Academic literature on the topic 'Anoxemia'

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Journal articles on the topic "Anoxemia"

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Peñaloza Ramella, Dante. "El test cardiológico de anoxemia." Anales de la Facultad de Medicina 34, no. 4 (October 18, 2014): 677. http://dx.doi.org/10.15381/anales.v34i4.9548.

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Es perfectamente conocida la importancia fundamental del diagnóstico de certeza del síndrome de Angina de Pecho. Según White, este dindrome constituye el 11.8% de las cardiopatías, lo que demuestra que no es tan infrecuente, sobre todo en las últimas décadas. Es bien sabido, asimismo, el pronóstico relativamente grave de la estenocardia; en la estadística de White, el término medio de vida, después del primer ataque, solo alcanza a 9.1 años. Finalmente, es conocido que, una parte esencial del tratamiento preventivo de los ataques de angor pectoris, es el cambio radical en el modo de vida, lo cual puede acarrear, en muchos casos, consecuencias muy serias para el paciente, desde el punto de vista económico y social. Esta suerte de tratamiento, que interferiría fundamentalmente en la vida del paciente, así como el pronóstico que, como ya hemos dicho, es de relativa gravedad, sólo pueden hacerse justificadamente sobre la base de un diagnóstico indudable del sindrome de angina de pecho.
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Horton, A., and C. Reynolds. "B-11Every Breath You Take: Anoxemia." Archives of Clinical Neuropsychology 31, no. 6 (August 31, 2016): 616.3–616. http://dx.doi.org/10.1093/arclin/acw043.86.

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Hurtado, Alberto, César Merino, and Ernesto Delgado Febres. "La influencia de la anoxemia sobre la actividad hematopoyética." Anales de la Facultad de Medicina 29, no. 2 (October 18, 2014): 125. http://dx.doi.org/10.15381/anales.v29i2.9636.

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Se han realizado investigaciones, al nivel del mar y en la altura, en varios grupos de sujetos (hombres), sanos y enfermos, concernientes a la influencia de la anoxia anóxica (anoxemia) temporal, intermitente y crónica, sobre la morfología y otras características de la sangre circulante. La literatura relacionada ha sido brevemente revisada.
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Larsen, Kaj. "Effect of Anoxemia on the Human Electrocardiogram." Acta Medica Scandinavica 90, S78 (April 24, 2009): 141–49. http://dx.doi.org/10.1111/j.0954-6820.1936.tb15932.x.

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Delgado Febres, Ernesto. "La Bilirrubinemia." Anales de la Facultad de Medicina 32, no. 1 (October 18, 2014): 29. http://dx.doi.org/10.15381/anales.v32i1.9583.

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Se ha estudiado la bilirrubinemia en 201 sujetos aduyltos y aparentemente sanos (159 hombres y 42 mujeres), lo que constituye la serie más numerosa que se ha dado sobre este particular. Asimismo se ha estudiado un grupoi de sujetos que, como única anormalidad aparente presentan cifras elevadas de bilirrubina de tipo indirecto y prueba de excreción para este pigmento (en todos los casos donde se estudió) insuficiente; condición ésta que, con diferentes nombres, ha sido estudiada por varios autores, cuyo conocimiento tiene gran valor. Igualmente se ha estudiado la bilirrubinemia y la función hepática relacionado con la excreción de este pigmento en diferentes condiciones de anoxemia; crónica, aguda (exposición por 4 horas y por 7 días); asimismo y desde ambos puntos de vista se estudió un grupo de sujetos nativos trasladados de Morocoha a Lima, a fin de observar el comportamiento de la bilirrubina de la sangre, y de la función hepática correspondiente, cuando se hace cesar la anoxemia. En condiciones patológicas se ha hecho un estudio comparativo y seriado en algunos casos en 144 enfermas, de los datos que proporciona la técnica de Malloy y Evelyn, son los que se suministra la clásica reacción de Van den Bergh.
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Kozlova, Elena, Ekaterina Sherstyukova, Viktoria Sergunova, Andrey Grechko, Artem Kuzovlev, Snezhanna Lyapunova, Vladimir Inozemtsev, Aleksandr Kozlov, and Aleksandr Chernysh. "Atomic Force Microscopy and High-Resolution Spectrophotometry for Study of Anoxemia and Normoxemia in Model Experiment In Vitro." International Journal of Molecular Sciences 24, no. 13 (July 3, 2023): 11043. http://dx.doi.org/10.3390/ijms241311043.

