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Surveys based on western populations have identified many risk factors for dysphagia in older people, but the potential risk factors consistent with the demographic characteristics of older, hospitalized Chinese patients require further study. This single-center prospective study aimed to determine the incidence of dysphagia in western China, and to develop and validate a model to predict the risk of dysphagia among older patients. A total of 343 inpatients (aged ≥ 65 years without dysphagia and cognitive impairment) were included. A score ≥ 2 on the Eating Assessment Tool-10 was defined as dysphagia. After a six-month follow-up, 70 (20.4%) patients were found to have dysphagia. The final model included age, wearing dentures, activities of daily living, cerebral vascular disease, coronary heart disease, and malignancy. The developed model has high predictive accuracy and can be easily implemented in daily practice.

The effect of Yb2O3 on the densification and corrosion resistance of MgAl2O4 spinel was studied. The phase structure, microscopic morphology and indentation diagonal length of the samples were analysed by using an X-ray diffractometer, scanning electron microscope and digital micro-hardness tester. Results showed that the apparent porosity and relative density of the sintered samples with 2 wt% Yb2O3 are 0% and 99.6%, respectively. The average grain size of MASY2 was the smallest, which was 17.51 μm. The second phase (Al5Yb3O12) was generated when Yb2O3 was added to the MgAl2O4 spinel. Appropriate addition of Yb2O3 can refine the crystal grains, and Al5Yb3O12 was mainly located at the grain boundary, thereby improving the densification of MAS ceramics. In addition, the hardness of the MASY2 sample was the largest, which was 1460 HV. The corrosion depth of the MASY2 sample was the smallest (71.59 μm). The most appropriate amount of Yb2O3 was 2 wt%.

Magnesium–aluminium spinel powder was prepared by microwave hydrothermal synthesis method. The phase structure of the samples was analysed using X-ray diffractometer. The microscopic morphology of the samples was analysed by scanning electron microscope. The particle size of the powder was characterised. The effects of different microwave hydrothermal reaction temperatures on the phase structure, micromorphology and particle size distribution of the precursors were studied. Results show that when hydrothermal reaction temperature was controlled at 140 °C-180 °C, pure magnesium–aluminium composite hydroxyl-hydrate precursor can be obtained after 200 min. The median diameter of magnesium–aluminium spinel precursor powder under 150 °C was 5.958 μm, which is the minimum. After calcination, the morphology of the powder underwent a process from flaking and particle stacking to development of complete flake morphology as the microwave hydrothermal reaction temperature increased. The agglomeration phenomenon was very serious when the synthesis temperature was greater than 150 °C.

Porous carbons derived from agricultural waste biomass are ideal active materials for eco-friendly and low-cost supercapacitors electrode materials. However, the challenge remains to further functional modification of biomass-based carbon to achieve high specific capacitance. Herein, PPD-modified porous carbon (MPC) was synthesized by KOH soaking coupled with facile carbonization method of natural corncob and covalently graft of p-phenylenediamine. The MPC exhibits a high specific capacitance of 393 F·g-1 at a scan rate of 5mV·s-1 in a three electrode system in a 1 M KOH aqueous electrolyte solution. MPC was expected to become promising active materials for high performance negative electrode materials.

The effects of various KClO3 concentrations and durations on polyacrylonitrile (PAN) fibers were investigated. The oxidation treatment of PAN fibers (PFs) in a KClO3/H2SO4 system is a new pretreatment method for carbon fiber oxidation stabilization. Wettability (droplet shape), chemical structures (Fourier transform infrared spectroscopy [FT-IR]), crystal structures (wide-angle X-ray diffraction), microscopic structures (scanning electron microscopy), and chemical components (X-ray photoelectron spectroscopy) were analyzed. The PFs had the smallest contact angle and the best wettability when the KClO3 concentration was 15 wt%. FT-IR analysis showed that the absorption peak of the fibers was the lowest when the KClO3 concentration was 15 wt%. The peak intensities of MPFs-15-60 and MPFs-15-90 at 2θ = 17° and 2θ = 29°, respectively, were close and lower than the peak intensities of others. The number of grooves present on the fiber surface decreased when the KClO3 concentration was 15 wt%. As the KClO3 concentration increased, the elemental C content decreased and the elemental O content increased. MPFs-15-60 had a low C content and the highest O content, indicating that it had the highest degree of oxidation. The best sample for PF oxidation treatment with KClO3 was MPFs-15-60. The optimal processing conditions were a KClO3 concentration of 15 wt% and duration of 60 min.

Sr(Ti0.6Fe0.4)1-xO3-δ precursors were prepared through the sol–gel method. The samples sintered in air at 1350 °C for 300 min were characterized in terms of conductivity, bulk density, microstructure and phase analysis via AC impedance, scanning electron microscope (SEM), Archimedes’ method and X-ray diffraction (XRD). The total electrical conductivity of Sr(Ti0.6Fe0.4)1-xO3-δ samples can be remarkably improved by B-site-deficient level (x). When x = 0.07, the total electrical conductivity reaches a maximum of 0.3445 S/cm at 800 °C. The microstructure of the sample becomes more porous as the B-site-deficient level increases. The relative density of samples is becoming lower with B-site-deficient level increases. Diffraction peaks without impurities appear in the X-ray diffraction pattern, indicating the formation of a single perovskite structure. In addition, the Sr(Ti0.6Fe0.4)1-xO3-δ/YSZ samples show a great chemical stability and compatibility.

