Relevant bibliographies by topics / Hypoxic burden

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Academic literature on the topic 'Hypoxic burden'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Hypoxic burden"

1

Hu, Junjie, Wangxiong Hu, and Yanmei Yang. "Hypoxia Confers Tumor with a Higher Immune Infiltration but Lower Mutation Burden in Gastrointestinal Cancer." Journal of Oncology 2022 (September 12, 2022): 1–9. http://dx.doi.org/10.1155/2022/4965167.

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Background. Hypoxia is one of the driving forces of cancer progression, recurrence, and metastasis. However, the association between the tumor hypoxic tumor microenvironment and the tumor mutation burden (TMB) is poorly understood in gastrointestinal cancer. Methods. Approximately 2,000 samples from colorectal cancer (CRC) and stomach adenocarcinoma (STAD) patients were obtained from the gene expression omnibus database and the cancer genome Atlas databases and were clustered and subtyped by nonnegative matrix factorization. Significant differentially expressed genes that were possibly related to survival differences between the hypoxic and normoxic groups were subjected to multivariate Cox regression. Results. Gastrointestinal cancer patients with CRC and STAD were further divided into two subgroups, namely, the hypoxia group and the normoxia group, and hypoxia was correlated with unfavorable outcomes. Notably, hypoxic tumors had lower TMB but significantly higher levels of immune and stromal infiltration. A signature of HEYL and NRP1 selected by LASSO classified gastrointestinal cancer patients into either a low or high-risk group, allowing for the combination of TMB status with markers of hypoxia in future clinical applications. Conclusions. Hypoxia is an independent prognostic factor and a strong immune infiltration indicator in gastrointestinal tumors of different organs, especially for cancers with low TMB.
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Kim, John S., Ali Azarbarzin, Rui Wang, Ina E. Djonlagic, Naresh M. Punjabi, Phyllis C. Zee, Brian B. Koo, Elsayed Z. Soliman, Magdy Younes, and Susan Redline. "Association of novel measures of sleep disturbances with blood pressure: the Multi-Ethnic Study of Atherosclerosis." Thorax 75, no. 1 (August 22, 2019): 57–63. http://dx.doi.org/10.1136/thoraxjnl-2019-213533.

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BackgroundMechanisms underlying blood pressure (BP) changes in obstructive sleep apnoea (OSA) are incompletely understood. We assessed the associations between BP and selected polysomnography (PSG) traits: sleep depth, airflow limitation measurements and OSA-specific hypoxic burden.MethodsThis cross-sectional analysis included 2055 participants from the Multi-Ethnic Study of Atherosclerosis who underwent PSG and BP measurements in 2010–2013. Sleep depth was assessed using the ‘OR product’, a continuous measure of arousability. Airflow limitation was assessed by duty cycle (Ti/Tt) and % of breaths with flow limitation, and hypoxia by ‘hypoxic burden’. Primary outcomes were medication-adjusted systolic BP (SBP) and diastolic BP (DBP). We used generalised linear models adjusted for age, sex, race/ethnicity, smoking, education, body mass index, alcohol use, periodic limb movements and alternative physiological disturbances.ResultsThe sample had a mean age of 68.4 years and apnoea–hypopnoea index of 14.8 events/hour. Sleep depth was not significantly associated with BP. Every 1 SD increment in log-transformed non-rapid eye movement duty cycle was associated with 0.9% decrease in SBP (95% CI: 0.1% to 1.6%), even after adjusting for sleep depth and hypoxic burden. Every 1 SD increment in log-transformed hypoxic burden was associated with a 1.1% increase in SBP (95% CI: 0.1% to 2.1%) and 1.9% increase in DBP (95% CI: 1.0% to 2.8%) among those not using hypertension medications.ConclusionsHigher duty cycle was associated with lower SBP overall and hypoxic burden with higher SBP and DBP among non-BP medication users. These findings suggest changes in both respiratory effort and oxygenation during sleep influence BP.
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Marallano, Valerie, Anirudh Sattiraju, Hongyan Zou, and Roland Friedel. "TAMI-61. EXAMINING THE ROLE OF HYPOXIA INDUCED GENES CXCR4 AND NXPH4 IN INVASION OF HYPOXIC GLIOBLASTOMA CELLS." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi211. http://dx.doi.org/10.1093/neuonc/noab196.843.