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The oxygen content in the blood may decrease under the influence of various physicochemical factors and different diseases. The state of hypoxemia is especially dangerous for critically ill patients. In this paper, we describe and analyze the changes in the characteristics of red blood cells (RBCs) with decreasing levels of oxygen in the RBC suspension from normoxemia to hypoxemia/anoxemia in an in vitro model experiment. The RBCs were stored in hypoxemia/anoxemia and normoxemia conditions in closed and open tubes correspondingly. For the quantitative study of RBC parameter changes, we used atomic force microscopy, digital spectrophotometry, and nonlinear curve fitting of the optical spectra. In both closed and open tubes, at the end of the storage period by day 29, only 2% of discocytes remained, and mainly irreversible types, such as microspherocytes and ghosts, were observed. RBC hemolysis occurred at a level of 25–30%. Addition of the storage solution, depending on the concentration, changed the influence of hypoxemia on RBCs. The reversibility of the change in hemoglobin derivatives was checked. Based on the experimental data and model approach, we assume that there is an optimal level of hypoxemia at which the imbalance between the oxidative and antioxidant systems, the rate of formation of reactive oxygen species, and, accordingly, the disturbances in RBCs, will be minimal.
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Ordóñez, J. Hernando. "Biología en la altura." Anales de la Facultad de Medicina 35, no. 1 (October 18, 2014): 193. http://dx.doi.org/10.15381/anales.v35i1.9350.

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La saturación de oxígeno en la sangre de la altura de Bogotá (2,640 metros; es normal o casi normal. En esta altura se han observado los siguientes datos: el pulso es anormal, la tensión arterial no está modificada, el electrocardiograma no muestra signos de anoxemia. No se han observado modificaciones del metabolismo, ni de la respiración ni del sistema nervioso. De una manera excepcional se han observado algunos síntomas leves del mal de las montañas crónicas. Se ha observado una melanosis generalizada la cual es por carencia de algunos factores en la alimentación y parece que la altura tenga un papel secundario en su patogenia. Hace falta estudiar más el comportamiento especial de algunas enfermedades, cardiopatías y neumopatías especialmente, en la altura. Otro tanto puede decirse de las condiciones del ejercicio en la altura.
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Voronina, T. A. "Antioxidants/antihypoxants: the missing puzzle piece in effective pathogenetic therapy for COVID-19." Infekcionnye bolezni 18, no. 2 (2020): 97–102. http://dx.doi.org/10.20953/1729-9225-2020-2-97-102.

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This review focuses on the specific characteristics of COVID-19 disease, which leads not only to respiratory impairments (bronchoalveolar epithelium does not retain oxygen, etc.), but also decreases the level of hemoglobin and its ability to transfer oxygen to the organs and tissues and increases the level of heme, resulting in anoxemia, hypoxia in all organs and tissues, and oxidative stress. Mexidol, a drug developed in Russia, is widely used in clinical practice, including the treatment of diseases accompanied by ischemia and hypoxia. Mexidol has antihypoxic and antioxidant effects, can treat mitochondrial respiratory dysfunction, thereby affecting the key processes in different cells of organs and tissues that develop due to hypoxia. Mexidol can be useful in the comprehensive therapy of patients with COVID-19. Key words: COVID-19, antioxidant, antihypoxant, hemoglobin, hypoxia, Mexidol, mitochondrial dysfunction, oxidative stress
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Monge M., Carlos. "La estimulación suprarrenal por la anoxemia aguda expresada en la variación de los eosinófilos circulantes." Anales de la Facultad de Medicina 37, no. 1 (October 18, 2014): 100. http://dx.doi.org/10.15381/anales.v37i1.9428.

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Los problemas de la vida en la altitud han suscitado interés y preocupación, e inducido a múltiples estudios a investigadores peruanos y extranjeros. El anhelo de comprensión ha sido tanto del hombre que viviendo allá tiene en equilibrio su fisiología frente al rigor ambiental, como del que habitando a nivel del mar asciende a las altas montañas, siendo sometido así a una "agresión anóxica", contra la que tiene que luchar.
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Richalet, Jean-Paul. "The invention of hypoxia." Journal of Applied Physiology 130, no. 5 (May 1, 2021): 1573–82. http://dx.doi.org/10.1152/japplphysiol.00936.2020.

