Optimization of the Layer Location of Extraction Wells Based on the Unpressurized Gas Transport Law.

Protective layer mining is one of the most effective measures to control outbursts of coal seam gas in coal mines. Accurately grasping the overlying rock movement and pressure-relief gas migration patterns under protective layer mining conditions is a prerequisite for efficient surface coalbed methane extraction; it is the basis for green emission reduction in coal mines. A physical model was established using the Ji15-33200 working face of Pingmei Shi Mine as the research object, and a method combining theoretical calculation and numerical simulation was used to obtain the overlying rock movement. In situ stress distribution characteristics of the stope after the upper protective layer was mined to explore the upper protective layer migration rules of pressure-relief gas after mining. On this basis, the location and layer of surface coalbed methane production wells was determined. The research results show that the coal and rock formations on the floor of the goaf experienced a deformation process of compression → expansion → rebalance during the mining process; the stress changes of the overlying and underlying coal strata in the goaf have experienced a process of increasing → decreasing → rebalance; and gas migrates upward through the fissure zone in the coal layer and slowly diffuses in other microfissure areas. When the pressure reaches a certain value, it is enriched in the crack development area and the upper part of the fissure zone; combined with the relevant geological conditions of the study area, it was determined that the upper part of the roof of the Ji16-17 coal seam is a gas-rich area. By comparing three mining vertical wells at different positions in the horizontal direction, it was found that the extraction effect was significant in the "O″ ring, near the excavation face.

Characteristics of Acid Leaching and Vibration Coupling Desorption of Gas-Saturated Coking Coal.

Permeability is a key factor affecting efficient gas drainage from coal seams, and acidification and vibration shock are effective means to increase permeability in original low-permeability coal seams. To study the gas desorption characteristics of coking coal under the coupling effect of mining disturbance and acidification permeability enhancement, taking the coal seam of Shoushan No. 1 coal as the research object, a self-built adsorption-desorption vibration test platform was used. Acid leaching vibration coupling desorption experiments at vibration frequencies of 0, 30, 60, and 100 Hz were conducted on selected particle coals with particle sizes of 0.18-0.25 and 1-3 mm. The experimental results show that the gas desorption amount of particle coal with the same particle size first increases and then decreases with the increase of vibration frequency, among which the desorption effect is the best under 60 Hz vibration condition. Under the condition of fixed vibration frequency, the desorption amount, initial desorption velocity, and velocity attenuation coefficient of particle coal increase as the particle size decreases. Under the same particle size and vibration frequency conditions, the acid leaching and vibration of coal samples have a synergistic effect on gas desorption, which is manifested in the promotion of gas desorption on the outer surface of the coal sample and the surface of open macropores. The research can provide theoretical reference for coal seam acidification and permeability enhancement under the influence of mining disturbance.

Effect of membrane thermal conductivity on ion current rectification in conical nanochannels under asymmetric temperature.

Nowadays, there have been extensively theoretical studies on the phenomenon of ion current rectification (ICR) induced by the asymmetric electrical double layer (EDL). As a key factor influencing the behavior of ion transport, temperature is given high priority by researchers. The thermal conductivity of the material commonly employed to prepare nanopores is 2-3 times higher than that of liquid solutions, which may affect ion transport within the nanochannel. However, it is often neglected in previous studies. Thus, we investigate the effect of membrane thermal conductivity on the ICR in conical nanochannels under asymmetric temperature. Based on the PNP-NS theoretical model, the ion current, the rectification ratio, as well as the temperature and ion concentration distributions along the nanochannel are calculated. It is found that the thermal conductivity of the solid membrane noticeably affects the temperature distribution across the nanochannel, altering the ion transport behavior. Larger membrane thermal conductivity tends to homogenize the temperature distribution in the nanochannel, leading to a decline of ionic thermal down-diffusion by a positive temperature difference and ionic thermal up-diffusion by a negative temperature difference, with the former promoting and the latter inhibiting ion current. As a result, the rectification ratio decreases under the positive temperature difference and increases under the negative temperature difference as the thermal conductivity of the membrane increases. These studies will be instructive for the design of nanofluidic diodes and biosensors.

