scholarly journals On the pathways feeding the H2 production process in nutrient-replete, hypoxic conditions. Commentary on the article “Low oxygen levels contribute to improve photohydrogen production in mixotrophic non-stressed Chlamydomonas cultures”, by Jurado-Oller et al., Biotechnology for Biofuels, published September 7, 2015; 8:149

2017 ◽  
Vol 10 (1) ◽  
Author(s):  
Alberto Scoma ◽  
Szilvia Z. Tóth
Keyword(s):  
Production Process ◽  
H2 Production ◽  
Low Oxygen ◽  
Oxygen Levels ◽  
Hypoxic Conditions

scholarly journals The effects of acute oxygen changes on heart rate in the freshwater crab Poppiana dentata (Randall, 1840)

2020 ◽  
Vol 48 (3) ◽  
pp. 480-487
Author(s):  
Delezia Shivani Singh ◽  
Mary Alkins-Koo ◽  
Luke Victor Rostant ◽  
Azad Mohammed
Keyword(s):  
Heart Rate ◽  
Invasive Technique ◽  
Cardiac Physiology ◽  
Low Oxygen ◽  
Heart Rates ◽  
Oxygen Levels ◽  
Non Invasive ◽  
Hypoxic Conditions ◽  
Cardiac Responses ◽  
Insight Into

Heart rate is a key physiological feature that can be used to assess the response of organisms to changing environmental conditions in aquatic habitats, such as acute fluctuations in oxygen levels and hypoxic conditions. This experiment, therefore, investigated cardiac responses in a freshwater brachyuran species, Poppiana dentata, exposed to low oxygen levels. Heart rate was derived from beats per minute (bpm) signals (n = 576) using an infrared, non-invasive technique over a 96 h period, under different dissolved oxygen (DO) conditions. These involved three regimes: normoxic (6.8 ± 0.1 mg L-1), decreasing DO to hypoxic levels (6.2 to 1.7 mg L-1), and recovery with normoxic levels (6.3 ± 0.1 mg L-1). Changes in heart rates among the three regimes were significant (P < 0.05); reflecting the shift in heart rate during different conditions of oxygen availability, normoxic (59 to 61 bpm), declining DO (54 to 62 bpm) and recovery DO (53 to 64 bpm). Additionally, the normal rhythmicity of heart rates under the normoxic condition was not maintained throughout most of the declining DO and recovery periods. P. dentata has demonstrated cardiac compensations in heart rate during low oxygen levels, providing insight into the species cardiac physiology.

scholarly journals Low oxygen levels caused by Noctiluca scintillans bloom kills corals in Gulf of Mannar, India

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
K. Diraviya Raj ◽  
G. Mathews ◽  
David O. Obura ◽  
R. L. Laju ◽  
M. Selva Bharath ◽  
...  
Keyword(s):  
Coral Reefs ◽  
Algal Blooms ◽  
Global Climate ◽  
Disease Outbreaks ◽  
Gulf Of Mannar ◽  
Coral Mortality ◽  
Low Oxygen ◽  
Noctiluca Scintillans ◽  
Oxygen Levels ◽  
Hypoxic Conditions

AbstractCoral reefs around the world are undergoing severe decline in the past few decades. Mass coral mortalities have predominantly been reported to be caused by coral bleaching or disease outbreaks. Temporary hypoxic conditions caused by algal blooms can trigger mass coral mortalities though are reported rarely. In this study in Gulf of Mannar (GoM), southeast India, we report a significant coral mortality caused by a bloom of the ciguatoxic dinoflagellate Noctiluca scintillans during September–October 2019. Dissolved oxygen levels declined below 2 mg l−1 during the bloom causing temporary hypoxia and mortality (up to 71.23%) in the fast growing coral genera Acropora, Montipora and Pocillopora. Due to global climate change, more frequent and larger algal blooms are likely in the future. Hence, it is likely that shallow water coral reefs will be affected more frequently by episodic hypoxic conditions driven by algal blooms. More studies are, however, required to understand the mechanism of coral mortality due to algal blooms, impacts on community composition and the potential for subsequent recovery.

