Abiotic aerobic oxidation pathways of stibnite revealed by oxygen and sulfur isotope systematics of sulfate.

The environmental threat posed by stibnite is an important geoenvironmental issue of current concern. To better understand stibnite oxidation pathways, aerobic abiotic batch experiments were conducted in aqueous solution with varying δ18OH2O value at initial neutral pH for different lengths of time (15-300 days). The sulfate oxygen and sulfur isotope compositions as well as concentrations of sulfur and antimony species were determined. The sulfur isotope fractionation factor (Δ34SSO4-stibnite) values decreased from 0.8‰ to -2.1‰ during the first 90 days, and increased to 2.6‰ at the 180 days, indicating the dominated intermediate sulfur species such as S2O32-, S0, and H2S (g) involved in Sb2S3 oxidation processes. The incorporation of O into sulfate derived from O2 (∼100%) indicated that the dissociated O2 was only directly adsorbed on the stibnite-S sites in the initial stage (0-90 days). The proportion of O incorporation into sulfate from water (27%-52%) increased in the late stage (90-300 days), which suggested the oxidation mechanism changed to hydroxyl attack on stibnite-S sites promoted by nearby adsorbed O2 on stibnite-Sb sites. The exchange of oxygen between sulfite and water may also contributed to the increase of water derived O into SO42-. The new insight of stibnite oxidation pathway contributes to the understanding of sulfide oxidation mechanism and helps to interpret field data.

Mechanism of extracellular electron transport and reactive oxygen mediated Sb(III) oxidation by Klebsiella aerogenes HC10.

Microbial oxidation and the mechanism of Sb(III) are key governing elements in biogeochemical cycling. A novel Sb oxidizing bacterium, Klebsiella aerogenes HC10, was attracted early and revealed that extracellular metabolites were the main fractions driving Sb oxidation. However, linkages between the extracellular metabolite driven Sb oxidation process and mechanism remain elusive. Here, model phenolic and quinone compounds, i.e., anthraquinone-2,6-disulfonate (AQDS) and hydroquinone (HYD), representing extracellular oxidants secreted by K. aerogenes HC10, were chosen to further study the Sb(III) oxidation mechanism. N2 purging and free radical quenching showed that oxygen-induced oxidation accounted for 36.78% of Sb(III) in the metabolite reaction system, while hydroxyl free radicals (·OH) accounted for 15.52%. ·OH and H2O2 are the main driving factors for Sb oxidation. Radical quenching, methanol purification and electron paramagnetic resonance (EPR) analysis revealed that ·OH, superoxide radical (O2•-) and semiquinone (SQ-•) were reactive intermediates of the phenolic induced oxidation process. Phenolic-induced ROS are one of the main oxidants in metabolites. Cyclic voltammetry (CV) showed that electron transfer of quinone also mediated Sb(III) oxidation. Part of Sb(V) was scavenged by the formation of the secondary Sb(V)-bearing mineral mopungite [NaSb(OH)6] in the incubation system. Our study demonstrates the microbial role of oxidation detoxification and mineralization of Sb and provides scientific references for the biochemical remediation of Sb-contaminated soil.

Oxygen atmosphere enhances ball milling remediation of petroleum-contaminated soil and reuse as adsorptive/catalytic materials for wastewater treatment.

