Photoanodes for Aqueous Solar Cells: Exploring Additives and Formulations Starting from a Commercial TiO2 Paste

Whereas the commercialization of dye‐sensitized solar cells (DSSCs) is finally proceeding taking advantage of their low cost and tunable optical features, such as colour and transparency for both indoor and building‐integrated applications, the corresponding aqueous counterpart is still at its infancy. As the TiO2 electrode is a fundamental component for hybrid solar cells, this work investigates the effect of different molecular (α‐terpineol, propylene carbonate) and polymeric (polyethylene oxide, polyethylene glycol, carboxymethyl cellulose and xanthan gum) additives that can be introduced into a commercial TiO2 paste for for screen‐printing (or doctor blade). Among all, the addition of polyethylene glycol leads to the best cell performances, with markedly increased short‐circuit current density (+18 %) and power conversion efficiency (+48 %) with respect to the pristine (commercial) counterpart. When further explored at different concentration levels, electrodes fabricated from polyethylene glycol‐based pastes show different morphologies, thicknesses and performances, which are investigated through (photo)electrochemical, structural, physical‐chemical and microscopic techniques

Photoanodes for Aqueous Solar Cells: Exploring Additives and Formulations Starting from a Commercial TiO2 Paste

Whereas the commercialization of dye‐sensitized solar cells (DSSCs) is finally proceeding taking advantage of their low cost and tunable optical features, such as colour and transparency for both indoor and building‐integrated applications, the corresponding aqueous counterpart is still at its infancy. As the TiO2 electrode is a fundamental component for hybrid solar cells, this work investigates the effect of different molecular (α‐terpineol, propylene carbonate) and polymeric (polyethylene oxide, polyethylene glycol, carboxymethyl cellulose and xanthan gum) additives that can be introduced into a commercial TiO2 paste for for screen‐printing (or doctor blade). Among all, the addition of polyethylene glycol leads to the best cell performances, with markedly increased short‐circuit current density (+18 %) and power conversion efficiency (+48 %) with respect to the pristine (commercial) counterpart. When further explored at different concentration levels, electrodes fabricated from polyethylene glycol‐based pastes show different morphologies, thicknesses and performances, which are investigated through (photo)electrochemical, structural, physical‐chemical and microscopic techniques

Platinum-free photoelectrochromic devices working with copper-based electrolytes for ultrastable smart windows

Photoelectrochromic systems are devices designed for large-scale manufacturing of smart windows, capable of changing their transmittance according to external environmental conditions. This communication proposes the replacement of the two most critical photoelectrochemical device components studied so far, namely the counter electrode and the redox mediator. Regarding the first, graphene nanoplatelets are used to replace platinum, maintaining both its optical and electrocatalytic properties, and at the same time reducing the device cost. Secondly, a copper-based redox pair was chosen to solve the corrosion problems typically encountered with the iodine-based mediator. The combination of the above components led to devices with high performance (coloration speeds in the order of seconds, with a maximum contrast ratio of 10.4 : 1), as well as the achievement of a long-term stability record (over 400 days) for these photoelectrochromic systems

Lignin-Based Polymer Electrolyte Membranes for Sustainable Aqueous Dye-Sensitized Solar Cells

In the quest for sustainable materials for quasi-solid-state (QS) electrolytes in aqueous dye-sensitized solar cells (DSSCs), novel bioderived polymeric membranes were prepared in this work by reaction of preoxidized kraft lignin with poly(ethylene glycol)diglycidylether (PEGDGE). The effect of the PEGDGE/lignin relative proportions on the characteristics of the obtained membranes was thoroughly investigated, and clear structure–property correlations were highlighted. In particular, the glass transition temperature of the materials was found to decrease by increasing the amount of PEGDGE in the formulation, indicating that polyethylene glycol chains act as flexible segments that increase the molecular mobility of the three-dimensional polymeric network. Concurrently, their swelling ability in liquid electrolyte was found to increase with the concentration of PEGDGE, which was also shown to influence the ionic transport efficiency within the membrane. The incorporation of these lignin-based cross-linked systems as QS electrolyte frameworks in aqueous DSSCs allowed the preparation of devices with excellent long-term stability under UV–vis light, which were found to be superior to benchmark QS-DSSCs incorporating state-of-the-art carboxymethylcellulose membranes. This study provides the first demonstration of lignin-based QS electrolytes for stable aqueous DSSCs, establishing a straightforward strategy to exploit the potential of lignin as a functional polymer precursor for the field of sustainable photovoltaic devices

