Self-assembled dendrimer polyamide nanofilms with enhanced effective pore area for ion separation.

Membrane technology using well-defined pore structure can achieve high ion purity and recovery. However, fine-tuning the inner pore structure of the separation nanofilm to be uniform and enhance the effective pore area is still challenging. Here, we report dendrimers with different peripheral groups that preferentially self-assemble in aqueous-phase amine solution to facilitate the formation of polyamide nanofilms with a well-defined effective pore range and uniform pore structure. The high permeabilities are maintained by forming asymmetric hollow nanostripe nanofilms, and their well-designed ion effective separation pore ranges show an enhancement, rationalized by molecular simulation. The self-assembled dendrimer polyamide membrane provides Cl-/SO42- selectivity more than 17 times that of its pristine polyamide counterparts, increasing from 167.9 to 2883.0. Furthermore, the designed membranes achieve higher Li purity and Li recovery compared to current state-of-the-art membranes. Such an approach provides a scalable strategy to fine-tune subnanometre structures in ion separation nanofilms.

The A53T mutation in α-synuclein enhances pro-inflammatory activation in human microglia.

Parkinson's disease (PD) is characterized by the aggregation of α-synuclein into Lewy bodies and Lewy neurites in the brain. Microglia-driven neuroinflammation may contribute to neuronal death in PD, however the exact role of microglia remains unclear and has been understudied. The A53T mutation in the gene coding for α-synuclein has been linked to early-onset PD, and exposure to A53T-mutant human α-synuclein increases the potential for inflammation of murine microglia. To date, its effect has not been studied in human microglia. Here, we used 2-dimensional cultures of human iPSC-derived microglia and transplantation of these cells into the mouse brain to assess the effects of the A53T mutation on human microglia. We found that A53T-mutant human microglia had an intrinsically increased propensity towards pro-inflammatory activation upon inflammatory stimulus. Additionally, A53T mutant microglia showed a strong decrease in catalase expression in non-inflammatory conditions, and increased oxidative stress. Our results indicate that A53T mutant human microglia display cell-autonomous phenotypes that may worsen neuronal damage in early-onset PD.

Preparation and Desalination of Semi-Aromatic Polyamide Reverse Osmosis Membranes (ROMs).

Reverse osmosis membrane (ROM) technology has a series of advantages, such as a simple process, no secondary pollution, high efficiency, energy saving, environmental protection, and good separation and purification effects. High-performance semi-aromatic polyamide reverse osmosis membranes (ROMs) were prepared by interfacial polymerization (IP) of novel cyclopentanecarbonyl chloride (CPTC) and m-phenylenediamine (MPD) monomers. The surface morphology, hydrophilicity and charge of the ROMs were characterized by field-emission scanning electron microscopy (SEM), a contact angle tester and a solid-surface zeta potential analyzer. The effects of CPTC concentration, MPD concentration, oil-phase solvent type, IP reaction time and additive concentration on the performance of semi-aromatic polyamide ROMs were studied. SEM morphology characterization showed that the surface of the prepared polyamide ROMs presented a multinodal structure. The performance test showed that when the concentration of MPD in the aqueous phase was 2.5 wt.%, the concentration of sodium dodecylbenzene sulfonate (SDBS) was 0.2%, the residence time in the aqueous phase was 2 min, the concentration of CPTC/cyclohexane in the oil phase was 0.13 wt.%, the IP reaction was 20 s, the NaCl rejection rate of the semi-aromatic polyamide ROM was 98.28% and the flux was 65.38 L/m2·h, showing good desalination performance. Compared with an NF 90 commercial membrane, it has a good anti-BSA pollution ability.

Fragile X Syndrome Patient-Derived Neurons Developing in the Mouse Brain Show FMR1-Dependent Phenotypes.

BACKGROUND: Fragile X syndrome (FXS) is characterized by physical abnormalities, anxiety, intellectual disability, hyperactivity, autistic behaviors, and seizures. Abnormal neuronal development in FXS is poorly understood. Data on patients with FXS remain scarce, and FXS animal models have failed to yield successful therapies. In vitro models do not fully recapitulate the morphology and function of human neurons. METHODS: To mimic human neuron development in vivo, we coinjected neural precursor cells derived from FXS patient-derived induced pluripotent stem cells and neural precursor cells derived from corrected isogenic control induced pluripotent stem cells into the brain of neonatal immune-deprived mice. RESULTS: The transplanted cells populated the brain and a proportion differentiated into neurons and glial cells. Immunofluorescence and single and bulk RNA sequencing analyses showed accelerated maturation of FXS neurons after an initial delay. Additionally, we found increased percentages of Arc- and Egr-1-positive FXS neurons and wider dendritic protrusions of mature FXS striatal medium spiny neurons. CONCLUSIONS: This transplantation approach provides new insights into the alterations of neuronal development in FXS by facilitating physiological development of cells in a 3-dimensional context.

