CO_2-triggered gelation for mobility control and channeling blocking during CO_2 flooding processes

CO2 flooding is regarded as an important method for enhanced oil recovery （EOR） and greenhouse gas control. However, the heterogeneity prevalently dis- tributed in reservoirs inhibits the performance of this technology. The sweep efficiency can be significantly reduced especially in the presence of ＂thief zones＂. Hence, gas channeling blocking and mobility control are important technical issues for the success of CO2 injection. Normally, crosslinked gels have the potential to block gas channels, but the gelation time control poses challenges to this method. In this study, a new method for selectively blocking CO2 channeling is proposed, which is based on a type of CO2-sensitive gel system （modified polyacry- lamide-methenamine-resorcinol gel system） to form gel in situ. A CO2-sensitive gel system is when gelation or solidification will be triggered by CO2 in the reservoir to block gas channels. The CO2-sensitivity of the gel system was demonstrated in parallel bottle tests of gel in N2 and CO2 atmospheres. Sand pack flow experiments were con- ducted to investigate the shutoff capacity of the gel system under different conditions. The injectivity of the gel system was studied via viscosity measurements. The results indi- cate that this gel system was sensitive to CO2 and had good performance of channeling blocking in porous media. Advantageous viscosity-temperature characteristics were achieved in this work. The effectiveness for EOR in heterogeneous formations based on this gel system was demonstrated using displacement tests conducted in double sand packs. The experimental results can provide guideli- nes for the deployment of theCO2-sensitive gel system for field applications.

MIMO Channel Measurement and Characterization at 6.0-6.4 GHz Under Typical Classroom Environment

An extensive 4 x 4 MIMO channel measurement is carried out at 6. 0-6. 4 GHz under a typical classroom environment with channel sounder based on vector network analyzer. Both LOS and NLOS scenarios are considered. The results on path loss, delay spread and spatial correlation are presented. The measurement shows that, for corridor coverage, 2x2 MIMO is more economical than 4x4 MIMO due to high correlation. In order to identify the unique characteristics at the high frequency band, the measured channel parameters at 6. 0-6.4 GHz are compared with those at 2. 45 GHz. The comparison shows that the shortened wavelength of this higher frequency band results in a great difference of channel characteristics. Therefore, our measurement results provide new gnidance for the design and development of the system working on 6. 0-6.4 GHz band.

Cognitive amplify-and-forward dual-hop relay networks over α-μ fading channels

This paper provides an analytic performance evaluation of dual-hop cognitive amplify-and-forward (AF) relaying networks over independent nonidentically distributed (i.n.i.d.) fading channels. Two different transmit power constraint strategies at the secondary network are proposed to investigate the performance of the secondary network. In the case of combined power constraint,the maximum tolerable interference power on the primary network and the maximum transmit power at the secondary network are considered. Closed-form lower bound and its asymptotic expression for the outage probability (OP) are achieved. Utilizing the above results,average symbol error probability (ABEP) at high signal-to-noise ratios (SNRs) are also derived. In order to further study the performance of dual-hop cognitive AF relaying networks,the Closed-form lower bounds and asymptotic expressions for OP with single power constraint of the tolerable interference on the primary network is also obtained. Both analytical and simulation are employed to validate the accuracy of the theoretical analysis. The results show that the secondary network obtains a better performance when higher power constraint is employed.

Multi-scale analysis of subgrid stress and energy dissipation in turbulent channel flow

In present study, the subgrid scale （SGS） stress and dissipation for multiscale formulation of large eddy simulation are analyzed using the data of turbulent channel flow at Ret = 180 obtained by direct numerical simulation. It is found that the small scale SGS stress is much smaller than the large scale SGS stress for all the stress components. The dominant contributor to large scale SGS stress is the cross stress between small scale and subgrid scale motions, while the cross stress between large scale and subgrid scale motions make major contributions to small scale SGS stress. The energy transfer from resolved large scales to subgrid scales is mainly caused by SGS Reynolds stress, while that between resolved small scales and subgrid scales are mainly due to the cross stress. The multiscale formulation of SGS models are evaluated a priori, and it is found that the small- small model is superior to other variants in terms of SGS dissipation.