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The word “hypoxia” has recently come to the attention of the general public on two occasions, the Nobel Prize in Medicine or Physiology in 2019 and the recent COVID-19 pandemic. In the academic environment, hypoxia is a current topic of research in biology, physiology, and medicine: in October 2020, there were more than 150,000 occurrences of “hypoxia” in the PubMed database. However, the first occurrence is dated to 1945, while the interest for the effects of oxygen lack on the living organisms started in the mid-19th century, when scientists explored high altitude regions and mainly used the terms “anoxia” or “anoxemia.” I therefore researched online through multiple databases to look for the first appearance of “hypoxia” and related terms “hypoxemia” and “hypoxybiosis” in scientific literature published in English, German, French, Italian, and Spanish. Viault and Jolyet used “Hypohématose” in 1894, but this term has not been used since. Hypoxybiosis first appeared in 1909 in Germany, then hypoxemia in 1923 in Austria, and hypoxia in 1938 in Holland. It was then exported to the United States where it appeared in 1940 in cardiology and anesthesiology. The clinical distinction between anoxia and hypoxia was clearly defined by Carl Wiggers in 1941. Hypoxia (decrease in oxygen), by essence variable in time and in localization in the body, in contrast with anoxia (absence of oxygen), illustrates the concept of homeodynamics that defines a living organism as a complex system in permanent instability, exposed to environmental and internal perturbations.
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Dissertations / Theses on the topic "Anoxemia"

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Kim, Song-Jung. "Hypoxemia Attenuates Coronary Autoregulation." Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc500734/.

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The effect of hypoxemia on coronary autoregulation was investigated in nine anesthetized, open-chest dogs. The anterior descending coronary artery (LAD) was cannulated and perfused with normoxic arterial blood and with moderately hypoxic blood (0₂ content = 10 + 1 ml 0₂ /dl). LAD blood flow was measured as perfusion pressure was varied from 140 to 40 mmHg. At perfusion pressures at and above 40 mmHg, hypoxemia significantly increased LAD flow. During normoxia, the autoregulatory closed-loop gain (Gc) was significantly greater than zero at perfusion pressures from 60 to 120 mmHg. During hypoxemia, Gc was greater than zero only at perfusion pressures from 80 to 100 mmHg. During hypoxemia, LAD blood flow increased sufficiently to maintain oxygen delivery and consumption constant, but the range and potency of autoregulation was attenuated.
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Vedam, Hima. "Short-term hypoxia and arterial stiffness." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28093.

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The studies in this thesis assess the ventilatory and vascular effects of short-term awake isocapnic hypoxia in healthy subjects and those with obstructive sleep apnoea (OSA). The particular focus of this thesis is the impact of the hypoxic stimulus on indices of arterial stiffness, in particular the augmentation index (AIx) and time to reflection (Tr). The role of nitric oxide in this response in healthy subjects is also examined.
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Saul, Lloyd. "The effect of repeat exercise on exercise-induced arterial hypoxemia /." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98792.

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Exercise-induced hypoxemia [EIAH, arterial PO2 < 90 mmHg and/or alveolar-arterial oxygen partial pressure gradient (A-a DO2) ≥ 25 mmHg] occurs during strenuous exercise in some healthy women. There is conflicting opinion if performing successive bouts of strenuous exercise reduces the severity of EIAH. The aim was to (a) test the hypothesis that the severity of EIAH would be reduced with three successive bouts of strenuous exercise, (b) to determine if repeated bouts of exercise increases hyperventilation thus improving arterial PO2. Seven fit female subjects with EIAH [arterial PO2 or PaO2= 88 +/- 2 mmHg, A-a DO 2 = 25 +/- 3 mmHg and 7 fit female control subjects (PaO2 = 100 +/- 5 mmHg, A-a DO2 = 16 +/- 5 mmHg) performed three bouts of intense exercise on a cycle ergometer at 236 +/- 27 watts [oxygen consumption at end of each set = 48 +/- 6 mL/kg/min, or 96 +/- 5% of maximum] for 5 min each with 10 min of rest between sets. Arterial PO 2 increased [EIAH Delta = +4 +/- 5 mmHg. 95% CI = 0.6 to 7.8; Control Delta = +2 +/- 2 mmHg. 95% CI = 0.4 to 3.6] and arterial PCO 2 or PaCO2 decreased [EIAH Delta = -5 +/- 4 mm Hg, 95% CI = -7.4 to -2.2; Control Delta = -4 +/- 2 mmHg, 95% CI = -5.8 to -2.4] between set 1 and set 3 (P< 0.05). Also, 34% of the variance in the change in PaO2, was explained by the variance in the change of PaCO2 (P < 0.05). In conclusion, repeat exercise improves PaO2, which is related to improved hyperventilation.
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Li, Jingping, and 李京平. "Role of tissue hypoxia in periodontitis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47849563.

