Cellulose-based light-management film exhibiting flame-retardant and thermal-healing properties.

The increased use and expansion of biomass applications offer a viable approach to diminish reliance on petroleum-derived resources and promote carbon neutrality. Cellulose, being the most abundant natural polymer on Earth, has garnered considerable attention. This study introduces a straightforward method to fabricate a cellulose-based multifunctional composite film designed for efficient light management, specifically featuring flame retardant and thermal-healing capabilities. The film incorporates a microfibrillated cellulose (MFC) matrix with functional components, namely benzoxazine resin (BR) and 2-hydroxyethyl methacrylate phosphate (HEMAP). Utilizing dynamic covalent crosslinking, the composite films exhibit satisfactory self-healing properties. The combined effects of BR and HEMAP contribute to the effective flame retardancy of the composite film. Furthermore, the resulting film shields ultraviolet and blue light, offering comfortable interior lighting by mitigating harsh light and extending light propagation. The film also demonstrates favorable water resistance and high tensile strength. The exceptional multifunctional properties, coupled with its safety and extended service life, position it as a potential optical management film for smart building materials.

Rapid fabricated in-situ polymerized lignin hydrogel sensor with highly adjustable mechanical properties.

Conductive hydrogels have been widely used as sensors owing to their tissue-like properties. However, the synthesis of conductive hydrogels with highly adjustable mechanical properties and multiple functions remains difficult to achieve yet highly needed. In this study, lignin hydrogel characterized by frost resistance, UV resistance, high conductivity, and highly adjustable mechanical properties without forming by-products was prepared through a rapid in-situ polymerization of acrylic acid/zinc chloride (AA/ZnCl2) aqueous solution containing lignin extract induced by the reversible quinone-catechol redox of the ZnCl2-lignin system at room temperature. Results revealed that the PAA/ZnCl2/lignin hydrogel exhibited mechanical properties with tensile stress (ranging from 0.08 to 3.28 MPa), adhesion to multiple surfaces (up to 62.05 J m-2), excellent frost resistance (-70-20 °C), UV resistance, and conductivity (0.967 S m-1), which further endow the hydrogel as potential strain and temperature sensor with wide monitor range (0-300 %), fatigue resistance, and quick response (70 ms for 150 % strain). This study proposed and developed a green, simple, economical, and efficient processing method for a hydrogel sensor in flexible wearable devices and man-machine interaction fields.

Bacopaside I alleviates depressive-like behaviors by modulating the gut microbiome and host metabolism in CUMS-induced mice.

Bacopaside I (BSI) is a natural compound that is difficult to absorb orally but has been shown to have antidepressant effects. The microbiota-gut-brain axis is involved in the development of depression through the peripheral nervous system, endocrine system, and immune system and may be a key factor in the effect of BSI. Therefore, this study aimed to investigate the potential mechanism of BSI in the treatment of depression via the microbiota-gut-brain axis and to validate it in a fecal microbiota transplantation model. The antidepressant effect of BSI was established in CUMS-induced mice using behavioral tests and measurement of changes in hypothalamicpituitaryadrenal (HPA) axis-related hormones. The improvement of stress-induced gut-brain axis damage by BSI was observed by histopathological sections and enzyme-linked immunosorbent assay (ELISA). 16 S rDNA sequencing analysis indicated that BSI could modulate the abundance of gut microbiota and increase the abundance of probiotic bacteria. We also observed an increase in short-chain fatty acids, particularly acetic acid. In addition, BSI could modulate the disruption of lipid metabolism induced by CUMS. Fecal microbiota transplantation further confirmed that disruption of the microbiota-gut-brain axis is closely associated with the development of depression, and that the microbiota regulated by BSI exerts a partial antidepressant effect. In conclusion, BSI exerts antidepressant effects by remodeling gut microbiota, specifically through the Lactobacillus and Streptococcus-acetic acid-neurotrophin signaling pathways. Furthermore, BSI can repair damage to the gut-brain axis, regulate HPA axis dysfunction, and maintain immune homeostasis.

