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1,693 results for “Hypoxia”
Both hypoxia and hypobaria impair baroreflex sensitivity but through different mechanisms
<p><strong>database using hypobaric hypoxia, normobaric hypoxia and hypobaric normoxia on pilot trainee</strong></p>
Data from: Divergent transcriptional patterns are related to differences in hypoxia tolerance between the intertidal and the subtidal sculpins
Transcriptionally mediated phenotypic plasticity as a mechanism of modifying traits in response to an environmental challenge remains an important area of study. We compared the transcriptional responses to low-oxygen (hypoxia) of the hypoxia tolerant intertidal fish, the tidepool sculpin (Oligocottus maculosus) with the closely related hypoxia intolerant subtidal fish, the silverspotted sculpin (Blepsias cirrhosus) to determine if these species use different mechanisms to cope with hypoxia. Individuals from each species were exposed to environmental O2 tensions chosen to yield a similar level of tissue hypoxia and gene transcription was assessed in the liver over time. There was an effect of time in hypoxia, where the greatest transcriptional change in the silverspotted sculpin occurred between 3 to 24 hours in contrast to the tidepool sculpin where the largest transcriptional change occurred between 24 and 72 hours of hypoxia. A number of genes showed similar hypoxia-induced transcription patterns in both species (e.g. genes associated with glycolysis and apoptosis) suggesting they are involved in a conserved hypoxia response. A large set of genes showed divergent transcriptional patterns in the two species, including fatty acid oxidation and oxidative phosphorylation, suggesting that these biological processes may contribute to explaining variation in hypoxia tolerance in these species. When both species were exposed to a single environmental O2 tension, large transcriptional responses were seen in the hypoxia intolerant silverspotted sculpin while almost no response was observed in the hypoxia tolerant tidepool sculpin. Overall, divergent transcription patterns in response to both magnitude and duration of hypoxia provide insights into the processes that may determine an animal's capacity to tolerate frequent bouts of hypoxia in the wild.
Independent losses of the Hypoxia-Inducible Factor (HIF) pathway within Crustacea
<p>Metazoans respond to hypoxic stress via the Hypoxia Inducible Factor (HIF) pathway, a mechanism thought to be extremely conserved due to its importance in monitoring cellular oxygen levels and regulating responses to hypoxia. However, recent work revealed that key members of the HIF pathway have been lost in specific lineages (a tardigrade and a copepod), suggesting alternative mechanisms have evolved but are still undescribed. Using genomic and transcriptomic data from 70 different species across 12 major crustacean groups, we assessed the degree to which the gene <i>HIF</i><i>a</i>, the master regulator of the HIF pathway, was conserved. Mining of protein domains, followed by phylogenetic analyses of gene families, uncovered group-level losses of <i>HIF</i><i>a</i>, including one across three orders within Cirripedia, and in three orders within Copepoda. For these groups, additional assessment showed losses of HIF repression machinery (EGLN, VHL). These results suggest the existence of alternative mechanisms for cellular response to low oxygen, and highlight these taxa as models useful for probing these evolutionary outcomes.</p>
Distal and proximal hypoxia response elements cooperate to regulate organ-specific erythropoietin gene expression
<p>While it is well-established that distal hypoxia response elements (HREs) regulate hypoxia-inducible factor (HIF) target genes such as erythropoietin (Epo), an interplay between multiple distal and proximal (promoter) HREs has not been described so far. Hepatic Epo expression is regulated by a HRE located downstream of the <i>EPO</i> gene, but this 3' HRE is dispensable for renal <i>EPO</i> gene expression. We previously identified a 5' HRE and could show that both HREs direct exogenous reporter gene expression. Here, we show that whereas in hepatic cells the 3' but not the 5' HRE is required, in neuronal cells both the 5' and 3' HREs contribute to endogenous Epo induction. Moreover, two novel putative HREs were identified in the <i>EPO</i> promoter. In hepatoma cells HIF interacted mainly with the distal 3' HRE, but in neuronal cells HIF most strongly bound the promoter, to a lesser extent the 3' HRE, and not at all the 5' HRE. Interestingly, mutation of either of the two distal HREs abrogated HIF binding to the 3' and promoter HREs. These results suggest that a canonical functional HRE can recruit multiple, not necessarily HIF, transcription factors to mediate HIF binding to different distant HREs in an organ-specific manner.</p>