Types of voltage-dependent calcium channels involved in high potassium depolarization-induced amylase secretion in the exocrine pancreatic tumour cell line AR4-2J

In the perifused fura-2 loaded exocrine pancreatic acinar cell line AR4-2J pulses of high potassium induced repetitive increases in intracellular calcium. Attached cells when stimulated with high potassium secreted large amount of amylase. High potassium-induced secretion was dependent both on the concentration of potassium and duration of stimulation. High potassium induced increases in intracellular calcium were inhibited by voltage-dependent calcium channel antagonists with an order of potency as follows: nifedipine > ω-agatoxin IVA > ω-conotoxin GVIA. In contrast, the L-type calcium channel antagonist nifedipine almost completely inhibited potassium-induced amylase secretion, whereas the N-type channel antagonist ω-conotoxin GVIA was without effect. The P-type channel antagonist ω-agatoxin IVA had a small inhibitory effect, but this inhibition was not significant at the level of amylase secretion. In conclusion, the AR4-2J cell line possesses different voltage-dependent calcium channels (L, P,N) with the L-type predominantly involved in depolarization induced amylase secretion.

Performance Analysis of Physical Layer Security over α-η-κ-μ Fading Channels

In this paper, we consider the secure data transmission over α-η-κ-μ fading channels, which are recently proposed to encompass nearly all the well-known statistical models adopted in the literature. In particular, we address the secrecy performance in terms of the average secrecy capacity(ASC) and the secrecy outage probability(SOP), for which novel analytical expressions are derived. Simulation results verify the analysis and demonstrate the impact of the physical parameters on the secrecy performance of this new channel fading model.

Study of depth-dependent tetragonal distortion of quaternary AlInGaN epilayer by Rutherford backscattering/channeling

A 240-nm thick Al0.4In0.02Ga0.58N layer is grown by metal organic chemical vapour deposition, with an over 1-μm thick GaN layer used as a buffer layer on a substrate of sapphire （0001）. Rutherford backscattering and channeling are used to characterize the microstructure of AlInGaN. The results show a good crystalline quality of AIInGaN （χmin = 1.5%） with GaN buffer layer. The channeling angular scan around an off-normal {1213} axis in the {1010} plane of the AlInGaN layer is used to determine tetragonal distortion eT, which is caused by the elastic strain in the AIInGaN. The resulting AlInGaN is subjected to an elastic strain at interracial layer, and the strain decreases gradually towards the near-surface layer. It is expected that an epitaxial AlInGaN thin film with a thickness of 850 nm will be fully relaxed （^eT = 0）.

Effects of information transmission delay and channel blocking on synchronization in scale-free Hodgkin-Huxley neuronal networks

In this paper,we investigate the evolution of spatiotemporal patterns and synchronization transitions in dependence on the information transmission delay and ion channel blocking in scale-free neuronal networks.As the underlying model of neuronal dynamics,we use the Hodgkin-Huxley equations incorporating channel blocking and intrinsic noise.It is shown that delays play a significant yet subtle role in shaping the dynamics of neuronal networks.In particular,regions of irregular and regular propagating excitatory fronts related to the synchronization transitions appear intermittently as the delay increases.Moreover,the fraction of working sodium and potassium ion channels can also have a significant impact on the spatiotemporal dynamics of neuronal networks.As the fraction of blocked sodium channels increases,the frequency of excitatory events decreases,which in turn manifests as an increase in the neuronal synchrony that,however,is dysfunctional due to the virtual absence of large-amplitude excitations.Expectedly,we also show that larger coupling strengths improve synchronization irrespective of the information transmission delay and channel blocking.The presented results are also robust against the variation of the network size,thus providing insights that could facilitate understanding of the joint impact of ion channel blocking and information transmission delay on the spatiotemporal dynamics of neuronal networks.