Hyperbaric oxygen combined with hydrogen-rich saline protects against acute lung injury.

Background: This study sought to investigate therapeutic effects of hydrogen-rich saline (HRS) combined with hyperbaric oxygen (HBO2) in an experimental rat model of acute lung injury (ALI). Method: Forty male Sprague-Dawley rats were randomly divided into sham, LPS, LPS + HBO2, LPS + HRS, and LPS + HBO2 + HRS groups. After an intratracheal injection of LPS-induced ALI, the rats were given a single-agent HBO2 or HRS or HBO2 + HRS treatment. The treatments were continued for three days in this experimental rat model of ALI. At the end of experiment, the lung pathological, inflammatory factors, and cell apoptosis in the pulmonary tissue were detected by Tunel method and cell apoptosis rate was calculated accordingly. Results: In the groups treated with HBO2 + HRS, pulmonary pathological data, wet-dry weight ratio, and inflammatory factors of pulmonary tissues and alveolar lavage fluid were significantly superior to those of the sham group (p≺0.05). Cell apoptosis detection revealed that no single agent treatment of HRS or HBO2, or combination treatment, could alleviate all cell apoptosis. HRS combined with HBO2 treatment was superior to single treatment (p≺0.05). Conclusion: HRS or HBO2 single treatment could decrease inflammatory cytokines release in lung tissue, reduce the accumulation of oxidative products and alleviate apoptosis of pulmonary cells, then lead to positive therapeutic effects on ALI induced by LPS. Furthermore, HBO2 combined with HRS treatment presented a synergy effect on cell apoptosis decrease and a decline in inflammatory cytokine release and related inflammatory product generation, compared with a single treatment.

Influence of exercise type and duration on cardiorespiratory fitness and muscular strength in post-menopausal women: a systematic review and meta-analysis.

Background and aim: Both cardiorespiratory fitness (CRF) and muscular strength are reported to decrease with age and menopause, which considered to be risk for cardiovascular diseases (CVDs). Previous relevant meta-analyses are inconclusive on the beneficial effects of exercise, particularly in post-menopausal women. In this systematic review and meta-analysis, we investigated the effects of exercise modalities on CRF and muscular strength in post-menopausal women, and identified the effective exercise type and duration. Methods: A comprehensive search was conducted on PubMed, Web of Science, CINAHL, and Medline to identify the randomized controlled trials, which evaluated exercise effect on CRF, lower- and upper-body muscular strength, and/or handgrip strength in post-menopausal women and compared the results with control. Standardized mean differences (SMD), weighted mean differences (WMD), and 95% confidence intervals (95% CIs) were calculated using random effects models. Results: A total of 129 studies comprising 7,141 post-menopausal women with mean age and BMI ranging from ∼53 to 90 years and 22 to 35 kg/m2, respectively, were included in the meta-analysis. Overall, exercise training effectively increased CRF (SMD: 1.15; 95% CI: 0.87, 1.42; p = 0.001), lower-body muscular strength (SMD: 1.06; 95% CI: 0.90, 1.22; p = 0.001), upper-body muscular strength (SMD: 1.11; 95% CI: 0.91, 1.31; p = 0.001), and handgrip strength (WMD: 1.78 kg; 95% CI: 1.24, 2.32; p = 0.001) in post-menopausal women. These increments were found to be irrespective of ages and intervention durations. Regarding exercise type, aerobic, resistance, and combined training significantly increased CRF and lower-body muscular strength, while resistance and combined training effectively increased handgrip strength. However, only resistance training increased the upper-body muscular strength in women. Conclusion: Our findings suggest that exercise training is effective in increasing CRF and muscular strength in post-menopausal women, which might be cardioprotective. Both aerobic and resistance training alone or in combination increased CRF and lower-body muscular strength, but only resistance training increased upper-body strength in women. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=283425, identifier: CRD42021283425.