A Hybrid Energy-Efficient, Area-Efficient, Low-Complexity Switching Scheme in SAR ADC for Biosensor Applications.

A hybrid energy-efficient, area-efficient, low-complexity switching scheme in SAR ADC for biosensor applications is proposed. This scheme is a combination of the monotonic technique, the MSB capacitor-splitting technique, and a new switching method. The MSB capacitor-splitting technique, as well as the reference voltage Vaq allow for more options for reference voltage conversion, resulting in higher area savings and higher energy efficiency. In a capacitor array, the circuit performs unilateral switching during all comparisons except for the second and last two comparisons, reducing the difficulty in designing the drive circuit. The proposed switching scheme saves 98.4% of the switching energy and reduces the number of unit capacitors by 87.5% compared to a conventional scheme. Furthermore, the SAR ADC employs low-noise and low-power dynamic comparators utilizing multi-clock control, low-sampling error-sampling switches based on the bootstrap technique, and dynamic SAR logic. The simulation results demonstrated that the proposed SAR ADC achieves 61.51 dB SNDR, 79.21 dB SFDR and consumes 0.278 µW of power in a 180 nm process with a 1 V power supply, a full swing input signal frequency of 23.33 kHz, and a sampling rate of 100 kS/s.

ΔNp63/p73 drive metastatic colonization by controlling a regenerative epithelial stem cell program in quasi-mesenchymal cancer stem cells.

Cancer stem cells (CSCs) may serve as the cellular seeds of tumor recurrence and metastasis, and they can be generated via epithelial-mesenchymal transitions (EMTs). Isolating pure populations of CSCs is difficult because EMT programs generate multiple alternative cell states, and phenotypic plasticity permits frequent interconversions between these states. Here, we used cell-surface expression of integrin ß4 (ITGB4) to isolate highly enriched populations of human breast CSCs, and we identified the gene regulatory network operating in ITGB4+ CSCs. Specifically, we identified ΔNp63 and p73, the latter of which transactivates ΔNp63, as centrally important transcriptional regulators of quasi-mesenchymal CSCs that reside in an intermediate EMT state. We found that the transcriptional program controlled by ΔNp63 in CSCs is largely distinct from the one that it orchestrates in normal basal mammary stem cells and, instead, it more closely resembles a regenerative epithelial stem cell response to wounding. Moreover, quasi-mesenchymal CSCs repurpose this program to drive metastatic colonization via autocrine EGFR signaling.

Hippocampal cells segregate positive and negative engrams.

The hippocampus is involved in processing a variety of mnemonic computations specifically the spatiotemporal components and emotional dimensions of contextual memory. Recent studies have demonstrated cellular heterogeneity along the hippocampal axis. The ventral hippocampus has been shown to be important in the processing of emotion and valence. Here, we combine transgenic and all-virus based activity-dependent tagging strategies to visualize multiple valence-specific engrams in the vHPC and demonstrate two partially segregated cell populations and projections that respond to appetitive and aversive experiences. Next, using RNA sequencing and DNA methylation sequencing approaches, we find that vHPC appetitive and aversive engram cells display different transcriptional programs and DNA methylation landscapes compared to a neutral engram population. Additionally, optogenetic manipulation of tagged cell bodies in vHPC is not sufficient to drive appetitive or aversive behavior in real-time place preference, stimulation of tagged vHPC terminals projecting to the amygdala and nucleus accumbens (NAc), but not the prefrontal cortex (PFC), showed the capacity drive preference and avoidance. These terminals also were able to change their capacity to drive behavior. We conclude that the vHPC contains genetically, cellularly, and behaviorally segregated populations of cells processing appetitive and aversive memory engrams.

The recombinant swinepox virus expressing sseB could provide piglets with strong protection against Salmonella typhimurium challenge.