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Abstract Hypoxia (low oxygen) has been associated with adverse effects in tumor biology by exaggerating the capabilities of invasion, proliferation, and survival of tumor cells within the tumor microenvironment. We engineered glioblastoma (GBM) proneural cells with a novel hypoxia reporter, HRE-UnaG, to study areas of tumor hypoxia and the effects that these hypoxic cells have on tumorigenesis. Single cell RNA-seq analysis from a mouse intracranially injected with our HRE dUnaG GBM cells revealed a shift to a mesenchymal state upon hypoxia (detected by expression of UnaG). Two genes, CXCR4 and NXPH4, were identified as being specifically induced in the hypoxic population. Our studies focus on the hypothesis that these two hypoxia induced genes, CXCR4 and NXPH4, are upregulated in hypoxic GBM cells, which may allow tumor cells to become more aggressive and resistant to conventional forms of therapies. GBM cells will be transduced with lentiviral vectors for Dox inducible shRNA knockdown of CXCR4 or NXPH4 to test specific contribution of these genes to the phenotype of the hypoxic population, with particular focus on the change in invasion and overall tumor burden upon gene silencing.
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Khouzam, Raefa Abou, Nagwa Ahmed Zeinelabdin, Mohak Sharda, Husam Nawafleh, Ayda shah Mahmood, Munazza Samar Khan, Goutham Hassan Venkatesh, Salem Chouaib, and Shyama Prasad Rao. "Abstract 5679: Application of a hypoxia metric to investigate tumor mutational burden and cancer cell immunogenicity in vitro." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5679. http://dx.doi.org/10.1158/1538-7445.am2022-5679.

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Abstract Hypoxia afflicts the microenvironment of solid tumors fueling tumor malignancy. Using an 8-gene in vitro hypoxia signature, we have recently shown that pancreatic cancer patients with highly hypoxic tumors experience worse survival and exhibit markers of an immunosuppressed microenvironment. Simultaneously, we obtained evidence of increased mutation count in more hypoxic tumors, which accommodates previous reports associating hypoxia with the regulation of tumor mutational burden (TMB) and genomic instability. These two features could enhance tumor immunogenicity by increasing neoantigen expression, enabling immune recognition and tumor eradication. In this work our aim is to further elucidate the underlying role of hypoxia in generating TMB and genomic instability, and how it contributes to cancer cells immunogenicity. To this end, we applied our recently identified 8-gene hypoxia signature to score the hypoxic response of different cancer cells, considering their median expression levels of the signature genes upon exposure to hypoxia (1% oxygen). The hypoxia score was then applied as a metric to distinguish between the highest and lowest scoring cells, enabling a novel approach for evaluating the intrinsic impact of hypoxia on immunogenicity. After twenty passages under hypoxic conditions (1% oxygen), scored cancer cells were subjected to whole exome sequencing (WES) using the Ion Chef System. Following data processing using appropriate bioinformatic tools, variants were called in the hypoxia-treated cells using their normoxic (21% oxygen) counterparts as controls. We first demonstrated that hypoxia induced an increase in TMB in all cell lines. More interestingly, higher scoring cells were found to display, on average, higher TMB than lower scoring cells, suggesting that cells that have a lower hypoxia score tend to be less mutable. Copy number alterations, mutational signature and neoantigen load predictions generated from the WES data will be discussed. The microarray analysis of transcriptomic data from these hypoxia-treated cells, as well as the relationship between the high TMB, high neoantigen load and increased activation of immune response pathways will also be illustrated. Citation Format: Raefa Abou Khouzam, Nagwa Ahmed Zeinelabdin, Mohak Sharda, Husam Nawafleh, Ayda shah Mahmood, Munazza Samar Khan, Goutham Hassan Venkatesh, Salem Chouaib, Shyama Prasad Rao. Application of a hypoxia metric to investigate tumor mutational burden and cancer cell immunogenicity in vitro [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5679.
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Weerackody, Roshan P., David J. Welsh, Roger M. Wadsworth, and Andrew J. Peacock. "Inhibition of p38 MAPK reverses hypoxia-induced pulmonary artery endothelial dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 5 (May 2009): H1312—H1320. http://dx.doi.org/10.1152/ajpheart.00977.2008.

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Hypoxia-induced endothelial dysfunction plays a crucial role in the pathogenesis of hypoxic pulmonary hypertension. p38 MAPK expression is increased in the pulmonary artery following hypoxic exposure. Recent evidence suggests that increased p38 MAPK activity is associated with endothelial dysfunction. However, the role of p38 MAPK activation in pulmonary artery endothelial dysfunction is not known. Sprague-Dawley rats were exposed to 2 wk hypobaric hypoxia, which resulted in the development of pulmonary hypertension and vascular remodeling. Endothelium-dependent relaxation of intrapulmonary vessels from hypoxic animals was impaired due to a reduced nitric oxide (NO) generation. This was despite increased endothelial NO synthase immunostaining and protein expression. Hypoxia exposure increased superoxide generation and p38 MAPK expression. The inhibition of p38 MAPK restored endothelium-dependent relaxation, increased bioavailable NO, and reduced superoxide production. In conclusion, the pharmacological inhibition of p38 MAPK was effective in increasing NO generation, reducing superoxide burden, and restoring hypoxia-induced endothelial dysfunction in rats with hypoxia-induced pulmonary hypertension. p38 MAPK may be a novel target for the treatment of pulmonary hypertension.
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Pardo, Andrea C. "Impact of Seizure Burden in Hypoxic Ischemic Encephalopathy." Pediatric Neurology Briefs 29, no. 10 (November 17, 2015): 74. http://dx.doi.org/10.15844/pedneurbriefs-29-10-1.