Performance comparison of three scaling algorithms in NMR-based metabolomics analysis.

Unit variance (UV) scaling, mean centering (CTR) scaling, and Pareto (Par) scaling are three commonly used algorithms in the preprocessing of metabolomics data. Based on our NMR-based metabolomics studies, we found that the clustering identification performances of these three scaling methods were dramatically different as tested by the spectra data of 48 young athletes' urine samples, spleen tissue (from mice), serum (from mice), and cell (from Staphylococcus aureus) samples. Our data suggested that for the extraction of clustering information, UV scaling could serve as a robust approach for NMR metabolomics data for the identification of clustering analysis even with the existence of technical errors. However, for the purpose of discriminative metabolite identification, UV scaling, CTR scaling, and Par scaling could equally extract discriminative metabolites efficiently based on the coefficient values. Based on the data presented in this study, we propose an optimal working pipeline for the selection of scaling algorithms in NMR-based metabolomics analysis, which has the potential to serve as guidance for junior researchers working in the NMR-based metabolomics research field.

Oxidative stress, dysfunctional energy metabolism, and destabilizing neurotransmitters altered the cerebral metabolic profile in a rat model of simulated heliox saturation diving to 4.0 MPa.

The main objective of the present study was to determine metabolic profile changes in the brains of rats after simulated heliox saturated diving (HSD) to 400 meters of sea water compared to the blank controls. Alterations in the polar metabolome in the rat brain due to HSD were investigated in cortex, hippocampus, and striatum tissue samples by applying an NMR-based metabolomic approach coupled with biochemical detection in the cortex. The reduction in glutathione and taurine levels may hypothetically boost antioxidant defenses during saturation diving, which was also proven by the increased malondialdehyde level, the decreased superoxide dismutase, and the decreased glutathione peroxidase in the cortex. The concomitant decrease in aerobic metabolic pathways and anaerobic metabolic pathways comprised downregulated energy metabolism, which was also proven by the biochemical quantification of the metabolic enzymes Na-K ATPase and LDH in cerebral cortex tissue. The significant metabolic abnormalities of amino acid neurotransmitters, such as GABA, glycine, and aspartate, decreased aromatic amino acids, including tyrosine and phenylalanine, both of which are involved in the metabolism of dopamine and noradrenaline, which are downregulated in the cortex. Particularly, a decline in the level of N-acetyl aspartate is associated with neuronal damage. In summary, hyperbaric decompression of a 400 msw HSD affected the brain metabolome in a rat model, potentially including a broad range of disturbing amino acid homeostasis, metabolites related to oxidative stress and energy metabolism, and destabilizing neurotransmitter components. These disturbances may contribute to the neurochemical and neurological phenotypes of HSD.

Effects of different simulated submarine escape depths by free ascent in animal models.

Objective: If a damaged submarine cannot be rescued in time, it is necessary to carry out a submarine escape by free ascent. Decompression illness is the greatest threat to the safety of submariners. The maximum depth at which a safe escape can be carried out is unknown. This study intends to explore the maximum safe escape depth by observing the effects of simulated submarine escape at different depths on animal models. Methods: We evaluated pulmonary function indexes, blood gas values, blood cell counts, the myocardial enzyme spectrum, coagulation parameters, and proinflammatory cytokine levels in rats, electrocardiographic activity in rabbits after simulated 150-m, 200-m, 220-m, and 250-m submarine escape by free ascent. Results: An escape depth of 150 m did not cause significant changes in the indicators. An escape depth of >200 m led to pulmonary ventilation and gas diffusion dysfunction, hypoxemia, myocardial ischemia, and activation of the fibrinolytic and inflammatory systems. The magnitudes of the changes in the indicators were proportional to escape depth. Conclusion: An escape depth of 150 m in animal models is safe, whereas escape at > 200 m can be harmful.

