Glucose-oxygen deprivation constrains HMGCR function and Rac1 prenylation and activates the NLRP3 inflammasome in human monocytes.

Hypoxia and low glucose abundance often occur simultaneously at sites of inflammation. In monocytes and macrophages, glucose-oxygen deprivation stimulates the assembly of the NLRP3 inflammasome to generate the proinflammatory cytokine IL-1ß. We found that concomitant glucose deprivation and hypoxia activated the NLRP3 inflammasome by constraining the function of HMG-CoA reductase (HMGCR), the rate-limiting enzyme of the mevalonate kinase pathway. HMGCR is involved in the synthesis of geranylgeranyl pyrophosphate (GGPP), which is required for the prenylation and lipid membrane integration of proteins. Under glucose-oxygen deprivation, GGPP synthesis was decreased, leading to reduced prenylation of the small GTPase Rac1, increased binding of nonprenylated Rac1 to the scaffolding protein IQGAP1, and enhanced activation of the NLRP3 inflammasome. In response to restricted oxygen and glucose supply, patient monocytes with a compromised mevalonate pathway due to mevalonate kinase deficiency or Muckle-Wells syndrome released more IL-1ß than did control monocytes. Thus, reduced GGPP synthesis due to inhibition of HMGCR under glucose-oxygen deprivation results in proinflammatory innate responses, which are normally kept in check by the prenylation of Rac1. We suggest that this mechanism is also active in inflammatory autoimmune conditions.

Hypoxia and the Hypoxia-Inducible Factors in Lymphocyte Differentiation and Function.

Molecular oxygen doubles as a biomolecular building block and an element required for energy generation and metabolism in aerobic organisms. A variety of systems in mammalian cells sense the concentration of oxygen to which they are exposed and are tuned to the range present in our blood and tissues. The ability to respond to insufficient O2 in tissues is central to regulation of erythroid lineage cells, but challenges also are posed for immune cells by a need to adjust to very different oxygen concentrations. Hypoxia-inducible factors (HIFs) provide a major means of making such adjustments. For adaptive immunity, lymphoid lineages are initially defined in bone marrow niches; T lineage cells arise in the thymus, and B cells complete maturation in the spleen. Lymphocytes move from these first stops into microenvironments (bloodstream, lymphatics, and tissues) with distinct oxygenation in each. Herein, evidence pertaining to functions of the HIF transcription factors (TFs) in lymphocyte differentiation and function is reviewed. For the CD4+ and CD8+ subsets of T cells, the case is very strong that hypoxia and HIFs regulate important differentiation events and functions after the naïve lymphocytes emerge from the thymus. In the B lineage, the data indicate that HIF1 contributes to a balanced regulation of B-cell fates after antigen (Ag) activation during immunity. A model synthesized from the aggregate literature is that HIF in lymphocytes generally serves to modulate function in a manner dependent on the molecular context framed by other TFs and signals.

Oxygen sensitivity of [FeFe]-hydrogenase: a comparative study of active site mimics inside vs. outside the enzyme.

[FeFe]-hydrogenase is nature's most efficient proton reducing and H2-oxidizing enzyme. However, biotechnological applications are hampered by the O2 sensitivity of this metalloenzyme, and the mechanism of aerobic deactivation is not well understood. Here, we explore the oxygen sensitivity of four mimics of the organometallic active site cofactor of [FeFe]-hydrogenase, [Fe2(adt)(CO)6-x(CN)x]x- and [Fe2(pdt)(CO)6-x(CN)x]x- (x = 1, 2) as well as the corresponding cofactor variants of the enzyme by means of infrared, Mössbauer, and NMR spectroscopy. Additionally, we describe a straightforward synthetic recipe for the active site precursor complex Fe2(adt)(CO)6. Our data indicate that the aminodithiolate (adt) complex, which is the synthetic precursor of the natural active site cofactor, is most oxygen sensitive. This observation highlights the significance of proton transfer in aerobic deactivation, and supported by DFT calculations facilitates an identification of the responsible reactive oxygen species (ROS). Moreover, we show that the ligand environment of the iron ions critically influences the reactivity with O2 and ROS like superoxide and H2O2 as the oxygen sensitivity increases with the exchange of ligands from CO to CN-. The trends in aerobic deactivation observed for the model complexes are in line with the respective enzyme variants. Based on experimental and computational data, a model for the initial reaction of [FeFe]-hydrogenase with O2 is developed. Our study underscores the relevance of model systems in understanding biocatalysis and validates their potential as important tools for elucidating the chemistry of oxygen-induced deactivation of [FeFe]-hydrogenase.