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Azarbarzin, Ali, Scott A. Sands, Luigi Taranto-Montemurro, Susan Redline, and Andrew Wellman. "Hypoxic burden captures sleep apnoea-specific nocturnal hypoxaemia." European Heart Journal 40, no. 35 (May 9, 2019): 2989–90. http://dx.doi.org/10.1093/eurheartj/ehz274.

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Azab, Abdel Kareem A., Phong Quang, Feda Azab, Brian Thompson, Patricia Maiso, Aldo M. Roccaro, Antonio Sacco, et al. "Dynamic Regulation of the Level of Hypoxia In the Bone Marrow Regulates Cell Dissemination In Multiple Myeloma." Blood 116, no. 21 (November 19, 2010): 4035. http://dx.doi.org/10.1182/blood.v116.21.4035.4035.

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Abstract Abstract 4035 INTRODUCTION: The interaction of multiple myeloma (MM) cells with the bone marrow (BM) microenvironment plays a crucial role in MM pathogenesis, implying that progression of MM occurs through continuous interaction between the BM and MM cells, which controls the ability of MM cells to egress out of the BM and home into new BM niches. We have previously shown that the CXCR4/SDF1 axis as well as Rho GTPases downstream of the receptor was important for chemotaxis, adhesion, homing and egress of MM cells. However, the driving force for MM cells to leave the BM and metastasize to other BM sites is not well understood. Regions of severe oxygen deprivation (hypoxia) arise in tumors due to rapid cell division and are associated with poor patient prognosis, cell motility, associated angiogenesis and metastasis. In this study, we tested the role of hypoxia in the dissemination of MM cells in vivo, as well as regulation of the retention/egress of MM cells in and out of the BM. METHODS: To test the effect of hypoxia on induction of MM egress, MM1s-GFP+/Luc+ cells were injected into 12 SCID mice, and then mice with different stages of tumor development (based on the tumor size detected by bioluminescence) were treated with the hypoxia marker pimonidazole. Blood was drawn and BM was obtained from the femur. Mononuclear cells were then fixed, permeabilized, and stained with antibodies against pimonidazole, followed with an APC- secondary antibody, PE-mouse-anti-human CXCR4, and anti-cadherin antibody followed by an Alexa-Fluor-594 secondary antibody. MM cells in BM and peripheral blood were identified by gating on cells with high GFP signal. To confirm the effects of severe hypoxia found in vivo compared to physiologic mild hypoxia found in the BM, we tested the effect of mild hypoxic conditions (6% O2) and severe hypoxic conditions (0.5% O2) on MM expression of cadherins and CXCR4, as well on functional adhesion of MM cells to stromal cells and chemotaxis. RESULTS: Twelve mice with different stages of MM tumor progression were used. A bi-phasic correlation between tumor progression and the percent of hypoxic cells in BM was found, showing that severe hypoxic conditions in the BM correlated with tumor burden. The correlation between the tumor burden and the number of circulating cells was not linear; however, a direct linear correlation was observed between the number of circulating MM cells and hypoxia in the BM. Moreover, hypoxia in BM correlated directly with the expression of CXCR4 and negatively correlated with the expression of cadherins in MM cells isolated from the BM. To test the effect of the severe hypoxic conditions induced by tumor progression compared to mild hypoxic conditions found physiologically in the BM, we tested the effect of 0.5% O2 (severe hypoxia) and 6% O2 (mild hypoxia) compared to normoxia (21%) on MM cell adhesion to BMSCs, as well as on chemotaxis in response to SDF1, as well as expression of CXCR4 and cadherins. We found that severe hypoxic conditions decreased MM expression of cadherins and adhesion to BMSCs, as well as increased expression of CXCR4 and chemotaxis to SDF1 compared to cells in normoxia. In contrast, mild hypoxic conditions did not alter the expression of CXCR4 and cadherins, adhesion of MM cells to BMSCs, or chemotaxis of MM to SDF1 compared to normoxic cells. CONCLUSION: Hypoxia in the BM directly correlates with the number of circulating MM cells, and with changes in expression of cadherins and CXCR4 in vivo. Severe hypoxic conditions, but not mild hypoxic conditions, induce hypoxic responses in MM cells. Based on these findings, further studies to manipulate hypoxia in order to regulate tumor dissemination as a therapeutic strategy in MM are warranted. Disclosures: Anderson: Millennium Pharmaceuticals: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau. Ghobrial:Celgene: Membership on an entity's Board of Directors or advisory committees; Millennium: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees.
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Wiese, Melanie, Roman G. Gerlach, Isabel Popp, Jasmin Matuszak, Mousumi Mahapatro, Kirstin Castiglione, Dipshikha Chakravortty, et al. "Hypoxia-Mediated Impairment of the Mitochondrial Respiratory Chain Inhibits the Bactericidal Activity of Macrophages." Infection and Immunity 80, no. 4 (January 17, 2012): 1455–66. http://dx.doi.org/10.1128/iai.05972-11.