Adaptation of Human CD4+ T Cells to Pathophysiological Hypoxia: A Transcriptome Analysis

2009 ◽  
Vol 36 (12) ◽  
pp. 2655-2669 ◽  
Author(s):  
TIMO GABER ◽  
THOMAS HÄUPL ◽  
GRIT SANDIG ◽  
KAROLINA TYKWINSKA ◽  
MONIQUE FANGRADT ◽  
...  
Keyword(s):  
T Cells ◽  
Synovial Tissue ◽  
Cd4 T Cells ◽  
Protein Modification ◽  
Quantitative Polymerase Chain Reaction ◽  
Low Oxygen ◽  
Rheumatoid Synovium ◽  
Tissue Samples ◽  
Oxygen Levels ◽  
Hypoxic Conditions

Objective.Inflamed tissues are usually characterized by low oxygen levels. We investigated whether pathophysiological hypoxia (pO2 < 1%) as found in the rheumatoid synovium modulates the transcriptome of human CD4+ T cells.Methods.We analyzed the extent to which hypoxia influences the transcriptome in the rheumatoid synovium according to a gene cluster reflecting adaptation to low oxygen levels. Hypoxia-inducible factor-1α (HIF-1α) was detected in the rheumatoid synovium using immunohistochemistry. Isolated human CD4+ T cells were exposed to hypoxia and analyzed using microarray analysis, quantitative polymerase chain reaction, and immunoblot detection.Results.In rheumatoid arthritis (RA) synovial tissue samples, hypoxia modulates the transcription profile. This profile is similar, but not identical, to that found in isolated CD4+ T cells incubated under hypoxic conditions. We show that HIF-1α is expressed in synovial tissue samples and in hypoxic CD4+ cells; and that hypoxia directly affects differential gene expression in human T cells with up to 4.8% modulation of the transcriptome. Functional genome analysis revealed substantial effects of hypoxia on immune response, transcriptional regulation, protein modification, cell growth and proliferation, and cell metabolism.Conclusion.Severe hypoxia, a feature of joint inflammation, considerably modulates the transcriptome of cells found in the rheumatoid synovium. Human CD4+ T cells adapt to hypoxic conditions mainly by HIF-1-driven effects on the transcriptome reflecting a profound influence on immune functions. Thus, hypoxia must be taken into account when therapeutically targeting inflammation.

scholarly journals A mathematical dissection of the adaptation of cell populations to fluctuating oxygen levels

2019 ◽  
Author(s):  
Aleksandra Ardaševa ◽  
Robert A Gatenby ◽  
Alexander R A Anderson ◽  
Helen M Byrne ◽  
Philip K Maini ◽  
...  
Keyword(s):  
Competitive Advantage ◽  
Phenotypic Variation ◽  
Evolutionary Dynamics ◽  
Chronic Hypoxia ◽  
Evolutionary Strategies ◽  
Metabolic Phenotype ◽  
Cell Populations ◽  
Low Oxygen ◽  
Oxygen Levels ◽  
Hypoxic Conditions

AbstractThe disordered network of blood vessels that arises from tumour angiogenesis results in variations in the delivery of oxygen into the tumour tissue. This brings about regions of chronic hypoxia (i.e. sustained low oxygen levels) and regions with alternating phases of low and relatively higher oxygen levels within vascularised tumours, and makes it necessary for cancer cells to adapt to fluctuating environmental conditions. We use a phenotype-structured model to dissect the evolutionary dynamics of cell populations exposed to fluctuating oxygen levels. In this model, the phenotypic state of every cell is described by a continuous variable that provides a simple representation of its metabolic phenotype, ranging from fully oxidative to fully glycolytic, and cells are grouped into two competing populations that undergo heritable, spontaneous phenotypic variations at different rates. Model simulations indicate that, depending on the rate at which oxygen is consumed by the cells, nonlinear dynamic interactions between cells and oxygen can stimulate chronic hypoxia and cycling hypoxia. Moreover, the model supports the idea that under chronic-hypoxic conditions lower rates of phenotypic variation lead to a competitive advantage, whereas higher rates of phenotypic variation can confer a competitive advantage under cycling-hypoxic conditions. In the latter case, the numerical results obtained show that bet-hedging evolutionary strategies, whereby cells switch between oxidative and glycolytic phenotypes, can spontaneously emerge. We explain how these results can shed light on the evolutionary process that may underpin the emergence of phenotypic heterogeneity in vascularised tumours.

scholarly journals Connectivity Map Analysis Indicates PI3K/Akt/mTOR Inhibitors as Potential Anti-Hypoxia Drugs in Neuroblastoma

