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Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
By studying the yak’s positive selection genes related to nutrient metabolism, we learn not only about the genetic features behind the important physiological traits of animals in high-altitude areas, but also receive potential clues about the various (hypoxia-related) high-altitude sickness conditions that affect humans. In addition, a careful study of the yak genome will help increase milk production and meat performance of these important economic animals in high-altitude areas.
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Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
By studying the yak’s positive selection genes related to nutrient metabolism, we learn not only about the genetic features behind the important physiological traits of animals in high-altitude areas, but also receive potential clues about the various (hypoxia-related) high-altitude sickness conditions that affect humans. In addition, a careful study of the yak genome will help increase milk production and meat performance of these important economic animals in highaltitude areas.
Therapeutic Use of Carbonic Anhydrase Inhibitors and Their Multiple Drug Interactions
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Andrea Angeli, Claudiu T. Supuran
Only α-CAs have been reported in vertebrates and, to date, in humans 16 α-CA isozymes or CA-related proteins have been described with different catalytic activity, subcellular localization, and tissue distribution (Hilvo et al., 2005; Thiry et al., 2006; Supuran et al., 2003). Only twelve isoforms showed catalytic activity, among these, they provided five cytosolic forms (CA I, CA II, CA III, CA VII and CA XIII), five membrane-bound isozymes (CA IV, CA IX, CA XII, CA XIV and CA XV), two mitochondrial forms (CA VA and CA VB), and one secreted CA isozyme (CA VI). Several studies demonstrated the important roles of CAs in a variety of physiological processes, and showed that abnormal levels or activities of these enzymes have been often associated with different human diseases (Suparan, 2008; Suparan et al., 2009). Specifically hCA I is found in many tissues and it is involved in retinal and cerebral edema, in this manner, its inhibition may be a valuable tool for fighting these conditions (Gao et al., 2007). hCA II is involved in several diseases, such as glaucoma, edema, epilepsy, and probably altitude sickness (Mincione et al., 2008; Suparan, 2008; De Simone et al., 2009). hCA III is involved in the oxidative stress, characterizing a lot of inflammatory diseases (Barreiro and Hussain, 2010; Brancaccio et al., 2010). hCA IV is surely a drug target for several pathologies, including glaucoma (together with hCA II and XII), retinitis pigmentosa and stroke (Matsui et al., 1996; Tang et al., 2006; Datta et al., 2009). The mitochondrial isoforms hCA VA and VB are targets for obtaining new antiobesity agents (De Simone and Supuran, 2007; Supuran et al., 2008), whereas CA VI is implicated in cariogenesis (Kiveläet al., 1999). CA VII has been noted for its contributions to epileptiform activity together with CA II and XIV (Ruusuvuori, et al., 2004). hCA IX is now a well-established marker of disease progression in many types of hypoxic tumors, and recently its inhibition has been shown to be associated with a significant inhibition of the growth of both primary tumors and metastases (Guler et al., 2010; De Simone and Supuran, 2010; Pastorekova et al., 2006). Finally, hCA XIV is involved in epileptogenesis and, similarly to hCA IV, in some retinopathies, thus, it may be a drug target for innovative agents useful in the management of such disorders (Shah et al., 2005; Ogilvie et al., 2007). Inhibitors of carbonic anhydrase (CAIs) are in clinically use since 1950s, but to date, no CAI showed selectivity for a specific isoform. Given this situation, patients often receive several or more drugs at the same time and, not surprising that an interaction may occur between them. For this reason, this chapter lays down the aspects of drug-drug interactions involving in the clinically used CAIs which all belong to the sulfonamide or sulfamate class (Supuran, 2008; Neri and Supuran, 2011).
