One-Pot Fabrication of Hierarchically Bicontinuous Polystyrene Monoliths with Homogeneous Skeletons and Glycopolymer Surfaces.

The hierarchically bicontinuous polystyrene monoliths (HBPMs) with homogeneous skeletons and glycopolymer surfaces are fabricated for the first time based on the medium internal phase emulsion (MIPE) templating method via activator generated by electron transfer for atom transfer radical polymerization (AGET ATRP). The synergistic self-assembly of amphiphilic diblock glycopolymer (ADG) and Pluronic F127 (PF127) at the oil/water interface via hydrogen bonding interaction contributes to the formation of bicontinuous MIPE with deformed neighboring water droplets, resulting in the highly interconnected HBPM after polymerization. There is a bimodal pore size distribution in the HBPM, that is, through pores (150-5000 nm) and mesopores (10-150 nm). The HBPMs as prepared show excellent biocompatibility, homogeneous skeletons, strong mechanical strength, and high bed permeability, overcoming the practical limitations of the second generation of polystyrene (PS) monoliths. Glycoprotein concanavalin A (Con A) can be easily and quickly separated by the HBPM in hydrophilic interaction chromatography (HILIC) mode. These results suggest the HBPMs have great potentials in catalysis, separations, and biomedical applications.

[Study on infrared spectroscopy of cationic polyacrylamide initiated by ultraviolet].

Cationic Polyacrylamide P(AM-DAC-BA) was synthesized by UV initiation, with acrylamide (AM), acryloyloxyethyl trimethyl ammonium chloride (DAC), butyl acrylate (BA) as the monomers. P(AM-DAC-BA). UV spectroscopy and infrared spectroscopy were employed to study the structural characteristics. Attributions of typical infrared vibrational frequencies in AM/DAC/BA/P(AM-DAC-BA) were analysed. By comparing with infrared spectroscopy of the monomers, symmetrical characteristic of P(AM-DAC-BA) increasesd, and the infrared spectroscopy of polymerization product was simpler. The intrinsic viscosity increased with the increase in light intensity, BA content, photoinitiator concentration and illumination time. The groups of -CONH2, -COOCH2(C=O), -COOCH2--(C-O-C), -CH2--N(CH3 )3 group in AM, DAC, BA were selected as characteristic absorption peaks for studying. With the increase in light intensity and BA content, the characteristic peak areas increased. With the increase in photoinitiator concentration, the characteristic peak areas decreased. The characteristic peak areas decreased firstly and then increased with increasing the illumination time. But the corresponding characteristic IR absorption peaks of P(AM-DAC-BA) were similar, and the positions of characteristic peaks were basically the same.

Exploring seasonal variations, assembly dynamics, and relationships of bacterial communities in different habitats of marine ranching.

Offshore coastal marine ranching ecosystems provide habitat for diverse and active bacterial communities. In this study, 16S rRNA gene sequencing and multiple bioinformatics methods were applied to investigate assembly dynamics and relationships in different habitats. The higher number of edges in the water network, more balanced ratio of positive and negative links, and more keystone species included in the co-occurrence network of water. Stochastic processes dominated in shaping gut and sediment community assembly (R2 < 0.5), while water bacterial community assembly were dominated by deterministic processes (R2 > 0.5). Dissimilarity-overlap curve model indicated that the communities in different habitats have general dynamics and interspecific interaction (P < 0.001). Bacterial source-tracking analysis revealed that the gut was more similar to the sediment than the water bacterial communities. In summary, this study provides basic data for the ecological study of marine ranching through the study of bacterial community dynamics.

[Ultraviolet-initiated synthesis and characterization of anionic polyacrylamide].