NaHS immersion alleviates the stress effect of chromium(III) on alfalfa seeds by affecting active oxygen metabolism.

OBJECTIVE: This study aimed to investigate the regulatory effects of exogenous hydrogen sulfide (H2S) on seed germination, seedling growth, and reactive oxygen species (ROS) homeostasis in alfalfa under chromium (Cr) ion (III) stress. METHODS: The effects of 0-4 mM Cr(III) on the germination and seedling growth of alfalfa were first assessed. Subsequently, following seed NaHS immersion, the influence of H2S on alfalfa seed germination and seedling growth under 2 mM Cr(III) stress was investigated, and the substance contents and enzyme activities associated with ROS metabolism were quantified. RESULTS: Compared to the control group, alfalfa plant germination was delayed under 2 mM Cr(III) stress for up to 48 h (p < 0.05). At 120 h, the total seedling length was approximately halved, and the root length was roughly one-third of the control. Treatment with 0.02-0.1 mM NaHS alleviated the delay in germination and root growth inhibition caused by 2 mM Cr(III) stress, resulting in an increased ratio of root length to hypocotyl length from 0.57 to 1 above. Additionally, immersion in 0.05 mM NaHS reduced hydrogen peroxide (H2O2) and oxygen-free radicals (O2· -) levels (p < 0.05), boosted glutathione (GSH) levels (p < 0.05), and notably enhanced catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR) activities (p < 0.05) compared to the 2 mM Cr(III) stress treatment group. CONCLUSION: Seed immersion in NaHS mitigated the delay in germination and inhibition of root elongation under 2 mM Cr(III) stress. This effect is likely attributed to the regulation of intracellular ROS homeostasis and redox balance through enzymatic and non-enzymatic systems; thus, providing a potential mechanism for combating oxidative stress.

Up-regulation of miR-126 via DNA methylation in hypoxia-preconditioned endothelial cells may contribute to hypoxic tolerance of neuronal cells.

BACKGROUND: Endothelial cells (ECs) can confer neuroprotection by secreting molecules. This study aimed to investigate whether DNA methylation contributes to the neuroprotective gene expression induced by hypoxia preconditioning (HPC) in ECs and to clarify that the secretion of molecules from HPC ECs may be one of the molecular mechanisms of neuroprotection. METHODS: Human microvascular endothelial cell-1 (HMEC-1) was cultured under normal conditions (C), hypoxia(H), and hypoxia preconditioning (HPC), followed by the isolation of culture medium (CM). SY5Y cell incubated with the isolated CM from HMEC-1 was exposed to oxygen-glucose deprivation (OGD). The DNA methyltransferases (DNMTs), global methylation level, miR-126 and its promotor DNA methylation level in HMEC-1 were measured. The cell viability and cell injury in SY5Y were detected. RESULTS: HPC decreased DNMTs level and global methylation level as well as increased miR-126 expression in HMEC-1. CM from HPC treated HMEC-1 also relieved SY5Y cell damage, while CM from HMEC-1 which over-expression of miR-126 can reduce injury in SY5Y under OGD condition. CONCLUSIONS: These findings indicate EC may secrete molecules, such as miR-126, to execute neuroprotection induced by HPC through regulating the expression of DNMTs.

Oxygen Saturation Curve Analysis in 2298 Hypoxia Awareness Training Tests of Military Aircrew Members in a Hypobaric Chamber.