Plateau effect on driver’s hazard perception response mode: Graph construction approach
Published in Journal of Transportation Safety & Security, 2023
Chenzhu Wang, Mingyu Hou, Fei Chen, Jiayun Zhu, Jianchuan Cheng, Wu Bo, Ping Zhang, Said M. Easa
Known as “the Roof of the World,” the Qinghai–Tibet Plateau in China has an average altitude of more than 4,500 m (H. Sun, 2010), where the partial pressure of oxygen (about 11 kPa) and atmospheric pressure (about 53 kPa) are lower than the those on the plain. Therefore, after entering the plateau, the respiratory center is indirectly stimulated through the peripheral chemoreceptors (mainly the carotid body), resulting in an early increase in ventilation and subsequent altitude sickness. Altitude sickness is the physiological discomfort caused by hypoxia, primarily as headache, dizziness, cardiopalmus, shortness of breath, and even temporary blackout (Anand & Wu, 2004). After being in a plateau area for some time, the body can adapt, with significantly relieved initial hypoxia symptoms and altitude acclimation. Then the body can inhale more oxygen to compensate, during a gradual transition to stable adaptation (around 1 to 3 months; Li et al., 2012).
Military customized fabric hyperbaric chamber - design and safety aspects
Published in The Journal of The Textile Institute, 2025
R. G. Revaiah, T. M. Kotresh, Balasubramanian Kandasubrmanian
Despite dissemination of knowledge to sojourners, trekkers and mountaineers and soldiers on high altitude illness, HAPO still remains as the most fatal high altitude casualty necessitating onsite treatment methods. Management of HAPO for the troops, sojourners, and mountaineers has been undergoing drastic changes in the positive direction, owing to pharmacological-prophylaxis, availability of HAPO chambers or a combination of both (Keller et al., 1995; Strickland & Kanaan, 2019). Evacuation of patients to a lower altitude for medical institutional admission may completely reverse HAPO conditions. However, in the field area, this has been largely impractical owing to logistic problems, tortuous terrains, and unforgiving mountain conditions. It has been reported that supplemental oxygen and simulated descent are equally effective in the treatment of high altitude sickness (Kasic et al., 1991). One of the best methods to treat a person having the symptoms of high altitude illness is the early treatment by suitable choice of medicines and descent (Dietz & Hackett, 2019) to enhance the partial pressure of the breathing gas. In case descent is not possible, simulate the virtual descent by subjecting the patient to enhanced partial pressure inside fabric hyperbaric chambers to prevent deterioration of the conditions and aid the recovery from impending and fatal HAPO and HACO. HAPO chambers have been used as lifesaving first aid devices for onsite treatment when medical facilities are not available (Dubois et al., 1994). The HAPO chamber is a foldable fabric structure, inflated above ambient pressure using foot/hand pump. Bleeding air regularly from the chamber is essential to avoid carbon dioxide build-up within the chamber.
Technical textiles for military applications
Published in The Journal of The Textile Institute, 2020
R. G Revaiah, T. M. Kotresh, Balasubramanian Kandasubramanian
AMS is most common problem in HAs, which is characterized by headache, nausea, vomiting, lethargy, disinclination towards work and general tiredness. AMS can occur to un-acclimatized lowlanders who ascend quickly to mountains. AMS can also occur to well-acclimatized soldier who performs physically taxing activities at HAs. AMS is generally self-limiting and gets resolved after 2–3 days bed rest. The pathophysiology, prevention and treatment of AMS is published by Imray, Wright, Subudhi, and Roach (2010). The serious form of altitude sickness is high altitude pulmonary oedema (HAPO), which is considered fatal (Korzeniewski, Nitsch-Osuch, Guzek, & Juszczak, 2015). Although HAPO is known to occur to at higher altitude, it has been reported to occur at moderate altitudes also (Gabry, Ledoux, Mozziconacci, & Martin, 2003). The pathogenesis of HAPO is still unknown, but strong evidence indicates that it is triggered by pulmonary hypertension as a result of hypoxic pulmonary vasoconstriction. Systemic blood vessels on exposure to hypoxic conditions dilate. In contrast, pulmonary blood vessels constrict during hypoxic exposure. This constriction is non-homogenous, probably reflects the distribution of smooth muscle in the walls of the arteries. It has been reported that HAPO is caused by an increase in capillary pressure (Maggiorini et al., 2001). It is likely that the hypoxic pulmonary vasoconstriction is patchy, with the result that some pulmonary capillaries are exposed to the high pressure. This causes damage to the capillary walls (stress failure), and they leak a high-protein oedema fluid with erythrocytes. Studies of alveolar fluid obtained by bronchoalveolar lavage in high-altitude pulmonary oedema have convincingly shown that this is a high-permeability type of oedema.