Lung function changes in divers after a single deep helium-oxygen dive.

INTRODUCTION: This study measured pulmonary function in divers after a single helium-oxygen (heliox) dive to 80, 100, or 120 metres of sea water (msw). METHODS: A total of 26 divers participated, of whom 15, five, and six performed a 80, 100, or 120 msw dive, respectively. While immersed, the divers breathed heliox and air, then oxygen during surface decompression in a hyperbaric chamber. Pulmonary function was measured twice before diving, 30 min after diving, and 24 h after diving. RESULTS: At 30 min after the 80 msw dive the forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ratio and the maximum expiratory flow at 25% of vital capacity (MEF25) values decreased (89.2% to 87.1% and 2.57 L·s⁻¹ to 2.35 L·s⁻¹, P = 0.04, P = 0.048 respectively) but FEV1/FVC returned to the baseline values by 24 h post-dive. Other pulmonary indicators exhibited downward trends at 30 min after the dive, but statistical significance was lacking. Interestingly, though several parameters decreased after the 100 msw dive, statistical significance was not reached. After the 120 msw dive, the FEV1/FVC and MEF75 decreased (90.4% to 85.6% and 8.05 L·s⁻¹ to 7.46 L·s⁻¹, P = 0.01, P = 0.007). The relatively small numbers of subjects who dived to 100 and 120 msw depths may explain the inconsistent results. The subjects diving to 100 and 120 msw were more trained / skilled, but this would not explain the inconsistencies in results between these depths. CONCLUSIONS: We conclude that single deep heliox dives cause a temporary decrease in FEV1/FEV and MEF25 or MEF75, but these changes can recover at 24 h after the dive.

Characteristics of Gut Microbial Profiles of Offshore Workers and Its Associations With Diet.

The composition of gut microbiota is not a static state in humans but fluctuates in response to changes in environments, diet, and lifestyle factors. Here, we explored differences in gut microbiota between populations worked offshore and onshore and further studied microbiota-associated variables in offshore workers (OFWs). We investigated the gut microbiota of 168 healthy subjects (offshore: 145 and onshore: 23) using 16S rRNA sequencing. Our results indicated that the marine environment caused significant changes in intestinal microbial structure, which was mainly reflected in the increase in bacterial diversity, changes in composition, and the emergence of more specific bacteria in OFWs. In addition, characteristics of gut microbiota in OFWs were further explored, and the genus Holdemanella was considered a potential contributor to the stable state of health. Besides, some dietary factors, namely, duck, mutton, dairy products, and algae vegetables were identified as the gut microbial covariates in the OFWs cohort and were positively correlated with the genus Holdemanella. This suggests the positive intervention of diet on Holdemanella. Our data highlight, for the first time to our knowledge, that the marine geographical environment plays an important role in shaping the gut mycobiome composition. And diet could be considered as the targeted intervention that alters the composition of the microbiome to improve host health.

[Effect of nuclear radiation on rat model of decompression sickness induced by large depth rapid floating escape].

Objective: To investigate the effects of different doses of nuclei exposure at different time on morbidity, mortality, and damage indicators in a rat model of decompression sickness caused by rapid flotation escape at a large depth. Methods: Eighty male SD rats were randomly divided into blank control group, escape control group and six intervention groups (escape at 4 hours after 4 Gy radiation, escape at 4 hours after 6 Gy radiation, escape at 4 hours after 12 Gy radiation, escape at 8 hours after 4 Gy radiation, escape at 8 hours after 6 Gy radiation, escape at 8 hours after 12 Gy radiation). Rats in intervention groups were exposed to different doses of γ-ray (4,6,12 Gy, respectively), and then were carried out a large depth and rapid buoyancy escape experiment (maximum pressure depth of 150 m). The changes of lung W/D, spleen index and plasma IL-1ß levels were analyzed. Results: Compared with the blank control group, decompression sickness incidence and mortality of rats in escape groups after nuclear exposure were increased significantly. In 4 Gy and 6 Gy irradiation groups, higher morbidity and mortality were observed in rats which escaped at 4 h post nuclear exposure when compared with rats in 8 h groups. Consistent with the changes in morbidity and mortality, the wet / dry ratio of lung tissue, the pathological damage of lung tissue, and the decrease of spleen index showed the same trends: the changes were obvious at 4 h after lower doses nuclear radiation (4 Gy and 6 Gy), not at 8 h. However, these indicators all changed markedly at 4 and 8 h after higher doses nuclear radiation (12 Gy). Plasma IL-1ß levels were significantly increased in each post-radiation exposure group when compared with the blank control group and the exposed control group. Conclusion: Nuclear radiation-induced lung injury, the damaged immune function and elevated plasma inflammatory factor concentrations increase the risk of decompression sickness after rapid ascent.