Regulation of adenosine triphosphate-sensitive potassium channels suppresses the toxic effects of amyloid-beta peptide(25-35)

In this study, we treated PC12 cells with 0-20 μM amyloid-β peptide （25-35） for 24 hours to induce cytotoxicity, and found that 5-20 μM amyloid-β peptide （25-35） decreased PC12 cell viability, but adenosine triphosphate-sensitive potassium channel activator diazoxide suppressed the decrease in PC12 cell viability induced by amyloid-β peptide （25-35）. Diazoxide protected PC12 cells against amyloid-β peptide （25-35）-induced increases in mitochondrial membrane potential and intracellular reactive oxygen species levels. These protective effects were reversed by the selective mitochondrial adenosine triphosphate-sensitive potassium channel blocker 5-hydroxydecanoate. An inducible nitric oxide synthase inhibitor, Nw-nitro-L-arginine, also protected PC12 cells from amyloid-β peptide （25-35）-induced increases in both mitochondrial membrane potential and intracellular reactive oxygen species levels. However, the H202-degrading enzyme catalase could not reverse the amyloid-β peptide （25-35）-induced increase in intracellular reactive oxygen species. A 24-hour exposure to amyloid-13 peptide （25-35） did not result in apoptosis or necrosis, suggesting that the increases in both mitochondrial membrane potential and reactive oxygen species levels preceded cell death. The data suggest that amyloid-β peptide （25-35） cytotoxicity is associated with adenosine triphosphate-sensitive potassium channels and nitric oxide. Regulation of adenosine triphosphate-sensitive potassium channels suppresses PC12 cell cytotoxicity induced by amyloid-β peptide （25-35）.

Enhancement of Multicast Security with Opportunistic Relaying Technique over κ-μ Shadowed Fading Channels

The effects of scatterers, fluctuation parameter and propagation clusters significantly affect the performance of κ-μ shadowed fading channel. On the other hand, opportunistic relaying is an efficient technique to improve the performance of fading channels reducing the effects of aforementioned parameters. Motivated by these issues, in this paper, a secure wireless multicasting scenario through κ-μ shadowed fading channel is considered in the presence of multiple eavesdroppers with opportunistic relaying. The main purpose of this paper is to ensure the security level in wireless multicasting compensating the loss of security due to the effects of power ratio between dominant and scattered waves, fluctuation parameter, and the number of propagation clusters, multicast users and eavesdroppers, by opportunistic relaying technique. The closed-form analytical expressions are derived for the probability of non-zero secrecy multicast capacity (PNSMC) and the secure outage probability for multicasting (SOPM) to understand the insight of the effects of above parameters. The results show that the loss of security in multicasting through κ-μ shadowed fading channel can be significantly enhanced using opportunistic relaying technique by compensating the effects of scatterers, fluctuation parameter, and the number of propagation clusters, multicast users and eavesdroppers.

PPAR -γ激动剂对 LPS 诱导的小鼠 ARDS 肺泡上皮钠通道-γ亚基的调控

目的：探讨过氧化物酶增殖体活化受体-γ（ PPAR-γ）激动剂对LPS诱导的小鼠ARDS的保护作用及其对肺泡上皮细胞钠通道-γ亚基（ ENaC-γ）的调控作用。方法40只雄性BALB/C小鼠随机分为对照组（ Control组）、模型组（ LPS组）、罗格列酮治疗组（ RGZ组，LPS＋罗格列酮）及GW9662干预组（ GW9662组，LPS＋GW9662＋罗格列酮），每组10只。处理后收集相关标本，ELISA测定肺泡灌洗液（ BALF）中IL-1β和TNF-α水平。肺组织湿/干比（ W/D）测定肺水肿程度。 HE染色观察肺组织病理变化并进行肺组织损伤评分。用免疫组织化学法和Western blot测定肺组织ENaC-γ蛋白的表达。 RT-PCR测定ENaC-γmRNA的表达。结果与Control组比较，LPS组、RGZ组和GW9662组中IL-1β和TNF-α水平、W/D值、HE染色肺组织损伤程度及评分明显升高（ P＜0．05）；与LPS组比较，RGZ组各指标水平及肺损伤评分明显下降（P＜0．05），但LPS组和GW9662组比较差异无统计学意义（P＞0．05）。 LPS造模后，LPS组（210±15IOD，0．18±0．02，0．22±0．04）、RGZ组（450±30IOD，0．43±0．03，0．45±0．03）、GW9662组（235±35IOD，0．21±0．03，0．25±0．02）肺组织ENaC-γ蛋白和mRNA的表达明显低于Control组（600±25IOD，0．64±0．01，0．67±0．02，P＜0．05），RGZ组与LPS组和GW9662比较差异有统计学意义（P＜0．05），但LPS组和GW9662组比较差异无统计学意义（P＞0．05）。结论 PPAR-γ受体激动剂可能从转录水平上调肺泡ENaC-γ的表达，从而减轻LPS诱导的小鼠ARDS肺水肿程度，发挥保护性作用。

