Access to safe drinking water is a human right, crucial to combat inequalities, reduce poverty and allow sustainable development. In many areas of the world, however, this right is not guaranteed, in part because of the lack of easily deployable diagnostic tools. Low-cost and simple methods to test water supplies onsite can protect vulnerable communities from the impact of contaminants in drinking water. Ideally such devices would also be easy to dispose of so as to leave no trace, or have a detrimental effect on the environment. To this aim, we here report the first paper microbial fuel cell (pMFC) fabricated by screen-printing biodegradable carbon-based electrodes onto a single sheet of paper, and demonstrate its use as a shock sensor for bioactive compounds (e.g. formaldehyde) in water. We also show a simple route to enhance the sensor performance by folding back-to-back two pMFCs electrically connected in parallel. This promising proof of concept work can lead to a revolutionizing way of testing water at point of use, which is not only green, easy-to-operate and rapid, but is also affordable to all.
Here we explore the electrochemical performance of pyrolyzed skins from the species A. bisporus, also known as the Portobello mushroom, as free-standing, binder-free, and current collector-free Li-ion battery anodes. At temperatures above 900 °C, the biomass-derived carbon nanoribbon-like architectures undergo unique processes to become hierarchically porous. During heat-treatment, the oxygen and heteroatom-rich organics and potassium compounds naturally present in the mushroom skins play a mutual role in creating inner void spaces throughout the resulting carbon nanoribbons, which is a process analogous to KOH-activation of carbon materials seen in literature. The pores formed in the pyrolytic carbon nanoribbons range in size from sub-nanometer to tens of nanometers, making the nanoribbons micro, meso, and macroporous. Detailed studies were conducted on the carbon nanoribbons using SEM and TEM to study morphology, as well as XRD and EDS to study composition. The self-supporting nanoribbon anodes demonstrate significant capacity increase as they undergo additional charge/discharge cycles. After a pyrolysis temperature of 1100 °C, the pristine anodes achieve over 260 mAh/g after 700 cycles and a Coulombic efficiency of 101.1%, without the use of harmful solvents or chemical activation agents.
We have developed an implantable fuel cell that generates power through glucose oxidation, producing 3.4 μW cm(-2) steady-state power and up to 180 μW cm(-2) peak power. The fuel cell is manufactured using a novel approach, employing semiconductor fabrication techniques, and is therefore well suited for manufacture together with integrated circuits on a single silicon wafer. Thus, it can help enable implantable microelectronic systems with long-lifetime power sources that harvest energy from their surrounds. The fuel reactions are mediated by robust, solid state catalysts. Glucose is oxidized at the nanostructured surface of an activated platinum anode. Oxygen is reduced to water at the surface of a self-assembled network of single-walled carbon nanotubes, embedded in a Nafion film that forms the cathode and is exposed to the biological environment. The catalytic electrodes are separated by a Nafion membrane. The availability of fuel cell reactants, oxygen and glucose, only as a mixture in the physiologic environment, has traditionally posed a design challenge: Net current production requires oxidation and reduction to occur separately and selectively at the anode and cathode, respectively, to prevent electrochemical short circuits. Our fuel cell is configured in a half-open geometry that shields the anode while exposing the cathode, resulting in an oxygen gradient that strongly favors oxygen reduction at the cathode. Glucose reaches the shielded anode by diffusing through the nanotube mesh, which does not catalyze glucose oxidation, and the Nafion layers, which are permeable to small neutral and cationic species. We demonstrate computationally that the natural recirculation of cerebrospinal fluid around the human brain theoretically permits glucose energy harvesting at a rate on the order of at least 1 mW with no adverse physiologic effects. Low-power brain-machine interfaces can thus potentially benefit from having their implanted units powered or recharged by glucose fuel cells.
