (HACE) would develop. Symptoms of AMS include headache, dizziness, nausea, and vomiting; HAPE is characterized by orthopnea, breathlessness at rest, cough, pink frothy sputum, and results in obvious pulmonary edema that poses significant harm to people; HACE is characterized by ataxia and decreased consciousness, leading to coma and brain herniation which would be fatal if not treated promptly. This review article provides a current understanding of the pathophysiology of these three forms of high altitude illness and elaborates the current prevention and treatment measures of these diseases.
•AHAI refers to a series of syndromes including AMS, HAPE and HACE.•HAPE is related with hypoxic pulmonary hypertension and alveolar fluid clearance.•AMS and HACE is related with cerebral hemodynamics and cytokines variation.•Current chemical drugs used to prevent AHAI have obvious toxic side effects.•Foodborne natural substances should be developed to prevent against AHAI.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Significance
The discovery of the archaic Denisovan hominins is one of the most significant findings in human evolutionary biology in the last decade. However, as of today, we have more questions ...than answers regarding this mysterious hominin group. This study leverages the information from the well-known example of adaptive introgression on the
EPAS1
gene in Tibetans, to gain insight on the history of our species’ interaction with Denisovans. We show that the Tibetan-
EPAS1
haplotype came from the East Asian-specific Denisovan introgression event, and it remained selectively neutral for a long time in the population before positive selection occurred, which may be concurrent with the permanent inhabitation of the Tibetan Plateau after the Last Glacial Maximum (LGM).
Recent studies suggest that admixture with archaic hominins played an important role in facilitating biological adaptations to new environments. For example, interbreeding with Denisovans facilitated the adaptation to high-altitude environments on the Tibetan Plateau. Specifically, the
EPAS1
gene, a transcription factor that regulates the response to hypoxia, exhibits strong signatures of both positive selection and introgression from Denisovans in Tibetan individuals. Interestingly, despite being geographically closer to the Denisova Cave, East Asian populations do not harbor as much Denisovan ancestry as populations from Melanesia. Recently, two studies have suggested two independent waves of Denisovan admixture into East Asians, one of which is shared with South Asians and Oceanians. Here, we leverage data from
EPAS1
in 78 Tibetan individuals to interrogate which of these two introgression events introduced the
EPAS1
beneficial sequence into the ancestral population of Tibetans, and we use the distribution of introgressed segment lengths at this locus to infer the timing of the introgression and selection event. We find that the introgression event unique to East Asians most likely introduced the beneficial haplotype into the ancestral population of Tibetans around 48,700 (16,000–59,500) y ago, and selection started around 9,000 (2,500–42,000) y ago. Our estimates suggest that one of the most convincing examples of adaptive introgression is in fact selection acting on standing archaic variation.
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Acute high-altitude illnesses are of great concern for physicians and people traveling to high altitude. Our recent article “Acute Mountain Sickness, High-Altitude Pulmonary Edema and High-Altitude ...Cerebral Edema, a View from the High Andes” was questioned by some sea-level high-altitude experts. As a result of this, we answer some observations and further explain our opinion on these diseases. High-Altitude Pulmonary Edema (HAPE) can be better understood through the Oxygen Transport Triad, which involves the pneumo-dynamic pump (ventilation), the hemo-dynamic pump (heart and circulation), and hemoglobin. The two pumps are the first physiologic response upon initial exposure to hypobaric hypoxia. Hemoglobin is the balancing energy-saving time-evolving equilibrating factor. The acid-base balance must be adequately interpreted using the high-altitude Van Slyke correction factors. Pulse-oximetry measurements during breath-holding at high altitude allow for the evaluation of high altitude diseases. The Tolerance to Hypoxia Formula shows that, paradoxically, the higher the altitude, the more tolerance to hypoxia. In order to survive, all organisms adapt physiologically and optimally to the high-altitude environment, and there cannot be any “loss of adaptation”. A favorable evolution in HAPE and pulmonary hypertension can result from the oxygen treatment along with other measures.