APAM was prepared under the action of composite initiator and UV irradiation, using acryl amide (AM), 2-acrylamido-2-methyl propane sulfonic acid (AMPS) and acrylic acid (AA) as raw materials. The paper studied the effect of proportion between monomers, monomer ratio, initiator concentration and other factors on intrinsic viscosity of the polymer, and optimized preparation conditions. The chemical structure and thermal stability of APAM were characterized by UV, FTIR, SEM and DTA-TGA respectively. The results showed that the APAM with the intrinsic viscosity 1.6 x 10(3) mL x g(-1) can prepared when the proportion between monomers was 70 : 10 : 10, the monomer ratio was 40%, initiator concentration was 0.20%, pH was 9 and the illumination time was 60 min.

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.

[The secondary metabolites of the HS-3 Alternaria sp. fungus associated with holothurians].

OBJECTIVE: The metabolites of HS-3 associated with holothurians were studied, which was identified by molecular biology as Alternaria sp.. METHODS: The holothurians were gathered from the Sea of Zhifu Islet, Shandong Province. HS-3 Alternaria sp. was culternitived in potato medium, and four compound was got by TLC, chromatography and HPLC, and 1-hydroxyl-3-methylanthracene-9,10-dione (1), chrysophanol (2), sterigmatocystin (3) and cerebroside (4) were elucated by modern spectrum. CONCLUSION: All of this provides scientific data for further study of holothurians, and the four coumpouns are isolated from the microbe associated with holothurians for the first time.

Application of iron/aluminum bimetallic nanoparticle system for chromium-contaminated groundwater remediation.

When the nanoscale zero valent iron (nZVI) is used for the reduction of hexavalent chromium (Cr6+) to trivalent chromium (Cr3+) in groundwater, the reduction efficiency is decreased due to the passivation of reactive sites by precipitation. The bimetallic nanoparticle (BNP) can be created with the addition of the second metal to achieve a higher activity and reduce the occurrence of the ferrous/ferric hydroxide precipitation. In this study, the iron-coated aluminum (Fe/Al) BNP and aluminum-coated iron (Al/Fe) BNP systems were designed for remediating Cr6+-contaminated groundwater. The chemical liquid-phase deposition and co-reduction method was applied to produce BNPs. Cr6+ removal rate by Fe/Al BNPs was directly proportional to the saturation concentration and reactive sites, which caused a higher Cr6+ removal rate. The pseudo-first-order kinetic model could be used to describe the Cr6+ adsorption mechanism by Fe/Al BNPs. Results show that Fe/Al BNPs and Al/Fe BNPs could reduce Cr6+ to Cr3+, and the removal efficiencies for Cr6+ were 1.47 g/g BNP and 0.07 g/g BNP, respectively. Detection of Cr3+ in the aqueous phase was observed during the Cr6+ removal process. Results from X-ray diffraction (XRD) analysis confirmed that Cr(OH)3 was present on the surface of BNPs. Main mechanisms caused Cr6+ removal included reduction, precipitation, and adsorption. The reduction of Cr6+ produced OH-, which created alkaline environment and facilitated the formation of chromium hydroxide precipitates [Cr(OH)3]. Thus, the migration of Cr3+ was prevented and the environmental risk was reduced. BNP had a higher activity and stability, and it was applicable for Cr6+-contaminated site remediation.

Negative regulation of neurogenesis and spatial memory by NR2B-containing NMDA receptors.

Several lines of evidence suggest involvement of NMDA receptors (NMDARs) in the regulation of neurogenesis in adults and the formation of spatial memory. Functional properties of NMDARs are strongly influenced by the type of NR2 subunits incorporated. In adult forebrain regions such as the hippocampus and cortex, only NR2A and NR2B subunits are available to form the receptor complex with NR1 subunit. NR2B is predominant NR2 subunit in any of rat or human neural stem cells (NSCs). Thus, we suppose that NR2B-containing NMDAR should be critical in regulating adult neurogenesis, and thereby playing a role in the formation of spatial memory. In the cultured NSCs derived from the embryonic brain of rats, NR2B subunit-specific NMDAR antagonist Ro25-6981 increased cell proliferation, whereas MK-801, non-selective open-channel blocker of NMDARs, inhibited cell proliferation. Blockade of NR2B-containing NMDAR stimulated neurogenesis in the adult hippocampus and facilitated the formation of spatial memory. The enhanced spatial memory dropped back to base level when the NR2B antagonist-induced neurogenesis was neutralized by 3'-azido-deoxythymidine, a telomerase inhibitor. In addition, blockade of NR2B inhibited neuronal nitric oxide synthase (nNOS) enzymatic activity. In null mutant mice lacking nNOS gene (nNOS-/-), the effects of NR2B antagonist on neurogenesis disappeared. Moreover, nitric oxide donor DETA/NONOate attenuated and nNOS inhibitor 7-nitroindazole enhanced the effect of Ro 25-6981 on NSCs proliferation. Our findings suggest that NR2B-containing NMDAR subtypes negatively regulate neurogenesis in the adult hippocampus by activating nNOS activity and thereby hinder the formation of spatial memory.