ABSTRACT Fe(II)-oxidizing aerobic bacteria are poorly understood, due in part to the difficulties involved in laboratory cultivation. Specific challenges include (i) providing a steady supply of electrons as Fe(II) while (ii) managing rapid formation of insoluble Fe(III) oxide precipitates and (iii) maintaining oxygen concentrations in the micromolar range to minimize abiotic Fe(II) oxidation. Electrochemical approaches offer an opportunity to study bacteria that require problematic electron donors or acceptors in their respiration. In the case of Fe(II)-oxidizing bacteria, if the electron transport machinery is able to oxidize metals at the outer cell surface, electrodes poised at potentials near those of natural substrates could serve as electron donors, eliminating concentration issues, side reactions, and mineral end products associated with metal oxidation. To test this hypothesis, the marine isolate Mariprofundus ferrooxydans PV-1, a neutrophilic obligate Fe(II)-oxidizing autotroph, was cultured using a poised electrode as the sole energy source. When cells grown in Fe(II)-containing medium were transferred into a three-electrode electrochemical cell, a cathodic (negative) current representing electron uptake by bacteria was detected, and it increased over a period of weeks. Cultures scraped from a portion of the electrode and transferred into sterile reactors consumed electrons at a similar rate. After three transfers in the absence of Fe(II), electrode-grown biofilms were studied to determine the relationship between donor redox potential and respiration rate. Electron microscopy revealed that under these conditions, M. ferrooxydans PV-1 attaches to electrodes and does not produce characteristic iron oxide stalks but still appears to exhibit bifurcate cell division. IMPORTANCE Electrochemical cultivation, supporting growth of bacteria with a constant supply of electron donors or acceptors, is a promising tool for studying lithotrophic species in the laboratory. Major pitfalls present in standard cultivation methods used for metal-oxidizing microbes can be avoided by the use of an electrode as the sole electron donor. Electrochemical cultivation also offers a window into the poorly understood metabolism of microbes such as obligate Fe(II), Mn(II), or S(0) oxidizers by replacing the electron source with the controlled surface of an electrode. The elucidation of redox-dependent behavior of these microbes could enhance industrial applications tuned to oxidation of specific metals, provide insight into how bacteria evolved to compete with oxygen for reactive metal species, and model geochemical impacts of their metabolism in the environment.
We have found that the addition of tin nanoparticles to a silicon-based anode provides dramatic improvements in performance in terms of both charge capacity and cycling stability. Using a simple procedure and off-the-shelf additives and precursors, we developed a structure in which the tin nanoparticles are segregated at the interface between the silicon-containing active layer and the solid electrolyte interface. Even a minor addition of tin, as small as ∼2% by weight, results in a significant decrease in the anode resistance, as confirmed by electrochemical impedance spectroscopy. This leads to a decrease in charge transfer resistance, which prevents the formation of electrically inactive “dead spots” in the anode structure and enables the effective participation of silicon in the lithiation reaction.
- Journal of neurology, neurosurgery, and psychiatry
- Published about 7 years ago
Transcranial direct current stimulation (tDCS), a non-invasive neuromodulation technique inducing prolonged brain excitability changes and promoting cerebral plasticity, is a promising option for neurorehabilitation. Here, we review progress in research on tDCS and language functions and on the potential role of tDCS in the treatment of post-stroke aphasia. Currently available data suggest that tDCS over language-related brain areas can modulate linguistic abilities in healthy individuals and can improve language performance in patients with aphasia. Whether the results obtained in experimental conditions are functionally important for the quality of life of patients and their caregivers remains unclear. Despite the fact that important variables are yet to be determined, tDCS combined with rehabilitation techniques seems a promising therapeutic option for aphasia.
Cytochrome P450 oxidoreductase (POR) is known as the sole electron donor in the metabolism of drugs by cytochrome P450 (CYP) enzymes in human. However, little is known about the effect of polymorphic variants of POR on drug metabolic activities of CYP3A4 and CYP2B6. In order to better understand the mechanism of the activity of CYPs affected by polymorphic variants of POR, six full-length mutants of POR (e.g., Y181D, A287P, K49N, A115V, S244C and G413S) were designed and then co-expressed with CYP3A4 and CYP2B6 in the baculovirus-Sf9 insect cells to determine their kinetic parameters. Surprisingly, both mutants, Y181D and A287P in POR completely inhibited the CYP3A4 activity with testosterone, while the catalytic activity of CYP2B6 with bupropion was reduced to approximately ~70% of wild-type activity by Y181D and A287P mutations. In addition, the mutant K49N of POR increased the CLint (Vmax/Km) of CYP3A4 up to more than 31% of wild-type, while it reduced the catalytic efficiency of CYP2B6 to 74% of wild-type. Moreover, CLint values of CYP3A4-POR (A115V, G413S) were increased up to 36% and 65% of wild-type respectively. However, there were no appreciable effects observed by the remaining two mutants of POR (i.e., A115V and G413S) on activities of CYP2B6. In conclusion, the extent to which the catalytic activities of CYP were altered did not only depend on the specific POR mutations but also on the isoforms of different CYP redox partners. Thereby, we proposed that the POR-mutant patients should be carefully monitored for the activity of CYP3A4 and CYP2B6 on the prescribed medication.