Reversible Ionic Liquid Intercalation for Electrically Controlled Thermal Radiation from Graphene Devices.

Using graphene as a tunable optical material enables a series of optical devices such as switchable radar absorbers, variable infrared emissivity surfaces, or visible electrochromic devices. These devices rely on controlling the charge density on graphene with electrostatic gating or intercalation. In this paper, we studied the effect of ionic liquid intercalation on the long-term performance of optoelectronic devices operating within a broad infrared wavelength range. Our spectroscopic and thermal characterization results reveal the key limiting factors for the intercalation process and the performance of the infrared devices, such as the electrolyte ion-size asymmetry and charge distribution scheme and the effects of oxygen. Our results provide insight for the limiting mechanism for graphene applications in infrared thermal management and tunable heat signature control.

Laser Synthesis of Nonprecious Metal-Based Single-Atom Catalysts for Oxygen Reduction Reaction.

Development of nonprecious metal-based single-atom catalysts (SACs) has provided opportunities to substitute Pt group metals and offer maximum atom utilization and unique coordination environments. Among these catalysts, Fe-N-C catalysts with atomically dispersed Fe-N4 active sites have emerged as some of the most promising oxygen reduction reaction (ORR) catalysts. However, furnace synthesis of Fe-N-C catalysts with carbon substrate derived from metal-organic framework (MOF) involves a high-temperature procedure, in which nitrogen from the carbonized MOF tends to be removed, subsequently leading to a low density of active sites. In this work, we developed a rapid and simple solid-state route to fabricate SACs through laser-induced thermal activation (LITA) of carbonized zeolitic imidazolate framework-8 (ZIF-8) adsorbed with Fe precursors. The results demonstrate that the laser process effectively avoids the loss of nitrogen in the nitrogen-doped carbon substrate and achieves a loading of Fe single atoms of 2.3 wt %, in comparison with that of 1.2 wt % from the conventional furnace treatment. The Fe-N-C catalyst synthesized in the study presents a half-wave potential of 0.91 V for ORR in alkaline media, which is higher than that of commercial Pt/C (0.87 V). When used as a cathode catalyst in zinc-air batteries (ZABs), the battery exhibits excellent electrochemical performance. This work also demonstrates the versatility of the technique through the successful synthesis of Co-N-C and Ni-N-C single atoms on nitrogen-doped carbon substrates.

[Effect of alpha-zearalanol on the generation of reactive oxygen species (ROS) and ROS-activated signal transduction in tumor necrosis factor alpha-stimulated human endothelial cells].

OBJECTIVE: To investigate the effects of alpha-zearalanol (alpha-ZAL) on the generation of reactive oxygen species (ROS) and ROS-activated signal transduction in the tumor necrosis factor (TNF-alpha)-stimulated human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were cultured and divided into 4 groups: (1) normal control group, (2) TNF-alpha stimulated group, undergoing TNF-alpha stimulation for 24 h, (3) alpha-ZAL retreatment group, undergoing re-treatment with alpha-ZAL of the concentrations of 1 x 10(-8), 1 x 10(-7), or 1 x 10(-6) mol/L for 1 h, then stimulation of TNF-alpha for 24 h, and (4) plasmid transfection group, transfected with p47(phox) siRNA for 24 h to block the NADPH oxidase protein subunit p47(phox) in the HUVECs, or transfected with blank plasmid as control. The intracellular ROS production was detected by using 2, 7-dichlorofluorescin diacetate as probe. Semi-quantitative RT-PCR and immunocytochemistry were used to detect the mRNA and protein expression of p47(phox). The activation of extracellular signal-regulated kinase (ERK) and nuclear translocation of nuclear factor-kappaB (NF-kappaB), stimulatory protein (SP)-1, and activator protein (AP)-1 were assessed with Western blotting. RESULTS: The ROS level in the HUVECs of the TNF-alpha group was higher than that of the control group by 155.4%, and alpha-ZAL reduced the ROS level dose-dependently. TNF-alpha treatment up-regulated the p47(phox) mRNA expression by 212.8%, and obviously increased the p47(phox) protein expression; and alpha-ZAL pretreatment attenuated the TNF-alpha-induced p47(phox) mRNA expression by 63.0%, and also markedly inhibited the p47(phox) protein expression. No obvious ROS was found in the HUVECs stimulated by TNF-alpha after the transfection of p47(phox) siRNA. The ERK activation and nuclear translocation of transcription factors SP-1 and NF-kappaB induced by TNF-alpha were abolished or markedly inhibited by alpha-ZAL pretreatment. CONCLUSION: alpha-ZAL has a potent inhibitory effect on the ROS production and ROS-activated signaling pathway in the TNF-alpha stimulated endothelial cells, mainly through the inhibition of NADPH oxidase.