The effects of modification temperature and time on polyacrylonitrile (PAN) fibers under various concentrations of KMnO4 were studied. Wettability, colouration, chemical structure (Fourier transform infrared spectroscopy), crystal structure (X-ray diffraction), stack domains (D), interlayer spacing (d), microscopic structure (Scanning electron microscopy) and elemental content (energy dispersive spectroscopy) were analysed. Aside from its good hydrophilicity, KMnO4 at 2 and 4 wt% are beneficial to the modification of PAN fibers. The colouration of the fiber at 80 °C is the most obvious. The clear peak of the pre-oxidised fibers at 2340 cm−1 corresponds to the conjugated structure of MnO4–C N. At 4 wt%, the degree of pre-oxidation is too high and the main infrared peak disappears. M2, 30 has a minimum D of 9.320 nm and 8.258 nm at 2θ = 16.883° and 2θ = 29.673°, respectively, and the fiber crystals are the finest. At a content of 4 wt%, the fibers are axially cracked and crystals appear on the surface. M2, 30 and M2, 60 have a close percentage of C element, whereas M2, 30 has a lower percentage of Mn element. The best modification conditions of KMnO4 are 2 wt%, 80 °C and 30 min.

Intermittent hyperbaric oxygen exposure (IE-HBO) can protect the body against oxygen toxicity, but the underlying mechanisms are not very clear. Peroxiredoxin 6 (Prdx6) is a special endogenous antioxidative protein. We explored if the protective effects of IE-HBO are related to Prdx6. Mice were exposed to 280 kPa O2 for 60 min, followed by 30-min exposure to 20% O2/N2 mixture with equal pressure, repeated for six cycles. The Prdx6 protein level and non-selenium glutathione peroxidase (NSGPx) activity in the brain and lungs were then measured and the injury degree of lung and the oxidation level of brain and lung were evaluated. On this basis, the relationship between Prdx6 and IE-HBO’s protection was explored. Generally, both IE-HBO and continuous exposure to HBO (CE-HBO) could increase the protein and mRNA levels of Prdx6, and such increases were more significant 24 h after cessation of exposure; moreover, the Prdx6 level of IE-HBO was higher than that of CE-HBO in both brain and lung, also more significantly 24 h after cessation of exposure. In addition, IE-HBO exposure could more effectively potentiate the activity of NSGPx and increase GSH content in brain and lung tissues. At the same time, it could reduce oxidation products in these tissues. IE-HBO could also provide protection for the lungs against injuries resulting from prolonged HBO exposure. These data showed that IE-HBO can potentiate the production and the activity of Prdx6 and consequently mitigate oxidative damages in brain and lungs. The influences of IE-HBO on Prdx6 may form an important basis for its protection against oxygen toxicity.

Polyacrylonitrile (PAN) precursor was modified with hydrogen peroxide, and oxidative stabilisation studies were carried out using conventional and microwave heating. Wetting property, bulk density, Fourier transform infrared spectroscopy (FT-IR), extent of reaction (EOR), X-ray diffraction (XRD), scanning electron microscopy (SEM), Raman spectroscopy and mechanical properties were also investigated. Results show that PAN fibers have excellent wettability with hydrogen peroxide. Hydrogen peroxide modification can shorten the oxidation stabilisation time of PAN fibers. The FT-IR spectrum shows that the stabilised fibers modified by hydrogen peroxide have a conjugated structure, and the EOR value of hydrogen peroxide-modified PAN fibers stabilised by microwave heating is the largest. XRD analysis shows that hydrogen peroxide-modified fibers stabilised by microwave heating have low stack domains and height of the interlayer spacing. The SEM and Raman spectra indicate that hydrogen peroxide can improve the surface finish of the fibers and reduce defects. In addition, hydrogen peroxide-modified fibers stabilised by microwave heating exhibit excellent mechanical properties, with fineness of 0.78 dtex, strength of 1.60 dtex, and elongation at break of 3.49%.

Central nervous system (CNS) oxygen toxicity (CNS-OT) is a toxic reaction that appears after the inhalation of gas at an excessive oxygen partial pressure during underwater operation or hyperbaric oxygen (HBO) treatment. The mechanism of CNS-OT has not been clearly characterized. Though it has been attributed to the excessive oxidative stress induced by HBO, evidences against this hypothesis have been reported. Here we find that Forkhead box protein O3 (FoxO3a) is important for CNS-OT protection. FoxO3a knock-out (KO) mice had a shorter latency to develop convulsions and greater number of seizures within a certain period of time. The acute lung injury (ALI) induced by CNS-OT was also more severe in FoxO3a KO mice. Further analysis reveals a significant decrease in the activity of catalase (CAT), an antioxidant enzyme and a significant increase in the content of malondialdehyde (MDA), an oxidative product, in brain tissues of FoxO3a KO mice. Short-time HBO exposure could increase FoxO3a expression level and trigger its nuclear translocation. The level of nuclear localized FoxO3a peaked at 8 h after exposure. Our results demonstrate that the activity of FoxO3a is highly sensitive to HBO exposure and FoxO3a plays important roles in protecting CNS-OT. Further mechanic analysis reveals that FoxO3a protects CNS-OT via activating antioxidative signaling pathway.