Human Physiological Responses to a Single Deep Helium-Oxygen Diving.

Objective: The objective of this study was to explore whether a single deep helium-oxygen (heliox) dive affects physiological function. Methods: A total of 40 male divers performed an open-water heliox dive to 80 m of seawater (msw). The total diving time was 280 min, and the breathing helium-oxygen time was 20 min. Before and after the dive, blood and saliva samples were collected, and blood cell counts, cardiac damage, oxidative stress, vascular endothelial activation, and hormonal biomarkers were assayed. Results: An 80 msw heliox dive induced a significant increase in the percentage of granulocytes (GR %), whereas the percentage of lymphocytes (LYM %), percentage of intermediate cells (MID %), red blood cell number (RBC), hematocrit (hCT), and platelets (PLT) decreased. During the dive, concentrations of creatine kinase (CK), a myocardial-specific isoenzyme of creatine kinase (CK-MB) in serum and amylase alpha 1 (AMY1), and testosterone levels in saliva increased, in contrast, IgA levels in saliva decreased. Diving caused a significant increase in serum glutathione (GSH) levels and reduced vascular cell adhesion molecule-1 (VCAM-1) levels but had no effect on malondialdehyde (MDA) and endothelin-1 (ET-1) levels. Conclusion: A single 80 msw heliox dive activates the endothelium, causes skeletal-muscle damage, and induces oxidative stress and physiological stress responses, as reflected in changes in biomarker concentrations.

Changes in acid-base status in oxygen toxicity at 230 kPa oxygen as a function of exposure time.

Breathing less than 50 kPa of oxygen over time can lead to pulmonary oxygen toxicity (POT). Vital capacity (VC) as the sole parameter for POT has its limitations. In this study we try to find out the changes of acid-base status in a POT rat model. Fifty male rats were randomly divided into five groups, exposed to 230 kPa oxygen for three, six, nine and 12 hours, respectively. Rats exposed to air were used as controls. After exposure the mortality and behavior of rats were observed. Arterial blood samples were collected for acid-base status detection and wet-dry (W/D) ratios of lung tissues were tested. Results showed that the acid-base status in rats exposed to 230 kPa oxygen presented a dynamic change. The primary status was in the compensatory period when primary respiratory acidosis was mixed with compensated metabolic alkalosis. Then the status changed to decompensated alkalosis and developed to decompensated acidosis in the end. pH, PCO2, HCO3-, TCO2, and BE values had two phases: an increase and a later decrease with increasing oxygen exposure time, while PaO2 and lung W/D ratio showed continuously increasing trends with the extension of oxygen exposure time. Lung W/D ratio was significantly associated with PaO2 (r = 0.6385, p = 0.002), while other parameters did not show a significant correlation. It is concluded that acid-base status in POT rats presents a dynamic change: in the compensatory period first, then turns to decompensated alkalosis and ends up with decompensated acidosis status. Blood gas analysis is a useful method to monitor the development of POT.

An easy-to-operate web-based calculator for predicting the progression of chronic kidney disease.