Reduced neuronal nitric oxide synthase is involved in ischemia-induced hippocampal neurogenesis by up-regulating inducible nitric oxide synthase expression.

Nitric oxide (NO), a free radical with signaling functions in the CNS, is implicated in some developmental processes, including neuronal survival, precursor proliferation, and differentiation. However, neuronal nitric oxide synthase (nNOS) -derived NO and inducible nitric oxide synthase (iNOS) -derived NO play opposite role in regulating neurogenesis in the dentate gyrus after cerebral ischemia. In this study, we show that focal cerebral ischemia reduced nNOS expression and enzymatic activity in the hippocampus. Ischemia-induced cell proliferation in the dentate gyrus was augmented in the null mutant mice lacking nNOS gene (nNOS-/-) and in the rats receiving 7-nitroindazole, a selective nNOS inhibitor, after stroke. Inhibition of nNOS ameliorated ischemic injury, up-regulated iNOS expression, and enzymatic activity in the ischemic hippocampus. Inhibition of nNOS increased and iNOS inhibitor decreased cAMP response element-binding protein phosphorylation in the ipsilateral hippocampus in the late stage of stroke. Moreover, the effects of 7-nitroindazole on neurogenesis after ischemia disappeared in the null mutant mice lacking iNOS gene (iNOS-/-). These results suggest that reduced nNOS is involved in ischemia-induced hippocampal neurogenesis by up-regulating iNOS expression and cAMP response element-binding protein phosphorylation.

Neuroprotective effect of curcumin on focal cerebral ischemic rats by preventing blood-brain barrier damage.

Curcumin, a member of the curcuminoid family of compounds, is a yellow colored phenolic pigment obtained from powdered rhizome of C. longa Linn. Recent studies have demonstrated that curcumin has protective effects against cerebral ischemia/reperfusion injury. However, little is known about its mechanism. Disruption of the blood-brain barrier occurs after stroke. Protection of the blood-brain barrier has become an important target of stroke interventions in experimental therapeutic. The objective of the present study was to determine whether curcumin prevents cerebral ischemia/reperfusion injury by protecting blood-brain barrier integrity. We report that a single injection of curcumin (1 and 2 mg/kg, i.v.) 30 min after focal cerebral ischemia/reperfusion in rats significantly diminished infarct volume, improved neurological deficit, decreased mortality, reduced the water content of the brain and the extravasation of Evans blue dye in ipsilateral hemisphere in a dose-dependent manner. In cultured astrocytes, curcumin significantly inhibited inducible nitric oxide synthase (iNOS) expression and NO(x) (Nitrites/nitrates contents) production induced by lipopolysaccharide (LPS)/tumor necrosis factor alpha (TNF(alpha)). Furthermore, curcumin prevented ONOO(-) donor SIN-1-induced cerebral capillaries endothelial cells damage. We concluded that curcumin ameliorates cerebral ischemia/reperfusion injury by preventing ONOO(-) mediated blood-brain barrier damage.

Perceived exertion during muscle fatigue as reflected in movement-related cortical potentials: an event-related potential study.