Ball milling is an environmentally friendly technology for the remediation of petroleum-contaminated soil (PCS), but the cleanup of organic pollutants requires a long time, and the post-remediation soil needs an economically viable disposal/reuse strategy due to its vast volume. The present paper develops a ball milling process under oxygen atmosphere to enhance PCS remediation and reuse the obtained carbonized soil (BCS-O) as wastewater treatment materials. The total petroleum hydrocarbon removal rates by ball milling under vacuum, air, and oxygen atmospheres are 39.83%, 55.21%, and 93.84%, respectively. The Langmuir and pseudo second-order models satisfactorily describe the adsorption capacity and behavior of BCS-O for transition metals. The Cu2+, Ni2+, and Mn2+ adsorbed onto BCS-O were mainly bound to metal carbonates and metal oxides. Furthermore, BCS-O can effectively activate persulfate (PDS) oxidation to degrade aniline, while BCS-O loaded with transition metal (BCS-O-Me) shows better activation efficiency and reusability. BCS-O and BCS-O-Me activated PDS oxidation systems are dominated by 1O2 oxidation and electron transfer. The main active sites are oxygen-containing functional groups, vacancy defects, and graphitized carbon. The oxygen-containing functional groups and vacancy defects primarily activate PDS to generate 1O2 and attack aniline. Graphitized carbon promotes aniline degradation by accelerating electron transfer. The paper develops an innovative strategy to simultaneously realize efficient remediation of PCS and sequential reuse of the post-remediation soil.

Roles of flavoprotein oxidase and the exogenous heme- and quinone-dependent respiratory chain in lactic acid bacteria.

Lactic acid bacteria (LAB) are a type of bacteria that convert carbohydrates into lactate through fermentation metabolism. While LAB mainly acquire energy through this anaerobic process, they also have oxygen-consuming systems, one of which is flavoprotein oxidase and the other is exogenous heme- or heme- and quinone-dependent respiratory metabolism. Over the past two decades, research has contributed to the understanding of the roles of these oxidase machineries, confirming their suspected roles and uncovering novel functions. This review presents the roles of these oxidase machineries, which are anticipated to be critical for the future applications of LAB in industry and comprehending the virulence of pathogenic streptococci.

Novel gas mixture combined with an auto-transfusion tourniquet enhances cerebral O2 transport and hemodynamic indices in CPR swine. Part B - A pilot experimental study.

Objectives: The cognitive outcome of CPR is poor. This study aims to evaluate if enhancing blood flow to the brain and oxygen dissociation from the hemoglobin improve cerebral O2 transport during CPR in cardiac arrest swine. Methods: Standard swine-CPR model of induced VF and recovery was treated with an auto-transfusion tourniquet (A-TT®; HemaShock® (HS) Oneg HaKarmel Ltd. Israel) and ventilation with a novel mixture of 30% Oxygen, 5% CO2, and 65% Argon (COXAR™). Five swine received the study treatment and 5 controls standard therapy. Animals were anesthetized, ventilated, and instrumented for blood draws and pressure measurements. Five minutes of no-CPR arrest were followed by 10 min of mechanical CPR with and without COXAR-HS™ enhancement followed by defibrillation and 45 min post ROSC follow-up. Results: All 5 COXAR-HS™ animals were resuscitated successfully as opposed to 3 of the control animals. Systolic (p < 0.05), and diastolic (p < 0.01) blood pressures, and coronary (p < 0.001) and cerebral (p < 0.05) perfusion pressures were higher in the COXAR-HS™ group after ROSC, as well as cerebral flow and O2 provided to the brain (p < 0.05). Blood pressure maintenance after ROSC required much higher doses of norepinephrine in the 3 resuscitated control animals vs. the 5 COXAR-HS™ animals (p < 0.05). jugular vein PO2 and SO2 exceeded 50 mmHg and 50%, respectively with COXAR-HS™. Conclusions: In this pilot experimental study, COXAR-HS™ was associated with higher diastolic blood pressure and coronary perfusion pressure with lower need of vasopressors after ROSC without significant differences prior to ROSC. The higher PjvO2 and SjvO2 suggest enhanced O2 provision to the brain mitochondria, while limb compression by the HS counteracts the vasodilatory effect of the CO2. Further studies are needed to explore and validate the COXAR-HS™ effects on actual post-ROSC brain functionality.

CaMKIIδ-dependent dysregulation of atrial Na+ homeostasis promotes pro-arrhythmic activity in an obstructive sleep apnea mouse model.