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In periodontitis, local oxygen supply and consumption in gingival tissues may be significantly altered due to the inflammatory process. The etiology agent of periodontal disease i.e. anaerobic bacterial biofilm is known to confer a low oxygen tension in the vicinity of periodontitis lesion. The oxygen shortage will lead to the stabilization of HIF-1α, the regulatory subunit of hypoxia-inducible factor (HIF)-1, which through controlling specific downstream genes transcription may modulate multiple cellular functions and hence shape the process of periodontitis. Lipopolysaccharide (LPS), a cell wall component of anaerobic bacteria, has been considered to be involved in the pathogenesis of periodontitis. Its interaction with host peptides including LPS-binding protein (LBP), CD14, MD-2 and Toll-like receptor (TLR) 4 may trigger the production of inflammatory cytokines. In this project we hypothesize that hypoxia and bacterial components may induce HIF-1α activity, which in turn impacts upon on the pathological process of periodontitis. This project aimed to detect in vivo expression of HIF-1α and TLR4 in human gingivae; to examine whether LPS could induce HIF-1α activity through pattern recognition receptor like TLR4 on human primary gingival fibroblasts (HGF); and to investigate the combined effect of hypoxia and LPS on type I collagen metabolism in HGF. Human gingival biopsies were collected from advanced periodontitis or clinically healthy sites. By immunohistochemistry, both HIF-1α and TLR4 peptides appeared to express in gingival epithelium. In periodontal pockets, there appeared a marked increase in HIF-1α and TLR4 expression in fibroblast-like and leukocyte-like cells. Human primary gingival keratinocytes (HGK) and fibroblasts (HGF) were cultured. Transcripts of TLR4, MD-2 and CD14 were identified in HGK, HGF and periodontal tissue using RT-PCR. Their protein products were identified in both cell types in vitro using immunoblotting. LBP transcript was only found in gingival biopsies but not in HGK and HGF culture. HGF treated by Escherichia coli LPS ranging from 0.2 μg/mL to 200 μg/mL showed nuclear accumulation of HIF-1α peptide, detectable by immunocytofluorescence and immunoblotting. This accumulation could be attenuated by treatment with TLR4-neutralizing antibody. Under hypoxia, LPS further increased HIF-1α accumulation. Using quantitative real-time PCR (qPCR), hypoxia and/or LPS appeared to enhance the transcription of certain enzymes or enzyme subunits that are related to collagen assembly and crosslink, including prolyl 4-hydroxylases, lysyl hydroxylases, lysyl oxidase and lysyl oxidase-like enzymes. These increased transcription could be downregulated by pretreatment with TLR4-neutralizing antibody or an HIF-α inhibitor, 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1). Finally, preliminary experiments showed KN-93 [Ca2+/Calmodulin-dependent protein kinase (CaMK) II inhibitor] or cyclosporine-A (calcineurin inhibitor) appeared able to attenuate the LPS-induced HIF-1α accumulation, indicating a possible role for intracellular calcium signal in regulating HIF-1α. In conclusions, human periodontitis is associated with increased expression of TLR4 and HIF-1α in gingivae; hypoxia causes and LPS/TLR4 signal associate with HIF-1α accumulation and activity in human gingival fibroblasts, and subsequently modulate in a certain extend collagen metabolism through upregulating the transcript expression of several collagen-related proteins. All these implicate possibility of an adaptive physiological or pathological response of human gingival fibroblasts towards gram-negative bacterial biofilm challenge in human periodontium.
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Dentistry
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Doctor of Philosophy
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Tam, Wai-kit, and 譚偉傑. "Role of hypoxia inducible factor-alpha (HIF-α) genes inchondrogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47849770.