BACKGROUND Recent studies indicated that ketone ester R,S-1,3-butanediol acetoacetate diester (BD-AcAc2) may be effective in preventing central nervous system oxygen toxicity (CNS-OT) and concomitant acute lung injury, a serious medical problem to be faced when breathing hyperbaric oxygen (HBO). This study aimed to further investigate the protective effects of BD-AcAc2 against CNS-OT and concomitant acute lung injury (ALI) in mice. METHODS Mice were treated with BD-AcAc2 in peanut oil vehicle (2.5, 5.0 or 10.0 g·kg⁻² body weight) by gavage 20 minutes before 600 kPa HBO exposure. Control mice received the vehicle only. Seizure latency was recorded. Malondialdehyde content in brain and lung tissues, total protein level in bronchoalveolar lavage fluid (BLF) and lung water content were measured 60 minutes after the hyperbaric exposure. Histopathology of lung tissue was undertaken. RESULTS Compared with the vehicle alone, BD-AcAc2 prolonged seizure latency in a dose-dependent manner (P < 0.01). The HBO-induced increase in brain malondialdehyde, BLF protein and lung water were significantly reduced by BD-AcAc2 (P < 0.01). CONCLUSION Oral administration of the ketone ester BD-AcAc2 significantly protected against CNS-OT and concomitant ALI. Alleviation of oxidative stress may be one underlying mechanism providing this effect.

Indium and iron were co-doped at the Ti site of strontium titanate (SrTiO3) as dopant to improve the electrical properties of the anode material for solid oxide fuel cells. The effect of B-site deficiency on the weight loss, phase, lattice parameter, density, microstructure and electrical properties of Sr(Ti0.8In0.1Fe0.1)1−xO3−δ (x = 0, 0.02, 0.06) samples was investigated. A compound solid solution was formed at 977 °C. Sr(Ti0.8In0.1Fe0.1)1−xO3−δ powders sintered at 1435 °C for 5 h in air exhibited a single-phas cubic perovskite structure. With increasing B-site deficiency level, the relative density and sinterability of (In, Fe) co-doped SrTiO3 decrease, whereas its lattice parameter, porosity and total conductivity increase.

The metabolism of adenosine (ADO) and nitric oxide (NO) in brain tissues is closely associated with the change of oxygen content. They have contrary effects in the onset of hyperbaric oxygen (HBO)-induced central nervous system oxygen toxicity (CNS OT): ADO can suppress the onset, while NO promotes it. We adopted the ADO-augmenting measure and NO-inhibiting measure in this study and found the combined use had a far superior preventive and therapeutic effect in protecting against CNS OT compared with the use of either measure alone. So we hypothesized that there is an interaction between ADO and NO which has an important impact on the onset of CNS OT. On this basis, we administered ADO-augmenting or ADO-inhibiting drugs to rats. After exposure to HBO, the onset of CNS OT was evaluated, followed by the measurement of NO content in brain tissues. In another experiment, rats were administered NO-augmenting or NO-inhibiting drugs. After exposure to HBO, the onset of CNS OT was evaluated, followed by measurement of the activities of ADO metabolism-related enzymes in brain tissues. The results showed that, following ADO augmentation, the content of NO and its metabolite was significantly reduced, and the onset of CNS OT significantly improved. After ADO inhibition, just the opposite was observed. NO promotion resulted in a decrease in the activity of ADO-producing enzyme, an increase in the activity of ADO-decomposing enzyme, and an aggravation in CNS OT. The above results were all reversed after an inhibition in NO content. Studies have shown that exposure to HBO has a significant impact on the content of ADO and NO in brain tissues as well as their biological effects, and ADO and NO might have an intense interaction, which might generate an important effect on the onset of CNS OT. The prophylaxis and treatment effects of CNS OT can be greatly enhanced by augmenting ADO and inhibiting NO.

BACKGROUND: Recent studies indicated that ketone ester R,S-1,3-butanediol acetoacetate diester (BD-AcAc(2)) may be effective in preventing central nervous system oxygen toxicity (CNS-OT) and concomitant acute lung injury, a serious medical problem to be faced when breathing hyperbaric oxygen (HBO). This study aimed to further investigate the protective effects of BD-AcAc(2) against CNS-OT and concomitant acute lung injury (ALI) in mice. METHODS: Mice were treated with BD-AcAc(2) in peanut oil vehicle (2.5, 5.0 or 10.0 g·kg(-1) body weight) by gavage 20 minutes before 600 kPa HBO exposure. Control mice received the vehicle only. Seizure latency was recorded. Malondialdehyde content in brain and lung tissues, total protein level in bronchoalveolar lavage fluid (BLF) and lung water content were measured 60 minutes after the hyperbaric exposure. Histopathology of lung tissue was undertaken. RESULTS: Compared with the vehicle alone, BD-AcAc(2) prolonged seizure latency in a dose-dependent manner (P < 0.01). The HBO-induced increase in brain malondialdehyde, BLF protein and lung water were significantly reduced by BD-AcAc(2) (P < 0.01). CONCLUSION: Oral administration of the ketone ester BD-AcAc(2) significantly protected against CNS-OT and concomitant ALI. Alleviation of oxidative stress may be one underlying mechanism providing this effect.