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ABSTRACTIn infected tissues oxygen tensions are low. As innate immune cells have to operate under these conditions, we analyzed the ability of macrophages (Mϕ) to killEscherichia coliorStaphylococcus aureusin a hypoxic microenvironment. Oxygen restriction did not promote intracellular bacterial growth but did impair the bactericidal activity of the host cells against both pathogens. This correlated with a decreased production of reactive oxygen intermediates (ROI) and reactive nitrogen intermediates. Experiments with phagocyte NADPH oxidase (PHOX) and inducible NO synthase (NOS2) double-deficient Mϕ revealed that inE. coli- orS. aureus-infected cells the reduced antibacterial activity during hypoxia was either entirely or partially independent of the diminished PHOX and NOS2 activity. Hypoxia impaired the mitochondrial activity of infected Mϕ. Inhibition of the mitochondrial respiratory chain activity during normoxia (using rotenone or antimycin A) completely or partially mimicked the defective antibacterial activity observed in hypoxicE. coli- orS. aureus-infected wild-type Mϕ, respectively. Accordingly, inhibition of the respiratory chain ofS. aureus-infected, normoxic PHOX−/−NOS2−/−Mϕ further raised the bacterial burden of the cells, which reached the level measured in hypoxic PHOX−/−NOS2−/−Mϕ cultures. Our data demonstrate that the reduced killing ofS. aureusorE. coliduring hypoxia is not simply due to a lack of PHOX and NOS2 activity but partially or completely results from an impaired mitochondrial antibacterial effector function. Since pharmacological inhibition of the respiratory chain raised the generation of ROI but nevertheless phenocopied the effect of hypoxia, ROI can be excluded as the mechanism underlying the antimicrobial activity of mitochondria.
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Ramzy, J. A., R. Rengan, M. Mandal, S. Rani, M. E. Vega Sanchez, F. Jaffe, G. D’Alonzo, et al. "0567 Hypoxic Burden and Apnea-Hypopnea Duration in Patients with Positional Obstructive Sleep Apnea." Sleep 43, Supplement_1 (April 2020): A217—A218. http://dx.doi.org/10.1093/sleep/zsaa056.564.

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Abstract Introduction Recently, the measurement of the hypoxic burden and apnea-hypopnea duration has been shown to correlate with mortality in patients with obstructive sleep apnea (OSA). We hypothesized that in patients with mild positional OSA (apnea-hypopnea index [AHI] < 5 events/hr in the non-supine position) the hypoxic burden would be increased and apnea-hypopnea duration shortened and similar to patients with non-positional OSA. Methods Fourteen patients with positional OSA and 24 patients non-positional OSA with similar severity of OSA based on the respiratory event index (REI) were included. All patients had a home sleep apnea test for suspected OSA. The hypoxic burden was calculated by the multiplication of REI and the mean area under the desaturation curves. Results Thirty-eight patients [12 (35%) males, 50±12 yrs, BMI 35±7 kg/m2, Epworth Sleepiness Scale (ESS) 11±8, REI 10±3 events/hr, apnea-hypopnea duration 19±4 sec, mean SaO2 94±2%, lowest SaO2 79±8%, % total sleep time (TST) SaO2 < 90% 11±16%, hypoxic burden 30±17 %min/hr] completed the study. Fourteen patients [9 (64%) males, 46±14 yrs, BMI 31±6 kg/m2, ESS 7±5, REI 9±3 events/hr, mean SaO2 94±2%, lowest SaO2 81±6%, %TST SaO2 < 90% 4±6%] had positional OSA (supine REI 16±7 events/hr, non-supine REI 3±1 events/hr) and 24 patients had non-positional OSA [3 (13%) males, 52±10 yrs, BMI 38±7 kg/m2, ESS 12±9, REI 10±3 events/hr, mean SaO2 94±2%, lowest SaO2 77±9%, %TST SaO2 < 90% 14±19%]. The hypoxic burden was elevated in both the positional and non-positional OSA patients with no difference between the groups (26±19 %min/hr and 32±15 %min/hr, respectively, p=0.13). The apnea-hypopnea duration was similar in positional and non-positional OSA patients (20±3 sec and 18±4 sec, respectively, p=0.08 sec). Conclusion In patients with mild positional OSA the hypoxic burden, which has been associated with cardiovascular mortality, is elevated and similar to patients with non-positional OSA. Support None
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Dissertations / Theses on the topic "Hypoxic burden"

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PERGER, ELISA. "SLEEP APNEA AND HYPOXIA: NEW THERAPEUTIC PROSPECTIVES." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2023. https://hdl.handle.net/10281/404617.