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2809
Author(s):  
Paolo Uva ◽  
Maria Carla Bosco ◽  
Alessandra Eva ◽  
Massimo Conte ◽  
Alberto Garaventa ◽  
...  
Keyword(s):  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Drug Repurposing ◽  
Enrichment Analysis ◽  
Mtor Inhibitors ◽  
Gene Set Enrichment Analysis ◽  
Low Oxygen ◽  
Connectivity Map ◽  
Hypoxic Conditions ◽  
Connectivity Score

Neuroblastoma (NB) is one of the deadliest pediatric cancers, accounting for 15% of deaths in childhood. Hypoxia is a condition of low oxygen tension occurring in solid tumors and has an unfavorable prognostic factor for NB. In the present study, we aimed to identify novel promising drugs for NB treatment. Connectivity Map (CMap), an online resource for drug repurposing, was used to identify connections between hypoxia-modulated genes in NB tumors and compounds. Two sets of 34 and 21 genes up- and down-regulated between hypoxic and normoxic primary NB tumors, respectively, were analyzed with CMap. The analysis reported a significant negative connectivity score across nine cell lines for 19 compounds mainly belonging to the class of PI3K/Akt/mTOR inhibitors. The gene expression profiles of NB cells cultured under hypoxic conditions and treated with the mTORC complex inhibitor PP242, referred to as the Mohlin dataset, was used to validate the CMap findings. A heat map representation of hypoxia-modulated genes in the Mohlin dataset and the gene set enrichment analysis (GSEA) showed an opposite regulation of these genes in the set of NB cells treated with the mTORC inhibitor PP242. In conclusion, our analysis identified inhibitors of the PI3K/Akt/mTOR signaling pathway as novel candidate compounds to treat NB patients with hypoxic tumors and a poor prognosis.

Composite Sr- and V-doped LaCrO 3 /YSZ sensor electrode operating at low oxygen levels

2011 ◽  
Vol 16 (6) ◽  
pp. 2113-2120 ◽  
Author(s):  
Anders Lund ◽  
Torben Jacobsen ◽  
Karin Vels Hansen ◽  
Mogens Mogensen
Keyword(s):  
Low Oxygen ◽  
Sensor Electrode ◽  
Oxygen Levels

Could studies on cell responses to low oxygen levels provide improved options for fruit storage and disinfestation?

1996 ◽  
Vol 7 (4) ◽  
pp. 289-299 ◽  
Author(s):  
Christian Chervin ◽  
Colin J. Brady ◽  
Brian D. Patterson ◽  
John D. Faragher
Keyword(s):  
Low Oxygen ◽  
Fruit Storage ◽  
Oxygen Levels ◽  
Cell Responses

scholarly journals Hypoxia-Induced Gene Expression Occurs Solely through the Action of Hypoxia-Inducible Factor 1α (HIF-1α): Role of Cytoplasmic Trapping of HIF-2α

2003 ◽  
Vol 23 (14) ◽  
pp. 4959-4971 ◽  
Author(s):  
Sang-ki Park ◽  
Agnes M. Dadak ◽  
Volker H. Haase ◽  
Lucrezia Fontana ◽  
Amato J. Giaccia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Activity ◽  
Hypoxia Inducible Factor ◽  
Low Oxygen ◽  
Hypoxic Conditions ◽  
Show Evidence ◽  
Dependent Protein ◽  
A Cell ◽  
Cell Type Specific ◽  
Inducible Genes

ABSTRACT The hypoxia-inducible factors 1α (HIF-1α) and 2α (HIF-2α) have extensive structural homology and have been identified as key transcription factors responsible for gene expression in response to hypoxia. They play critical roles not only in normal development, but also in tumor progression. Here we report on the differential regulation of protein expression and transcriptional activity of HIF-1α and -2α by hypoxia in immortalized mouse embryo fibroblasts (MEFs). We show that oxygen-dependent protein degradation is restricted to HIF-1α, as HIF-2α protein is detected in MEFs regardless of oxygenation and is localized primarily to the cytoplasm. Endogenous HIF-2α remained transcriptionally inactive under hypoxic conditions; however, ectopically overexpressed HIF-2α translocated into the nucleus and could stimulate expression of hypoxia-inducible genes. We show that the factor inhibiting HIF-1 can selectively inhibit the transcriptional activity of HIF-1α but has no effect on HIF-2α-mediated transcription in MEFs. We propose that HIF-2α is not a redundant transcription factor of HIF-1α for hypoxia-induced gene expression and show evidence that there is a cell type-specific modulator(s) that enables selective activation of HIF-1α but not HIF-2α in response to low-oxygen stress.

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