Hyperbaric oxygen (HBO) has been used widely in many underwater missions and clinical work. However, exposure to extremely high oxygen pressure may cause central nervous system oxygen toxicity (CNS-OT). The regulation of astrocyte glutamate metabolism is closely related to epilepsy. This study aimed to observe the effects of HBO exposure on glutamate metabolism in astrocytes and confirm the role of glutamate metabolism in CNS-OT. Anesthetized rats were exposed to 5 atmosphere absolute HBO for 80 min and microdialysis samples of brain interstitial fluid were continuously collected. Extracellular glutamate and glutamine concentrations were also detected. Freely moving rats were exposed to HBO of the same pressure for 20 min and glutamine synthetase (GS) activity in brain tissues was measured. Finally, we observed the effects of different doses of drugs related to glutamate metabolism on the latency of CNS-OT. Results showed that HBO exposure significantly increased glutamate content, whereas glutamine content was significantly reduced. Moreover, HBO exposure significantly reduced GS activity. Glutamate transporter-1 (GLT-1) selective antagonist ceftriaxone prolonged CNS-OT latency, whereas GLT-1 selective inhibitor dihydrokainate shortened CNS-OT latency. In summary, HBO exposure improved glutamate concentration and reduced glutamine concentration by inhibition of GS activity. GLT-1 activation also participated in the prevention of HBO-induced CNS-OT. Our research will provide a potential new target to terminate or attenuate CNS-OT.

Al/α-PbO2–CeO2–TiO2 composite electrodes are prepared by electrowinning. The effects of current density on the thickness, hardness, density, morphology, and elemental composition of Al/α-PbO2–CeO2–TiO2 composites are investigated by metallographic microscopy, micro-hardness testing, scanning electron microscopy and energy dispersive analysis of x-rays. Results show that after incorporating nano-TiO2 and CeO2, the thickness increases significantly at a current density of less than 4 mA cm−2. When the current density is 5.5 mA cm−2, the micro-hardness values of α-PbO2 and α-PbO2–CeO2–TiO2 reach 540 and 584 Hv, respectively. The current density measures 4–4.5 mA cm−2, and the minimum coating densities of α-PbO2 and α-PbO2–CeO2–TiO2 total 6.03 and 7.21 g cm−3, respectively.

Diabetic retinopathy is the leading cause of blindness in the working population of the developed countries and also a significant cause of blindness in the elderly. This study aimed at examining the protective effect of H(2) saline on diabetic retinopathy in a streptozotocin-induced diabetic rat model.Sprague-Dawley male rats were divided into 3 groups as follows: (1) nondiabetic control group (non-DM control); (2) diabetic control group (DM control); and (3) diabetic rats receiving H(2) saline therapy (DM H(2) saline). Rats in DM H(2) saline group were intraperitoneally injected with H(2) saturated saline (5 mL/kg) every day for 4 weeks. Retinal vascular permeability was assessed by measuring Evans blue leakage into the retina. Retinal apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining and measuring caspase-3 activity. Retinal thickness was observed by hematoxylin and eosin staining.Our results showed that H(2) saline treatment could depress the caspase activity, reduce the retinal apoptosis, and vascular permeability. The H(2) saline could also prominently attenuate the retinal parenchyma thickening that resulted from diabetic retinopathy.Our preliminary studies indicated that H(2) saline may have potentials in the clinical treatment of diabetic retinopathy.

INTRODUCTION Hydrogen (H2) has been reported to be effective in the treatment of oxidative injury, which plays an important role in the process of decompression sickness (DCS). This study was designed to test whether H2-rich saline (saline saturated with molecular hydrogen) protected rats against DCS. METHODS Models of DCS were induced in male Sprague-Dawley rats weighing 300-310 g. H2-rich (0.86 mmol x L(-1)) saline was administered intraperitoneally (10 ml x kg(-1)) at 24 h, 12 h, immediately before compression, and right after fast decompression. RESULTS H2-rich saline significantly decreased the incidence of DCS from 67.57 to 35.14% and partially counteracted the increases in the total concentration of protein in the bronchoalveolar lavage from 0.33 +/- 0.05 to 0.14 +/- 0.01 mg x ml(-1) (mean +/- SD; P < 0.05), myeloperoxidase activity from 0.86 +/- 0.16 to 0.44 +/- 0.13 U/g, levels of malondialdehyde (MDA) from 0.80 +/- 0.10 to 0.48 +/- 0.05 nmol x mg(-1), 8-hydroxydeoxyguanosine from 253.7 +/- 9.3 to 191.2 +/- 4.8 pg x mg(-1) in the lungs, and MDA level from 1.77 +/- 0.20 to 0.87 +/- 0.23 nmol x mg(-1) in the spinal cord in rat DCS models. The histopathology results also showed that H2-rich saline ameliorated DCS injuries. DISCUSSION It is concluded that H2-rich saline may have a protective effect against DCS, possibly due to its antioxidant action.

A novel compound, 4-{1′-hydroxy-1′-mercapto-1′-[1′′-2′′(N→O)-isoquinolyl]}yl-1-benzoic acid (1), together with six known compounds, 6-hydroxykaempferol-3-O-β-D-glucopyranoside (2), rutin (3), quercetin-3-O-β-D-glucopyranoside (4), kaempferol-3-O-β-D-glucopyranoside (5), cartormin (6), hydroxysafflor yellow A (7), were isolated by chromatography from the n-BuOH fraction of 50% ethanol extraction of Flos carthami. Their structures were elucidated on the basis of spectral analysis and comparison with published data. Among them, compound 1 was shown to possess a weak protective effect against cerebral ischemic damage in rats.