Background: Obstructive sleep apnea (OSA) has been linked to various pathologies, including arrhythmias such as atrial fibrillation. Specific treatment options for OSA are mainly limited to symptomatic approaches. We previously showed that increased production of reactive oxygen species (ROS) stimulates late sodium current through the voltage-dependent Na+ channels via Ca2+/calmodulin-dependent protein kinase IIδ (CaMKIIδ), thereby increasing the propensity for arrhythmias. However, the impact on atrial intracellular Na+ homeostasis has never been demonstrated. Moreover, the patients often exhibit a broad range of comorbidities, making it difficult to ascertain the effects of OSA alone. Objective: We analyzed the effects of OSA on ROS production, cytosolic Na+ level, and rate of spontaneous arrhythmia in atrial cardiomyocytes isolated from an OSA mouse model free from comorbidities. Methods: OSA was induced in C57BL/6 wild-type and CaMKIIδ-knockout mice by polytetrafluorethylene (PTFE) injection into the tongue. After 8 weeks, their atrial cardiomyocytes were analyzed for cytosolic and mitochondrial ROS production via laser-scanning confocal microscopy. Quantifications of the cytosolic Na+ concentration and arrhythmia were performed by epifluorescence microscopy. Results: PTFE treatment resulted in increased cytosolic and mitochondrial ROS production. Importantly, the cytosolic Na+ concentration was dramatically increased at various stimulation frequencies in the PTFE-treated mice, while the CaMKIIδ-knockout mice were protected. Accordingly, the rate of spontaneous Ca2+ release events increased in the wild-type PTFE mice while being impeded in the CaMKIIδ-knockout mice. Conclusion: Atrial Na+ concentration and propensity for spontaneous Ca2+ release events were higher in an OSA mouse model in a CaMKIIδ-dependent manner, which could have therapeutic implications.

Synergistic enhancement of Zn-air battery performance via integration of Ni-doped cobalt sulfide nanoparticles within N, S-doped carbon matrix.

Exploring precious metal-free bifunctional electrocatalysts for both the oxygen reduction reaction (ORR) and the oxygen evolution reaction (OER) is essential for the practical application of rechargeable Zn-air battery (ZAB). Herein, Ni-doped Co9S8 nanoparticles embedded in a defect-rich N, S co-doped carbon matrix (d-NixCo9-xS8@NSC) are synthesized via a facile pyrolysis and acid treatment process. The introduction of abundant defects in both the carbon matrix and metal sulfide provides numerous active sites and significantly enhances the electrocatalytic performances for both the ORR and OER. d-NixCo9-xS8@NSC exhibits a superior half-wave potential of 0.841 V vs. RHE for the ORR and delivers a low overpotential of 0.329 V at 10 mA cm-2 for the OER. Additionally, Zn-air secondary battery using d-NixCo9-xS8@NSC as the air cathode displays a higher specific capacity of 734 mAh gZn-1 and a peak power density of 148.03 mW cm-2 compared to those of state-of-the-art Pt/C-RuO2 (673 mAh gZn-1 and 136.9 mW cm-2, respectively). These findings underscore the potential of d-NixCo9-xS8@NSC as a high-performance electrocatalyst for secondary ZABs, offering new perspectives on the design of efficient noble metal-free electrocatalysts for future energy storage and conversion applications.

Oxygen-to-ammonium-nitrogen ratio as an indicator for oxygen supply management in microoxic bioanodic ammonium oxidation.