We aim to provide reference values for military aircrews participating in hypoxia awareness training (HAT). We describe several parameters with potential biomedical interest based on selected segments and slopes of the changes in oxygen saturation (SatO2) during a standard HAT. A retrospective analysis of 2298 records of the SatO2 curve was performed, including 1526 military men aged 30.48 ± 6.47 years during HAT in a hypobaric chamber. HAT consisted of pre-oxygenation at 100% and an ascent to 7620 m, followed by O2 disconnection starting the phase of descent of SatO2 until reaching the time of useful consciousness (TUC), and finally reconnection to 100% O2 in the recovery phase. Using an ad hoc computational procedure, the time taken to reach several defined critical values was computed. These key parameters were the time until desaturation of 97% and 90% (hypoxia) after oxygen mask disconnection (D97/D90) and reconnection (R97/R90) phases, the time of desaturation (TUC-D97) and hypoxia (TUC-D90) during disconnection, the total time in desaturation (L97) or hypoxia (L90), and the slopes of SatO2 drop (SDSAT97 and SDSAT90) and recovery (SRSAT97). The mean of the quartiles according to TUC were compared by ANOVA. The correlations between the different parameters were studied using Pearson's test and the effect size was estimated with ω2. Potentially useful parameters for the HAT study were those with statistical significance (p < 0.05) and a large effect size. D97, D90, R97, and R90 showed significant differences with small effect sizes, while TUC-D97, TUC-D90, L97, L90, and SDSAT97 showed significant differences and large effect sizes. SDSAT97 correlated with TUC (R = 0.79), TUC-D97 (R = 0.81), and TUC-D90 (R = 0.81). In conclusion, several parameters of the SatO2 curve are useful for the study and monitoring of HAT. The SDSAT97 measured during the test can estimate the TUC and thus contribute to taking measures to characterize and protect the aircrew members.

Shionone relieves oxygen-glucose deprivation/reoxygenation induced SH-SY5Y cells injury by inhibiting the p38 MAPK/NF-κB pathway.

BACKGROUND: Cerebral ischemia-reperfusion injury (I/R) can affect patient outcomes and can even be life-threatening. This study aimed to explore the role of Shionone in cerebral I/R and reveal its mechanism of action through the cerebral I/R in vitro model. METHODS: SH-SY5Y cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to induce cerebral I/R in vitro model. SH-SY5Y cells were treated with different concentrations of Shionone. Cell counting kit-8 and flow cytometry assays were used to detect cell viability and apoptosis levels. The levels of superoxide dismutase, catalase, and malondialdehyde were determined using their corresponding kits to examine the level of oxidative stress. The inflammation response was detected by IL-6, IL-1ß, and TNF-α levels, using enzyme-linked-immunosorbent-assay. RT-qPCR was performed to measure the mRNA levels of p38 and NF-κB. Western blotting was used to quantify the apoptosis-related proteins and p38MAPK/NF-κB signaling pathway proteins. RESULTS: Shionone exhibited no toxic effects on SH-SY5Y cells. Shionone inhibited OGD/R-induced cell apoptosis, improved the inflammatory response caused by OGD/R, and reduced the level of oxidative stress in cells. Western blot assay results showed that Shionone alleviated OGD/R-induced injury by inhibiting the activity of the p38 MAPK/NF-κB signaling pathway. The p38/MAPK agonist P79350 reversed the beneficial effects of Shionone. CONCLUSION: Shionone alleviates cerebral I/R and may thus be a novel therapeutic strategy for treating cerebral I/R.

The Impact of Virgin and Aged Microstructured Plastics on Proteins: The Case of Hemoglobin Adsorption and Oxygenation.

Plastic particles, particularly micro- and nanoparticles, are emerging pollutants due to the ever-growing amount of plastics produced across a wide variety of sectors. When plastic particles enter a biological medium, they become surrounded by a corona, giving them their biological identity and determining their interactions in the living environment and their biological effects. Here, we studied the interactions of microstructured plastics with hemoglobin (Hb). Virgin polyethylene microparticles (PEMPs) and polypropylene microparticles (PPMPs) as well as heat- or irradiation-aged microparticles (ag-PEMPs and ag-PPMPs) were used to quantify Hb adsorption. Polypropylene filters (PP-filters) were used to measure the oxygenation of adsorbed Hb. Microstructured plastics were characterized using optical microscopy, SAXS, ATR-FTIR, XPS, and Raman spectroscopy. Adsorption isotherms showed that the Hb corona thickness is larger on PPMPs than on PEMPs and Hb has a higher affinity for PPMPs than for PEMPs. Hb had a lower affinity for ag-PEMPs and ag-PPMPs, but they can be adsorbed in larger amounts. The presence of partial charges on the plastic surface and the oxidation rate of microplastics may explain these differences. Tonometry experiments using an original method, the diffuse reflection of light, showed that adsorbed Hb on PP-filters retains its cooperativity, but its affinity for O2 decreases significantly.

