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Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
At high altitude, people are exposed to chronic hypoxia. For example, if the barometric pressure at sea level is 760 mmHg then the inspired partial pressure of oxygen (PIO2) will be 149 mmHg, 101 mmHg in a settlement at 3,000 m, 89 mmHg at 4,000 m and 78 mmHg at 5,000 m. Such hypoxia is a great challenge to the human body and of the more than 140 million people that live above 250 m, 5–10% are at risk of developing chronic mountain sickness. Chronic mountain sickness is a major health problem which is associated with a high haemoglobin concentration and haematocrit, a reduced oxygen saturation and often a high blood pressure in the lung circuit, termed pulmonary hypertension (22). Thus, the questions are: Are populations that live permanently at high altitudes genetically adapted to chronic hypoxia? Do they carry DNA sequence variants such as those possessed by a Finnish family, where a heterozygous EPO receptor gene (EPOR) mutation increased haematocrit (23)?
Radiobiology of Tumours
Published in W. P. M. Mayles, A. E. Nahum, J.-C. Rosenwald, Handbook of Radiotherapy Physics, 2021
Gordon Steel, Catharine West, Alan Nahum
During the 1960s and 1970s, tumour hypoxia was perceived to be one of the principal causes of failure in radiation therapy, and much research effort was directed at developing ways of selectively killing hypoxic cells: high-linear energy transfer (LET) radiations (see Section 6.11.5), hyperbaric oxygen, chemical radiosensitisers, etc. Although the results of individual studies were equivocal, meta-analyses showed that hypoxia modification of radiotherapy worked (Overgaard 1994, 2011). The most recent randomised trials confirmed that targeting hypoxia improves radiotherapy outcomes in head and neck (Overgaard et al. 1998; Janssens et al. 2012) and bladder (Hoskin et al. 2010) cancers. There is also a large body of evidence indicating that hypoxia is an adverse prognostic factor. For example, studies using Eppendorf pO2 microelectrodes showed that hypoxia identified prior to the start of radiotherapy is associated with the treatment failure of cervical (Hockel et al. 1996), head and neck (Nordsmark et al. 2005) and prostate (Movsas et al. 2002; Milosevic et al. 2012) carcinomas and of sarcomas (Nordsmark et al. 2001). There is also good evidence that patients with the most hypoxic tumours benefit most from the addition of hypoxia-modifying agents (e.g. Toustrup et al. 2012; Eustace et al. 2013).
The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
There is, however, a ‘programmed’ form of cell death that is called apoptosis. In this process, the cell shrinks and wraps important chemicals and structures in plasma membranes and signals to phagocytic cells to dispose of them. Apoptosis is usually associated with development. The webs between our toes and fingers, found in the embryo, are removed in this way. More significantly, it happens in severely hypoxic cells, particularly in relation to myocardial infarction and stroke (Marieb and Hoehn 2019). This is one of the reasons why patients are very carefully monitored if any hypoxia is suspected.
Sigma receptor ligands haloperidol and ifenprodil attenuate hypoxia induced dopamine release in rat striatum
Published in Neurological Research, 2022
Murat Gursoy, Zulfiye Gul, R. Levent Buyukuysal
Hypoxia in the brain is a major cause of morbidity and mortality in humans culminating in pathological consequences such as loss of motor activity, speech deficit, gradual muscle weakness and to a few names [35]. These symptoms, namely disruption of spontaneous motor activity, may be linked to altered dopaminergic neurotransmission in the striatum which is a brain region that subserves sensorimotor functions. In striatum, hypoxia causes a depletion in ATP content which leads to neurodegeneration [36,37] via a mechanism involving a massive release of neurotransmitters, mainly dopamine and glutamate [38–42]. In addition to these studies, it has been demonstrated that mild hypoxaemic hypoxia increases extracellular dopamine concentration in the striatum without any change in glutamate release [43] and energy metabolism [44–46]. These findings suggest that hypoxia-induced dopamine toxicity should be a primer therapeutic target for the treatment of hypoxia in various degrees.
Impact of prehospital pediatric asthma management protocol adherence on clinical outcomes
Published in Journal of Asthma, 2022
Alexandra L. Cheetham, Nidhya Navanandan, Jan Leonard, Kelsey Spaur, Geoffrey Markowitz, Kathleen M. Adelgais
EMS interventions stratified by PAS are shown in Table 2. Patient encounters with higher severity distress had a measurably lower EMS contact time, however, there was no difference in the overall documentation of labored breathing by EMS. EMS administered bronchodilators to the majority of patients with no difference based on severity of presentation, yet, only 16.7% of those with a severe presentation (PAS >12) received IM Epinephrine. Intravenous access was obtained in 21.0% (n = 61), however corticosteroids were only given to 7.6% (n = 22) and IV Magnesium Sulfate was not administered during any of the encounters. Overall, protocol adherence occurred in 68.3% of encounters. Reasons for non-adherence in our study population include a failure to administer bronchodilators in 26.9% and failure to administer IM Epinephrine in 83.3% of patients with a severe presentation. All hypoxic patients were treated with oxygen.
Abusive head trauma in India: imaging raises the curtain
Published in International Journal of Injury Control and Safety Promotion, 2022
Hima Pendharkar, Shumyla Jabeen, Nupur Pruthi, K. V. L. N Narasinga Rao, Dhaval Shukla, Nitish Kamble, Kavita V. Jangam, John Vijay Sagar Kommu, Thennarasu Kandavel, Senthil Amudhan
Hypoxic-ischemic injury (HII) is another manifestation that is seen in these children. In young children (<36 months) presenting with acute head trauma, HII more commonly occurs in AHT than in accidental head trauma (Ichord et al., 2007; McKinney et al., 2008). In our study, 22/48 (45.8%) cases showed imaging features of hypoxia. This incidence is higher when compared to the incidence reported by Ichord et al. (2007) and Zimmerman et al. (2007). The CT appearance of HII in our cases (Figure 2A, B) is what is referred to as the ‘Big Black Brain (BBB)’ – a term coined in 1993 by Duhaime et al. (1993) to describe cases of AHT associated with subdural hematoma(s), brain swelling and uni- or bilateral hypo-density involving the entire supratentorial compartment on CT imaging. Whereas unilateral BBB is specific to AHT, bilateral BBB may be seen in hypoxic-ischemic encephalopathy. The area involved by HII undergoes rapid atrophy and the outcome is usually poor. In four of our patients, the part of the cerebral hemisphere that had HII underwent severe atrophy (within eleven to fifteen days). A word of caution is warranted here: by itself, HII in young children is not a determinant of AHT, and correlation with the clinical, imaging and legal scenario is essential.