Microbial electrolysis cells (MECs) have been proven effective for oxidizing ammonium (NH4+), where the anode acts as an electron acceptor, reducing the energy input by substituting oxygen (O2). However, O2 has been proved to be essential for achieving high removal rates MECs. Thus, precise control of oxygen supply is crucial for optimizing treatment performance and minimizing energy consumption. Unlike previous studies focusing on dissolved oxygen (DO) levels, this study introduces the O2/NH4+-N ratio as a novel control parameter for balancing oxidation rates and the selectivity of NH4+ oxidation towards dinitrogen gas (N2) under limited oxygen condition. Our results demonstrated that the O2/NH4+-N ratio is a more relevant oxygen supply indicator compared to DO level. Oxygen served as a more favorable electron acceptor than the electrode, increasing NH4+ oxidation rates but also resulting in more oxidized products such as nitrate (NO3-). Additionally, nitrous oxide (N2O) and N2 production were higher with the electrode as the electron acceptor compared to oxygen alone. An O2/NH4+-N ratio of 0.5 was found to be optimal, achieving a balance between product selectivity for N2 (51.4 % ± 4.5 %) and oxidation rates (344.6 ± 14.7 mg-N/L*d), with the columbic efficiency of 30.7 % ± 2.0 %. Microbial community analysis revealed that nitrifiers and denitrifiers were the primary bacteria involved, with oxygen promoting the growth of nitrite-oxidizing bacteria, thus facilitating complete NH4+ oxidation to NO3-. Our study provides new insights and guidelines on the appropriate oxygen dosage, offering strategies into optimizing operational conditions for NH4+ removal using MECs.

Bavachinin, a main compound of Psoraleae Fructus, facilitates GSDMD-mediated pyroptosis and causes hepatotoxicity in mice.

Psoraleae Fructus (PF, Psoralea corylifolia L.), a traditional medicine with a long history of application, is widely used clinically for the treatment of various diseases. However, the reports of PF-related adverse reactions, such as hepatotoxicity, phototoxic dermatitis, and allergy, are increasing year by year, with liver injury being the mostly common. Our previous studies have demonstrated that PF and its preparations can cause liver injury in lipopolysaccharide (LPS)-mediated susceptibility mouse model, but the mechanism of PF-related liver injury is unclear. In this study, we showed that PF and bavachinin, a major component of PF, can directly induce the expression of caspase-1 and interleukin-1ß (IL-1ß), indicating that PF and bavachinin can directly triggered the activation of inflammasome. Furthermore, pretreatment with NLR family pyrin domain-containing 3 (NLRP3), NLR family CARD domain containing 4 (NLRC4) or absent in melanoma 2 (AIM2) inflammasome inhibitors, containing MCC950, ODN TTAGGG (ODN) and carnosol, all significantly reversed bavachinin-induced inflammasome activation. Mechanistically, bavachinin dose-dependently promote Gasdermin D (GSDMD) post-shear activation and then induce mitochondrial reactive oxygen species (mtROS) production and this effect is markedly inhibited by pretreatment with N-Acetylcysteine amide (NAC). In addition, combination treatment of LPS and bavachinin significantly induced liver injury in mice, but not LPS or bavachinin alone, and transcriptome analysis further validated these results. Thus, PF and bavachinin can induce the activation of inflammasome by promoting GSDMD cleavage and cause hepatotoxicity in mice. Therefore, PF, bavachinin, and PF-related preparations should be avoided in patients with inflammasome activation-associated diseases.

Optimizing selective withdrawal strategies to mitigate hypoxia under water-level reduction in Germany's largest drinking water reservoir.

Water-level reduction frequently occurs in deep reservoirs, but its effect on dissolved oxygen concentration is not well understood. In this study we used a well-established water quality model to illustrate effects of water level dynamics on oxygen concentration in Rappbode Reservoir, Germany. We then systematically elucidated the potential of selective withdrawal to control hypoxia under changing water levels. Our results documented a gradual decrease of hypolimnetic oxygen concentration under decreasing water level, and hypoxia occurred when the initial level was lower than 410 m a.s.l (71 m relative to the reservoir bottom). We also suggested that changes of hypoxic region, under increasing hypolimnetic withdrawal discharge, followed a unimodal trajectory with the maximum hypoxic area projected under the discharge between 3 m3/sec and 4 m3/sec. Besides, our results illustrated the extent of hypoxia was most effectively inhibited if the withdrawal strategy was applied at the end of stratification with the outlet elevation at the deepest part of the reservoir. Moreover, hypoxia can be totally avoided under a hybrid elevation withdrawal strategy using surface withdrawal during early and mid stratification, and deep withdrawal at the end of stratification. We further confirmed the decisive role of thermal structure in the formation of hypoxia under water-level reduction and withdrawal strategies. We believe the conclusions from this study can be applied to many deep waters in the temperate zone, and the results should guide stakeholders to mitigate negative impacts of hypoxia on aquatic ecosystems.