BACKGROUND: This study aimed to establish and validate an easy-to-operate novel scoring system based on simple and readily available clinical indices for predicting the progression of chronic kidney disease (CKD). METHODS: We retrospectively evaluated 1045 eligible CKD patients from a publicly available database. Factors included in the model were determined by univariate and multiple Cox proportional hazard analyses based on the training set. RESULTS: Independent prognostic factors including etiology, hemoglobin level, creatinine level, proteinuria, and urinary protein/creatinine ratio were determined and contained in the model. The model showed good calibration and discrimination. The area under the curve (AUC) values generated to predict 1-, 2-, and 3-year progression-free survival in the training set were 0.947, 0.931, and 0.939, respectively. In the validation set, the model still revealed excellent calibration and discrimination, and the AUC values generated to predict 1-, 2-, and 3-year progression-free survival were 0.948, 0.933, and 0.915, respectively. In addition, decision curve analysis demonstrated that the model was clinically beneficial. Moreover, to visualize the prediction results, we established a web-based calculator ( https://ncutool.shinyapps.io/CKDprogression/ ). CONCLUSION: An easy-to-operate model based on five relevant factors was developed and validated as a conventional tool to assist doctors with clinical decision-making and personalized treatment.

Simulation stress model of the undersea environment activates the central nervous, neuroendocrine and immune systems and anxiety in rats.

The present study was designed to assess the stress responses to a simulation model of the undersea environment that is similar to some undersea working conditions such as submarine rescue, underwater salvage and underwater construction. Restraint, hyperbaric air and immersion were chosen to produce the simulation stress model in rats for four hours. Rats were randomized into five groups: control group, restraint (R) group, hyperbaric air (H) group, restraint plus hyperbaric air (RH) group, and restraint plus hyperbaric air plus immersion (RHI) group. The results showed that the responses to the simulation stress model of the undersea environment induced by R, H, RH and RHI involved the upregulated norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT) of the central nervous system (CNS), upregulated adrenocorticotropic hormone (ACTH), corticosterone (CORT) and blood glucose of the neuroendocrine system, upregulated interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) of the immune system, and increased anxiety in rats. Compared with hyperbaric air, restraint tended to activate stronger stress responses. Conclusively, this work established a simulation stress model of the undersea environment induced by restraint, hyperbaric air and immersion. It further provided experimental data of such a model that showed significant activation of the CNS, neuroendocrine and immune systems and anxiety in rats. In this experiment we provided an experimental basis for undersea work such as working aboard a submarine.

[Edaravone has a protective role in a mouse model of pulmonary oxygen toxicity].

OBJECTIVE: To find if edaravone can play a protective role in a mouse model of pulmonary oxygen toxicity and explore the intervention mechanism. METHODS: Thirty male C57BL/6 mice were randomly divided into 3 groups(Air +Vehicle, Hyperbaric oxygen(HBO) +Vehicle and HBO + Edaravone). Mice were either given edaravone (5 mg/(kg·d)) in sterilized water or a sterilized water vehicle for 3 days before oxygen exposure. Mice in HBO groups were exposed to 0.23 MPa hyperoxia (≥95% O2) for 6 h. Lung tissues were collected and the wet/dry ratio of lung were analyzed. For histologic analysis, lung sections were stained with hematoxylin and eosin (HE). Proinflammatory cytokine levels and antioxidant enzyme activities in lungs were determined by using ELISA kits. The expression levels of pro-apoptosis protein were determined with Western blot analysis. RESULTS: Edaravone treatment could significantly reduce lung permeability, decrease tissue pro-apoptosis protein (cleaved-caspase3) and inflammation (IL-1ß). However, edaravone treatment had no effect on antioxidant enzyme activities. CONCLUSION: These results showed that edaravone treatment had a protective role in pulmonary oxygen toxicity through curbing inflammation and apoptosis.