Lignin as polymer electrolyte precursor for stable and sustainable potassium batteries

Potassium batteries show interesting peculiarities as large-scale energy storage systems and, in this scenario, the formulation of polymer electrolytes obtained from sustainable resources or waste-derived products represents a milestone activity. In this study, a lignin-based membrane is designed by crosslinking a pre-oxidized Kraft lignin matrix with an ethoxylated difunctional oligomer, leading to self-standing membranes that are able to incorporate solvated potassium salts. The in-depth electrochemical characterization highlights a wide stability window (up to 4 V) and an ionic conductivity exceeding 10−3 S cm−1 at ambient temperature. When potassium metal cell prototypes are assembled, the lignin-based electrolyte attains significant electrochemical performances, with an initial specific capacity of 168 mAh g−1 at 0.05 A g−1 and an excellent operation for more than 200 cycles, which is an unprecedented outcome for biosourced systems in potassium batteries

Cardanol-Derived Epoxy Resins as Biobased Gel Polymer Electrolytes for Potassium-Ion Conduction

In this study, biobased gel polymer electrolyte (GPE) membranes were developed via the esterification reaction of a cardanol-based epoxy resin with glutaric anhydride, succinic anhydride, and hexahydro-4-methylphthalic anhydride. Nonisothermal differential scanning calorimetry was used to assess the optimal curing time and temperature of the formulations, evidencing a process activation energy of ∼65–70 kJ mol–1. A rubbery plateau modulus of 0.65–0.78 MPa and a crosslinking density of 2 × 10–4 mol cm–3 were found through dynamic mechanical analysis. Based on these characteristics, such biobased membranes were tested for applicability as GPEs for potassium-ion batteries (KIBs), showing an excellent electrochemical stability toward potassium metal in the −0.2–5 V voltage range and suitable ionic conductivity (10–3 S cm–1) at room temperature. This study demonstrates the practical viability of these biobased materials as efficient GPEs for the fabrication of KIBs, paving the path to increased sustainability in the field of next-generation battery technologies

Metformin overdose causes platelet mitochondrial dysfunction in humans

Introduction. We have recently demonstrated that metformin intoxication causes mitochondrial dysfunction in several porcine tissues, including platelets. The aim of the present work was to clarify whether it also causes mitochondrial dysfunction (and secondary lactate overproduction) in human platelets, in-vitro and ex-vivo. Methods. Human platelets were incubated for 72 h with saline or increasing dose of metformin (in-vitro experiments). Lactate production, respiratory chain complex activities (spectrophotometry), mitochondrial membrane potential (flow-cytometry after staining with JC-1) and oxygen consumption (Clark-type electrode) were then measured. Platelets were also obtained from ten patients with lactic acidosis (arterial pH 6.97\ub10.18 and lactate 16\ub17 mmol/l) due to accidental metformin intoxication (serum drug level 32\ub114 mg/l) and ten healthy volunteers of similar sex and age. Respiratory chain complex activities were measured as above (ex-vivo experiments). Results. In-vitro, metformin dose-dependently increased lactate production (p<0.001), decreased respiratory chain complex I activity (p=0.009), mitochondrial membrane potential (p=0.003) and oxygen consumption (p<0.001) of human platelets. Ex-vivo, platelets taken from intoxicated patients had significantly lower complex I (p=0.045) and complex IV (p<0.001) activity compared to controls. Conclusions. Depending on dose, metformin can cause mitochondrial dysfunction and lactate overproduction in human platelets in-vitro and, possibly, in-vivo. Trial registration. NCT 0094212

Clinical-genetic features and peculiar muscle histopathology in infantile DNM1L-related mitochondrial epileptic encephalopathy