Methanogenesis in the presence of oxygenic photosynthetic bacteria may contribute to global methane cycle.

Accumulating evidences are challenging the paradigm that methane in surface water primarily stems from the anaerobic transformation of organic matters. Yet, the contribution of oxygenic photosynthetic bacteria, a dominant species in surface water, to methane production remains unclear. Here we show methanogenesis triggered by the interaction between oxygenic photosynthetic bacteria and anaerobic methanogenic archaea. By introducing cyanobacterium Synechocystis PCC6803 and methanogenic archaea Methanosarcina barkeri with the redox cycling of iron, CH4 production was induced in coculture biofilms through both syntrophic methanogenesis (under anoxic conditions in darkness) and abiotic methanogenesis (under oxic conditions in illumination) during the periodic dark-light cycles. We have further demonstrated CH4 production by other model oxygenic photosynthetic bacteria from various phyla, in conjunction with different anaerobic methanogenic archaea exhibiting diverse energy conservation modes, as well as various common Fe-species. These findings have revealed an unexpected link between oxygenic photosynthesis and methanogenesis and would advance our understanding of photosynthetic bacteria's ecological role in the global CH4 cycle. Such light-driven methanogenesis may be widely present in nature.

Unveiling a new oceanic anoxic event at the Norian/Rhaetian boundary (Late Triassic).

The latest Triassic was characterised by protracted biotic extinctions concluding in the End-Triassic Extinction (~ 200 Ma) and a global carbon cycle perturbation. The onset of declining diversity is closely related to reducing conditions that spread globally from upper Sevatian (uppermost Norian) to across the Norian-Rhaetian boundary, likely triggered by unusually high volcanic activity. We correlate significant organic carbon cycle perturbations to an increase of CO2 in the ocean-atmosphere system, likely outgassed by the Angayucham igneous province, the onset of which is indicated by the initiation of a rapid decline in 87Sr/86Sr and 188Os/187Os seawater values. A possible causal mechanism involves elevated CO2 levels causing global warming and accelerating chemical weathering, which increased nutrient discharge to the oceans and greatly increased biological productivity. Higher export production and oxidation of organic matter led to a global O2 decrease in marine water across the Norian/Rhaetian boundary (NRB). Biotic consequences of dysoxia/anoxia include worldwide extinctions in some fossil groups, such as bivalves, ammonoids, conodonts, radiolarians.

Effect of Hb conformational changes on oxygen transport physiology. / Hb构象变化对氧转运生理功能的影响.

Red blood cells (RBCs) are the primary mediators of oxygen transport in the human body, and their function is mainly achieved through conformational changes of hemoglobin (Hb). Hb is a tetramer composed of four subunits, with HbA being the predominant Hb in healthy adults, existing in two forms: tense state (T state) and relaxed state (R state). Endogenous regulators of Hb conformation include 2,3-diphosphoglyceric acid, carbon dioxide, protons, and chloride ions, while exogenous regulators include inositol hexaphosphate, inositol tripyrophosphate, benzabate, urea derivative L35, and vanillin, each with different mechanisms of action. The application of Hb conformational regulators provides new insights into the study of hypoxia oxygen supply issues and the treatment of sickle cell disease.

Measures of overnight oxygen saturation to characterize sleep apnea severity and predict postoperative respiratory depression.