About 140 million people worldwide live at an altitude above 2500 m. Studies have showed an increase of the incidence of hyperuricemia among plateau populations, but little is known about the ...possible mechanisms. This study aims to assess the effects of high altitude on hyperuricemia and explore the corresponding mechanisms at the histological, inflammatory and molecular levels. This study finds that intermittent hypobaric hypoxia (IHH) exposure results in an increase of serum uric acid level and a decrease of uric acid clearance rate. Compared with the control group, the IHH group shows significant increases in hemoglobin concentration (HGB) and red blood cell counts (RBC), indicating that high altitude hyperuricemia is associated with polycythemia. This study also shows that IHH exposure induces oxidative stress, which causes the injury of liver and renal structures and functions. Additionally, altered expressions of organic anion transporter 1 (OAT1) and organic cation transporter 1 (OCT1) of kidney have been detected in the IHH exposed rats. The adenosine deaminase (ADA) expression levels and the xanthione oxidase (XOD) and ADA activity of liver of the IHH exposure group have significantly increased compared with those of the control group. Furthermore, the spleen coefficients, IL-2, IL-1β and IL-8, have seen significant increases among the IHH exposure group. TLR/MyD88/NF-κB pathway is activated in the process of IHH induced inflammatory response in joints. Importantly, these results jointly show that IHH exposure causes hyperuricemia. IHH induced oxidative stress along with liver and kidney injury, unusual expression of the uric acid synthesis/excretion regulator and inflammatory response, thus suggesting a potential mechanism underlying IHH-induced hyperuricemia.
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•High altitude hypoxia exposure induced hyperuricemia, which was associated with polycythemia.•Liver and kidney injury induced by oxidative stress is one of the possible mechanisms of high altitude hyperuricemia.•TLR/MyD88/NF-κB pathway participated in the high altitude hyperuricemia induced inflammatory response in the joint.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
This study aimed to explore the neural mechanisms underlying high‐altitude (HA) adaptation and deadaptation in perceptual processes in lowlanders. Eighteen healthy lowlanders were administered a ...facial S1‐S2 matching task that included incomplete face (S1) and complete face (S2) photographs combined with ERP technology. Participants were tested at four time points: shortly before they departed the HA (Test 1), twenty‐five days after entering the HA (Test 2), and one week (Test 3) and one month (Test 4) after returning to the lowlands. Compared with those at sea level (SL), shorter reaction times (RTs), shorter latencies of P1 and N170, and larger amplitudes of complete face N170 were found in HAs. After returning to SL, compared with that of HA, the amplitude of the incomplete face P1 was smaller after one week, and the complete face was smaller after one month. The right hemisphere N170 amplitude was greater after entering HA and one week after returning to SL than at baseline, but it returned to baseline after one month. Taken together, the current findings suggest that HA adaptation increases visual cortex excitation to accelerate perceptual processing. More mental resources are recruited during the configural encoding stage of complete faces after HA exposure. The perceptual processes affected by HA exposure are reversible after returning to SL, but the low‐level processing stage differs between incomplete and complete faces due to neural compensation mechanisms. The configural encoding stage in the right hemisphere is affected by HA exposure and requires more than one week but less than one month to recover to baseline.