Hypoxia-inducible factor induces cysteine dioxygenase and promotes cysteine homeostasis in Caenorhabditis elegans
<p>Dedicated genetic pathways regulate cysteine homeostasis. For example, high levels of cysteine activate cysteine dioxygenase, a key enzyme in cysteine catabolism in most animal and many fungal species. The mechanism by which cysteine dioxygenase is regulated is largely unknown. In an unbiased genetic screen for mutations that activate cysteine dioxygenase (<em>cdo-1</em>) in the nematode <em>C. elegans, </em>we isolated loss-of-function mutations in <em>rhy-1 </em>and <em>egl-9, </em>which encode proteins that negatively regulate the stability or activity of the oxygen-sensing hypoxia-inducible transcription factor (<em>hif-1</em>). EGL-9 and HIF-1 are core members of the conserved eukaryotic hypoxia response. However, we demonstrate that the mechanism of HIF-1-mediated induction of <em>cdo-1 </em>is largely independent of EGL-9 prolyl hydroxylase activity and the von Hippel-Lindau E3 ubiquitin ligase, the classical hypoxia signaling pathway components. We demonstrate that <em>C. elegans cdo-1 </em>is transcriptionally activated by high levels of cysteine and <em>hif-1</em>. <em>hif-1-</em>dependent activation of <em>cdo-1</em> occurs downstream of an H<sub>2</sub>S-sensing pathway that includes <em>rhy-1, cysl-1, </em>and <em>egl-9.</em> <em>cdo-1 </em>transcription is primarily activated in the hypodermis where it is also sufficient to drive sulfur amino acid metabolism. Thus, the regulation of <em>cdo-1 </em>by <em>hif-1 </em>reveals a negative feedback loop that maintains cysteine homeostasis. High levels of cysteine stimulate the production of an H<sub>2</sub>S signal. H<sub>2</sub>S then acts through the <em>rhy-1/cysl-1/egl-9 </em>signaling pathway to increase HIF-1-mediated transcription of <em>cdo-1, </em>promoting the degradation of cysteine via CDO-1.</p>
Thermal-metabolic phenotypes of the lizard Podarcis muralis differ across elevation, but converge in high elevation hypoxia
<p>In response to a warming climate, many montane species are shifting upslope to track the emergence of preferred temperatures. Characterizing patterns of variation in metabolic, physiological and thermal traits along an elevational gradient, and the plastic potential of these traits, is necessary to understand current and future responses to abiotic constraints at high elevations, including limited oxygen availability. We performed a transplant experiment with the upslope-colonizing common wall lizard (<em>Podarcis</em> <em>muralis</em>) in which we measured nine aspects of thermal physiology and aerobic capacity in lizards from replicate low- (400 m above sea level, ASL) and high-elevation (1700 m ASL) populations. We first measured traits at their elevation of origin and then transplanted half of each group to extreme high elevation (2900 m ASL; above the current elevational range limit of this species), where oxygen availability is reduced by ∼25% relative to sea level. After 3 weeks of acclimation, we again measured these traits in both the transplanted and control groups. The multivariate thermal–metabolic phenotypes of lizards originating from different elevations differed clearly when measured at the elevation of origin. For example, high-elevation lizards are more heat tolerant than their low-elevation counterparts (counter-gradient variation). Yet, these phenotypes converged after exposure to reduced oxygen availability at extreme high elevation, suggesting limited plastic responses under this novel constraint. Our results suggest that high-elevation populations are well suited to their oxygen environments, but that plasticity in the thermal–metabolic phenotype does not pre-adapt these populations to colonize more hypoxic environments at higher elevations.</p>
Fish carcass deposition to suppress invasive lake trout through hypoxia causes limited, non-target effects on benthic invertebrates in Yellowstone Lake