BACKGROUND: Sleep apnea syndrome, characterized by recurrent cessation (apnea) or reduction (hypopnea) of breathing during sleep, is a major risk factor for postoperative respiratory depression. Challenges in sleep apnea assessment have led to the proposal of alternative metrics derived from oxyhemoglobin saturation (SpO2), such as oxygen desaturation index (ODI) and percentage of cumulative sleep time spent with SpO2 below 90% (CT90), as predictors of postoperative respiratory depression. However, their performance has been limited with area under the curve of 0.60 for ODI and 0.59 for CT90. Our objective was to propose novel features from preoperative overnight SpO2 which are correlated with sleep apnea severity and predictive of postoperative respiratory depression. METHODS: Preoperative SpO2 signals from 235 surgical patients were retrospectively analyzed to derive seven features to characterize the sleep apnea severity. The features included entropy and standard deviation of SpO2 signal; below average burden characterizing the area under the average SpO2; average, standard deviation, and entropy of desaturation burdens; and overall nocturnal desaturation burden. The association between the extracted features and sleep apnea severity was assessed using Pearson correlation analysis. Logistic regression was employed to evaluate the predictive performance of the features in identifying postoperative respiratory depression. RESULTS: Our findings indicated a similar performance of the proposed features to the conventional apnea-hypopnea index (AHI) for assessing sleep apnea severity, with average area under the curve ranging from 0.77 to 0.81. Notably, entropy and standard deviation of overnight SpO2 signal and below average burden showed comparable predictive capability to AHI but with minimal computational requirements and individuals' burden, making them promising for screening purposes. Our sex-based analysis revealed that compared to entropy and standard deviation, below average burden exhibited higher sensitivity in detecting respiratory depression in women than men. CONCLUSION: This study underscores the potential of preoperative SpO2 features as alternative metrics to AHI in predicting postoperative respiratory.

Low-oxygen-induced root bending is altered by phytoglobin1 through mediation of ethylene response factors (ERFs) and auxin signaling.

MAIN CONCLUSION: phytoglobin1 positively regulates root bending in hypoxic Arabidopsis roots through regulation of ethylene response factors and auxin transport. Hypoxia-induced root bending is known to be mediated by the redundant activity of the group VII ethylene response factors (ERFVII) RAP2.12 and HRE2, causing changes in polar auxin transport (PAT). Here, we show that phytoglobin1 (Pgb1), implicated in hypoxic adaptation through scavenging of nitric oxide (NO), can alter root direction under low oxygen. Hypoxia-induced bending is exaggerated in roots over-expressing Pgb1 and attenuated in those where the gene is suppressed. These effects were attributed to Pgb1 repressing both RAP2.12 and HRE2. Expression, immunological and genetic data place Pgb1 upstream of RAP2.12 and HRE2 in the regulation of root bending in oxygen-limiting environments. The attenuation of slanting in Pgb1-suppressing roots was associated with depletion of auxin activity at the root tip because of depression in PAT, while exaggeration of root bending in Pgb1-over-expressing roots with the retention of auxin activity. Changes in PIN2 distribution patterns, suggestive of redirection of auxin movement during hypoxia, might contribute to the differential root bending responses of the transgenic lines. In the end, Pgb1, by regulating NO levels, controls the expression of 2 ERFVIIs which, in a cascade, modulate PAT and, therefore, root bending.

Conserved C-Terminal Tail Is Responsible for Membrane Localization and Function of Pseudomonas aeruginosa Hemerythrin.

Many bacteria have hemerythrin (Hr) proteins that bind O2, including Pseudomonas aeruginosa, in which microoxia-induced Hr (Mhr) provide fitness advantages under microoxic conditions. Mhr has a 23 amino-acid extension at its C-terminus relative to a well-characterized Hr from Methylococcus capsulatus, and similar extensions are also found in Hrs from other bacteria. The last 11 amino acids of this extended, C-terminal tail are highly conserved in gammaproteobacteria and predicted to form a helix with positively charged and hydrophobic faces. In cellular fractionation assays, wild-type (WT) Mhr was found in both membrane and cytosolic fractions, while a MhrW143* variant lacking the last 11 residues was largely in the cytosol and did not complement Mhr function in competition assays. MhrL112Y, a variant that has a much longer-lived O2-bound form, was fully functional and had a similar localization pattern to that of WT Mhr. Both MhrW143* and MhrL112Y had secondary structures, stabilities, and O2-binding kinetics similar to those of WT Mhr. Fluorescence studies revealed that the C-terminal tail, and particularly the fragment corresponding to its last 11 residues, was sufficient and necessary for association with lipid vesicles. Molecular dynamics simulations and subsequent cellular analysis of Mhr variants have demonstrated that conserved, positively charged residues in the tail are important for Mhr interactions with negatively charged membranes and the contribution of this protein to competitive fitness. Together, these data suggest that peripheral interactions of Mhr with membranes are guided by the C-terminal tail and are independent of O2-binding.

Metaproteomics-informed stoichiometric modeling reveals the responses of wetland microbial communities to oxygen and sulfate exposure.

