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Recent advances in microfluidic devices put a high demand on small, robust and reliable pumps suitable for high-throughput applications. Here we demonstrate a compact, low-cost, directly attachable (clip-on) electroosmotic pump that couples with standard Luer connectors on a microfluidic device. The pump is easy to make and consists of a porous polycarbonate membrane and poly(3,4-ethylenedioxythiophene) polystyrene sulfonate (PEDOT:PSS) electrodes. The soft electrode and membrane materials make it possible to incorporate the pump into a standard syringe filter holder, which in turn can be attached to commercial chips. The pump is less than half the size of the microscope slide used for many commercial lab-on-a-chip devices, meaning that these pumps can be used to control fluid flow in individual reactors in highly parallelized chemistry and biology experiments. Flow rates at various electric current and device dimensions are reported. We demonstrate the feasibility and safety of the pump for biological experiments by exposing endothelial cells to oscillating shear stress (up to 5 dyn/cm2) and by controlling the movement of both micro- and macroparticles, generating steady or oscillatory flow rates up to ± 400 μL/min.

In nearly all cases, electrophoresis in gels is driven via the electrolysis of water at the electrodes, where the process consumes water and produces electrochemical by-products. We have previously demonstrated that π-conjugated polymers such as poly(3,4-ethylenedioxythiophene) (PEDOT) can be placed between traditional metal electrodes and an electrolyte to mitigate electrolysis in liquid (capillary electroosmosis/electrophoresis) systems. In this report, we extend our previous result to gel electrophoresis, and show that electrodes containing PEDOT can be used with a commercial polyacrylamide gel electrophoresis system with minimal impact to the resulting gel image or the ionic transport measured during a separation.

Electroosmotic pumps employing silica frits synthesized from potassium silicate as a stationary phase show strong electroosmotic flow velocity and resistance to pressure-driven flow. We characterize these pumps and measure an electroosmotic mobility of 2.5 × 10(-8) m(2)/V s and hydrodynamic resistance per unit length of 70 × 10(17) Pa s/m(4) with a standard deviation of less than 2% even when varying the amount of water used in the potassium silicate mixture. Furthermore, we demonstrate the simple integration of these pumps into a proof-of-concept PDMS lab-on-a-chip device fabricated from a 3D-printed template.

Static p–n junctions in inorganic semiconductors are exploited in a wide range of today’s electronic appliances. Here, we demonstrate the in situ formation of a dynamic p–n junction structure within an organic semiconductor through electrochemistry. Specifically, we use scanning kelvin probe microscopy and optical probing on planar light-emitting electrochemical cells (LECs) with a mixture of a conjugated polymer and an electrolyte connecting two electrodes separated by 120 μm. We find that a significant portion of the potential drop between the electrodes coincides with the location of a thin and distinct light-emission zone positioned >30 μm away from the negative electrode. These results are relevant in the context of a long-standing scientific debate, as they prove that electrochemical doping can take place in LECs. Moreover, a study on the doping formation and dissipation kinetics provides interesting detail regarding the electronic structure and stability of the dynamic organic p–n junction, which may be useful in future dynamic p–n junction-based devices. The light-emitting electrochemical cell (LEC) is one application of organic semiconductors. Scanning kelvin probe microscopy and light-emission data obtained from operational planar LECs provide insight into the devices. The measured electrostatic potential profiles confirm that there is in situ formation of a dynamic p–n junction in the organic semiconductor during operation.

In this study, the authors show that MeCP2 interacts with the NCoR/SMRT co-repressor complex and that a discrete cluster of Rett syndrome–causing mutations in the C-terminal domain of MeCP2 disrupts this interaction, impairing transcriptional repression. Knock-in mice expressing one of these MeCP2 missense mutations exhibit severe motor phenotypes. Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the DNA-binding domain of MeCP2, suggesting that association with chromatin is critical for its function. We identified a second mutational cluster in a previously uncharacterized region of MeCP2. We found that RTT mutations in this region abolished the interaction between MeCP2 and the NCoR/SMRT co-repressor complexes. Mice bearing a common missense RTT mutation in this domain exhibited severe RTT-like phenotypes. Our data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP2 'bridge' between the NCoR/SMRT co-repressors and chromatin.

A large-area, fabric-like pump would potentially have applications, for example, in controlling water transport through a garment, such as a rain jacket, regardless of the external temperature and humidity. This paper presents an all-plastic, flexible electroosmotic pump, constructed from commercially available materials: A polycarbonate membrane combined with the electrochemically active polymer poly(3,4-ethylenedioxythiophene) polystyrene sulfonate that actively transports water using an electric potential that can be supplied by a small battery. By using electrochemically active polymer electrodes instead of metal electrodes, the electrochemical reaction that drives flow avoids the oxygen and hydrogen gas production or pH changes associated with water electrolysis. We observe a water mass flux up to 23 mg min −1  per cm 2 polycarbonate membrane (porosity 10–15%), at an applied potential of 5 V, and a limiting operating pressure of 0.3 kPa V −1 , similar to previously reported membrane-based electroosmotic pumps.