Salmonella spp. poses a great threat to the livestock, food safety and public health. A recombinant swinepox virus expressing a protective antigen sseB was constructed by homologous recombination to develop a vaccine against Salmonella infection. The rSPV-sseB was verified using PCR, Western blot and indirect immunofluorescence assay. The immune responses and protective efficacy of rSPV-sseB were assessed in piglets. Forty piglets were immunized with rSPV-sseB, inactive Salmonella vaccine, wild-type SPV (wtSPV), or PBS. The results showed that the level of the sseB-specific antibody of the rSPV-sseB-vaccinated piglets was significantly higher at all time points post-vaccination than those of the inactivated Salmonella vaccine (P < 0.05), wtSPV (P < 0.001) or mock treated piglets (P < 0.001). The IL-4 and IFN-γ in the rSPV-sseB group were significantly higher than the other three groups at all post-infection time points. rSPV-sseB provided piglets with strong protection against the challenge of S. typhimurium with lethal dose. These results suggest the possibility of using recombinant swinepox virus rSPV-sseB as a promising vaccine to prevent Salmonella infection.

Increased expression of TIGIT and KLRG1 correlates with impaired CD56bright NK cell immunity in HPV16-related cervical intraepithelial neoplasia.

BACKGROUND: The onset and progression of cervical intraepithelial neoplasia (CIN) are closely associated with the persistent infection of high-risk HPV (especially type16), which is mainly caused by immune escape. Natural killer (NK) cells play an important role against virally infected cells and tumor cells through a fine balance of signals from multiple surface receptors. Overexpression of non-MHC-I specific inhibitory receptors TIGIT, KLRG1, Siglec-7, LAIR-1, and CD300a on NK cells correlates with cellular exhaustion and immune evasion, but these receptors have not been investigated in CIN. The aim of the present study was to examine the potential role of NK cell non-MHC-I specific inhibitory receptors expression in immune escape from HPV16(+)CIN patients. METHODS: The subset distribution, IFN-γ and TNF-α expression levels and immunophenotype of TIGIT, KLRG1, Siglec-7, LAIR-1, and CD300a of NK cells were investigated in peripheral blood mononuclear cell samples by flow cytometry from 82 women who were HPV16(+) with CIN grades 0, I, II-III or HPV(-) CIN 0. Immunohistochemistry was applied to detect the expression of ligands for NK receptors in the cervical tissues. HPV types were identified by PCR assays. RESULTS: The HPV16(+) subjects with high-grade lesions had an increased number of circulating peripheral blood CD56bright NK cells with reduced functionality and IFN-γ secretion. The expression levels of the inhibitory molecules TIGIT and KLRG1 on CD56bright NK cells increased in parallel with increasing CIN grade. In addition, TIGIT and KLRG1 related ligands, Poliovirus receptor (PVR), N-Cadherin and E-Cadherin expression level was also elevated with increasing CIN grade. CONCLUSIONS: Our results suggest that up-regulation of the inhibitory TIGIT, KLRG1 and their ligands may negatively regulate cervical CD56bright NK-mediated immunity to HPV16 and contribute to the progression of CIN. These results may facilitate the development of early-warning immune predictors and therapeutic strategies for HPV16(+) CIN based on the TIGIT and KLRG1 inhibitory pathways of NK cells.

Loading ferric lignin on polyethylene film and its influence on arsenic-polluted soil and growth of romaine lettuce plant.

This work developed a composite (Pe-FeLs) which loaded ferric lignin on polyethylene film (PE film) by chemical modification and physico-chemically characterized by Microscope, FESEM with elemental mapping analysis, and XRD. Microscope pictures showed that chemical modification did not destroy the appearance of PE film. The FESEM images of Pe-FeLs showed the well-distributed clusters could be clearly seen and most of the particles were spherical morphology. Elemental mapping of individual element on Pe-FeLs clearly indicated the existing of iron. The XRD pattern showed the amorphous hydroxides of iron on Pe-FeLs. In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic. For making Pe-FeLs work well in the soil, a Pe-FeLs system was set up with plastic grid plate, PE film with holes, Pe-FeLs, PE film, and plastic grid plate from the upper to bottom in order. With applying Pe-FeLs system under the soil, arsenic was significantly reduced by 25.5 ~ 53.4% in heavily, moderately, and lower arsenic-polluted soils, the biomass of the romaine lettuce increased and arsenic accumulation in the romaine lettuce decreased.

Au3+ Species Boost the Catalytic Performance of Au/ZnO for the Semi-hydrogenation of Acetylene.