<p class="MsoNormal">Invasive species can have negative effects on native biodiversity and ecosystem function, and suppression is often required to minimize the effects. However, management actions to suppress invasive species may cause negative, unintended effects on non-target taxa. Across the USA, lake trout (<em>Salvelinus namaycush</em>) are invasive in many freshwater ecosystems, reducing native fish abundance and diversity through predation and competition. In an integrated pest management approach, lake trout embryos in Yellowstone Lake, Wyoming are suppressed by depositing lake trout carcasses onto spawning sites; the carcasses reduce dissolved oxygen concentrations as they decay, causing embryo mortality. We conducted a field experiment during one ice-free season at four sites in Yellowstone Lake to investigate the non-target effects of carcass treatment on benthic invertebrates, which could have consequences for native fish diets. While overall invertebrate density and biomass did not respond to carcass treatment, Chironomidae midges and Sphaeriidae fingernail clams decreased in abundance. Carcass treatment altered invertebrate community structure based on density, but not biomass. Carcass treatment to suppress invasive fish embryos has spatially localized, non-target effects on some benthic invertebrate taxa. Given the small spatial extent of carcass treatment within the lake, we conclude it is unlikely that carcass treatment will alter food availability for native fishes.</p>
Data from: Long-term severe hypoxia adaptation induces non-canonical EMT and a novel Wilms Tumor 1 (WT1) isoform
<p>The majority of cancer deaths are caused by solid tumors, where the four most prevalent cancers (breast, lung, colorectal and prostate) account for more than 60% of all cases (1). Tumor cell heterogeneity driven by variable cancer microenvironments, such as hypoxia, is a key determinant of therapeutic outcome. We developed a novel culture protocol, termed the Long-Term Hypoxia (LTHY) time course, to recapitulate the gradual development of severe hypoxia seen in vivo to mimic conditions observed in primary tumors. Cells subjected to LTHY underwent a non-canonical epithelial to mesenchymal transition (EMT) based on miRNA and mRNA signatures as well as displayed EMT-like morphological changes. Concomitant to this, we report production of a novel truncated isoform of WT1 transcription factor (tWt1), a non-canonical EMT driver, with expression driven by a yet undescribed intronic promoter through hypoxia-responsive elements (HREs). We further demonstrated that tWt1 initiates translation from an intron-derived start codon, retains proper subcellular localization and DNA binding. A similar tWt1 is also expressed in LTHY-cultured human cancer cell lines as well as primary cancers and predicts long-term patient survival. Our study not only demonstrates the importance of culture conditions that better mimic those observed in primary cancers, especially with regards to hypoxia, but also identifies a novel isoform of WT1 which correlates with poor long-term survival in ovarian cancer.</p>
Data from: Nutrient sources, phytoplankton blooms, and hypoxia along the Chinese coast in the East China Sea: Insight from summer 2014
<p>This dataset contains data collected onboard the <em>R/V Ocean Researcher I</em> during the summer of 2014 (August 20–31) East China Sea described in the paper: "C.-C. Chen, W.-C. Chou, and C.-C. Hung (2024). Nutrient sources, phytoplankton blooms, and hypoxia along the Chinese coast in the East China Sea: Insight from summer 2014, Marine Pollution Bulletin (accepted on July 4 2024)".</p>
Seasonal and Interannual Variability of Areal Extent of the Gulf Hypoxia from a Coupled Physical-Biogeochemical Model: A New Implication for Management Practice
<p>netcdf data and code for JGR manuscript: seasonal and interannual variability of areal extent of the Gulf Hypoxia from a coupled physical-biogeochemical model: A new implication for management practice</p>
Data from: Organic matter loading by hippopotami causes subsidy overload resulting in downstream hypoxia and fish kills
Organic matter and nutrient loading into aquatic ecosystems affects ecosystem structure and function and can result in eutrophication and hypoxia. Hypoxia is usually attributed to anthropogenic pollution and is rarely documented in unpolluted systems, particularly in rivers. Here we show that organic matter loading from hippopotami causes the repeated occurrence of hypoxia in the Mara River, East Africa. We documented 49 high flow events over three years that caused dissolved oxygen decreases, including 13 events resulting in hypoxia, and 9 fish kills over five years. Evidence from experiments and modeling demonstrates a strong mechanistic link between the flushing of hippo pools and decreased dissolved oxygen. This phenomenon may have been more widespread throughout Africa before hippo populations were severely reduced. Frequent hypoxia may be a natural part of tropical river ecosystem function, which directly challenges our notions of the reference state of rivers in the absence of human influence.