Rett syndrome is caused by mutations in MeCP2, and this study identifies a site on MeCP2, T308, whose phosphorylation is regulated by neuronal activity: phosphorylation of T308 blocks the interaction of MeCP2 with the NCoR co-repressor complex, suppressing MeCP2's ability to repress transcription, and mice carrying mutations of MeCP2 T308 show Rett-syndrome-related symptoms. Causation of Rett syndrome The childhood neurodevelopmental disorder Rett syndrome is caused by mutations in MeCP2, a protein that regulates transcription in neurons. Michael Greenberg and colleagues identify a site on MeCP2, threonine 308 (T308), whose phosphorylation is regulated by neuronal activity. T308 phosphorylation blocks the interaction of MeCP2 with the NCoR co-repressor complex, suppressing MeCP2's ability to repress transcription. Mice carrying mutations of MeCP2 T308 show Rett syndrome-related symptoms, suggesting that this activity-dependent phosphorylation and regulation of MeCP2–NCoR interaction may have a causal role in Rett syndrome. Rett syndrome (RTT) is an X-linked human neurodevelopmental disorder with features of autism and severe neurological dysfunction in females. RTT is caused by mutations in methyl-CpG-binding protein 2 (MeCP2), a nuclear protein that, in neurons, regulates transcription, is expressed at high levels similar to that of histones, and binds to methylated cytosines broadly across the genome 1 , 2 , 3 , 4 , 5 . By phosphotryptic mapping, we identify three sites (S86, S274 and T308) of activity-dependent MeCP2 phosphorylation. Phosphorylation of these sites is differentially induced by neuronal activity, brain-derived neurotrophic factor, or agents that elevate the intracellular level of 3′,5′-cyclic AMP (cAMP), indicating that MeCP2 may function as an epigenetic regulator of gene expression that integrates diverse signals from the environment. Here we show that the phosphorylation of T308 blocks the interaction of the repressor domain of MeCP2 with the nuclear receptor co-repressor (NCoR) complex and suppresses the ability of MeCP2 to repress transcription. In knock-in mice bearing the common human RTT missense mutation R306C, neuronal activity fails to induce MeCP2 T308 phosphorylation, suggesting that the loss of T308 phosphorylation might contribute to RTT. Consistent with this possibility, the mutation of MeCP2 T308A in mice leads to a decrease in the induction of a subset of activity-regulated genes and to RTT-like symptoms. These findings indicate that the activity-dependent phosphorylation of MeCP2 at T308 regulates the interaction of MeCP2 with the NCoR complex, and that RTT in humans may be due, in part, to the loss of activity-dependent MeCP2 T308 phosphorylation and a disruption of the phosphorylation-regulated interaction of MeCP2 with the NCoR complex.

Cells and tissues use finely regulated ion fluxes for their intra- and intercellular communication. Technologies providing spatial and temporal control for studies of such fluxes are however, limited. We have developed an electrophoretic ion pump made of poly(3,4-ethylenedioxythiophene) doped with poly(styrene sulphonate) (PEDOT:PSS) to mediate electronic control of the ion homeostasis in neurons. Ion delivery from a source reservoir to a receiving electrolyte via a PEDOT:PSS thin-film channel was achieved by electronic addressing. Ions are delivered in high quantities at an associated on/off ratio exceeding 300. This induces physiological signalling events that can be recorded at the single-cell level. Furthermore, miniaturization of the device to a 50-μm-wide channel allows for stimulation of individual cells. As this technology platform allows for electronic control of ion signalling in individual cells with proper spatial and temporal resolution, it will be useful in further studies of communication in biological systems.

We compare three different methods to quantify the monosaccharide fucose in solutions using the displacement of a large glycoprotein, lactoferrin. Two microfluidic analysis methods, namely fluorescence detection of (labeled) lactoferrin as it is displaced by unlabeled fucose and the displacement of (unlabeled) lactoferrin in SPR, provide fast responses and continuous data during the experiment, theoretically providing significant information regarding the interaction kinetics between the saccharide groups and binding sites. For comparison, we also performed a static displacement ELISA. The stationary binding site in all cases was immobilized S2-AAL, a monovalent polypeptide based on Aleuria aurantia lectin. Although all three assays showed a similar dynamic range, the microfluidic assays with fluorescent or SPR detection show an advantage in short analysis times. Furthermore, the microfluidic displacement assays provide a possibility to develop a one-step analytical platform.

This study reports an approach to tailoring the temperature-sensitive conductivity behavior of poly(ethylene oxide) (PEO)-based polymer electrolytes to match a concrete hardening model, for use in temperature-sensitive organic electronics. Plasticized PEO/MX (M = Li, Na; X = TFSI, Tf) polymer electrolytes were designed to fit a specific temperature-sensitive behavior of the ionic conductivity within a temperature range of 20–60 °C. Polymer electrolytes with varying concentrations of plasticizing solvents (propylene carbonate and ethylene carbonate; PC and EC) and short-chain polyether homologs such as poly(ethylene glycol)-dimethyl ether were produced. Some of the investigated electrolytes displayed useful and stable temperature-sensitive conductivity for applications in process monitoring or quality control of temperature-sensitive products; the best being either a 40:60 PEO:PEGDME blend by w/w containing NaCF 3 SO 3 at a Na:O ratio 1:10 and with 10 wt% PC or PEO with LiTFSI or NaTFSI at a salt:O ratio 1:25 and 30 wt% PC. Analysis of variance indicates the adequacy of temperature-sensitive poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate) (PEDOT:PSS) electrochromic monitoring devices based on these electrolytes relative to a standard model for the concrete hardening process. Graphical Abstract