The aim of this study was to explore the mechanism on perceived exertion during muscle fatigue. A total of 15 individuals in the fatigue group and 13 individuals in the nonfatigue group were recruited into this study, performing 200 intermittent handgrip contractions with 30% maximal voluntary contraction. The force, surface electromyography (sEMG), movement-related cortical potentials (MRCPs), and rating perception of effort (RPE) were combined to evaluate the perceived exertion during muscle fatigue. The maximal handgrip force significantly decreased (P<0.01), the root mean square of sEMG over each block significantly increased (P<0.01), and SD of force at plateau increased (P<0.01) during muscle fatigue. The RPE scores reported by the individuals and the motor potential amplitude of MRCPs in the fatigue group significantly increased (P<0.001). However, as for the individuals in the nonfatigue group, the other indexes showed no significant changes except for a little increase in the RPE. The within-subject correlation coefficients showed that there were significant correlations between RPE and motor potential amplitude of MRCPs at the C1 site (r=-0.609, P<0.001) and between RPE and root mean square of sEMG (r=0.541, P<0.001). Our results substantiate that the perceived exertion correlates with the central motor command during movement execution rather than the preparatory process. The perceived exertion not only reflects central fatigue but could also reflect the peripheral local muscle fatigue.

Glutamate Transporters/Na(+), K(+)-ATPase Involving in the Neuroprotective Effect as a Potential Regulatory Target of Glutamate Uptake.

The glutamate (Glu) transporters GLAST and GLT-1, as the two most important transporters in brain tissue, transport Glu from the extracellular space into the cell protecting against Glu toxicity. Furthermore, GLAST and GLT-1 are sodium-dependent Glu transporters (GluTs) that rely on sodium and potassium gradients generated principally by Na(+), K(+)-ATPase to generate ion gradients that drive Glu uptake. There is an interaction between Na(+), K(+)-ATPase and GluTs to modulate Glu uptake, and Na(+), K(+)-ATPase α, ß or γ subunit can be directly coupled to GluTs, co-localizing with GLAST or GLT-1 in vivo to form a macromolecular complex and operate as a functional unit to regulate glutamatergic neurotransmission. Therefore, GluTs/Na(+), K(+)-ATPase may be involved in the neuroprotective effect as a potential regulatory target of Glu uptake in neurodegenerative diseases induced by Glu-mediated neurotoxicity as the final common pathway.

Neuroprotective effect of resveratrol against glutamate-induced excitotoxicity.

As the major neurotransmitter in the mammalian central nervous system (CNS), excessive extracellular glutamate (Glu) can activate the Glu receptors and neuronal calcium (Ca2+) overload, then produce neurotoxicity, which is a common pathway for neuronal injury or death, and is associated with acute and chronic neurodegenerative diseases. Therefore, it has been a therapeutic strategy to investigate neuroprotective effects against Glu-induced neurotoxicity for treating both acute and chronic forms of neurodegeneration. Resveratrol (Res), as a naturally occurring polyphenol mainly found in grapes and red wine, has shown a neuroprotective effect in a variety of experimental models for neurodegenerative diseases in vitro and in vivo. This review will focus on the neuroprotective effect of Res against Glu-induced excitotoxicity in neurodegenerative diseases by blocking different Glu receptors and Ca2+ ion channels.

Induction of SARS-nucleoprotein-specific immune response by use of DNA vaccine.

Induction of effective cytotoxic T lymphocyte (CTL) and/or a specific antibody against conserved viral proteins may be essential to the development of a safe and effective severe acute respiratory syndrome coronavirus (SARS-Cov) vaccine. DNA vaccination represents a new strategy for induction of humoral and cellular immune response. To determine the ability of SARS-Cov nucleoprotein (N protein) to induce antiviral immunity, in this report, we established a stable C2C12 line expressing SARS-Cov N protein, which was used as a target for specific CTL assay. We also expressed recombinant N proteins in Escherichia coli and prepared N protein-specific polyclonal antibodies. C3H/He mice were immunized with N protein-expressible pcDN-fn vector by intramuscular injections. We found that the DNA vaccination induced both N protein-specific antibody and specific CTL activity to the target. When C3H/He mice were immunized by three separate injections, high antibody titre (1:3200-1:6400, average titre is 1:4580) and high CTL activity (67.4+/-8.4% (E:T = 25:1), 69.6+/-6.7% (E:T = 50:1) and 71.8+/-6.2% (E:T = 100:1)) were observed. In the case of two vaccine injections, CTL activity was also high (56.6+/-12.7% (E:T = 25:1), 57.4+/-11.7% (E:T = 50:1) and 63.0+/-6.3% (E:T = 100:1)) However, antibody titres were much lower (1:200-1:3200, average titre is 1:980). Our results suggest that SARS-Cov nucleocapsid gene might be a candidate gene for SARS DNA vaccination.