Au nanoparticles have garnered remarkable attention in the chemoselective hydrogenation due to their extraordinary selectivity. However, the activity is far from satisfactory. Knowledge of the structure-performance relationship is a key prerequisite for rational designing of highly efficient Au-based hydrogenation catalysts. Herein, diverse Au sites were created through engineering their interactions with supports, specifically via adjusting the support morphology, that is, flower-like ZnO (ZnO-F) and disc-like ZnO (ZnO-D), and the catalyst pretreatment atmosphere, that is, 10 vol % O2/Ar and 10 vol % H2/Ar (denoted as -O and -H, respectively). The four samples of Au/ZnO were characterized by various techniques and evaluated in the semi-hydrogenation of acetylene. The transmission electron microscopy results indicated that the Au particle sizes are almost similar for our Au/ZnO catalysts. The charge states of Au species demonstrated by X-ray photoelectron spectroscopy, diffuse reflectance infrared Fourier transform spectroscopy with CO as the probe molecule, and simulation based on density functional theory, however, are greatly dependent on the ZnO shape and pretreatment atmosphere, that is, the percentage of Au3+ reduces following the order of Au/ZnO-F-O > Au/ZnO-F-H > Au/ZnO-D-O > Au/ZnO-D-H. The testing results showed that the Au/ZnO-F-O catalyst containing maximum of Au3+ possesses the optimal activity with 1.8 × 10-2 s-1 of specific activity at 200 °C, around 16.5-fold of that for Au/ZnO-D-H. More interestingly, the specific rate at 200 °C and the average conversion/selectivity in the entire operating temperature range are well correlated with the redox states of the Au species, indicating that Au3+ sites are more active for acetylene hydrogenation. A plausible explanation is that the Au3+ species not only facilitate acetylene adsorption via electrostatic interactions but also favor the heterolysis of H2 via constructing frustrated Lewis pairs with O.

Asymmetric polyamide nanofilms with highly ordered nanovoids for water purification.

Tailor-made structure and morphology are critical to the highly permeable and selective polyamide membranes used for water purification. Here we report an asymmetric polyamide nanofilm having a two-layer structure, in which the lower is a spherical polyamide dendrimer porous layer, and the upper is a polyamide dense layer with highly ordered nanovoids structure. The dendrimer porous layer was covalently assembled in situ on the surface of the polysulfone (PSF) support by a diazotization-coupling reaction, and then the asymmetric polyamide nanofilm with highly ordered hollow nanostrips structure was formed by interfacial polymerization (IP) thereon. Tuning the number of the spherical dendrimer porous layers and IP time enabled control of the nanostrips morphology in the polyamide nanofilm. The asymmetric polyamide membrane exhibits a water flux of 3.7-4.3 times that of the traditional monolayer polyamide membrane, showing an improved divalent salt rejection rate (more than 99%), which thus surpasses the upper bound line of the permeability-selectivity performance of the existing various structural polyamide membranes. We estimate that this work might inspire the preparation of highly permeable and selective reverse osmosis (RO), organic solvent nanofiltration (OSNF) and pervaporation (PV) membranes.

Phosphocholine accumulation and PHOSPHO1 depletion promote adipose tissue thermogenesis.

Phosphocholine phosphatase-1 (PHOSPHO1) is a phosphocholine phosphatase that catalyzes the hydrolysis of phosphocholine (PC) to choline. Here we demonstrate that the PHOSPHO1 transcript is highly enriched in mature brown adipose tissue (BAT) and is further induced by cold and isoproterenol treatments of BAT and primary brown adipocytes. In defining the functional relevance of PHOPSPHO1 in BAT thermogenesis and energy metabolism, we show that PHOSPHO1 knockout mice are cold-tolerant, with higher expression of thermogenic genes in BAT, and are protected from high-fat diet-induced obesity and development of insulin resistance. Treatment of mice with the PHOSPHO1 substrate phosphocholine is sufficient to induce cold tolerance, thermogenic gene expression, and allied metabolic benefits. Our results reveal a role of PHOSPHO1 as a negative regulator of BAT thermogenesis, and inhibition of PHOSPHO1 or enhancement of phosphocholine represent innovative approaches to manage the metabolic syndrome.

Neuroprotective Effects of Grape Seed Procyanidins on Ethanol-Induced Injury and Oxidative Stress in Rat Hippocampal Neurons.