Elevating expression of MeCP2 T158M rescues DNA binding and Rett syndrome-like phenotypes.

Mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome (RTT), a neurological disorder affecting cognitive development, respiration, and motor function. Genetic restoration of MeCP2 expression reverses RTT-like phenotypes in mice, highlighting the need to search for therapeutic approaches. Here, we have developed knockin mice recapitulating the most common RTT-associated missense mutation, MeCP2 T158M. We found that the T158M mutation impaired MECP2 binding to methylated DNA and destabilized MeCP2 protein in an age-dependent manner, leading to the development of RTT-like phenotypes in these mice. Genetic elevation of MeCP2 T158M expression ameliorated multiple RTT-like features, including motor dysfunction and breathing irregularities, in both male and female mice. These improvements were accompanied by increased binding of MeCP2 T158M to DNA. Further, we found that the ubiquitin/proteasome pathway was responsible for MeCP2 T158M degradation and that proteasome inhibition increased MeCP2 T158M levels. Together, these findings demonstrate that increasing MeCP2 T158M protein expression is sufficient to mitigate RTT-like phenotypes and support the targeting of MeCP2 T158M expression or stability as an alternative therapeutic approach.

Inhibitory effects of alpha-zearalenol on angiotensin II-induced integrin beta3 mRNA via suppression of nuclear factor-kappaB.

OBJECTIVE: To investigate the effect of alpha-zearalenol on angiotensin II-induced beta3 integrin mRNA expression in human umbilical vein endothelial cells (HUVECs). METHODS: The mRNA level in integrin beta3 was determined by reverse transcription-polymerase chain reaction. Endothelial NF-kappaB activity was determined by the luciferase activity assay of plasmid NF-kappaB-LUC. RESULTS: The angiotensin II-induced beta3 integrin mRNA expression was inhibited by alpha-zearalenol and 17beta-estradiol (10 nmol/L -1 micromol/L), but not influenced by ICI 182, 780, a pure competitive antagonist for estrogen receptor or a nitric oxide inhibitor Nomega-Nitro-L-arginine methyl ester hydrochloride. Alpha-zearalenol and 17beta-estradiol suppressed the angiotensin II-induced activation of NF-kappaB in endothelial cells. CONCLUSION: Alpha-zearalenol inhibits angiotensin II-induced integrin beta3 mRNA expression by suppressing NF-kappaB activation in endothelial cells.

Web-Based Access to Positive Airway Pressure Usage with or without an Initial Financial Incentive Improves Treatment Use in Patients with Obstructive Sleep Apnea.