Movement-related cortical potentials during muscle fatigue induced by upper limb submaximal isometric contractions.

The aim of this study was to examine the central neurophysiological mechanisms during fatigue induced by submaximal isometric contractions. A total of 23 individuals participated in the study and were assigned to fatigue and nonfatigue groups. Handgrip force, root mean square (RMS) of surface electromyography (sEMG) signal and movement-related cortical potentials during self-paced submaximal handgrip isometric contractions were assessed for each participant. The experimental data showed significant decreases in both maximal voluntary contraction [-24.3%; F(3, 42)=19.62, P<0.001, ηp=0.48] and RMS [-30.1%; F(3, 42)=19.01, P<0.001, ηp=0.57] during maximal voluntary contractions and a significant increase [F(3, 42)=14.27, P<0.001, ηp=0.50] in the average RMS of sEMG over four blocks in the fatigue group. There was no significant difference in the readiness potential between the fatigue and the nonfatigue groups at early stages, and at late stages, significant differences were observed only at the Fp1 and FC1 sites. Motor potential amplitudes were significantly higher in the fatigue group than in the nonfatigue group irrespective of block or electrode positions. Positive waveforms were observed in the prefrontal cortex in states without muscle fatigue, whereas a negative waveform pattern was observed with muscle fatigue. Significant within-subject correlations were observed between motor potential at the C1 site and RMS of sEMG (r=-0.439, P=0.02, ηp=0.11). Neurophysiological evidence indicates that cortical activity increases in the prefrontal cortex, primary motor cortex and supplementary motor cortex with muscle fatigue. Muscle fatigue appears to have considerable effects on the components of movement-related cortical potentials during movement execution, whereas the readiness potential before movement is sensitive to cognitive demands during prolonged exercise. Our results provide additional evidence for a link between central motor command during movement execution and motor unit recruitment.

[Surface characteristics of alkali modified activated carbon and the adsorption capacity of methane].

Coconut shell based activated carbon was modified by alkali with different concentrations. The surface structures of tested carbons were observed and analyzed by SEM and BET methods. Boehm's titration and SEM/EDS methods were applied to assay the functional groups and elements on the carbon surface. The adsorption of methane on tested carbons was investigated and adsorption behavior was described by the adsorption isotherms. Results showed that surface area and pore volume of modified carbon increased and surface oxygen groups decreased as the concentration of the alkali used increased, with no obvious change in pore size. When concentration of alkali was higher than 3.3 mol x L(-1), the specific surface area and pore volume of modified carbon was larger than that of original carbon. Methane adsorption capacity of alkali modified carbon increased 24%. Enlargement of surface area and pore volume, reduction of surface oxygen groups will benefit to enhance the methane adsorption ability on activated carbon. Adsorption behavior of methane followed the Langmuir isotherm and the adsorption coefficient was 163.7 m3 x mg(-1).

Na⁺-K⁺-ATPase, a potent neuroprotective modulator against Alzheimer disease.