Mechanisms Governing Target Search and Binding Dynamics of Hypoxia-Inducible Factors
<p>Raw fast SPT data for Hypoxia-Inducible Factors:</p> <p><strong>HIF2a_HIF1b_KIN_Clones.zip </strong>corresponds to Figure 2A-C and Figure 2-Figure supplement 2A-B, contains fast SPT data for Halo-HIF-2α KIN clone A31 and clone B50, Halo-HIF-1β KIN clone A21 and clone B89.</p> <p><strong>HIF1b_with_HIF2a_overexpression.zip </strong>corresponds to Figure 2D-E and Figure 2-Figure supplement 2C, contains fast SPT data for: Halo-HIF-1β KIN clone A21, Halo-HIF-1β KIN clone A21 with HIF-2α stably over-expressed, and Halo-HIF-1β KIN clone A21 with a dimerization mutant form of HIF-2α (R171A/V192D) stably over-expressed.</p> <p><strong>Belzutifan_dosage.zip </strong>corresponds to Figure 3-Figure supplement 1, contains fast SPT data for: Halo-HIF-2α KIN clone A31, treated with 0.0002 uM, 0.002 uM, 0.005 uM, 0.01 uM, 0.02 uM, and 0.2 uM of Belzutifan.</p> <p><strong>HIF1b_with_HIFa_chimera_overexpression_and_Belzutifan.zip </strong>corresponds to Figure 3 and Figure 3-Figure supplement 2, contains fast SPT data for: Parental Halo-HIF-1β KIN clone A21 cells and cells stably over-expressing either a certain form of HIF-α (WT or domain swap), treated with either Belzutifan or DMSO. </p> <p><strong>HIFa_domain_swap.zip </strong>corresponds to Figure 4 and Figure 4-Figure supplement 2, contains fast SPT data for: Halo-HIF-2α KIN clone A31, WT 786-O cells stably express V5-Halo-HIF-2α with an L30 promoter, WT 786-O cells stably express V5-Halo-HIF-2α/1α with an L30 promoter, WT 786-O cells stably express V5-Halo-HIF-1α with an L30 promoter, and WT 786-O cells stably express V5-Halo-HIF-1α/2α with an L30 promoter. </p> <p><strong>DBD_mutant.zip </strong>corresponds to Figure 5A-C, contains fast SPT data for: WT 786-O cells stably express V5-Halo-HIF-2α with an L30 promoter, WT 786-O cells stably express a DBD mutant form of V5-Halo-HIF-2α (R27E) with an L30 promoter, WT 786-O cells stably express V5-Halo-HIF-1α with an L30 promoter, and WT 786-O cells stably express a DBD mutant form of V5-Halo-HIF-1α (R30E) with an L30 promoter.</p> <p><strong>Dimerization_mutant.zip </strong>corresponds to Figure 5D-F, contains fast SPT data for: WT 786-O cells stably express V5-Halo-HIF-2α with an L30 promoter, WT 786-O cells stably express a dimerization mutant form of V5-Halo-HIF-2α (R171A/V192D) with an L30 promoter, WT 786-O cells stably express V5-Halo-HIF-1α with an L30 promoter, and WT 786-O cells stably express a dimerization mutant form of V5-Halo-HIF-1α (R170A/V191D) with an L30 promoter.<br> </p>
Long non-coding RNA Neat1 and paraspeckle components are translational regulators in hypoxia
<p>Internal ribosome entry sites (IRESs) drive translation initiation during stress. In response to hypoxia, (lymph)angiogenic factors responsible for tissue revascularization in ischemic diseases are induced by the IRES-dependent mechanism. Here we searched for IRES <em>trans</em>-acting factors (ITAFs) active in early hypoxia in mouse cardiomyocytes. Using knock-down and proteomics approaches, we show a link between a stressed-induced nuclear body, the paraspeckle, and IRES-dependent translation. Furthermore, smiFISH experiments demonstrate the recruitment of IRES-containing mRNA into paraspeckle during hypoxia. Our data reveal that the long non-coding RNA Neat1, an essential paraspeckle component, is a key translational regulator, active on IRESs of (lymph)angiogenic and cardioprotective factor mRNAs. In addition, paraspeckle proteins p54<sup>nrb</sup> and PSPC1 as well as nucleolin and Rps2, two p54<sup>nrb</sup>-interacting proteins identified by mass spectrometry, are ITAFs for IRES subgroups. Paraspeckle thus appears as a platform to recruit IRES-containing mRNAs and possibly host IRESome assembly. Polysome PCR array shows that Neat1 isoforms regulate IRES-dependent translation and, more widely, translation of mRNAs involved in stress response.</p>
Data for: Seasonal variability in resilience of a coral reef fish to marine heatwaves and hypoxia