Synthesis and photodynamic activity of new 5-[(E)-2-(3-alkoxy-1-phenyl-1H-pyrazol-4-yl)ethenyl]-2-phenyl-3H-indoles.

A series of new indole-pyrazole hybrids 8a-m were synthesized through the palladium-catalyzed ligandless Heck coupling reaction from easily accessible unsubstituted, methoxy- or fluoro-substituted 4-ethenyl-1H-pyrazoles and 5-bromo-3H-indoles. These compounds exerted cytotoxicity to melanoma G361 cells when irradiated with blue light (414 nm) and no cytotoxicity in the dark at concentrations up to 10 µM, prompting us to explore their photodynamic effects. The photodynamic properties of the example compound 8d were further investigated in breast cancer MCF-7 cells. Evaluation revealed comparable anticancer activities of 8d in both breast and melanoma cancer cell lines within the submicromolar range. The treatment induced a massive generation of reactive oxygen species, leading to different types of cell death depending on the compound concentration and the irradiation intensity.

Clinical impact of hyperbaric oxygen therapy combined with steroid treatment for sudden sensorineural hearing loss: A case-control study.

Objectives: The aim of present study was to evaluate the clinical efficacy of hyperbaric oxygen therapy (HBOT) as a primary therapy combined with standard systemic corticosteroid treatment for sudden sensorineural hearing loss (SSNHL) compared to treatment without the use of HBOT (non-HBOT) through clinical data and advanced analytical approaches. Study Design: Case-control study. Methods: Conducted across three Japanese medical centers involving 298 SSNHL patients diagnosed between 2020 and 2023. Inclusion criteria encompassed first onset and treatment, WHO grade 3 or 4 initial hearing impairment, receipt of systemic corticosteroid therapy within 14 days of symptom onset, and initiation of HBOT within the same timeframe for the case group. The primary outcome measure was the difference in hearing improvement (mean hearing level in decibels, dB) between the two groups, assessed by pure-tone audiometry at baseline and 3 months post-treatment, using the inverse probability of treatment weighting (IPTW) method adjusted for covariate differences. Results: The study included 67 patients in the HBOT group and 68 in the non-HBOT group. The HBOT group exhibited significantly greater hearing improvement (IPTW-adjusted difference: 7.6 dB, 95% CI 0.4-14.7; p = 0.038). Patients without vertigo in the HBOT group demonstrated substantial hearing improvement (11.5 dB, 95% CI 2.3-20.6; p = 0.014), whereas those with vertigo showed no significant improvement (-1.8 dB, 95% CI -11.8-8.3; p = 0.729). The HBOT group also had a significantly higher association with complete recovery (IPTW-adjusted odds ratio: 2.57, 95% CI 1.13-5.85; p = 0.025). Conclusion: In SSHNL, HBOT combination therapy yielded slightly but significantly improved hearing outcomes compared to non-HBOT treatment. Level of Evidence: 4.

CARDIOGENIC SHOCK AND GLOBUS PALLIDUS INJURY AS A PRESENTATION OF CARBON MONOXIDE POISONING.