Climate changes significantly impact greenhouse gas emissions from wetland soil. Specifically, wetland soil may be exposed to oxygen (O2) during droughts, or to sulfate (SO42-) as a result of sea level rise. How these stressors - separately and together - impact microbial food webs driving carbon cycling in the wetlands is still not understood. To investigate this, we integrated geochemical analysis, proteogenomics, and stoichiometric modeling to characterize the impact of elevated SO42- and O2 levels on microbial methane (CH4) and carbon dioxide (CO2) emissions. The results uncovered the adaptive responses of this community to changes in SO42- and O2 availability and identified altered microbial guilds and metabolic processes driving CH4 and CO2 emissions. Elevated SO42- reduced CH4 emissions, with hydrogenotrophic methanogenesis more suppressed than acetoclastic. Elevated O2 shifted the greenhouse gas emissions from CH4 to CO2. The metabolic effects of combined SO42- and O2 exposures on CH4 and CO2 emissions were similar to those of O2 exposure alone. The reduction in CH4 emission by increased SO42- and O2 was much greater than the concomitant increase in CO2 emission. Thus, greater SO42- and O2 exposure in wetlands is expected to reduce the aggregate warming effect of CH4 and CO2. Metaproteomics and stoichiometric modeling revealed a unique subnetwork involving carbon metabolism that converts lactate and SO42- to produce acetate, H2S, and CO2 when SO42- is elevated under oxic conditions. This study provides greater quantitative resolution of key metabolic processes necessary for the prediction of CH4 and CO2 emissions from wetlands under future climate scenarios.

Development of graphitic carbon nitride quantum dots-based oxygen self-sufficient platforms for enhanced corneal crosslinking.

Keratoconus, a disorder characterized by corneal thinning and weakening, results in vision loss. Corneal crosslinking (CXL) can halt the progression of keratoconus. The development of accelerated corneal crosslinking (A-CXL) protocols to shorten the treatment time has been hampered by the rapid depletion of stromal oxygen when higher UVA intensities are used, resulting in a reduced cross-linking effect. It is therefore imperative to develop better methods to increase the oxygen concentration within the corneal stroma during the A-CXL process. Photocatalytic oxygen-generating nanomaterials are promising candidates to solve the hypoxia problem during A-CXL. Biocompatible graphitic carbon nitride (g-C3N4) quantum dots (QDs)-based oxygen self-sufficient platforms including g-C3N4 QDs and riboflavin/g-C3N4 QDs composites (RF@g-C3N4 QDs) have been developed in this study. Both display excellent photocatalytic oxygen generation ability, high reactive oxygen species (ROS) yield, and excellent biosafety. More importantly, the A-CXL effect of the g-C3N4 QDs or RF@g-C3N4 QDs composite on male New Zealand white rabbits is better than that of the riboflavin 5'-phosphate sodium (RF) A-CXL protocol under the same conditions, indicating excellent strengthening of the cornea after A-CXL treatments. These lead us to suggest the potential application of g-C3N4 QDs in A-CXL for corneal ectasias and other corneal diseases.

Impacts of ocean warming on fish size reductions on the world's hottest coral reefs.

The impact of ocean warming on fish and fisheries is vigorously debated. Leading theories project limited adaptive capacity of tropical fishes and 14-39% size reductions by 2050 due to mass-scaling limitations of oxygen supply in larger individuals. Using the world's hottest coral reefs in the Persian/Arabian Gulf as a natural laboratory for ocean warming - where species have survived >35.0 °C summer temperatures for over 6000 years and are 14-40% smaller at maximum size compared to cooler locations - we identified two adaptive pathways that enhance survival at elevated temperatures across 10 metabolic and swimming performance metrics. Comparing Lutjanus ehrenbergii and Scolopsis ghanam from reefs both inside and outside the Persian/Arabian Gulf across temperatures of 27.0 °C, 31.5 °C and 35.5 °C, we reveal that these species show a lower-than-expected rise in basal metabolic demands and a right-shifted thermal window, which aids in maintaining oxygen supply and aerobic performance to 35.5 °C. Importantly, our findings challenge traditional oxygen-limitation theories, suggesting a mismatch in energy acquisition and demand as the primary driver of size reductions. Our data support a modified resource-acquisition theory to explain how ocean warming leads to species-specific size reductions and why smaller individuals are evolutionarily favored under elevated temperatures.