STUDY OBJECTIVES: We tested whether providing adults with obstructive sleep apnea (OSA) with daily Web-based access to their positive airway pressure (PAP) usage over 3 mo with or without a financial incentive in the first week improves adherence and functional outcomes. SETTING: Academic- and community-based sleep centers. PARTICIPANTS: One hundred thirty-eight adults with newly diagnosed OSA starting PAP treatment. INTERVENTIONS: Participants were randomized to: usual care, usual care with access to PAP usage, or usual care with access to PAP usage and a financial incentive. PAP data were transmitted daily by wireless modem from the participants' PAP unit to a website where hours of usage were displayed. Participants in the financial incentive group could earn up to $30/day in the first week for objective PAP use ≥ 4 h/day. MEASUREMENTS AND RESULTS: Mean hours of daily PAP use in the two groups with access to PAP usage data did not differ from each other but was significantly greater than that in the usual care group in the first week and over 3 mo (P < 0.0001). Average daily use (mean ± standard deviation) during the first week of PAP intervention was 4.7 ± 3.3 h in the usual care group, and 5.9 ± 2.5 h and 6.3 ± 2.5 h in the Web access groups with and without financial incentive respectively. Adherence over the 3-mo intervention decreased at a relatively constant rate in all three groups. Functional Outcomes of Sleep Questionnaire change scores at 3 mo improved within each group (P < 0.0001) but change scores of the two groups with Web access to PAP data were not different than those in the control group (P > 0.124). CONCLUSIONS: Positive airway pressure adherence is significantly improved by giving patients Web access to information about their use of the treatment. Inclusion of a financial incentive in the first week had no additive effect in improving adherence.

[Identification of a novel splice mutation of low density lipoprotein receptor gene in a Chinese family with familial hypercholesterolemia].

OBJECTIVE: To identify the mutation of low density lipoprotein receptor(LDLR) gene in a large Chinese family with familial hypercholesterolemia(F H) and make a discussion on the pathogenesis of FH at the molecular level. METHODS: Investigations were made on a patient with the clinical phenotype of homozygous FH and his parents for mutations of promoter and all 18 exons of LDLR gene. Screening was carried out using Touch down PCR and a g arose gel electrophoresis, combined with DNA sequence analysis. The results were compared with the normal sequences in GenBank and FH database (www.ucl.uk/fh) t o find the mutation. Then the mutation was identified in other members of the family. In addition, the authors screened the apolipoprotein B(100) (apoB(100)) gene f or known mutations (R3500Q) that cause familial defective apoB(100) (FDB) by PCR-RFLP. RESULTS: A novel homozygous IN III 5' GT --> AT mutation in the splice donor of LDLR intron 3 was detected in the homozygote propositus with FH. The mutation was also identified in four heterozygous carriers in his family. No mutations R3500Q of apoB(100)were observed. CONCLUSION: A homozygous G --> A splice mutation in LDLR gene was first reported. The change of the splice donor in LDLR intron 3 may cause skipping of exon 3, which is responsible for FH. Perhaps it is a particular pathogenesis for Chinese people.

Angiotensin II stimulates endothelial integrin beta3 expression via nuclear factor-kappaB activation.

The present study examined the effect and part mechanism of angiotensin II-stimulated integrin beta3 gene expression in human umbilical vein endothelial cells. Protein level and mRNA level of integrin beta3 expression were determined using enzyme-linked immunoadsorbent assay and reverse transcription-polymerase chain reaction. Four plasmids of 5'-different deletion of integrin beta3 gene promoter were constructed to transiently transfected into cells to uncover the region in response to angiotensin II. Blockade of nuclear factor-kappaB (NF-kappaB) signaling pathway effect on integrin beta3 expression was analyzed by cotransfection with mutant plasmids for NF-kappaB-inducing kinase, inhibitory proteins alpha and beta of NF-kappaB kinase, respectively, together with the integrin beta3 plasmid including the sequence -1486 approximately - 900. The study found that 10(-8) mol/L,10(-7) mol/L, 10(-6) mol/L, and 10(-5) mol/L angiotensin II increased integrin beta(3) protein level by 45%, 52%, 62%, and 73% respectively. Angiotensin II at 10(-6) mol/L increased integrin beta3 mRNA level by 67%. The luciferase activity of the integrin beta3 plasmid PGL3 - 1486 approximately - 900 increased by 84.72% in response to angiotensin II. N-acetylcysteine blocked angiotensin II-induced NF-kappaB activity and integrin beta3 expression. Blockade of NF-kappaB signaling pathway abolished the stimulation of angiotensin II. These results suggest that angiotensin II stimulates integrin beta3 expression partly by NF-kappaB activation.