Carbon monoxide poisoning is one of the leading causes of mortality and morbidity by poisoning in the world. Signs and symptoms are nonspecific and related to impaired oxygen delivery to tissues, with the brain being the most affected organ due to its high oxygen demand. CO-Hb is a poor indicator of severity and long-term outcome, with clinicians relying more on clinical features such as level of consciousness and need for intubation, organ dysfunction and shock and also pH level. A 45-year-old female was found unconscious in her home with the fireplace lit and smoke all over the house. She was last seen well 18 hours before. She was brought to the emergency department and was admitted to the ICU in coma and cardiogenic shock, with a metabolic acidosis with hyperlactacidemia and a CO-Hb level of 15.5%. Laboratorial investigation revealed hepatic cytolysis, acute renal failure, rhabdomyolysis and a troponin I level of 338 ng/L. ECG showed no acute myocardial ischemia. Echocardiogram revealed diffuse hypokinesia with an ejection fraction of 25%. Head CT scan showed bilateral and symmetrical hypodensities of the globus pallidus. The patient underwent hyperbaric oxygen treatment with full neurological and cardiac recovery, allowing extubation 48 hours after admission. This rare severe case of coma due to carbon monoxide intoxication with globus pallidus injury and cardiogenic shock was successfully treated with hyperbaric oxygen, showing that it can be the right treatment choice in these cases, with an excellent impact on neurological and cardiac outcome.

L'intoxication au CO est une des causes principales de décès par empoisonnement dans le monde. Les signes, non spécifiques, sont dus à l'hypoxie cellulaire et le cerveau est le plus souvent atteint en raison de sa consommation d'oxygène élevée. Le taux d'HbCO est un indice peu fiable de la gravité initiale et du risque de séquelles si bien que l'on préfère se baser sur la clinique (conscience, nécessité d'intubation, dysfonctions d'organe, choc) et le pH sanguin. Une femme de 45 ans a été trouvée inconsciente à son domicile entièrement enfumé, cheminée allumée. Le dernier contact remontait à 18 heures. Elle a été hospitalisée en réanimation en coma et choc cardiogénique, avec une acidose lactique et une HbCO à 15,5%. La biologie retrouvait une cytolyse hépatique, une insuffisance rénale aiguë, une rhabdomyolyse et une troponine I à 338 ng/L. L'ECG ne trouvait pas d'ischémie, l'échocardiographie objectivait une hypokinésie globale et évaluait la fraction d'éjection à 25%. La TDM cérébrale montrait une hypodensité pallidale bilatérale. L'oxygénothérapie hyperbare (OHB) a permis une récupération neurologique et cardiaque complètes, permettant l'extubation à h48. Cette récupération complète après OHB confirme qu'il peut s'agir du traitement idoine des intoxications graves au CO, avec un excellent impact sur les devenirs cardiaque et neurologique.

Mitochondrial GRIM19 Loss Induces Liver Fibrosis through NLRP3/IL33 Activation via Reactive Oxygen Species/NF-кB Signaling.

Background and Aims: Hepatic fibrosis (HF) is a critical step in the progression of hepatocellular carcinoma (HCC). Gene associated with retinoid-IFN-induced mortality 19 (GRIM19), an essential component of mitochondrial respiratory chain complex I, is frequently attenuated in various human cancers, including HCC. Here, we aimed to investigate the potential relationship and underlying mechanism between GRIM19 loss and HF pathogenesis. Methods: GRIM19 expression was evaluated in normal liver tissues, hepatitis, hepatic cirrhosis, and HCC using human liver disease spectrum tissue microarrays. We studied hepatocyte-specific GRIM19 knockout mice and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein-9 (Cas9) lentivirus-mediated GRIM19 gene-editing in murine hepatocyte AML12 cells in vitro and in vivo. We performed flow cytometry, immunofluorescence, immunohistochemistry, western blotting, and pharmacological intervention to uncover the potential mechanisms underlying GRIM19 loss-induced HF. Results: Mitochondrial GRIM19 was progressively downregulated in chronic liver disease tissues, including hepatitis, cirrhosis, and HCC tissues. Hepatocyte-specific GRIM19 heterozygous deletion induced spontaneous hepatitis and subsequent liver fibrogenesis in mice. In addition, GRIM19 loss caused chronic liver injury through reactive oxygen species (ROS)-mediated oxidative stress, resulting in aberrant NF-кB activation via an IKK/IкB partner in hepatocytes. Furthermore, GRIM19 loss activated NLRP3-mediated IL33 signaling via the ROS/NF-кB pathway in hepatocytes. Intraperitoneal administration of the NLRP3 inhibitor MCC950 dramatically alleviated GRIM19 loss-driven HF in vivo. Conclusions: The mitochondrial GRIM19 loss facilitates liver fibrosis through NLRP3/IL33 activation via ROS/NF-кB signaling, providing potential therapeutic approaches for earlier HF prevention.