接触蛋白相关蛋白-2抗体阳性的自免脑炎1例报告

接触蛋白相关蛋白-2（contactin-associated protein-like 2,Caspr2）是轴突蛋白超家族成员之一,在中枢神经（主要是海马、小脑）和周围神经都有表达,Caspr2同抗富亮氨酸胶质瘤失活1蛋白（leucine-rich glioma inactiveted protein1,LGI1）一起构成了电压门控钾离子通道（voltage-gated potassium channel,VGKC）复合体抗原,

(-)-Stepholodine induced enhancement of cardiac muscle contractions mediated by D_1 receptors

Objective To investigate the effect of(-)-Stepholidine(SPD)on enhancing D1 receptor mediated contraction of cardiac muscle in isolated rat heart and to examine whether SPD has a direct effect on the heart dopamine D1 receptors.SPD an active ingredient of the Chinese herb Stephania intermedia,binds to dopamine D1 and D2 like receptors.Biochemical,electrophysiological and behavioural experiments have provided strong evidence that SPD is both a D(1/5)agonist and a D(2/4)antagonist,which could indicate unique antipsychotic properties.Methods Normal adult rat working hearts were isolated by Langendorff technique.Results SPD significantly increased the cardiac muscle contraction in a dose-dependent manner.The selective D1 dopamine receptor antagonist SCH23390(1 μM)blocked the SPD induced heart contraction,however,neither the β-receptor antagonist propranolol(1 μM)nor the α1-receptor antagonist prazosin(1 μM)had any effect on blocking SPD induced heart contractions.Moreover,the L-type Ca2+ channel inhibitor nimodipine(1 μM)completely blocked the effect of SPD on cardiac muscle contraction.Conclusions SPD show the effect on enhancing contraction of isolated rat heart through activating L-type Ca2+ channel mediated by heart D1 receptors.

Evaluation of Fast Flood Diffusion through a Drainage Channel: A Flood Disaster Case Study of Japan’s Kinugawa River, September 10, 2015

On September 10, 2015, unprecedented flood was occurred in Kinugawa River basin located on eastern Japan. It inundated 40 km2 of flood plain in Joso city, Ibaraki Prefecture, and more than 4000 people there called for help despite supposedly having sufficient time to evacuate. Some said that small initial flood before main severe flood arrived made them make a mistake in deciding whether to evacuate or stay there, despite having to actually evacuate in reality. This study focused on flood behaviour in this area, in particular, the effect of a small drainage channel lying on the flood plain which caused fast flood diffusion in case of occurring huge overflowing. Field investigations starting on time of the disaster with high-resolution positioning system were conducted to obtain spatial maps of flood depth and height. For appropriate modelling of the effect of small channel, we applied simulation model coupling 1-dimensional (1D) and 2-dimensional (2D) hydraulic scheme on the field and compared results from the 1D/2D coupled model and model without 1D scheme. The models provided information that the flood could reach 4 hours earlier to the city central of Joso city comparing in case of model without 1D scheme. The water depth rose irregularly and it was more confusing and difficult for the victims to make appropriate evacuation act.