AIMS: Ethanol is a small molecule capable of interacting with numerous targets in the brain, the mechanisms of which are complex and still poorly understood. Studies have revealed that ethanol-induced hippocampal neuronal injury is associated with oxidative stress. Grape seed procyanidin (GSP) is a new type of antioxidant that is believed to scavenge free radicals and be anti-inflammatory. This study evaluated the ability and mechanism by which the GSP improves ethanol-induced hippocampal neuronal injury. METHODS: Primary cultures of hippocampal neurons were exposed to ethanol (11, 33 and 66 mM, 1, 4, 8, 12 and 24 h) and the neuroprotective effects of GSP were assessed by evaluating the activity of superoxide dismutase (SOD), the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and cell morphology. RESULTS: Our results indicated that GSP prevented ethanol-induced neuronal injury by reducing the levels of MDA and LDH, while increasing the activity of SOD. In addition, GSP increased the number of primary dendrites and total dendritic length per cell. CONCLUSION: Together with previous findings, these results lend further support to the significance of developing GSP as a therapeutic tool for use in the treatment of alcohol use disorders.

Ultrathin Polyamide Membrane with Decreased Porosity Designed for Outstanding Water-Softening Performance and Superior Antifouling Properties.

Poly(piperazine-amide)-based nanofiltration membranes exhibit a smooth surface and superior antifouling properties but often have lower Ca2+ and Mg2+ rejection due to their larger inner micropore and thus cannot be extensively used in water-softening applications. To decrease the pore size of poly(piperazine-amide) membranes, we designed and synthesized a novel monomer, 1,2,3,4-cyclobutane tetracarboxylic acid chloride (BTC), which possesses a smaller molecular conformation than trimesoyl chloride (TMC). The thickness of the prepared BTC-piperazine (PIP) polyamide nanofilm via interfacial polymerization is as thin as 15 nm, significantly lower than the 50 nm thickness of the TMC-PIP nanofilm. The surface characterization reveals that the BTC-PIP polyamide membrane exhibits an enhanced hydrophilicity, a smooth surface, and a decreased surface-negative charge. The desalination performance (both rejection and water flux) of these membranes in terms of Ca2+ and Mg2+ exceeds that of the current commercial water-softening membranes. In addition, the BTC-PIP polyamide membrane also exhibits superior antifouling properties compared to the TMC-based polyamide membrane. More importantly, molecular simulations show that the BTC-PIP membrane has a lower average pore size than that of the TMC-PIP membrane, which demonstrates an enhanced steric hindrance effect, as confirmed by desalination performance. Our results demonstrate that in the household and industrial water-softening market, BTC-PIP membrane with decreased porosity, enhanced hydrophilicity, and smooth surface is preferred alternative to the conventional TMC-based polyamide membranes.

Rescue of Fragile X Syndrome Neurons by DNA Methylation Editing of the FMR1 Gene.

Fragile X syndrome (FXS), the most common genetic form of intellectual disability in males, is caused by silencing of the FMR1 gene associated with hypermethylation of the CGG expansion mutation in the 5' UTR of FMR1 in FXS patients. Here, we applied recently developed DNA methylation editing tools to reverse this hypermethylation event. Targeted demethylation of the CGG expansion by dCas9-Tet1/single guide RNA (sgRNA) switched the heterochromatin status of the upstream FMR1 promoter to an active chromatin state, restoring a persistent expression of FMR1 in FXS iPSCs. Neurons derived from methylation-edited FXS iPSCs rescued the electrophysiological abnormalities and restored a wild-type phenotype upon the mutant neurons. FMR1 expression in edited neurons was maintained in vivo after engrafting into the mouse brain. Finally, demethylation of the CGG repeats in post-mitotic FXS neurons also reactivated FMR1. Our data establish that demethylation of the CGG expansion is sufficient for FMR1 reactivation, suggesting potential therapeutic strategies for FXS.

Efficient derivation of microglia-like cells from human pluripotent stem cells.

Microglia, the only lifelong resident immune cells of the central nervous system (CNS), are highly specialized macrophages that have been recognized to have a crucial role in neurodegenerative diseases such as Alzheimer's, Parkinson's and adrenoleukodystrophy (ALD). However, in contrast to other cell types of the human CNS, bona fide microglia have not yet been derived from cultured human pluripotent stem cells. Here we establish a robust and efficient protocol for the rapid production of microglia-like cells from human (h) embryonic stem (ES) and induced pluripotent stem (iPS) cells that uses defined serum-free culture conditions. These in vitro pluripotent stem cell-derived microglia-like cells (termed pMGLs) faithfully recapitulate the expected ontogeny and characteristics of their in vivo counterparts, and they resemble primary fetal human and mouse microglia. We generated these cells from multiple disease-specific cell lines and find that pMGLs derived from an hES model of Rett syndrome are smaller than their isogenic controls. We further describe a platform to study the integration and live behavior of pMGLs in organotypic 3D cultures. This modular differentiation system allows for the study of microglia in highly defined conditions as they mature in response to developmentally relevant cues, and it provides a framework in which to study the long-term interactions of microglia residing in a tissue-like environment.