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Cartilage is an essential skeletal connective tissue in vertebrates. It comprises extracellular matrix components, especially for collagens and proteoglycans. Once the cartilage is damaged, it has limited self-repair capacity. Thus, by understanding the dynamic cellular process of chondrogenesis and chondrocyte differentiation would be necessary in developing therapeutic approaches for cartilage repair. Currently, there is a great interest in the development of cell therapy to repair damaged tissues. In particularly, human mesenchymal stem cells (hMSCs) are attractive candidates for the treatment of skeletal system disorders because they can be greatly expanded ex vivo and they readily differentiate into chondrocytes upon stimulation. Studies have demonstrated low environmental oxygen tension could affect the chondrogenic differentiation of hMSCs. The three basic helix-loop-helix (bHLH) motif-containing hypoxia inducible factor α (HIF-α) subunits (i.e. HIF-1α, HIF-2α and HIF-3α) are the major oxygen-sensitive transcription factors regulating physiological responses under hypoxia. Of significance, HIF-1α has been reported to induce a hyaline chondrocyte-like phenotype in human articular chondrocytes. The aim of this study was to investigate the roles of all three human HIF-α paralogues in chondrogenesis, particularly for the transcriptional regulation of chondrocyte-specific genes, including type II collagen (COL2A1) and aggrecan (AGC1). The effect of all three human HIF-α paralogues on the chondrogenic differentiation of hMSCs could then be investigated. Self-inactivating lentivirus vector (SIN-LV) shuttle plasmids coding for murine SOX9, wild-type and oxygen-insensitive versions of human HIF-1α and HIF-2α or wild-type HIF-3α were generated. These plasmids were used in luciferase-based promoter assays and to generate SIN-LV particles for overexpression studies. Our data revealed that SOX9, a key transactivator of chondrogenesis, strongly activates the transcription of COL2A1 and AGC1. Ectopic expression of HIF-2α could also induce the transcription of COL2A1 and AGC1. Strikingly, a cooperative transcriptional up-regulation of COL2A1 and AGC1 via the overexpression of HIF-1α and SOX9 was observed. Furthermore, HIF-3α was shown to inhibit the SOX9–dependent transcriptional up-regulation of COL2A1 and AGC1. Here, the multipotency of hMSCs cultured under hypoxia (1% O2 tension) was also illustrated. A pilot study for overexpressing exogenous gene in chondrogenic stimulated hMSC pellets via SIN-LV particles is described. Eventually, a rationale is provided for manipulating HIF-α expression in chondrogenic stimulated hMSC pellet via SIN-LVs encoding HIF-α subunits to study the contribution of HIF-α paralogues on promoting the chondrogenic differentiation of hMSCs.
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Orthopaedics and Traumatology
Doctoral
Doctor of Philosophy
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Dinkelacker, Stephen A. "Ecological physiology of overwintering in hatchling Blanding's turtles (Emydoidea blandingii) insights into anoxia tolerance and freeze tolerance /." Oxford, Ohio : Miami University, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=miami1091035075.

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Ma, Shufen. "Seasonal anoxia in the Delaware Inland Bays its development and its effects on nutrient and algal community structure /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 172 Mb., 1.33 p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3200545.

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Schwab, David Earl. "Electron paramagnetic resonance investigations of adducts of human hemoglobin." Thesis, Montana State University, 2010. http://etd.lib.montana.edu/etd/2010/schwab/SchwabD0510.pdf.