Alzheimer disease (AD) is a neurodegenerative disorder clinically characterized by progressive cognitive and memory dysfunction, which is the most common form of dementia. Although the pathogenesis of neuronal injury in AD is not clear, recent evidences suggest that Na⁺-K⁺-ATPase plays an important role in AD, and may be a potent neuroprotective modulator against AD. This review aims to provide readers with an in-depth understanding of Na⁺-K⁺-ATPase in AD through these modulations of some factors that are as follows, which leads to the change of learning and memory in the process of AD. 1. The deficiency in Na⁺, K⁺-ATPase α1, α2 and α3 isoform genes induced learning and memory deficits, and α isoform was evidently changed in AD, revealing that Na⁺, K⁺-ATPase α isoform genes may play an important role in AD. 2. Some factors, such as ß-amyloid, cholinergic and oxidative stress, can modulate learning and memory in AD through the mondulation of Na⁺-K⁺-ATPase activity. 3. Some substances, such as Zn, s-Ethyl cysteine, s-propyl cysteine, citicoline, rivastigmine, Vit E, memantine, tea polyphenol, curcumin, caffeine, Alpinia galanga (L.) fractions, and Bacopa monnieri could play a role in improving memory performance and exert protective effects against AD by increasing expression or activity of Na⁺, K⁺-ATPase.

Crosstalk between dopamine receptors and the Na⁺/K⁺-ATPase (review).

Dopamine (DA) receptors, which belong to the G protein-coupled receptor family, are the target of ~50% of all modern medicinal drugs and constitute a large and diverse class of proteins whose primary function is to transduce extracellular stimuli into intracellular signals. Na+/K+-ATPase (NKA) is ubiquitous and crucial for the maintenance of intracellular ion homeostasis and excitability. Furthermore, it plays a critical role in diverse effects, including clinical cardiotonic and cardioprotective effects, ischemic preconditioning in the brain, natriuresis, lung edema clearance and other processes. NKA regulation is of physiological and pharmacological importance and has species- and tissue-specific variations. The activation of DA receptors regulates NKA expression/activity and trafficking in various tissues and cells, for example in the kidney, lung, intestine, brain, non-pigmented ciliary epithelium and the vascular bed. DA receptor-mediated regulation of NKA mediates a diverse range of cellular responses and includes endocytosis/exocytosis, phosphorylation/dephosphorylation of the α subunit of NKA and multiple signaling pathways, including phosphatidylinositol (PI)-phospholipase C/protein kinase (PK) C, cAMP/PKA, PI3K, adaptor protein 2, tyrosine phosphatase and mitogen-activated protein kinase/extracellular signal-regulated protein kinase. Furthermore, in brain and HEK293T cells, D1 and D2 receptors exist in a complex with NKA. Among D1 and D2 receptors and NKA, regulations are reciprocal, which leads to crosstalk between DA receptors and NKA. In the present study, the current understanding of signaling mechanisms responsible for the crosstalk between DA receptors and NKA, as well as with specific consequent functions, is reviewed.

Reduced spatial learning in mice treated with NVP-AAM077 through down-regulating neurogenesis.

NR2A-containing N-methyl-D-aspartate (NMDA) receptors have important roles in influencing the long-term potentiation and spatial memory. Here using Morris water maze, we found that inhibition of NR2A-containing NMDA receptors by [(R)-[(S)-1-(4-bromophenyl)-ethylamino]-(2, 3-dioxo-1,2,3,4-tetrahydroquinoxalin-5-yl)-methyl]-phosphonic acid (NVP-AAM077) hindered the formation of spatial memory. An increasing number of reports suggest that adult hippocampal neurogenesis is involved in hippocampal-mediated learning. To explore the possible mechanisms understanding the reduced spatial memory by NVP-AAM077, we investigated the effects of NVP-AAM077 on neurogenesis. We found that NVP-AAM077 inhibited progenitor cells proliferation in the subventricular zone and dentate gyrus and reduced the survival of newborn cells in the dentate gyrus in the adult mice. In null mutant mice lacking neuronal nitric oxide synthase (nNOS) gene (nNOS(-/-)), the effects of NVP-AAM077 on neurogenesis disappeared. In addition, NVP-AAM077 increased nNOS enzymatic activity. Our findings suggest that NVP-AAM077 reduced spatial learning through down-regulating neurogenesis in the adult hippocampus.