This study tested the hypothesis that spinal cord ischemic tolerance induced by hyperbaric oxygen preconditioning (HBO-PC) is mediated by inhibition of early apoptosis. Male Sprague-Dawley rats were preconditioned with consecutive 4 cycles of 1-h HBO exposures (2.5 atmospheres absolute [ATA], 100% O(2)) at a 12-h interval. At 24 h after the last HBO pretreatment, rats underwent 9 min of spinal cord ischemia induced by occlusion of the descending thoracic aorta in combination with systemic hypotension (40 mmHg). Spinal cord ischemia produced marked neuronal death and neurological dysfunction in animals. HBO-PC enhanced activities of Mn-superoxide dismutase (Mn-SOD) and catalase, as well as the expression of Bcl-2 in the mitochondria in the normal spinal cord at 24 h after the last pretreatment (before spinal cord ischemia), and retained higher levels throughout the early reperfusion in the ischemic spinal cord. In parallel, superoxide and hydrogen peroxide levels in mitochondria were decreased, cytochrome c release into the cytosol was reduced at 1 h after reperfusion, and activation of caspase-3 and -9 was subsequently attenuated. HBO-PC improved neurobehavioral scores and reduced neuronal apoptosis in the anterior, intermediate, and dorsal gray matter of lumbar segment at 24 h after spinal cord ischemia. HBO-PC increased nitric oxide (NO) production. L-nitroarginine-methyl-ester (L-NAME; 10 mg/kg), a nonselective NO synthase (NOS) inhibitor, applied before each HBO-PC protocol abolished these beneficial effects of HBO-PC. We conclude that HBO-PC reduced spinal cord ischemia-reperfusion injury by increasing Mn-SOD, catalase, and Bcl-2, and by suppressing mitochondrial apoptosis pathway. NO may be involved in this neuroprotection.

Four novel bakkenolides - bakkenolide-Ia ( 1), bakkenolide-IIa ( 2), bakkenolide-IIIa ( 3) and bakkenolide-IVa ( 4) - were isolated from the extract of the rhizome of Petasites tricholobus. The structures were characterized by using NMR ( (1)H, (13)C, (1)H- (1)H COSY, HMQC, HMBC, and NOESY) and mass spectrometry. The neuroprotective activity of the compounds 1 - 4 was assayed with primary cultured neurons exposed to oxygen-glucose deprivation and oxidative insults. Antioxidant activity of the bakkenolides was evaluated by cell-free bioassays. The IN VITRO assay results showed that all these compounds exhibited significant neuroprotective and antioxidant activities. To our knowledge, this is the first report on the neuroprotective and antioxidant activities of bakkenolides.

Exposure to hyperbaric oxygen (HBO) can lead to seizures, the etiology of which is not completely understood. Glutamic acid decarboxylase (GAD) plays a very important role in maintaining excitatory-inhibitory balance of the central nervous system (CNS). In the present study we investigated the effects of HBO on the activity and content of GAD in vivo and in primarily cultured neurons to probe in detail its effect on the formation of convulsion induced by HBO exposure. The results obtained from in vivo and in vitro experiments were identical. In the latent period before the onset of seizure, the GAD activity followed a rise-and-fall pattern with the prolongation of HBO exposure. At the time of the onset of seizure, GAD activity descended to the normal level. Besides, in the latent period, GAD content also reduced. Such reduction came from a GAD subtype, GAD67, while the content of another GAD subtype, GAD65, remained almost unchanged. Our investigations indicated that GAD is indeed an enzyme highly sensitive to the effect of HBO exposure. The rapid reduction in GAD67 content may be very closely related to seizures induced by HBO exposure.

Decompression sickness (DCS) is a specific diving injury which sometimes may be life-threatening. Previous studies suggested that simvastatin (SIM) can protect against pathological inflammation and tissue damage. This study aimed to investigate whether SIM pretreatment could exert its beneficial effects on DCS. SIM was administered orally to adult male Sprague-Dawley rats for two weeks (2 mg/kg/day), then rats were subjected to a simulated dive at 700 kPa air pressure for 100 minutes before rapid decompression. After 30 minutes of symptom observation, lung tissue and blood samples were collected for further analysis. Compared to the vehicle-control, SIM pretreatment significantly decreased the incidence of DCS and ameliorated all parameters of pulmonary injuries, including lung dry/wet weight ratio, bronchoalveolar lavage fluid protein concentration, lung tissue malondialdehyde level and morphology. Moreover, SIM pretreatment abolished increases in systemic and pulmonary inflammation by reducing tumor necrosis factor-α levels in blood plasma and lung tissue. The results indicate that SIM may offer a novel pharmacological protection against injuries in DCS rats by inhibiting inflammatory responses. Further study is needed to understand the exact mechanisms.