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Un terzo della popolazione europea è affetta da apnee ostruttive del sonno (OSA), patologia che ha conseguenze negative su morbilità cardiovascolare e qualità della vita. L’OSA è caratterizzata da ripetuti episodi di collasso delle alte vie respiratorie che determinano ipossia intermittente, modifiche della pressione intratoracica e risvegli corticali. L’ipossia intermittente ha un ruolo chiave nel determinare le conseguenze cardiovascolari dei disturbi del respiro nel sonno e può sovrapporsi, peggiorandone la prognosi, a condizioni caratterizzate da ipossia tonica quali l’alta quota o le patologie respiratorie croniche o infettive, esacerbando lo stress ossidativo, l’angiogenesi e quindi l’attivazione del sistema nervoso simpatico con conseguenti incrementi della pressione arteriosa, della frequenza cardiaca e dell’infiammazione. Il trattamento gold standard per l’OSA è la terapia ventilatoria che risulta però non tollerata dalla metà dei pazienti che ne fanno uso. Nuove strategie terapeutiche sono pertanto auspicabili. Recentemente sono stati identificati specifici fattori fisiopatologici che contribuiscono allo sviluppo dell’OSA: un’elevata collassabilità delle vie aeree superiori, l’instabilità del sistema di controllo del respiro, una ridotta soglia di arousal ed una ridotta risposta compensatoria dei muscoli dilatatori della faringe. Quest’ultima è dovuta alla perdita di attività noradrenergica e aumento delle influenze muscariniche alle alte vie aeree. Il riconoscimento di questi tratti fisiopatologici ha permesso di ipotizzare e sviluppare nuove strategie terapeutiche per l’OSA. Obiettivo: Valutare l’efficacia della somministrazione per 1 settimana della combinazione di reboxetina (noradrenergico) ed ossibutinina (antimuscarinico) sul trattamento dell’OSA e dell’effetto dei farmaci sugli endotipi fisiopatologici. Metodi: E’ stato condotto uno studio randomizzato controllato cross-over in doppio cieco per comparare 4mg di reboxetina più 5mg di ossibutinina (reb-oxy) in pazienti con OSA. I pazienti sono stati sottoposti ad una polisonnografia basale (PSG), una dopo 7 notti di assunzione di reb-oxy ed una dopo 7 notti di assunzione di placebo per confrontare l’indice di apnea-ipopnea (AHI–outcome primario). Outcome secondari comprendevano il carico ipossico, modifiche degli endotipi, la variabilità della frequenza cardiaca, test di vigilanza. Risultati: Hanno completato lo studio 16 pazienti con età 57 [51-61] anni (mediana [range interquartilico]) ed indice di massa corporea 30 [26-36] kg/m2. Reb-oxy ha determinato una riduzione di AHI da 49 [35-57] eventi/h al basale a 18 [13-21] eventi/h (59% di riduzione mediana) e 39 [29-48] eventi/h (6% riduzione mediana) confrontato con il placebo (p<0·001). La frequenza cardiaca mediana durante la PSG è stata 65 [60-69] bpm al basale ed è aumentata fino a 69 [64-77] bpm dopo reb-oxy e 66 [59-70] bpm dopo placebo (p=0.02). La somministrazione di reb-oxy non ha comportato modifiche di variabilità della frequenza cardiaca, pressione arteriosa nelle 24 ore. Il test di vigilanza si è ridotto da 250 [239-312] ms al basale a 223 [172-244] ms dopo reb-oxy versus 264 [217-284] ms dopo placebo (p<0·001). Conclusioni: Il miglioramento delle conoscenze della fisiopatologia dell’OSA ha permesso di identificare la responsività muscolare delle alte vie come target principale di strategia terapeutica per l’OSA, predisponendo il percorso verso la medicina di precisione anche nel contesto dei disturbi del respiro nel sonno. Il nostro studio ha evidenziato il dato pionieristico dell’effetto positivo della somministrazione di reboxetina più ossibutinina sulla gravità dell’OSA e sull’ipossia associata agli eventi ostruttivi nel sonno. I risultati del nostro studio sottolineano la possibilità di una terapia personalizzata con farmaci per trattare l’OSA ed il carico ipossico ad essa relato.
Introduction: Obstructive sleep apnea (OSA) affects one third of the population in Europe and has major negative consequences for cardiovascular disease and quality of life. OSA is characterized by recurrent episodes of apneas and hypopneas associated with repetitive episodes of intermittent hypoxemia, intrathoracic pressure changes, and arousals. Intermittent hypoxemia, particularly with concomitant hypercapnia, activates the sympathetic nervous system and it is the major contributor to negative cardiovascular consequences. Intermittent hypoxia might also worsen concomitant tonic hypoxia due to high altitude or due to acute or chronic respiratory diseases by promoting oxidative stress and angiogenesis, thus increasing sympathetic activation with blood pressure elevation, inflammation and endothelial dysfunction. Although OSA and its hypoxic consequence are effectively alleviated with positive airways pressure, this treatment is yet unsatisfactory, being poorly tolerated by up to half of patients. Thus, new treatment strategies are strongly needed. With the aim of better understand OSA physiopathology, key contributors of its development have been identified and include upper airway collapsibility, ventilatory instability, low arousal threshold and reduced pharyngeal dilator muscle responsiveness during sleep, due to loss of noradrenergic drive and enhanced muscarinic influences to upper airway muscles. The recognition of these pathophysiological traits permitted to advance the research in the field of OSA new therapeutic perspectives. Aim: The aim of this study was to evaluate the effect of 1-week of reboxetine (a noradrenergic) plus oxybutynin (an antimuscarinic) on OSA severity (primary outcome) and their effect on endotypic traits and cardiovascular autonomic modulation. Methods: We performed a randomized, placebo-controlled, double-blind, crossover trial comparing 4 mg reboxetine plus 5 mg oxybutynin (reb–oxy) to placebo in OSA subjects. After a baseline in-lab polysomnogram (PSG), patients performed PSGs after 7 nights of reb-oxy and 7 nights of placebo to compare apnea-hypopnea index (AHI, primary outcome). Secondary outcomes included hypoxic burden, heart rate variability, blood pressure and heart rate changes and psychomotor vigilance test. Home oximetry evaluated overnight oxygen desaturation throughout treatment. Results: 16 subjects aged 57[51-61] years (median [interquartile range]) with body mass index 30[26-36] kg/m2 completed the study. Reb-oxy lowered AHI from 49[35-57] events/h at baseline to 18[13-21] events/h (59% median reduction) compared with 39[29-48] events/h (6% median reduction) on placebo (p<0·001). Response rate for reb-oxy was 81% versus 13% for placebo p<0·001). Median nocturnal heart rate during the PSG was 65 [60-69] bpm at baseline and increased to 69 [64-77] bpm on reb-oxy vs 66 [59-70] bpm on placebo (p=0.02). Reb-oxy administration was not associated with any modification in heart rate variability, 24-hour, day-time and night-time systolic and diastolic blood pressure. The psychomotor vigilance test decreased from 250[239-312] ms on baseline to 223[172-244] ms on reb-oxy versus 264[217-284] ms on placebo (p<0·001). Home oximetry illustrated acute and sustained improvement in oxygen desaturation index on reb-oxy versus placebo. Conclusions: The recent understanding of OSA pathophysiological mechanisms brought to hypothesize that, among the others, muscle responsiveness would be the main target to develop a precision medicine to treat OSA. We demonstrated that OSA severity and OSA-related hypoxic consequences are greatly decrease by the administration of reboxetine-plus-oxybutynin. These results highlight potential possibilities for personalized medicine with pharmacological therapy to treat OSA and its related hypoxic burden.
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Erupaka, Kinnera. "DETERMINATION OF THE EXTRAVASCULAR BURDEN OF CARBON MONOXIDE (CO) ON HUMAN HEART." UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_theses/501.