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Hemoglobin transports oxygen to the tissues of the body. The delivery of oxygen to tissues by hemoglobin is dependent on blood flow, which is determined by vessel tension regulated by local oxygen gradients. Dilation of the blood vessels in the microcirculation of tissues under high metabolic demand is induced by the endothelium-derived relaxation factor, nitric oxide, in a process known as hypoxic vasodilation. Although the means of nitric oxide bioactivity preservation and transportation in the blood are disputed, it is clear that S-nitrosohemoglobin, a nitrosylated variant of hemoglobin, plays a pivotal role. The details surrounding S-nitrosohemoglobin formation in vivo, however, remain uncertain. Using electron paramagnetic resonance (EPR) spectroscopy, in conjunction with detailed spectral simulation and least-squares fitting, various hemoglobin species which possibly participate in the formation of S-nitrosohemoglobin were characterized. The EPR spectrum of methemoglobin-nitrite, a purported precursor to S-nitrosohemoglobin formation, was determined to be a composite spectrum arising from the presence of two species, the origin of which is proposed to lie in the differences between the distal heme pockets and histidine residues of the alpha- and beta-subunits of hemoglobin. By direct measurement of methemoglobin-nitrite by EPR spectroscopy, the weak affinity of methemoglobin for nitrite was confirmed, precluding nitrite-methemoglobin from having a direct role in physiological hypoxic vasodilation. Furthermore, the temperature dependence of the EPR spectra of the various species of neat methemoglobin was determined, as was the temperature dependence of the nitrosyl-hemoglobin (Hb(NO)â‚„) spectrum at high frequency. The high frequency spectrum of Hb(NO)â‚„ provided additional resolution of the axial and rhombic components of the spectrum, but revealed no evidence of distinct subunit spectra. Finally, synthetic routes to generate Fe(II)NO/Fe(III)-Hb hybrids have been presented, which, among other things, demonstrated that bolus addition of nitric oxide can produce similar results as the addition of time and condition dependent nitric oxide donors. Overall, this work expands the understanding of hemoglobin, specifically with regard to hemoglobin species with possible involvement in S-nitrosohemoglobin formation.
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Mc, Govern Naomi Nuala. "The effects of hypoxia on neutrophil biology." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609111.

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Woodside, John. "Redox regulation of vascular NO bioavailability during hypoxia : implications for oxygen transport and exercise performance." Thesis, University of South Wales, 2010. https://pure.southwales.ac.uk/en/studentthesis/redox-regulation-of-vascular-no-bioavailability-during-hypoxia(9f798152-e88b-408d-85bc-b6dda49a7e6b).html.

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The reduction in O2peak at altitude is well documented. Maximal exercise in hypoxia is accelerated through a reduction in O2 supply with contributions from central and peripheral origins of fatigue. Changes in cerebral and muscle oxygenation have not been well characterised during incremental exercise in hypoxia. It is possible attainment of O2peak is driven by the oxygenation profile of these tissues whilst changes in molecular biomarkers of endothelial function could provide some insight into the mechanisms driving systemic and regional O2 delivery and vascular hypoxic sensing capabilities. The first study of this thesis examined the impact of acute hypoxia (FIO2 = 0.12) on the cerebral and muscle oxygenation response to incremental cycling exercise using NIRS (n = 14; age: 23 ± 5yr; height: 1.80 ± 0.07m; weight: 84 ± 8kg). The profiles were characterised at equivalent relative and absolute exercise intensities and molecular blood-borne markers of O2 sensing and function were measured before and immediately after maximal exercise for changes in oxidative stress (A• and 3-NT), NO metabolites (NOx, NO3•, NO2• and RSNO) and cell adhesion molecules (sICAM-1 and sVCAM-1). The key observations from this study were: 1) O2peak decreased by 22% and the magnitude of cerebral and muscle deoxygenation (↓O2Hb and ↑HHb) was greater in hypoxia, 2) the slope for the relative HHb response was similar between conditions whereas there was an accelerated slope across the absolute workloads in hypoxia implying cycling performance was driven by a premature attainment of maximal O2 extraction capacity of the muscle, 3) there was no evidence suggesting cerebral O2 metabolism was impaired in hypoxia however since SaO2 was 78 ± 4% at PPO it is possible the reduction in systemic O2 delivery could have influenced central fatigue, 4) there was a tendency for a rightward shift in the cerebral THb profile in hypoxia and although muscle THb peaked at 80% PPO in both trials, the response also tended to be lower in hypoxia, 5) there was no change in oxidative stress markers and NOx after exercise, 6) RSNO increased and NO2• decreased after maximal exercise. The decline in NO2• was attenuated in hypoxia possibly due to a blunted NO2•-HHb-NO pathway and may explain the systemic hypoperfusion response, 7) The increase in sICAM-1 and sVCAM-1 after exercise was augmented in normoxia, 8) Only when normoxia and hypoxia data was pooled was there a correlation between sVCAM-1 pre-post exercise and O2peak. Intermittent hypoxia (IH) may be used to improve the efficiency of exercise training and as a pre-acclimatisation strategy prior to high altitude ascent. The purpose of the second study was to evaluate the efficacy of a 10 day IH regime consisting of 9x 5 min daily exposures of 9.5% O2 breathing followed by equal periods of normoxia on submaximal and maximal cardiorespiratory responses to exercise in hypoxia. Additionally, cerebral and muscle oxygenation was monitored throughout incremental cycling to exhaustion and changes in NO metabolites (NO3•, NO2• and RSNO) and CAMs (sICAM-1 and sVCAM-1) were measured before and immediately after maximal exercise. The key observations from this study were: 1) a tendency for IH to reduce submaximal O2 and increase O2peak in hypoxia, 2) IH increased the muscle THb response to exercise due an increased intercept for both the muscle O2Hb and HHb in the absence of any change in slope, 4) cerebral oxygenation increased (↑O2Hb) at rest and during exercise, 4) the reduction in nitrite was attenuated in the IH group whilst resting sICAM-1 decreased and the pre-post maximal exercise increase in sICAM-1 was augmented after IH. It is concluded that exercise performance in acute hypoxia is driven by the magnitude of hypoxaemia and an accelerated rate of cerebral and muscle deoxygenation. Molecular biomarkers of endothelial function in particular, NO2• and CAMs, are also influenced by hypoxia and may contribute to the reduction in O2peak. IH may be used to improve exercise economy and O2peak in hypoxia by improving cerebral and muscle oxygenation in the absence of any change in central O2 delivery. It is possible a recalibration of mechanisms that affect NO bioactivation could have enhanced vascular hypoxic sensitivity, O2 delivery and adaptation within brain and muscle tissue which ultimately translated to an improved hypoxic exercise performance. These results give motivation for athletes and mountaineers to incorporate an IH strategy prior to athletic performance at altitude.
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Books on the topic "Anoxemia"