This study aimed to investigate the protective effects of pravastatin on hyperbaric hyperoxia-induced lung injury (HILI). C57BL/6 mice were randomly assigned into three groups: control group, HILI group and pravastatin (Pra) group. Mice in the HILI and Pra groups were subjected to exposure to pure oxygen at 2.5 atm abs for six hours. Mice in the Pra group were intraperitoneally treated with pravastatin at 15 mg/kg. immediately after exposure. At 24 hours, the lungs were collected for HE staining, TUNEL staining and detection of lung edema, myeloperoxidase (MPO) activity and cytokines, and bronchoalveolar lavage fluid (BALF) was harvested for cell-counting. Pravastatin treatment significantly improved the pathology of the lung after HILI (reduction in thickness of alveolar septum, attenuation of lung edema, fracturing of alveolar septa and decrease in infiltrated leukocytes); reduced the number of apoptotic cells; inhibited lung MPO activity; and regulated the balance between pro-inflammatory and anti-inflammatory cytokines. Our findings suggest that pravastatin may exert a protective effect on lung injury after hyperbaric hyperoxia exposure by inhibiting inflammation.

Nicotiflorin is a single component extracted from traditional Chinese medicine Flos Carthami. In this study, we investigated its neuroprotection in permanent focal cerebral ischemia model in rats, and in an in vitro model of ischemia. At doses of 2.5, 5 and 10 mg/kg, nicotiflorin administered immediately after the onset of ischemia markedly reduced brain infarct volume and neurological deficits. For primarily cultured neurons suffered 2 h hypoxia followed by 24 h reoxygenation, nicotiflorin significantly attenuated cell death and reduced LDH release. Morphological observation also directly confirmed its protective effect on neuron. These results provided strong pharmacological basis for its potential therapeutic role in cerebral ischemic illness.

Hyperbaric oxygen therapy is one of the most widely used clinical interventions to counteract insufficient pulmonary oxygen delivery in patients with severe lung injury. However, prolonged exposure to hyperoxia leads to inflammation and acute lung injury. This study aimed to investigate the protective effect of hydrogen sulfide on hyperbaric hyperoxia-induced lung injury. Rats were intraperitoneally treated with sodium hydrosulphide (NaHS) at 28 μmol/kg immediately before hyperoxia exposure and then exposed to pure oxygen at 2.5 atmospheres absolute (atm abs) with continuous ventilation for six hours, Immediately after hyperoxia exposure, rats were sacrificed via anesthesia. The bronchoalveolar lavage fluid (BALF) was harvested for the detection of protein concentration and IL-1 content, and the lungs were collected for HE staining, TUNEL staining and detection of wet/dry weight ratio. Our results showed hyperbaric hyperoixa exposure could significantly damage the lung (HE staining), increase the protein and IL-13 in the BALF, elevate the wet/dry Weight ratio and raise the TUNEL positive cells. However, pre-treatment with hydrogen sulfide improved the lung morphology, reduced the TUNEL positive cells and attenuated the lung inflammation (reduction in IL-13 of BALF and HE staining). Taken together, our findings indicate that hydrogen sulfide pretreatment may exert protective effects on hyperbaric hyperoxia-induced lung injury.

Oxygen therapy is one of the most widely used clinical interventions to counteract insufficient pulmonary oxygen delivery in patients with severe lung injury. However, prolonged exposure to hyperoxia at elevated partial pressure leads to inflammation and acute lung injury. The population at risk for this condition has markedly increased with the advent of efficient systems for delivery of high concentrations of oxygen in hospitals. Thus, the therapy of hyperoxia-induced lung injury has been a focus in studies of pediatrics and pulmonary medicine. In this paper, we briefly summarized the advances in the therapies of hyperoxia-induced lung injury on the basis of its pathogenesis. We hope our summary will help provide evidence for further investigation of therapeutic measures for hyperoxia-induced lung injury.

In this study, we investigated whether nuclear factor erythroid 2-related factor 2 (Nrf2) activation in astrocytes contributes to the neuroprotection induced by a single hyperbaric oxygen preconditioning (HBO-PC) against spinal cord ischemia/reperfusion (SCIR) injury. In vivo: At 24 h after a single HBO-PC at 2.5 atmospheres absolute for 90 min, the male ICR mice underwent SCIR injury by aortic cross-clamping surgery and observed for 48 h. HBO-PC significantly improved hindlimb motor function, reduced secondary spinal cord edema, ameliorated the reactivity of spinal motor-evoked potentials, and slowed down the process of apoptosis to exert neuroprotective effects against SCIR injury. At 12 h or 24 h after HBO-PC without aortic cross-clamping surgery, Western blot, enzyme-linked immunosorbent assay, realtime-polymerase chain reaction and double-immunofluorescence staining were used to detect the Nrf2 activity of spinal cord tissue, such as mRNA level, protein content, DNA binding activity, and the expression of downstream gene, such as glutamate-cysteine ligase, γ-glutamyltransferase, multidrug resistance protein 1, which are key proteins for intracellular glutathione synthesis and transit. The Nrf2 activity and downstream genes expression were all enhanced in normal spinal cord with HBO-PC. Glutathione content of spinal cord tissue with HBO-PC significantly increased at all time points after SCIR injury. Moreover, Nrf2 overexpression mainly occurs in astrocytes. In vitro: At 24 h after HBO-PC, the primary spinal astrocyte-neuron co-cultures from ICR mouse pups were subjected to oxygen-glucose deprivation (OGD) for 90 min to simulate the ischemia-reperfusion injury. HBO-PC significantly increased the survival rate of neurons and the glutathione content in culture medium, which was mainly released from asctrocytes. Moreover, the Nrf2 activity and downstream genes expression induced by HBO-PC were mainly enhanced in astrocytes, but not in neurons. In conclusion, our findings demonstrated that spinal cord ischemic tolerance induced by HBO-PC may be mainly related to Nrf2 activation in astrocytes.