TSC-36/FRP inhibits vascular smooth muscle cell proliferation and migration.

OBJECTIVE: In-stent restenosis is a vascular proliferation/migration disorder characterized by hyperplasia of vascular smooth muscle cells (VSMCs). Because mounting evidence suggests that the therapeutic potential of anti-proliferation and anti-migration therapy, we investigated possible inhibitory effects of the matricellular protein TGF-beta-stimulated clone 36 (TSC-36) on vascular smooth muscle cell proliferation and migration in vitro and in vivo. METHODS: Human umbilical artery smooth muscle cells (SMCs) were treated with inducting agents daidzein or estradiol. TSC-36 expression was detected by nested competitive PCR and in situ hybridization. TSC-36 was expressed in Origami (DE3) cells. The recombinant protein was used to immunize rabbits to produce polyclonal antibodies. VSMCs were treated with various concentrations of recombinant TSC-36 (rTSC-36) protein and daidzein. The MTT assay was used to analyze for cell proliferation. A transwell system was used to detect cell migration. Flow cytometry was used to detect cell phase. A rat carotid artery balloon injury model was duplicated. The rats were treated with daidzein or solvent control. Animals were sacrificed 5 weeks later, and injured arteries were taken for pathology and histology. RESULTS: TSC-36 mRNA and protein expression was induced in SMCs. Cell proliferation and migration were inhibited by rTSC-36. rTSC-36 caused accumulation of SMCs in G2 phase. The inducting agent daidzein decreased neo-intima proliferation. TSC-36 mRNA and protein expression was induced and expressed in the neo-intima. CONCLUSION: TSC-36 can be induced in VSMCs and inhibits VSMCs proliferation in vitro and in vivo.

Roles of NF-kappaB and SP-1 in oxidative stress-mediated induction of platelet-derived growth factor-B by TNFalpha in human endothelial cells.

Platelet-derived growth factor-B (PDGF-B) is upregulated by proinflamatory stimuli in the early stages of atherosclerosis. However, its mechanisms are not fully elucidated. In the present study, by using the antioxidant N-acetylcysteine (NAC), we investigated in human umbilical vein endothelial cells (HUVECs) the roles of oxidative stress in PDGF-B expression induced by tumor necrosis factor alpha (TNFalpha) and its underlying mechanisms. Exposure of HUVECs to TNFalpha (200 U/ml) for 24 hours caused significant increases of both the PDGF-B expression and its promoter/enhancer activity, which were abolished by NAC (20 mmol/L). Accordingly, a prolonged oxidative stress was induced by TNFalpha and that was prevented by pretreatment with NAC. Electrophoresis mobility shift assay (EMSA) and Western blot analysis showed that both the nuclear factor-kappaB (NF-kappaB) and the specificity protein-1 (SP-1) were activated by TNFalpha. However, NAC only partially inhibited the TNFalpha-induced activation of NF-kappaB, but abolished the activation of SP-1. Mutation of the NF-kappaB binding site resulted in a moderate reduction in the TNFalpha-induced activity of PDGF-B promoter/enhancer, whereas mutation of SP-1 binding site resulted in an absence of induction by TNFalpha. These results suggest that oxidative stress mediates the TNFalpha-induced expression of PDGF-B in HUVECs through redox-sensitive transcription factors, predominantly the SP-1 and possibly, to some extent of NF-kappaB.