<p>Climate change projections indicate more frequent and severe tropical marine heatwaves (MHWs) and accompanying hypoxia year-round. However, most studies have focused on peak summer peak conditions under the assumption that annual maximum temperatures will induce the greatest physiological consequences. This study challenges this idea by characterizing seasonal MHWs (i.e., mean, maximum, and cumulative intensities, durations, heating rates, and mean annual occurrence) and comparing metabolic traits (i.e., standard metabolic rate (SMR), Q10 of SMR, maximum metabolic rate (MMR), aerobic scope, and critical oxygen tension (<em>P</em><sub>crit</sub>)) of winter- and summer-acclimatized convict tang (<em>Acanthurus</em> <em>triostegus</em>) to the combined effects of MHWs and hypoxia. Fish were exposed to one of six MHW treatments with seasonally varying maximum intensities (winter: 24.5, 26.5, 28.5°C; summer: 28.5, 30.5, 32.5°C), representing past and future MHWs under IPCC projections (i.e., +0, +2, +4°C). Surprisingly, MHW characteristics did not significantly differ between seasons, yet SMR was more sensitive to winter MHWs (mean Q10 = 2.92) than summer MHWs (mean Q10 = 1.81), despite higher absolute summer temperatures. Concurrently, MMR increased similarly among winter +2°C and +4°C treatments (i.e., 26.5, 28.5°C) and all summer MHW treatments, suggesting a ceiling for maximal MMR increase. Aerobic scope did not significantly differ between seasons nor among MHW treatments. While mean <em>P</em><sub>crit</sub> did not significantly vary between seasons, warming of +4°C during winter (i.e., 28.5°C) significantly increased <em>P</em><sub>crit</sub> relative to the winter control group. Contrary to the idea of increased sensitivity to MHWs during the warmest time of year, our results reveal heightened sensitivity to the deleterious effects of winter MHWs, and that seasonal acclimatization to warmer summer conditions may bolster metabolic resilience to warming and hypoxia. Consequently, physiological sensitivity to MHWs and hypoxia may extend across larger parts of the year than previously expected, emphasizing the importance of evaluating climate change impacts during cooler seasons when essential fitness-related traits such as reproduction occur in many species.</p>
Raw Data for the article: High-Resolution Secretome Analysis of Chemical Hypoxia Treated Cells Identifies Putative Biomarkers of Chondrosarcoma
<p>Chondrosarcoma is the second most common bone tumor, accounting for 20% of all cases. Little is known about the pathology and molecular mechanisms involved in the development and in the metastatic process of chondrosarcoma. As a consequence, there are no approved therapies for this tumor and surgical resection is the only treatment currently available. Moreover, there are no available biomarkers for this type of tumor, and chondrosarcoma classification relies on operator-dependent histopathological assessment. Reliable biomarkers of chondrosarcoma are urgently needed, as well as greater understanding of the molecular mechanisms of its development for translational purposes. Hypoxia is a central feature of chondrosarcoma progression. The hypoxic tumor microenvironment of chondrosarcoma triggers a number of cellular events, culminating in increased invasiveness and migratory capability. Herein, we analyzed the effects of chemically-induced hypoxia on the secretome of SW 1353, a human chondrosarcoma cell line, using high-resolution quantitative proteomics. We found that hypoxia induced unconventional protein secretion and the release of proteins associated to exosomes. Among these proteins, which may be used to monitor chondrosarcoma development, we validated the increased secretion in response to hypoxia of glyceraldehyde 3-phosphate dehydrogenase (GAPDH), a glycolytic enzyme well-known for its different functional roles in a wide range of tumors. In conclusion, by analyzing the changes induced by hypoxia in the secretome of chondrosarcoma cells, we identified molecular mechanisms that can play a role in chondrosarcoma progression and pinpointed proteins, including GAPDH, that may be developed as potential biomarkers for the diagnosis and therapeutic management of chondrosarcoma.</p>
Taurine depletion impairs cardiac function and affects tolerance to hypoxia and high temperatures in brook char (Salvelinus fontinalis)