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Noninvasive measurements of myocardial carboxymyoglobin levels (%MbCO) and oxygen tensions (PtO2) are difficult to obtain experimentally. We have developed a compartmental model which allows prediction of myocardial %MbCO levels and PtO2 for varied carbon monoxide (CO) exposures. The cardiac compartment in the model consists of vascular subcompartments which contain two tissue subcompartments varying in capillary density. Mass-balance equations for oxygen (O2) and CO are applied for all compartments. Myocardial oxygen consumption and blood flow are quantified from predictive formulas based on heart rate. Model predictions are validated with experimental data at normoxia, hypoxia, exercise and hyperoxia. CO exposures of varying concentration and time (short-high, long-low), CO rebreathing during 100% O2, and exposure during exercise is simulated. Results of the simulations demonstrate that during CO exposures and subsequent therapies, the temporal changes of %MbCO in the heart differ from those of carboxyhemoglobin levels (%HbCO). Analysis of correlation between %HbCO, %MbCO and PtO2 was done to understand myocardial injury due to CO hypoxia. This thesis demonstrates that the model is able to anticipate the uptake and distribution of CO in the human myocardium and thus can be used to estimate the extravascular burden (MbCO, PtO2 ) of CO on the human heart.
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Books on the topic "Hypoxic burden"

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Froio, Sara, and Franco Valenza. Aspiration of gastric contents in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0106.

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This chapter focuses on the pathophysiology, clinical features, management and prevention of aspiration pneumonitis, aspiration pneumonia, and airway obstruction. Aspiration is defined as the inhalation of oropharyngeal or gastric contents into the larynx and lower respiratory tract. Pulmonary syndromes caused by aspiration are different, depending on the amount and nature of the aspirated material, the frequency of aspiration and the host’s response. This results in a chemical burn of tracheobronchial tree and pulmonary parenchyma. The caustic effects of the low pH of the aspirate cause an intense inflammatory reaction. As a consequence, severe hypoxaemia and infiltrates on chest radiograph occur. If colonized oropharyngeal material enters the lungs, aspiration pneumonia develops and antibiotics are needed. Even if not toxic per se, large volumes of fluids may cause suffocation by mechanical obstruction. Prevention of aspiration is of vital importance and the patient at risk must be identified. The major therapeutic approach is to correct hypoxia, support pulmonary function, and prevent pneumonia development.
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Book chapters on the topic "Hypoxic burden"

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Toro-Urrego, Nicolas, Marco Avila-Rodriguez, María Inés Herrera, Andrea Aguilar, Lucas Udovin, and Juan P. Luaces. "Neuroactive Steroids in Hypoxic–Ischemic Brain Injury: Overview and Future Directions." In Neuroprotection - New Approaches and Prospects. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93956.