We demonstrated that high‐altitude adaptation accompanies increased occipital lobe excitation, and more neural resources are recruited during the configural encoding stage. Moreover, this change is reversible after returning to the lowlands, and the neural compensation mechanism exists. It provided new insights for understanding how hypoxia affects nonprefrontal lobe functions.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
The key elements in acclimatization aim at securing the oxygen supply to tissues and organs of the body with an optimal oxygen tension of the arterial blood. In acute exposure, ventilation and heart ...rate are elevated with a minimum reduction in stroke volume. In addition, plasma volume is reduced over 24–48 h to improve the oxygen‐carrying capacity of the blood, and is further improved during a prolonged sojourn at altitude through an enhanced erythropoiesis and larger Hb mass, allowing for a partial or full restoration of the blood volume and arterial oxygen content. Most of these adaptations are observed from quite low altitudes ∼1000 m above sea level (m a.s.l.) and become prominent from 2000 m a.s.l. At these higher altitudes additional adaptations occur, one being a reduction in the maximal heart rate response and consequently a lower peak cardiac output. Thus, in spite of a normalization of the arterial oxygen content after 4 or more weeks at altitude, the peak oxygen uptake reached after a long acclimatization period is essentially unaltered compared with acute exposure. What is gained is a more complete oxygenation of the blood in the lungs, i.e. SaO2 is increased. The alteration at the muscle level at altitude is minor and so is the effect on the metabolism, although it is debated whether a possible reduction in blood lactate accumulation occurs during exercise at altitude. Transient acute mountain sickness (headache, anorexia, and nausea) is present in 10–30% of subjects at altitudes between 2500 and 3000 m a.s.l. Pulmonary edema is rarely seen below 3000 m a.s.l. and brain edema is not seen below 4000 m a.s.l. It is possible to travel to altitudes of 2500–3000 m a.s.l., wait for 2 days, and then gradually start to train. At higher altitudes, one should consider a staged ascent (average ascent rate 300 m/day above 2000 m a.s.l.), primarily in order to sleep and feel well, and minimize the risk of mountain sickness. A new classification of altitude levels based on the effects on performance and well‐being is proposed and an overview given over the various modalities using hypoxia and altitude for improvement of performance.
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BFBNIB, FSPLJ, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
To provide guidance to clinicians about best preventive and therapeutic practices, the Wilderness Medical Society (WMS) convened an expert panel to develop evidence-based guidelines for prevention ...and treatment of acute mountain sickness, high altitude cerebral edema, and high altitude pulmonary edema. Recommendations are graded based on the quality of supporting evidence and the balance between the benefits and risks/burdens according to criteria put forth by the American College of Chest Physicians. The guidelines also provide suggested approaches to prevention and management of each form of acute altitude illness that incorporate these recommendations. This is an updated version of the original WMS Consensus Guidelines for the Prevention and Treatment of Acute Altitude Illness published in 2010 and subsequently updated as the WMS Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness in 2014.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The unexpectedly high flux of cosmic-ray positrons detected at Earth may originate from nearby astrophysical sources, dark matter, or unknown processes of cosmic-ray secondary production. We report ...the detection, using the High-Altitude Water Cherenkov Observatory (HAWC), of extended tera–electron volt gamma-ray emission coincident with the locations of two nearby middle-aged pulsars (Geminga and PSR B0656+14). The HAWC observations demonstrate that these pulsars are indeed local sources of accelerated leptons, but the measured tera–electron volt emission profile constrains the diffusion of particles away from these sources to be much slower than previously assumed. We demonstrate that the leptons emitted by these objects are therefore unlikely to be the origin of the excess positrons, which may have a more exotic origin.
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High-altitude environments present strong stresses for living organisms, which have driven striking phenotypic and genetic adaptations. While previous studies have revealed multiple genetic ...adaptations in high-altitude species, how evolutionary history (i.e., phylogenetic background) contributes to similarity in genetic adaptations to high-altitude environments is largely unknown, in particular in a group of birds. We explored this in 3 high-altitude passerine birds from the Qinghai-Tibet Plateau and their low-altitude relatives in lowland eastern China. We generated transcriptomic data for 5 tissues across these species and compared sequence changes and expression shifts between high- and low-altitude pairs. Sequence comparison revealed that similarity in all 3 high-altitude species was high for genes under positive selection (218 genes) but low in amino acid substitutions (only 4 genes sharing identical amino acid substitutions). Expression profiles for all genes identified a tissue-specific expression pattern (i.e., all species clustered by tissue). By contrast, an altitude-related pattern was observed in genes differentially expressed between all 3 species pairs and genes associated with altitude, suggesting that the high-altitude environment may drive similar expression shifts in the 3 high-altitude species. Gene expression level, gene connectivity, and the interactions of these 2 factors with altitude were correlated with evolutionary rates. Our results provide evidence for how gene sequence changes and expression shifts work in a concerted way in a group of high-altitude birds, leading to similar evolution routes in response to high-altitude environmental stresses.
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