Fullerol-reinforced antioxidantive 3D-printed bredigite scaffold for accelerating bone healing.

Reactive oxygen species play a vital role in tissue repair, and nonequilibrium of redox homeostasis around bone defect can compromise osteogenesis. However, insufficient antioxidant capacity and weak osteogenic performance remain major obstacles for bone scaffold materials. Herein, integrating the mussel-inspired polydopamine (PDA) coating and 3D printing technologies, we utilized the merits of both osteogenic bredigite and antioxidative fullerol to construct 3D-printed porous, biodegradable acid-buffering, reactive oxygen species (ROS) -scavenging and robust osteogenic bio-scaffold (denoted "FPBS") for in situ bone defect restoration under oxidative stress microenvironment. Initially, fullerol nanoparticles were attached to the surface of the bredigite scaffold via covalently inter-crosslinking with PDA. Upon injury, extracellular ROS capturing triggered the oxidative degradation of PDA, releasing fullerol nanoparticles to enter into cells for further intracellular ROS scavenging. In vitro, FPBS had good biocompatibility and excellent antioxidative capability. Furthermore, FPBS promoted the osteogenesis of stem cells with significant elevation of osteogenic markers. Finally, in vivo implantation of FPBS remarkably enhanced new bone formation in a rat critical calvarial defect model. Overall, with amelioration of the ROS microenvironment of injured tissue and enhancement of osteogenic differentiation of stem cells simultaneously, FPBS may hold great potential towards bone defect repair.

The Impact of Using Nesting Care on Heart Rate, Oxygen Saturation, and Pain Among Premature Neonates in Neonatal Intensive Care Units in Saudi Arabia: A Quasi-Experimental Study.

BACKGROUND: Supportive positioning may mimic the intrauterine environment and enhance neonates' physiological and developmental outcomes. Limited research in Saudi Arabia examined the effect of supportive positioning aids (nesting) on infant outcomes in neonatal intensive care units (NICUs). OBJECTIVE: This study compared nesting care to non-nesting care in the short-term outcomes of premature neonates (heart rate, oxygen saturation, and pain) in Saudi NICUs. METHODS: A quasi-experimental design compared two groups of premature neonates from two NICUs regarding their heart rate, oxygen saturation, and pain level. Nesting was used in the first group, and not in the second group. Seventy premature neonates (35 per group) were recruited. An independent t-test was used to compare the two groups. RESULTS: Heart rate was significantly lower in the nesting group than the non-nesting group at baseline and after procedures (136bpm and 139bpm vs 144bpm and 148bpm, P ≤ 0.05). The pain level was significantly lower in the nesting group than the non-nesting group at baseline and after procedures (3.7 and 3.8 vs 4.7 and 4.6, P ≤ 0.05). There was no significant difference between the two groups in oxygen saturation. CONCLUSION: Nesting care supported premature neonates in the NICU. It helped stabilize the heart rate and pain. NICUs in Saudi Arabia would benefit from educating NICU nurses and informing NICU managers and policymakers of nesting care.

Body-Wide Inactivation of the Myc-Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence.