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Hypoxic–ischemic brain injury is a number one cause of long-term neurologic disability and death worldwide. This public health burden is mainly characterized by a decrease in oxygen concentration and blood flow to the tissues, which lead to an inefficient supply of nutrients to the brain. This condition induces cell death by energy depletion and increases free radical generation and inflammation. Hypoxic–ischemic brain injury may occur in ischemic-stroke and over perinatal asphyxia, being both leading causes of morbidity in adults and children, respectively. Currently, there are no effective pharmaceutical strategies to prevent the triggering of secondary injury cascades, including oxidative stress and metabolic dysfunction. Neuroactive steroids like selective estrogen receptor modulators, SERMs, and selective tissue estrogenic activity regulators, STEARs, exert several neuroprotective effects. These encompass mitochondrial survival, a decrease in reactive oxygen species, and maintenance of cell viability, among others. In this context, these neurosteroids constitute promising molecules, which could modify brain response to injury. Here we show an updated overview of the underlying mechanisms of hypoxic–ischemic brain injury. We also highlight the neuroprotective effects of neurosteroids and their future directions.
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Preda, Carmen-Monica, and Doina Istrătescu. "Etiology of Ulcerative Colitis." In Ulcerative Colitis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106842.

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Ulcerative colitis (UC) is a chronic immune-mediated inflammatory disorder of the colon, related to a complex contribution of environmental and host factors that increase the susceptibility of individuals. Genetics, environmental factors, dysbiosis, and dysregulated immune system: all these components together are necessary to trigger IBD. The temporal sequence of events leading to UC is unknown. UC is not a classically transmitted genetic affliction. The risk of developing the disease is increased in first-degree relatives but there is no evidence that it is related to genetics or environmental factors exposure early in childhood. The environmental factors associated with ulcerative colitis development are diet, smoking, breastfeeding, use of antibiotics or NSAIDs, urban location, pollution exposure, appendectomy, and hypoxia. In normal intestinal homeostasis environment, both innate and adaptive immune systems are integrated with various mediators and immune cells to maintain tolerance to commensal organisms. In UC patients, the innate immune system is responsible for inducing inflammatory reactions, while the adaptive immune system is crucial in the evolution of chronic inflammatory events. With the shifting global burden of ulcerative colitis, more research is needed to better understand the illness’s etiology in order to prevent and find potential novel therapeutic targets or predictors of disease burden in the future.
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Sharma, Anuj, and Deepesh Arora. "Role of Inflammation in Diabetic Retinopathy." In Diabetic Eye Disease - From Therapeutic Pipeline to the Real World [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100175.

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As the global burden of diabetes is increasing there is a corresponding increase in the complications associated with the same. Diabetic retinopathy is a sight threatening complication of diabetes mellitus which was considered to be a microvasculopathy. Recent evidence however, has brought to light that inflammation may be a key player in the pathogenesis of this condition. Levels of inflammatory mediators like Hypoxia inducible factor, TNF-α, IL-6 and IL-1B amongst others have been noted to be elevated in the diabetic vitreous gel. The concept of the neurovascular unit better explains the changes that take place resulting in the breakdown of the blood retinal barriers and how these inflammatory mediators affect the morphology of the retina at a cellular level. Glial cells form a key instrument of this neurovascular structure and are also the cells from where the inflammatory response is initiated. Understanding of the pathogenesis of diabetic retinopathy will help us in finding targeted therapies which may provide long term benefits and possible cure. Few anti-inflammatory medications have shown promise albeit in a small clinical or experimental laboratory setting. However, future research may lead to better understanding of the disease and a better pharmacological intervention.
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Mishra, Rakesh K. "Potential Role of Nuclear Factor κB in Cardiovascular Disease." In Emerging Applications, Perspectives, and Discoveries in Cardiovascular Research, 43–52. IGI Global, 2017. http://dx.doi.org/10.4018/978-1-5225-2092-4.ch003.

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Lung and Cardiovascular disease creating a major health burden in developed countries and primary cause of deaths. Although treatments have progressed, the development of novel treatments for patients with cardiovascular diseases remains a major research goal. Despite modern advances in pharmacological and interventional cardiology, cardiovascular disease still remains a leading cause of morbidity and mortality in all over the world. The nuclear factor (NF)-?B super family of transcription factors has been implicated in the regulation of immune cell maturation, cell survival, and inflammation in many cell types, including cardiac myocytes. Recent studies have shown that NF-?B is cardioprotective during acute hypoxia and reperfusion injury. NF-kB regulates the gene expression of major pro-inflammatory cytokines (TNF-a, IL-b), chemokines [macrophage inflammatory protein (MIP-2), cytokine-induced neutrophil chemoattractant (CINC)], and adhesion molecules (ICAM-1, E selectin) (2), all of which play a major role in lung injury. However, prolonged activation of NF-?B appears to be detrimental and promotes heart failure by eliciting signals that trigger chronic inflammation through enhanced elaboration of cytokines. In this review, we summarize progresses in understanding the NF-kB pathway in lung and cardio-vascular disease development as well as in modulating NF-kB for prevention and therapy.
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Conference papers on the topic "Hypoxic burden"

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Azarbarzin, A., S. A. Sands, K. L. Stone, L. T. Taranto-Montemurro, D. Vena, K. Yaffe, R. Wang, D. P. White, A. Wellman, and S. Redline. "Mechanisms Underlying Increased Hypoxic Burden in Patients with Sleep Apnea." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2592.