Decompression sickness (DCS) is a major concern in diving and space walk. Hyperbaric oxygen (HBO) preconditioning has been proved to enhance tolerance to DCS via nitric oxide. Heat-shock protein (HSP) 70 was also found to have protective effects against DCS. We hypothesized that the beneficial effects of HBO preconditioning on DCS was related to levels of elevated HSP70. HSPs (70, 27 and 90) expressed in tissues of spinal cord and lung in rats was detected at different time points following HBO exposure by Western blot. HSP27 and HSP90 showed a slight but not significant increase after HBO. HSP70 increased and reached highest at 18 h following exposure before decreasing. Then rats were exposed to HBO and subjected to simulated air dive and rapid decompression to induce DCS 18 h after HBO. The severity of DCS, along with levels of HSP70 expression, as well as the extent of oxidative and apoptotic parameters in the lung and spinal cord were compared among different groups of rats pretreated with HBO, HBO plus NG-nitro-L-arginine-methyl ester (l-NAME), HBO plus quercetin or normobaric air. HBO preconditioning significantly reduced the morbidity of DCS (from 66.7% to 36.7%), reduced levels of oxidation (malondialdehyde, 8-hydroxyguanine and hydrogen peroxide) and apoptosis (caspase-3 and 9 activities and the number of apoptotic cells). l-NAME or quercetin eliminated most of the beneficial effects of HBO on DCS, and counteracted the stimulation of HSP70 by HBO. Bubbles in pulmonary artery were detected using ultrasound imaging to observe the possible effect of HBO preconditioning on DCS bubble formation. The amounts of bubbles in rats pretreated with HBO or air showed no difference. These results suggest that HSP70 was involved in the beneficial effects of HBO on DCS in rats, suspected be by the antioxidation and antiapoptosis effects.

Perfluorocarbon (PFC) has been hypothesized to potentially increase the risk of central nervous system oxygen toxicity (CNS-OT) under hyperbaric oxygen (HBO) conditions. However, little is known about the effects, mechanism and prevention of PFC-facilitated CNS-OT. A rat model of CNS-OT was used to evaluate the effects of intravenously-administered PFC emulsion. The electroencephalogram (EEG) was recorded during treatment with HBO 2 at 6.0 ATA in the presence and absence of PFC. Concentrations of malondialdehyde (MDA), nitric oxide (NO) and hydrogen peroxide (H 2 O 2 ) in the brain cortex and hippocampus were quantified. Changes in the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and NO synthase (NOS) in the brain cortex and hippocampus were also determined. Edaravone, a potent antioxidant, was used to prevent PFC-facilitated CNS-OT. The results showed that after PFC administration, the latency to first electrical discharge in EEG was significantly shortened; MDA, H 2 O 2 , NO levels and NOS activity increased; and SOD, GPx and CAT activities decreased. Edaravone effectively protected against CNS-OT and the adverse effects of PFC. The results clearly demonstrate that PFC administered before HBO 2 would promote the occurrence of CNS-OT, and edaravone could serve as a promising chemoprophylactic agent to prevent CNS-OT.

Exposure to high oxygen concentrations leads to acute lung injury, including lung tissue and alveolar edema formation, congestion, intra-alveolar hemorrhage, as well as endothelial and epithelial cell apoptosis or necrosis. Several studies have reported that molecular hydrogen is an efficient antioxidant by gaseous rapid diffusion into tissues and cells. Moreover, consumption of water with dissolved molecular hydrogen to a saturated level (hydrogen water) prevents stress-induced cognitive decline in mice and superoxide formation in mice. The purpose of the present study was to investigate the effect of saturated hydrogen saline on pulmonary injury-induced exposure to98% oxygen at 2.5 ATA for five hours. Adult male Sprague-Dawley (SD) rats were randomly divided into three groups: control group, saline group and saturated hydrogen saline group. Hematoxylin and eosin (HE) staining were used to examine histological changes. The lung wet to dry (W/D) weight ratio was calculated. The concentration of protein and total cell counts in bronchoalveolar lavage fluid (BALF) were measured. Lactate dehydrogenase (LDH) in serum and BALF were measured by spectrophotometer. The light microscope findings showed that saturated hydrogen saline reduced the impairment when compared with the saline group: Saturated hydrogen saline decreased lung edema, reduced LDH activity in BALF and serum, and decreased total cells and protein concentration in BALF. These results demonstrated that saturated hydrogen saline alleviated hyperoxia-induced pulmonary injury, which was partly responsible for the inhibition of oxidative damage.