Mitochondria are highly dynamic organelles, undergoing continuous fission and fusion. The DNM1L gene encodes for the DRP1 protein, an evolutionary conserved member of the dynamin family, responsible for fission of mitochondria, and having a role in the division of peroxisomes, as well. DRP1 impairment is implicated in several neurological disorders and associated with either de novo dominant or compound heterozygous mutations. In five patients presenting with severe epileptic encephalopathy we identified 5 de novo dominant DNM1L variants, the pathogenicity of which was validated in a yeast model. Fluorescence microscopy revealed abnormally elongated mitochondria and aberrant peroxisomes in mutant fibroblasts, indicating impaired fission of these organelles. Moreover, a very peculiar finding in our cohort of patients was the presence, in muscle biopsy, of core like areas with oxidative enzyme alterations, suggesting an abnormal distribution of mitochondria in the muscle tissue

Purkinje cell COX deficiency and mtDNA depletion in an animal model of spinocerebellar ataxia type 1

Spinocerebellar ataxias (SCAs) are a genetically heterogeneous group of cerebellar degenerative disorders, characterized by progressive gait unsteadiness, hand incoordination, and dysarthria. Ataxia type 1 (SCA1) is caused by the expansion of a CAG trinucleotide repeat in the SCA1 gene resulting in the atypical extension of a polyglutamine (polyQ) tract within the ataxin-1 protein. Our main objective was to investigate the mitochondrial oxidative metabolism in the cerebellum of transgenic SCA1 mice. SCA1 transgenic mice develop clinical features in the early life stages (around 5 weeks of age) presenting pathological cerebellar signs with concomitant progressive Purkinje neuron atrophy and relatively little cell loss; this evidence suggests that the SCA1 phenotype is not the result of cell death per se, but a possible effect of cellular dysfunction that occurs before neuronal demise. We studied the mitochondrial oxidative metabolism in cerebellar cells from both homozygous and heterozygous transgenic SCA1 mice, aged 2 and 6 months. Histochemical examination showed a cytochrome-c-oxidase (COX) deficiency in the Purkinje cells (PCs) of both heterozygous and homozygous mice, the oxidative defect being more prominent in older mice, in which the percentage of COX-deficient PC was up to 30%. Using a laser-microdissector, we evaluated the mitochondrial DNA (mtDNA) content on selectively isolated COX-competent and COX-deficient PC by quantitative Polymerase Chain Reaction and we found mtDNA depletion in those with oxidative dysfunction. In conclusion, the selective oxidative metabolism defect observed in neuronal PC expressing mutant ataxin occurs as early as 8 weeks of age thus representing an early step in the PC degeneration process in SCA1 disease

Transcriptomic profiling of TK2 deficient human skeletal muscle suggests a role for the p53 signalling pathway and identifies growth and differentiation factor-15 as a potential novel biomarker for mitochondrial myopathies

Background Mutations in the gene encoding thymidine kinase 2 (TK2) result in the myopathic form of mitochondrial DNA depletion syndrome which is a mitochondrial encephalomyopathy presenting in children. In order to unveil some of the mechanisms involved in this pathology and to identify potential biomarkers and therapeutic targets we have investigated the gene expression profile of human skeletal muscle deficient for TK2 using cDNA microarrays. Results We have analysed the whole transcriptome of skeletal muscle from patients with TK2 mutations and compared it to normal muscle and to muscle from patients with other mitochondrial myopathies. We have identified a set of over 700 genes which are differentially expressed in TK2 deficient muscle. Bioinformatics analysis reveals important changes in muscle metabolism, in particular, in glucose and glycogen utilisation, and activation of the starvation response which affects aminoacid and lipid metabolism. We have identified those transcriptional regulators which are likely to be responsible for the observed changes in gene expression. Conclusion Our data point towards the tumor suppressor p53 as the regulator at the centre of a network of genes which are responsible for a coordinated response to TK2 mutations which involves inflammation, activation of muscle cell death by apoptosis and induction of growth and differentiation factor 15 (GDF-15) in muscle and serum. We propose that GDF-15 may represent a potential novel biomarker for mitochondrial dysfunction although further studies are required