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Bondia Real, Elvira, Jaime Signes-Costa, Jose Gavara, César Ríos-Navarro, Vicente Bodí, Paolo Racugno, Maria Pilar Lopez-Lereu, et al. "Hypoxic burden and angiogenic factors in patients with myocardial infarction and obstructive sleep apnea." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa897.

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Azarbarzin, A., S. A. Sands, L. Taranto Montemurro, D. Vena, T. Sofer, S. W. Kim, D. P. White, D. A. Wellman, and S. S. Redline. "Hypoxic Burden Predicts Incident Heart Failure in Adults with Sleep Apnea: The Sleep Heart Health Study." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7369.

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Strassberger, Christian, Ludger Grote, Kaj Stenlöf, Jan Hedner, and Ding Zou. "Reduced hypoxic burden following carbonic anhydrase inhibition in obstructive sleep apnea – a randomized placebo-controlled study." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa747.

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Vena, D., A. Azarbarzin, R. Radmand, B. Radmand, L. Gell, L. Taranto-Montemurro, G. Labarca, et al. "Effect of Oral Appliances on Blood Pressure in Obstructive Sleep Apnea Patients with Elevated Hypoxic Burden." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3735.

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Labarca, G. P., S. Op De Beeck, D. Vena, S. A. Sands, D. P. White, S. S. Redline, A. Wellman, P. J. Strollo, and A. Azarbarzin. "Effect of Hypoglossal Nerve Stimulation on Hypoxic Burden and Sleepiness: Secondary analysis of the STAR trial." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4818.

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Beauperthuy Levy, T., G. Oscullo Yepez, M. Inglés Azorín, A. García-Ortega, J. D. Gómez-Olivas, A. Bekki, and M. Á. Martínez-García. "Hypoxic burden in patients with Obstructive Sleep Apnea and its correlation with other polygraphic parameters and subjective hypersomnia." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3026.

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Trzepizur, Wojciech, Margaux Blanchard, Timothée Ganem, Frédéric Balusson, Mathieu Feuilloy, Jean-Marc Girault, Nicole Meslier, et al. "Association of symptom subtypes and obstructive sleep apnoea-specific hypoxic burden with cardiovascular morbidity and all-cause mortality." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2491.

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Azarbarzin, A., S. A. Sands, M. K. Younes, L. Taranto Montemurro, D. Vena, R. Sadeghi, S. W. Kim, et al. "Post-Event Tachycardia Combined with Sleep Apnea-Specific Hypoxic Burden Is a Strong Predictor of Cardiovascular Morbidity and Mortality." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2526.

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Raju, S., M. C. McCormack, S. R. Patel, K. M. Kunisaki, J. H. Cho, G. D'Souza, S. Wolinksy, T. T. Brown, and N. M. Punjabi. "The Combined Influence of Sleep Disordered Breathing and Impaired Diffusing Capacity on Nocturnal Hypoxemic Burden." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4708.

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Reports on the topic "Hypoxic burden"

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Wu, Xiaoqi, Maoxia Fan, Yaobo Pan, and Dona Guo. Quality of Evidence Supporting the Effects of Ginkgo Terpene Lactone Preparations in Ischemic Stroke: An Overview of Systematic Reviews and Meta-Analyses. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0124.

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Review question / Objective: 2.2.1 Type of studies SRs/MAs of Randomized Controlled Trials (RCTs) of GTLP for IS in any language. 2.2.2 Type of Participants Included patients were diagnosed with IS according to international or national standards, regardless of race, age, gender, time of onset, and source of cases. 2.2.3 Type of Intervention The intervention method in the control group was routine treatment, and the intervention method in the intervention group was GTLP treatment or GTLP combined with the treatment of the control group. 2.2.4 Types of outcomes Conclusions at least need to include clinical efficacy analysis and National Institute of Health Stroke Scale (NIHSS). Condition being studied: Stroke is the second leading cause of death and third leading cause of disability globally.Among them, ischemic stroke (IS) accounts for 70% of all stroke types. It is a central nervous system disease caused by cerebral blood circulation disorder, ischemia and hypoxia .The incidence rate is high and increasing year by year, the age of onset is younger, the disability rate is high, and most patients have different degrees of limb motor dysfunction.In order to reduce the burden of stroke on the society and the patient's family, many articles proposed to strengthen the primary stroke prevention - behavior change and drug intervention.
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