<p>Physiological and environmental stressors can cause osmotic stress in fish hearts, leading to a reduction in intracellular taurine concentration. Taurine is a beta amino acid known to regulate cardiac function in other animal models but its role in fish has not been fully elucidated. We generated a model of cardiac taurine-deficiency (TD) by feeding brook char (<em>Salvelinus</em> <em>fontinalis</em>) a diet enriched in β-alanine, which inhibits cardiomyocyte taurine uptake. Cardiac taurine levels were reduced by 21%, and stress-induced changes in normal taurine handling were observed in TD brook char. Responses to exhaustive exercise and acute thermal and hypoxia tolerance were then assessed using a combination of in vivo, in vitro, and biochemical approaches. Critical thermal maximum was higher in TD brook char despite significant reductions in maximum heart rate. In vivo, TD brook char exhibited a lower resting heart rate, blunted hypoxic bradycardia, and a severe reduction in time to loss of equilibrium under hypoxia. In vitro function was similar between control and TD hearts under oxygenated conditions, but stroke volume and cardiac output were severely compromised in TD hearts under anoxia. Aspects of mitochondrial structure and function were also impacted in TD permeabilized cardiomyocytes, but overall effects were modest. High levels of intracellular taurine are required to achieve maximum cardiac function in brook char and cardiac taurine efflux may be necessary to support heart function under stress. Taurine appears to play a vital, previously unrecognized role in supporting cardiovascular function and stress tolerance in fish.</p>
Near-bed stratification controls bottom hypoxia in ice-covered alpine lakes
<p>Dataset supporting the study of the development of near-bottom hypoxia in high-altitude lakes.</p> <p>Herein, hypoxia is set for dissolved oxygen concentrations equal to or below 2 mg/l</p> <p>Variables: Lake (name of the lake), Year (corresponding winter of measurements),Max_depth (lake'smax depth, in m),Lake_surface (lake's surface area in m2), Drainage_ratio (unitless), Percent_macrophyte_cover (lake's average macrophyte cover, in %), Catchement_NDVI (unitless),Secchi (Secchi depth in m, measured over the previous summer), ice_duration (estimated duration of the ice cover, in days), T_ice_on (average water column temperature at the date of ice_on, in °C), DOinit (average concentration in dissolved oxygen at ice-on, in mg/l), DOinitsat (average saturation in dissolved oxygen_DO_ at ice-on, in %), time_under_hypoxia (duration in days of near-bottom hypoxia under the ice), time_to_hypoxia (time in days to reach near-bottom hypoxia under the ice, after the onset of ice), Kexp (near_bottom DO decay rate under the ice, in /d), Klm (rate of near_bottom DO decrease under the ice, in mg/l/d), Kheat (deep warming rate under the ice, in /d).</p> <p>see the corresponding paper for more details</p> <p> </p>
Effects of the oral angiotensin II type 2 receptor agonist C21 in Sugen-hypoxia induced pulmonary hypertension in rats
<p><span><span>Substantial evidence supports involvement of the renin-angiotensin system in pulmonary hypertension (PH), and the angiotensin II type 2 receptor (AT<sub>2</sub>R) is known to exert tissue-protective actions. The effect of the selective AT<sub>2</sub>R agonist C21 (also known as Compound 21 or buloxibutid) was evaluated in the rat Sugen-hypoxia PH model. After a single injection of Sugen 5416 and hypoxia for 21 days, </span><span>C21</span><span> (2 or 20 mg/kg) or vehicle was administered perorally twice daily from Day 21 to Day 55. On Day 56, hemodynamic assessments were performed, and lung and heart tissue were prepared for quantification of cardiac and vascular remodeling and fibrosis. Treatment with C21 20 mg/kg improved cardiac output and stroke volume and decreased right ventricular hypertrophy (all p<0.05). Treatment with C21 2 mg/kg significantly decreased vessel wall and muscular layer thickness and increased the luminal opening in vessels >100 </span><span>μ</span><span>m (all p<0.05). There were no significant differences between the two C21 doses on any parameter, and <em>post hoc</em> analyses </span><span>comparing the merged C21 groups with the vehicle group showed that C21 treatment reduced vascular remodeling (reduced endothelial proliferation and thickening of the vascular wall) in vessels of all sizes; moreover, the diastolic pulmonary artery pressure and right ventricular pressure were reduced along with reduction of right ventricular hypertrophy. Sugen 5416 and hypoxia increased pulmonary collagen deposition, which was counteracted by C21 20 mg/kg. In conclusion, the effects of C21 on vascular remodeling, hemodynamic alterations, and fibrosis suggest that AT<sub>2</sub>R agonists may have a role in Group 1 and 3 PH treatment.</span><br></span></p>
Supplementary material 1 for Thesis Chapter 2 - An obligate aerobe hybridises hydrogen fermentation and carbon storage to adapt to hypoxia
<p>Supplementary material for paired comparative metabolomics and proteomics on <em>Mycobacterium smegmatis </em>mc<sup>2</sup>155 during hypoxia, as part of chapter 2 for the thesis "Biochemistry and physiology of mycobacterial adaptations to energy starvation".</p> <p>Description below is identical to that provided in 'Summary.docx'. </p> <p>Proteomics_analysis.xlsx</p> <p>Includes raw and annotated data for comparative proteomics experiments for chapter 2.</p> <p>The tab ‘Annotated comparisons’ contains fold change and p values for the comparisons for each protein from <em>Mycobacterium smegmatis </em>mc<sup>2</sup>155 derived from LFQ-Analyst. Functional annotations are derived from KEGG pathways and modules, which utilise the spreadsheets in ‘MSMEG gene annotation’ ‘Protein ids to KEGG pathway’ and ‘KEGG Pathway and Modules’ to link KEGG annotations to MSMEG_XXXX gene identifiers and MSMEG_XXXX to Uniprot ID. Output from LFQ-Analyst is provided in the ‘Full_dataset’, ‘Imputed_matrix’ and ‘Original_matrix’ tabs.</p> <p>Data provided by the Monash Proteomics and Metabolomics Facility for upload into LFQ-analyst are provided as the ‘combined_protein.tsv’ and ‘LFQ-Analyst_experimental_design.txt’.</p> <p> </p> <p>Metabolism_analysis.xlsx</p> <p>Includes annotated data for comparative metabolomics experiments for chapter 2. Within the spreadsheet, TR refers to transition, ST refers to stationary phase and EXP refers to exponential phase. The tabs ‘TRvsEXP’, ‘STvsTR’ and ‘STvsEXP’ contain fold change and p values for each metabolite detected for each comparison. The remaining tabs categorise the metabolites based on KEGG database and IDEOM annotations. For broader categories (‘Lipid metabolism’,’ Carbohydrate metabolism’, ‘Cofactor metabolism’, ‘Nucleotide metabolism’, ‘Amino acid metabolism’ and ‘Peptides’ tabs), annotations were derived directly from filtering the ‘Map’ column of ‘Comparisons’ tab of the IDEOM worksheet (IDEOM_analysis.xlsb). Screenshots are pasted into each tab to show the filtering settings. The remaining tabs comprise narrower categories which were manually annotated with reference to KEGG pathways and maps, and also include rows corresponding to the proteomics data for these categories, so the proteomics and metabolomics data can be interpreted together. The ‘Proteomics’ tab contains the proteomics data referenced by these tabs, which is a copy of the ‘Annotated comparisons’ tab from the ‘Proteomics_analysis.xlsx’ file. A value of ‘N’ indicates the metabolite or protein (at least according to the name in the same row) was not found in these datasets.</p> <p>The IDEOM worksheet (IDEOM_analysis.xlsb) was provided by the Monash Proteomics and Metabolomics Facility and was used for further analysis and for annotations. ‘Data_for_MA_no_normalization.csv’ was also provided by the Monash Proteomics and Metabolomics Facility for upload into Metaboanalyst (https://www.metaboanalyst.ca/).</p>
Dataset on biomarkers for the project "Intermittent hypoxia differentially affects metabolic and oxidative stress responses in two species of cyprinid fish"
<p>The file contains the data for the tissue-level biomarkers evaluating the impact of short-term hypoxia on oxidative stress and metabolic parameters in silver carp <em>Hypophthalmichthys molitrix </em>and gibel carp <em>Carassius gibelio.</em></p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.