Activation of metabotropic glutamate receptor 1 regulates hippocampal CA1 region excitability in rats with status epilepticus by suppressing the HCN1 channel

Dysregulation of hyperpolarization-activated cyclic nucleotide-gated cation(HCN)channels alters neuronal excitability.However,the role of HCN channels in status epilepticus is not fully understood.In this study,we established rat models of pentylenetetrazole-induced status epilepticus.We performed western blot assays and immunofluorescence staining.Our results showed that HCN1 channel protein expression,particularly HCN1 surface protein,was significantly decreased in the hippocampal CA1 region,whereas the expression of HCN2 channel protein was unchanged.Moreover,metabolic glutamate receptor 1(mGluR1)protein expression was increased after status epilepticus.The mGluR1 agonist(RS)-3,5-dihydroxyphenylglycine injected intracerebroventricularly increased the sensitivity and severity of pentylenetetrazole-induced status epilepticus,whereas application of the mGluR1 antagonist(+)-2-methyl-4-carboxyphenylglycine(LY367385)alleviated the severity of pentylenetetrazole-induced status epilepticus.The results from double immunofluorescence labeling revealed that mGluR1 and HCN1 were co-localized in the CA1 region.Subsequently,a protein kinase A inhibitor(H89)administered intraperitoneally successfully reversed HCN1 channel inhibition,thereby suppressing the severity and prolonging the latency of pentylenetetrazole-induced status epilepticus.Furthermore,H89 reduced the level of mGluR1,downregulated cyclic adenosine monophosphate(cAMP)/protein kinase A expression,significantly increased tetratricopeptide repeat-containing Rab8b-interacting protein(TRIP8b)(1a-4)expression,and restored TRIP8b(1b-2)levels.TRIP8b(1a-4)and TRIP8b(1b-2)are subunits of Rab8b interacting protein that regulate HCN1 surface protein.

Arsenic exposure decreases rhythmic contractions of vascular tone through sodium transporters and K^+ channels

Arsenic-contaminated drinking water is a public health problem in countries such as Taiwan, Bangladesh, United States, Mexico, Argentina, and Chile. The chronic ingestion of arsenic-contaminated drinking water increases the risk for ischemic heart disease, cerebrovascular disease, and prevalence of hypertension. Although toxic arsenic effects are controversial, there is evidence that a high concentration of arsenic may induce hypertension through increase in vascular tone and resistance. Vascular tone is regulated by the rhythmic contractions of the blood vessels, generated by calcium oscillations in the cytosol of vascular smooth muscle cells. To regulate the cytosolic calcium oscillations, the membrane oscillator model involves the participation of Ca2+ channels, calcium-activated K+ channels, Na+/Ca2+exchange, plasma membrane Ca2+-ATPase, and the Na+/K+-ATPase. However, little is known about the role of K+ uptake by sodium transporters [Na+/K+-ATPase or Na+-K+-2Cl-(NKCC1)] on the rhythmic contractions.Vascular rhythmic contractions, or vasomotion are a local mechanism to regulate vascular resistance andblood flow. Since vascular rhythmic contractions of blood vessels are involved in modulating the vascular resistance, the blood flow, and the systemic pressure,we suggest a model explaining the participation of the sodium pump and NKCC1 co-transporter in low dose arsenic exposure effects on vasomotion and vascular dysfunction.

Nonstationary Filtering for Markov Jumping Systems with Fading Channel and Multiplicative Noises

This paper studies the nonstationary filtering problem of Markov jump system under l2 - l∞ performance. Due to the difference in propagation channels, signal strength and phase will inevitably change randomly and cause the waste of signals resources. In response to this problem, a channel fading model with multiplicative noise is introduced. And then a nonstationary filter, which receives signals more efficiently is designed. Meanwhile Lyapunov function is constructed for error analysis. Finally, the gain matrix for filtering is obtained by solving the matrix inequality, and the results showed that the nonstationary filter converges to the stable point more quickly than the traditional asynchronous filter, the stability of the designed filter is verified.