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H, Hackett Peter, Roach Robert C. 1956-, Wagner P. D, and International Hypoxia Symposium (11th : 1999 : Edmonton, Alta.), eds. Hypoxia: Into the next millennium. New York: Kluwer Academic/Plenum Publishers, 1999.

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1950-, Rabalais Nancy N., United States. Minerals Management Service. Gulf of Mexico OCS Region, and Louisiana Universities Marine Consortium, eds. Influence of hypoxia on the interpretation of effects of petroleum production activities. New Orleans, La: U.S. Dept. of the Interior, Minerals Management Service, Gulf of Mexico OCS Region, 1993.

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Westerländer Gespräche (7th 1992 Westerland, Germany). Tissue reactions in response to hypoxia and ischemia: 7. Westerländer Gespräch Erwin Riesch-Symposium, Westerland, 24 to 27 September 1992. Stuttgart: Gustav Fischer Verlag, 1996.

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Prof, Kaur Charanjit, ed. Hypoxia and the central nervous system. Trivandrum: Transworld Research Network, 2007.

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M, Seredenko M., and Instytut fiziolohiï im. O.O. Bohomolʹt͡s︡i͡a︡., eds. Mekhanizmy razvitii͡a︡ i kompensat͡s︡ii gemicheskoĭ gipoksii. Kiev: Nauk. dumka, 1987.

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6

International, Hypoxia Symposium (7th 1991 Lake Louise Alta ). Hypoxia and mountain medicine: Proceedings of the 7th International Hypoxia Symposium, held at Lake Louise, Canada, February 1991. Oxford: Pergamon Press, 1992.

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7

United, States Congress Senate Committee on Commerce Science and Transportation Subcommittee on Oceans and Fisheries. Harmful algal blooms: Hearing before the Subcommittee on Oceans and Fisheries of the Committee on Commerce, Science, and Transportation, United States Senate, One Hundred Fifth Congress, second session, May 20, 1998. Washington: U.S. G.P.O., 1999.

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8

Chŏn, Yang-suk. Chongyang ŭi sansŏnghwa e ŭihan HIF-1[alpha] kwabarhyŏn kijŏn kyumyŏng kwa saeroun hangam chʻiryo tʻaget ŭi palgul =: Mechanism of HIF-1[alpha] overexpression in acidified tumor and novel target for anticancer therapy. [Seoul]: Pogŏn Pokchibu, 2007.

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9

1921-, Monge Cassinelli Carlos, ed. Hypoxia, polycythemia, and chronic mountain sickness. Baltimore: Johns Hopkins University Press, 1987.

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10

Sharpe, Ann. Studies in perinatal lamb mortality in prolific sheep. Dublin: University College Dublin, 1998.

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