Numerical simulation of gas–liquid flow in the bubble column using Wray–Agarwal turbulence model coupled with population balance model

In this paper,an improved computational fluid dynamic(CFD)model for gas-liquid flow in bubble column was developed using the one-equation Wary-Agarwal(WA)turbulence model coupled with the population balance model(PBM).Through 18 orthogonal test cases,the optimal combination of interfacial force models,including drag force,lift force,turbulent dispersion force.The modified wall lubrication force model was proposed to improve the predictive ability for hydrodynamic behavior near the wall of the bubble column.The values simulated by optimized CFD model were in agreement with experimental data,and the errors were within±20%.In addition,the axial velocity,turbulent kinetic energy,bubble size distribution,and the dynamic characteristic of bubble plume were analyzed at different superficial gas velocities.This research work could provide a theoretical basis for the extension of the CFD-PBM coupled model to other multiphase reactors..

Neuropeptide Y protects cerebral cortical neurons by regulating microglial immune function

Neuropeptide Y has been shown to inhibit the immunological activity of reactive microglia in the rat cerebral cortex, to reduce N-methyl-D-aspartate current（INMDA） in cortical neurons, and protect neurons. In this study, after primary cultured microglia from the cerebral cortex of rats were treated with lipopolysaccharide, interleukin-1β and tumor necrosis factor-α levels in the cell culture medium increased, and mRNA expression of these cytokines also increased. After primary cultured cortical neurons were incubated with the lipopolysaccharide-treated microglial conditioned medium, peak INMDA in neurons increased. These effects of lipopolysaccharide were suppressed by neuropeptide Y. After addition of the neuropeptide Y Y1 receptor antagonist BIBP3226, the effects of neuropeptide Y completely disappeared. These results suggest that neuropeptide Y prevents excessive production of interleukin-1β and tumor necrosis factor-α by inhibiting microglial reactivity. This reduces INMDA in rat cortical neurons, preventing excitotoxicity, thereby protecting neurons.

Neuropeptide Y gene transfection inhibits post-epileptic hippocampal synaptic reconstruction

Exogenous neuropeptide Y has antiepileptic effects; however, the underlying mechanism and optimal administration method for neuropeptide Y are still unresolved. Previous studies have used intracerebroventricular injection of neuropeptide Y into animal models of epilepsy. In this study, a recombinant adeno-associated virus expression vector carrying the neuropeptide Y gene was injected into the lateral ventricle of rats, while the ipsilateral hippocampus was injected with kainic acid to establish the epileptic model. After transfection of neuropeptide Y gene, mossy fiber sprouting in the hippocampal CA3 region of epileptic rats was significantly suppressed, hippocampal synaptophysin （p38） mRNA and protein expression were inhibited, and epileptic seizures were reduced. These experimental findings indicate that a recombinant adeno-associated virus expression vector carrying the neuropeptide Y gene reduces mossy fiber sprouting and inhibits abnormal synaptophysin expression, thereby suppressing post-epileptic synaptic reconstruction.

Anti-epileptic effects of neuropeptide Y gene transfection into the rat brain

Neuropeptide Y gene transfection into normal rat brain tissue can provide gene overexpression, which can attenuate the severity of kainic acid-induced seizures. In this study, a recombinant adeno-associated virus carrying the neuropeptide Y gene was transfected into brain tissue of rats with kainic acid-induced epilepsy through stereotactic methods. Following these transfections, we verified overexpression of the neuropeptide Y gene in the epileptic brain. Electroencephalograms showed that seizure severity was significantly inhibited and seizure latency was significantly prolonged up to 4 weeks after gene transfection. Moreover, quantitative fluorescent PCR and western blot assays revealed that the mRNA and protein expression of the N-methyI-D-aspartate receptor subunits NR1, NR2A, and NR2B was inhibited in the hippocampus of epileptic rats. These findings indicate that neuropeptide Y may inhibit seizures via down-regulation of the functional expression of N-methyI-D-aspartate receptors.

Functional characterization of powdery mildew resistance gene MIIW172,a new Pm60 allele and its allelic variation in wild emmer wheat

Wild emmer wheat(Triticum dicoccoides,WEW)is an immediate progenitor of both the cultivated tetraploid and hexaploid wheats and it harbors rich genetic diversity against powdery mildew caused by Blumeria graminis f.sp.tritici(Bgt).A powdery mildew resistance gene Ml I^(W172)originated from WEW accession I^(W172)(G-797-M)is fine mapped in a 0.048 centimorgan(c M)genetic interval on 7 AL,corresponding to a genomic region spanning 233 kb,1 Mb and 800 kb in Chinese Spring,WEW Zavitan,and T.urartu G1812,respectively.Ml I^(W172)encodes a typical NLR protein NLRI^(W172)and physically locates in an NBS-LRR gene cluster.NLRI^(W172)is subsequently identified as a new allele of Pm60,and its function is validated by EMS mutagenesis and transgenic complementation.Haplotype analysis of the Pm60 alleles reveals diversifications in sequence variation in the locus and presence and absence variations(PAV)in WEW populations.Four common single nucleotide variations(SNV)are detected between the Pm60 alleles from WEW and T.urartu,indicative of speciation divergence between the two different wheat progenitors.The newly identified Pm60 alleles and haplotypes in WEW are anticipated to be valuable for breeding powdery mildew resistance wheat cultivars via marker-assisted selection.

神经肽Y在人脑局灶性皮层发育不良不同Palmini病理亚型间的表达差异

目的探讨不同Palmini病理亚型局灶性脑皮层发育不良(FCD)与正常人脑中神经肽Y(NPY)表达的差异,以及FCD诱发癫痫的机制。方法收集河北省人民医院神经外科自2007年5月至2011年10月收治的行癫痫手术后病理结果符合FCD的患者58例作为试验组。以Palmini分类标准,按病理亚型分为4组:ⅠA组9例、ⅠB组26例、ⅡA组10例、ⅡB组13例。同时取10例正常人脑组织设为对照组。观察FCD患者癫痫发病临床特点,FCD患者及正常人脑中NPY免疫反应阳性细胞数目差异。结果FCDⅡB组癫痫发作频率明显高于其他病理亚型组。FCDⅡB组NPY免疫反应阳性细胞数目与对照组比较明显增加,差异有统计学意义(P<0.05);FCD组中FCDⅠA、FCDⅠB、FCDⅡA各亚型与对照组比较,差异无统计学意义(P>0.05)。结论FCD各病理亚型中FCDⅡB型的NPY免疫反应阳性细胞反应明显,FCDⅡB致痫机制可能与NPY的表达增高有关。