Acetazolamide has been recognized as an effective treatment for acute mountain sickness. The efficacy of acetazolamide is related to metabolic acidosis, which promotes chemoreceptors to respond to hypoxic stimuli at altitude. In this study, adult male Sprague-Dawley rats were treated with acetazolamide (100mg/kg or 50mg/kg, I.P.) for 3 days. Primary cultured cortical neurons and PC12 cell lines were exposed to acidosis-permissive (pH 6.5) or standard (pH 7.2) media for 20h. HIF-1alpha and its target genes were assayed by Western blot, real-time PCR, HIF-1 DNA-binding assay and chloramphenicol acetyltransferase reporter gene assay. HIF-1alpha protein level and HIF-1 DNA-binding activities were increased in cerebral cortices of rats treated with acetazolamide. Moreover, the mRNA levels of erythropoietin, vascular endothelial growth factor, and glucose transporter-1 also increased. The HIF-1alpha protein level and activity of HIF-driven chloramphenicol acetyltransferase reporters of cortical neurons and PC12 cells treated with acidosis media were significantly enhanced. We conclude that the normoxic induction of HIF-1alpha and HIF-1 mediated genes by acetazolamide may mediate the effect of acetazolamide in the reduction of symptoms of acute mountain sickness.

Cerebral hypoxia-ischemia (HI) represents a major cause of brain damage in the term newborn. This study aimed to examine the short and long-term neuroprotective effect of hydrogen saline (H(2) saline) using an established neonatal HI rat pup model. Seven-day-old rat pups were subjected to left common carotid artery ligation and then 90 min hypoxia (8% oxygen at 37 degrees C). H(2) saturated saline was administered by peritoneal injection (5 ml/kg) immediately and again at 8 h after HI insult. At 24 h after HI, the pups were decapitated and brain morphological injury was assessed by 2,3,5-triphenyltetrazolium chloride (TTC), Nissl, and TUNEL staining. Acute cell death, inflammation and oxidative stress were evaluated at 24 h by studying caspase-3 activity, MDA measurement as well as Iba-1 immunochemistry in the brain. At 5 weeks after HI, spontaneous activity test and Morris water maze test were conducted. We observed that H(2) saline treatment reduced the caspase activity, MDA, Iba-1 levels, the infarct ratio, and improved the long-term neurological and neurobehavioral functions. H(2) saline has potentials in the clinical treatment of HI and other ischemia-related cerebral diseases.

A newly synthesized flavanone derivative, (+/-)-(3aRS,4SR)-2-(2-chloro-4-methyl- sulfonylphenyl)-4'-chloro-3a,4-diethoxy-flavane[4,3-d]-Delta-1,2,3-thiadiazoline (MSFTZ), was investigated for its antileukemia activity and molecular mechanisms. Cytotoxicity assay confirmed the high antiproliferative efficiency of MSFTZ in six leukemia cell lines (including two drug-resistant cell lines), with 50% inhibition of cell viability values ranging from 1.0 to 9.2 micromol/l. The results of flow cytometry assay showed that the percentage of apoptotic HL-60 cells was 68.3% after 48 h treatment with MSFTZ, suggesting that the activation of the apoptosis pathway was an anticancer property of MSFTZ. Furthermore, the protein changes related to apoptosis were investigated. Exposure of HL-60 cells to MSFTZ induced pro-caspase-9 and pro-caspase-3 cleavage, X-linked inhibitor of apoptosis protein and Bcl-X(L) downregulation, and poly(ADP-ribose) polymerase degradation. Treatment of cells with MSFTZ resulted in a time-dependent reduction in phosphorylation (activation) of extracellular signal-regulated kinase 1/2 and an increase in phosphorylation (activation) of Jun N-terminal kinase. Taken together, our results demonstrated that activation of mitogen-activated protein kinase and apoptotic cascade is involved in MSFTZ-induced antileukemia activity. All data suggest that MSFTZ is a promising chemotherapy drug.

A series of 2,4-diarylchromane[4,3-d]-Delta(1,9b)-1,2,3-thiadiazolines have been synthesized by cyclization of corresponding 2-arylchroman-4-one-arylhydrazones with SOCl(2) then treated with alcohol. All the compounds have been tested for their antiproliferative activity in vitro against six human tumor cell lines, and the highly potent derivative 11a exhibited in vivo inhibitory effect on tumor growth. Mechanism research indicated that it is due to 11a that induces DNA fragmentation.

Nicotiflorin is a flavonoid glycoside extracted from a traditional Chinese medicine Flos Carthami. In the current study, we investigated the neuroprotective effect of nicotiflorin on a transient focal cerebral ischemia–reperfusion model in rats. Nicotiflorin (2.5–10 mg/kg) administered after onset of ischemia markedly reduced brain infarct volume by 24.5–63.2% and neurological deficits. Also the effect of nicotiflorin on endothelial nitric oxide synthase (eNOS) activity, mRNA and protein expression after hypoxia–reoxygenation (H–R) treatment was investigated in an in vitro model mimic cerebrum ischemia–reperfusion in vivo. After total 4 h hypoxia and 12 h reoxygenation, eNOS activity, mRNA and protein levels in the primarily cultured rat cerebral blood vessel endothelial cells treated with nicotiflorin (25–100 μg/ml) 2 h after onset of hypoxia were significantly higher than eNOS activity, mRNA and protein levels in the pure H–R cells and also higher than eNOS activity, mRNA and protein levels in cells cultured under normoxic conditions. The results demonstrated that nicotiflorin had a protective effect against cerebral ischemic damage. The results also gave an important elucidation for the mechanism underlying the protective effect at the cellular level.