The "Mlx" and "Myc" transcription factor networks cross-communicate and share many common gene targets. Myc's activity depends upon its heterodimerization with Max, whereas the Mlx Network requires that the Max-like factor Mlx associate with the Myc-like factors MondoA or ChREBP. The current work demonstrates that body-wide Mlx inactivation, like that of Myc, accelerates numerous aging-related phenotypes pertaining to body habitus and metabolism. The deregulation of numerous aging-related Myc target gene sets is also accelerated. Among other functions, these gene sets often regulate ribosomal and mitochondrial structure and function, genomic stability, and aging. Whereas "MycKO" mice have an extended lifespan because of a lower cancer incidence, "MlxKO" mice have normal lifespans and a higher cancer incidence. Like Myc, the expression of Mlx, MondoA, and ChREBP and their control over their target genes deteriorate with age in both mice and humans. Collectively, these findings underscore the importance of lifelong and balanced cross-talk between the two networks to maintain proper function and regulation of the many factors that can affect normal aging.

Nanopriming boost seed vigor: Deeper insights into the effect mechanism.

Nanopriming, an advanced seed priming technology, is highly praised for its environmental friendliness, safety, and effectiveness in promoting sustainable agriculture. Studies have shown that nanopriming can enhance seed germination by stimulating the expression of aquaporins and increasing amylase production. By applying an appropriate concentration of nanoparticles, seeds can generate reactive oxygen species (ROS), enhance their antioxidant capacity, improve their response to oxidative stress, and enhance their tolerance to both biotic and abiotic stresses. This positive impact extends beyond the seed germination and seedling growth stages, persisting throughout the entire life cycle. This review offers a comprehensive overview of recent research progress in seed priming using various nanoparticles, while also addressing current challenges and future opportunities for sustainable agriculture.

Proton-Enriched Alginate-Graphene Hydrogel Microreactor for Enhanced Hydrogen Peroxide Photosynthesis.

Efficient synthesis of H2O2 via photocatalytic oxygen reduction without sacrificial agents is challenging due to inadequate proton supply from water and difficulty in maintaining O-O bond during O2 activation. Herein, we developed a straightforward strategy involving a proton-rich hydrogel cross-linked by metal ions [M(n)], which is designed to facilitate the selective production of H2O2 through proton relay and metal ion-assisted detachment of crucial intermediates. The hydrogel comprises CdS/graphene and alginate cross-linked by metal ions via O=C-O-M(n) bonds. Efficient O2 reduction and hydrogenation occurred, benefitting from the collaboration between proton-rich alginate and the photocatalytically active CdS/graphene. Meanwhile, the O=C-O-M(n) bonds enhance the electron density of α-carbon sites on graphene, crucial for O2 activation and *OOH intermediate detachment, preventing deeper O-O bond cleavage. The role of metal ions in promoting *OOH desorption was evident through Lewis acidity-dependent activity, with Y(III) demonstrating the highest activity followed by Lu(III), La(III), and Ca(II).

N-Phenyl-2-Pyridone-Derived Endoperoxide Suppressing both Lung Cancer and Idiopathic Pulmonary Fibrosis Progression by Three-Pronged Action.

We report an endoperoxide compound (E5) which can deliver three therapeutic components by a thermal cycloreversion, namely, singlet oxygen, triplet oxygen and 3-methyl-N-phenyl-2-pyridone, thus targeting multiple mechanisms for treating non-small cell lung cancer and idiopathic pulmonary fibrosis. In aqueous environment, E5 undergoes clean reaction to afford three therapeutic components with a half-life of 8.3 hours without the generation of other by-products, which not only achieves good cytotoxicity toward lung cancer cells and decreases the levels of HIF-1α protein, but also inhibits the TGF-ß1 induced fibrosis in vitro. In vivo experiments also demonstrated the efficacy of E5 in inhibiting tumor growth and relieving idiopathic pulmonary fibrosis, while exhibiting good biocompatibility. Many lines of evidence reveal the therapeutic efficacy of singlet oxygen and 3-methyl-N-phenyl-2-pyridone, and triplet oxygen could downregulate HIF-1α and relieve tumor hypoxia which is a critical issue in conventional PDT. Unlike other combination therapies, in which multiple therapeutic agents are given in independent formulations, our work demonstrates single molecule endoperoxide prodrugs could be developed as new platforms for treatment of cancers and related diseases.