Disruption of intestinal oxygen balance in acute colitis alters the gut microbiome.

The juxtaposition of well-oxygenated intestinal colonic tissue with an anerobic luminal environment supports a fundamentally important relationship that is altered in the setting of intestinal injury, a process likely to be relevant to diseases such as inflammatory bowel disease. Herein, using two-color phosphorometry to non-invasively quantify both intestinal tissue and luminal oxygenation in real time, we show that intestinal injury induced by DSS colitis reduces intestinal tissue oxygenation in a spatially defined manner and increases the flux of oxygen from the tissue into the gut lumen. By characterizing the composition of the microbiome in both DSS colitis-affected gut and in a bioreactor containing a stable human fecal community exposed to microaerobic conditions, we provide evidence that the increased flux of oxygen into the gut lumen augments glycan degrading bacterial taxa rich in glycoside hydrolases which are known to inhabit gut mucosal surface. Continued disruption of the intestinal mucus barrier through such a mechanism may play a role in the perpetuation of the intestinal inflammatory process.

Efficiency of aerobic biodegradation of sugar beet distillery stillage under dissolved oxygen tension-controlled conditions.

The efficiency of aerobic biodegradation of distillery wastewater using various microbial cultures is intricately linked to process conditions. The study aimed to examine the aerobic biodegradation by a Bacillus bacteria under controlled dissolved oxygen tension (DOT) conditions as a novel approach in the treatment of sugar beet distillery stillage. The processes were conducted in a 2-L Biostat®B stirred-tank reactor (STR), at a temperature of 36°C, with aeration of 1.0 L/(L·min), and uncontrolled pH of the medium (an initial pH of 8.0). Each experiment was performed at a different DOT setpoint: 75%, 65% and 55% saturation, controlled through stirrer rotational speed adjustments. The study showed that the DOT setpoint did not influence the process efficiency, determined by the pollutant load removal expressed as COD, BOD5 and TOC. In all three experiments, the obtained reduction values of these parameters were comparable, falling within the narrow ranges of 78.6-78.7%, 97.3-98.0% and 75.0-76.4%, respectively. However, the DOT setpoint did influence the rate of process biodegradation. The removal rate of the pollutant load expressed as COD, was the lowest when DOT was set at 55% (0.48 g O2/(L•h)), and the highest when DOT was set at 65% (0.55 g O2/(L•h)). For biogenic elements (nitrogen and phosphorus), a beneficial effect was observed at a low setpoint of controlled DOT during biodegradation. The maximum extent of removal of both total nitrogen (54%) and total phosphorus (67.8%) was achieved at the lowest DOT setpoint (55%). The findings suggest that conducting the batch aerobic process biodegradation of sugar beet stillage at a relatively low DOT setpoint in the medium might achieve high efficiency pollutant load removal and potentially lead to a reduction in the process cost.

High oxygen exposure's impact on newborn mice: Temporal changes observed via micro-computed tomography.

INTRODUCTION: Bronchopulmonary dysplasia (BPD) impacts life expectancy and long-term quality of life. Currently, BPD mouse models exposed to high oxygen are frequently used, but to reevaluate their relevance to human BPD, we attempted an assessment using micro-computed tomography (µCT). METHODS: Newborn wildtype male mice underwent either 21% or 95% oxygen exposure for 4 days, followed until 8 wk. Weekly µCT scans and lung histological evaluations were performed independently. RESULTS: Neonatal hyperoxia for 4 days hindered lung development, causing alveolar expansion and simplification. Histologically, during the first postnatal week, the exposed group showed a longer mean linear intercept, enlarged alveolar area, and a decrease in alveolar number, diminishing by week 4. Weekly µCT scans supported these findings, revealing initially lower lung density in newborn mice, increasing with age. However, the high-oxygen group displayed higher lung density initially. This difference diminished over time, with no significant contrast to controls at 3 wk. Although no significant difference in total lung volume was observed at week 1, the high-oxygen group exhibited a decrease by week 2, persisting until 8 wk. CONCLUSION: This study highlights µCT-detected changes in mice exposed to high oxygen. BPD mouse models might follow a different recovery trajectory than humans, suggesting the need for further optimization.