JAK2 V617F stimulates proliferation of erythropoietin-dependent erythroid progenitors and delays their differentiation by activating Stat1 and other nonerythroid signaling pathways.

JAK2 V617F is a mutant-activated JAK2 kinase found in most polycythemia vera (PV) patients; it skews normal proliferation and differentiation of hematopoietic stem and progenitor cells and simulates aberrant expansion of erythroid progenitors. JAK2 V617F is known to activate some signaling pathways not normally activated in mature erythroblasts, but there has been no systematic study of signal transduction pathways or gene expression in erythroid cells expressing JAK2 V617F undergoing erythropoietin (Epo)-dependent terminal differentiation. Here we report that expression of JAK2 V617F in murine fetal liver Epo-dependent progenitors allows them to divide approximately six rather than the normal approximately four times in the presence of Epo, delaying their exit from the cell cycle. Over time, the number of red cells formed from each Epo-dependent progenitor increases fourfold, and these cells eventually differentiate into normal enucleated reticulocytes. We report that purified fetal liver Epo-dependent progenitors express many cytokine receptors additional to the EpoR. Expression of JAK2 V617F triggers activation of Stat5, the only STAT normally activated by Epo, as well as activation of Stat1 and Stat3. Expression of JAK2 V617F also leads to transient induction of many genes not normally activated in terminally differentiating erythroid cells and that are characteristic of other hematopoietic lineages. Inhibition of Stat1 activation blocks JAK2 V617F hyperproliferation of erythroid progenitors, and we conclude that Stat1-mediated activation of nonerythroid signaling pathways delays terminal erythroid differentiation and permits extended cell divisions.

Propylene/propane permeation properties of ethyl cellulose (EC) mixed matrix membranes fabricated by incorporation of nanoporous graphene nanosheets.

Nanopore containing graphene nanosheets were synthesized by graphene oxide and a reducing agent using a facile hydrothermal treatment in sodium hydroxide media. The as-prepared nanoporous graphene was incorporated into ethyl cellulose (EC) to prepare the mixed matrix membranes (MMMs) for C3H6/C3H8 separation. Transmission electron microscopy (TEM) photograph and X-ray photoelectron spectroscopy (XPS) analysis of nanoporous graphene nanosheets indicated that the structure of nano-pore was irregular and the oxygen-containing groups in the surface were limited. More importantly, the as-prepared MMMs presented better separation performance than that of pristine EC membrane due to simultaneous enhancement of C3H6 permeability and ideal selectivity. The ideal selectivity of the MMMs with 1.125 wt‰ nanoporous graphene content for C3H6/C3H8 increased from 3.45 to 10.42 and the permeability of C3H6 increased from 57.9 Barrer to 89.95 Barrer as compared with the pristine membrane. The presumed facilitated mechanism was that the high specific surface area of nanoporous graphene in polymer matrix increased the length of the tortuous pathway formed by nanopores for the gas diffusion as compared with the pristine graphene nanosheets, and generated a rigidified interface between the EC chains and fillers, thus enhanced the diffusivity selectivity. Therefore, it is expected that nanoporous graphene would be effective material for the C3H6/C3H8 separation.

MERAV: a tool for comparing gene expression across human tissues and cell types.

The oncogenic transformation of normal cells into malignant, rapidly proliferating cells requires major alterations in cell physiology. For example, the transformed cells remodel their metabolic processes to supply the additional demand for cellular building blocks. We have recently demonstrated essential metabolic processes in tumor progression through the development of a methodological analysis of gene expression. Here, we present the Metabolic gEne RApid Visualizer (MERAV, http://merav.wi.mit.edu), a web-based tool that can query a database comprising ∼4300 microarrays, representing human gene expression in normal tissues, cancer cell lines and primary tumors. MERAV has been designed as a powerful tool for whole genome analysis which offers multiple advantages: one can search many genes in parallel; compare gene expression among different tissue types as well as between normal and cancer cells; download raw data; and generate heatmaps; and finally, use its internal statistical tool. Most importantly, MERAV has been designed as a unique tool for analyzing metabolic processes as it includes matrixes specifically focused on metabolic genes and is linked to the Kyoto Encyclopedia of Genes and Genomes pathway search.