PDTC ameliorates decompression induced-lung injury caused by unsafe fast buoyancy ascent escape via inhibition of NF-κB pathway.

Nuclear factor kappa B (NF-κB) is the critical transcriptional factor in the pathogenesis of acute lung injury (ALI). NF-κB regulates the expression changes of inflammatory factors such as tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß) and interleukin 6 (IL-6). In a previous study we showed that decompression sickness (DCS) caused by simulated unsafe fast buoyancy ascent escape (FBAE) could result in ALI, which was characterized by expression changes of inflammatory factors in rat lung tissue. The purpose of the present work was to study the roles of NF-κB and TNF-α in the process of DCS-induced rat lung injury caused by simulated unsafe FBAE. The research methods aimed to detect the rat lung tissue messenger ribonucleic acid (mRNA) and protein level variations of NF-κB, inhibitory ×B (I×B), TNF-α, IL-1ß, IL-6, IL-10 and IL-13 by using pretreatment of the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and TNF-α antibody (Ab). Our experimental results demonstrated that PDTC could improve the survival rate of the rats with DCS caused by unsafe FBAE more effectively than TNF-α Ab. However, the inhibition of TNF-α Ab on the nuclear translocated protein expression of NF-κB was more effective than PDTC. Both PDTC and TNF-α Ab can abrogate the increment of the rat lung tissue mRNA levels of TNF-α, IL-1ß, IL-6 and protein levels of NF-κB, TNF-α, IL-1ß effectively and increase the rat lung tissue content of I×B significantly. In conclusion, TNF-α-mediated NF-κB signaling may be one of the critical signaling pathways in the pathogenesis of DCS-induced rat lung injury caused by simulated unsafe FBAE. PDTC may ameliorate this type of injury partly through inhibiting the NF-κB pathway.

Hepatic PHD2/HIF-1α axis is involved in postexercise systemic energy homeostasis.

Exercise plays an important role in the prevention and treatment of chronic liver disease and associated metabolic disorders. A single bout of exercise induces tissue blood flow redistribution, which decreases splanchnic circulation and leads to physiologic hypoxia in the gastrointestinal system and liver. The transcription factor, hypoxia inducible factor-1α (HIF-1α), and its regulator, prolylhydroxylase 2 (PHD2), play pivotal roles in the response to oxygen flux by regulating downstream gene expression levels in the liver. We hypothesized that exercise increases the HIF-1α levels in the liver, and that the hepatic PHD2/HIF-1α axis is involved in postexercise restoration of systemic energy homeostasis. Through constant O2 consumption, CO2 production, food and water intake, and physical activity detection with metabolic chambers, we observed that one 30-min session of swimming exercise enhances systemic energy metabolism in mice. By using the noninvasive bioluminescence imaging ROSA26 oxygen-dependent domain Luc mouse model, we reveal that exercise increases in vivo HIFα levels in the liver. Intraperitoneal injections of the PHD inhibitor, dimethyloxalylglycine, mimicked exercise-induced HIFα increase, whereas the HIF-1α inhibitor, PX-478, blocked this effect. We next constructed liver-specific knockout (LKO) mouse models with albumin- Cre-mediated, hepatocyte-specific Hif1a and Phd2 deletion. Compared with their controls, Hif1a-LKO and Phd2-LKO mice exhibited distinct patterns of hepatic metabolism-related gene expression profiles. Moreover, Hif1a-LKO mice failed to restore systemic energy homeostasis after exercise. In conclusion, the current study demonstrates that a single bout of exercise disrupts systemic energy homeostasis, increasing the HIF-1α levels in the liver. These findings also provide evidence that the hepatic PHD2/HIF-1α axis is involved in postexercise systemic metabolic homeostasis.-Luo, B., Xiang, D., Wu, D., Liu, C., Fang, Y., Chen, P., Hu, Y.-P. Hepatic PHD2/HIF-1α axis is involved in postexercise systemic energy homeostasis.