Functional analysis of calcium channel-mediated exocytosis in synaptic terminals by FM imaging technique

Objective Presynaptic voltage-gated Ca^2＋ channels mediate rapid Ca^2＋ influx into the synaptic terminal which triggers synaptic vesicle exocytosis and neurotransmitter release. The FM 1-43 dye was firstly introduced as a fluorescence probe by Betz and his colleagues in 1992, and has been used to monitor exocytosis, endocytosis and endosomal traffic in a variety of cell types. The present study aims to investigate the feasibility of applying the FM 1-43 dye in the functional analysis of calcium channel-mediated exocytosis in synaptic terminals. Methods The hippocampi were isolated from embryos of pregnant rats, and hippocampal neurons were then transfected with Ds-Red conjugated plasmid. The neurons were then loaded with 8 μmol/L FM 1-43 and 47 mmol/L KCl for 90 s after transfection. After that, 90 mmol/L KCI was employed to induce FM dye destaining, which was recorded by FM imaging system. Results The neuron synaptic terminals of rat hippocampus could be effectively stained by the FM 1-43 dye. Besides, the destaining of the labeled neuron terminals was in accordance with the transmitter release, which could be blocked by the application of nifedipine （inhibitor for L-type calcium channel）. Conclusion The FM imaging technique is an advanced and effective method for analyzing synaptic vesicle exocytosis and neurotransmitter release, and can be applied in various synaptic functional studies.

Ionic liquids inhibit the dynamic transition fromα-helices toβ-sheets in peptides

Abnormalities in the transition betweenα-helices andβ-sheets(α-βtransition)may lead to devastating neurodegenerative diseases,such as Parkinson's syndrome and Alzheimer's disease.Ionic liquids(ILs)are potential drugs for targeted therapies against these diseases because of their excellent bioactivity and designability of ILs.However,the mechanism through which ILs regulate the aα-βtransition remains unclear.Herein,a combination of GPU-accelerated microsecond molecular dynamics simulations,correlation analysis,and machine learning was used to probe the dynamicalα-βtransition process induced by ILs of 1-alkyl-3-methylimidazolium chloride([C_(n)mim]cl)and its molecular mechanism.Interestingly,the cation of [C_(n)mim]+in ILs can spontaneously insert into the peptides as free ions(n≤10)and clusters(n≥11).Such insertion can significantly inhibit theα-β,transition and the inhibiting ability for the clusters is more significant than that of free ions,where[Ciomim]+and[C_(12)mim]+can reduce the maximumβ-sheet content of the peptide by 18.5% and 44.9%,respectively.Furthermore,the correlation analysis and machine learning method were used to develop a predictive model accounting for the influencing factors on theα-βtransition,which could accurately predict the effect of ILs on theα-βtransition.Overall,these quantitative results may not only deepen the understanding of the role of ILs in theα-βtransition but also guide the development of the IL-based treatments for related diseases.

Salt Stress Triggers Phosphorylation of the Arabidopsis Vacuolar K＋ Channel TPK1 by Calcium-Dependent Protein Kinases （CDPKs）

14-3-3 proteins play an important role in the regulation of many cellular processes. The Arabidopsis vacuolar two-pore K＋ channel 1 （TPK1） interacts with the 14-3-3 protein GRF6 （GF14-λ）. Upon phosphorylation of the putative binding motif in the N-terminus of TPK1, GRF6 binds to TPK1 and activates the potassium channel. In order to gain a deeper understanding of this 14-3-3-mediated signal transduction, we set out to identify the respective kinases, which regulate the phosphorylation status of the 14-3-3 binding motif in TPK1. Here, we report that the calcium-dependent protein kinases （CDPKs） can phosphorylate and thereby activate the 14-3-3 binding motif in TPK1. Focusing on the stress-activated kinase CPK3, we visualized direct and specific interaction of TPK1 with the kinase at the tonoplast in vivo. In line with its proposed role in K＋ homeostasis, TPK1 phosphorylation was found to be induced by salt stress in planta, and both cpk3 and tpkl mutants displayed salt-sensitive phenotypes. Molecular modeling of the TPK1-CPK3 interaction domain provided mechanistic insights into TPK1 stress-regulated phosphorylation responses and pinpointed two arginine residues in the N-terminal 14-3-3 binding motif in TPK1 critical for kinase interaction. Taken together, our studies provide evidence for an essential role of the vacuolar potassium channel TPK1 in salt-stress adaptation as a target of calcium-regulated stress signaling pathways involving Ca2＋, Ca2＋-dependent kinases, and 14-3-3 proteins.