ABSTRACT Shewanella oneidensis strain MR-1 is widely studied for its ability to respire a diverse array of soluble and insoluble electron acceptors. The ability to breathe insoluble substrates is defined as extracellular electron transfer and can occur via direct contact or by electron shuttling in S. oneidensis. To determine the contribution of flavin electron shuttles in extracellular electron transfer, a transposon mutagenesis screen was performed with S. oneidensis to identify mutants unable to secrete flavins. A multidrug and toxin efflux transporter encoded by SO_0702 was identified and renamed bfe (bacterial flavin adenine dinucleotide [FAD] exporter) based on phenotypic characterization. Deletion of bfe resulted in a severe decrease in extracellular flavins, while overexpression of bfe increased the concentration of extracellular flavins. Strains lacking bfe had no defect in reduction of soluble Fe(III), but these strains were deficient in the rate of insoluble Fe(III) oxide reduction, which was alleviated by the addition of exogenous flavins. To test a different insoluble electron acceptor, graphite electrode bioreactors were set up to measure current produced by wild-type S. oneidensis and the Δbfe mutant. With the same concentration of supplemented flavins, the two strains produced similar amounts of current. However, when exogenous flavins were not supplemented to bioreactors, bfe mutant strains produced significantly less current than the wild type. We have demonstrated that flavin electron shuttling accounts for ~75% of extracellular electron transfer to insoluble substrates by S. oneidensis and have identified the first FAD transporter in bacteria. IMPORTANCE Extracellular electron transfer by microbes is critical for the geochemical cycling of metals, bioremediation, and biocatalysis using electrodes. A controversy in the field was addressed by demonstrating that flavin electron shuttling, not direct electron transfer or nanowires, is the primary mechanism of extracellular electron transfer employed by the bacterium Shewanella oneidensis. We have identified a flavin adenine dinucleotide transporter conserved in all sequenced Shewanella species that facilitates export of flavin electron shuttles in S. oneidensis. Analysis of a strain that is unable to secrete flavins demonstrated that electron shuttling accounts for ~75% of the insoluble extracellular electron transfer capacity in S. oneidensis.
The aim of this study was to examine the effect of ACS14, a hydrogen sulfide (H(2)S)-releasing derivative of aspirin (Asp), on Asp-induced gastric injury. Gastric hemorrhagic lesions were induced by intragastric administration of Asp (200 mg/kg, suspended in 0.5% carboxymethyl cellulose solutions) in a volume of 1 ml/100 g body weight. ACS14 (1, 5 or 10 mg/kg) was given 30 min before the Asp administration. The total area of gastric erosions, H(2)S concentration and oxidative stress in gastric tissues were measured three hours after administration of Asp. Treatment with Asp (200 mg/kg), but not ACS14 (430 mg/kg, at equimolar doses to 200 mg/kg Asp), for 3 h significantly increased gastric mucosal injury. The damage caused by Asp was reversed by ACS14 at 1-10 mg/kg in a concentration-dependent manner. ACS14 abrogated Asp-induced upregulation of COX-2 expression, but had no effect on the reduced PGE(2) level. ACS14 reversed the decreased H(2)S concentrations and blood flow in the gastric tissue in Asp-treated rats. Moreover, ACS14 attenuated Asp-suppressed superoxide dismutase-1 (SOD-1) expression and GSH activity, suggesting that ACS14 may stimulate antioxidants in the gastric tissue. ACS14 also obviously inhibited Asp-induced upregulation of protein expression of oxidases including XOD, p47(phox) and p67(phox). In conclusion, ACS14 protects Asp induced gastric mucosal injury by inhibiting oxidative stress in the gastric tissue.
A somatic activating mutation in AKT1, c.49G>A, pGlu17Lys, that results in elevated AKT signaling in mutation-positive cells, is responsible for the mosaic overgrowth condition, Proteus syndrome. ARQ 092 is an allosteric pan-AKT inhibitor under development for treatment in cancer. We tested the efficacy of this drug for suppressing AKT signaling in cells and tissues from patients with Proteus syndrome. ARQ 092 reduced phosphorylation of AKT and downstream targets of AKT in a concentration-dependent manner in as little as two hours. While AKT signaling was suppressed with ARQ 092 treatment, cells retained their ability to respond to growth factor stimulation by increasing pAKT levels proportionally to untreated cells. At concentrations sufficient to decrease AKT signaling, little reduction in cell viability was seen. These results indicate that ARQ 092 can suppress AKT signaling and warrants further development as a therapeutic option for patients with Proteus syndrome.