Simvastatin decreases hyperbaric oxygen-induced acute lung injury by upregulating eNOS.

Statins, which are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase competitive inhibitors, not only lower blood cholesterol but also exert pleiotropic and beneficial effects in various diseases. However, the effects of statins on acute lung injury (ALI) induced by hyperbaric oxygen (HBO) have not been investigated. The present study is the first to investigate the effects of simvastatin in ALI induced by HBO in 8- to 9-wk-old C57BL/6 mice exposed to 0.23 MPa [=2.3 atmosphere absolute (ATA)] hyperoxia (≥95% O2) for 6 h. Mice were either given simvastatin (20 mg·kg·-1·day-1) in saline or a saline vehicle for 3 days before oxygen exposure. Lung tissue, serum, and bronchoalveolar lavage fluid (BALF) were collected for analysis of proapoptotic proteins, low-density lipoprotein cholesterol (LDL-C) levels, and lung inflammation. Simvastatin treatment significantly reduced lung permeability, serum LDL-C levels, tissue apoptosis, and inflammation. However, simvastatin treatment had no effect on antioxidant enzyme activity, nicotinamide adenine dinucleotide phosphate oxidase 4 (NADPH4) expression, and Akt phosphorylation levels. Furthermore, we investigated the role of endothelial nitric oxide synthase (eNOS) in simvastatin protection through inhibiting eNOS activity with NG-nitro-l-arginine methyl ester (l-NAME; 20 mg/kg). Results showed that the beneficial effects of simvastatin on ALI induced by HBO (antiinflammatory, antiapoptotic, lipid lowering, and reduction in lung permeability) were reversed. These results showed that simvastatin curbs HBO-induced lung edema, permeability, inflammation, and apoptosis via upregulating eNOS expression and that simvastatin could be an effective therapy to treat prolonged HBO exposure.

Simulated High Altitude Helium-Oxygen Diving.

BACKGROUND: Experience with commercial heliox diving at high altitude is limited. The purpose of this study was to evaluate the effects of acute high-altitude exposure on fitness to dive and the safety of decompression after heliox diving while using U.S. Navy heliox decompression tables with Cross correction. METHOD: Four professional male divers were consecutively decompressed in a hypo- and hyperbaric chamber to altitudes of 3000 m (9842.5 ft), 4000 m (13,123.4 ft), and 5200 m (17,060.4 ft) during the 8-d study. The dive profiles tested were to 30 m (98.4 ft) for 60 min at all three altitudes and, in addition, a dive to 50 m (164 ft) for 60 min at 5200 m altitude. The decompression followed the U.S. Navy heliox decompression table. The safety of decompression was evaluated by precordial Doppler venous gas emboli (VGE) monitoring during the decompression stages and postdive monitoring of the divers for symptoms of decompression sickness (DCS). Effects of altitude exposure were measured as subjective rating and EEG signs of sleepiness and fatigue, clinical symptoms of high altitude disease, and fitness to dive. RESULTS: A total of 24 person-dives were conducted. There were no VGE detected during the decompression and no postdive symptoms of decompression illness. Both the EEG findings and subjective evaluation indicated increased sleepiness and fatigue at 3000 m, 4000 m, and 5200 m, all compared with the sea level baseline. During the diving phase, both the EEG findings and subjective evaluation scores returned to the baseline and the divers successfully completed diving. DISCUSSION: Diving at high altitude with a short acclimatization period appears safe despite divers exhibiting clinical symptoms and EEG signs of impairment by hypoxia at high altitude. Despite a small number of dives, the results of this study indicate that our application of U.S. Navy standard heliox decompression tables with Cross correction is effective and could be used for underwater constructions up to 5200 m altitude, with due caution.Shi L, Zhang Y, Tetsuo K, Shi Z, Fang Y, Denoble PJ, Li Y. Simulated high altitude helium-oxygen diving. Aerosp Med Hum Perform. 2017; 88(12):1088-1093.