Electro-extractive fermentation for efficient biohydrogen production

Electrodialysis, an electrochemical membrane technique, was found to prolong and enhance the production of biohydrogen and purified organic acids via the anaerobic fermentation of glucose by Escherichia coli. Through the design of a model electrodialysis medium using cationic buffer, pH was precisely controlled electrokinetically, i.e. by the regulated extraction of acidic products with coulombic efficiencies of organic acid recovery in the range 50–70% maintained over continuous 30-day experiments. Contrary to\ud previous reports, E. coli produced H2 after aerobic growth in minimal medium without inducers and with a mixture of organic acids dominated by butyrate. The selective separation of organic acids from fermentation provides a potential nitrogen-free carbon source for further biohydrogen production in a parallel photofermentation. A parallel study incorporated this fermentation system into an integrated biohydrogen refinery (IBR) for the conversion of organic waste to hydrogen and energy

The contributions of molecular vibrations and higher triplet levels to the intersystem crossing mechanism in metal-free organic emitters.

Intense, simultaneous, room temperature phosphorescence (RTP) and thermally activated delayed fluorescence (TADF) is observed in a series of donor-acceptor-donor (D–A–D) molecules. This dual-luminescence is stronger in the “angular” isomers, compared to their “linear” regioisomers, which is consistent with an enhanced intersystem crossing (ISC) in the former. Herein, we demonstrate that the small energy gap between the triplet levels, T1-Tn, below the lowest singlet state, S1, in the “angular” regioisomers, enhances the coupling between S1 and T1 states and favors ISC and reverse ISC (rISC). This is consistent with a spin-vibronic mechanism. In the absence of this “triplet ladder”, due to the larger energy difference between T1 and Tn in the “linear” regioisomers, the ISC and rISC are not efficient. Remarkably the enhancement on the ISC rate in the “angular” regioisomers is accompanied by an increase on the rate of internal conversion (IC). These results highlight the contributions of higher triplet excited states and molecular vibronic coupling to harvest triplet states in organic compounds, and casts the TADF and RTP mechanisms into a common conceptual framework

Mapping Time-course Mitochondrial Adaptations in the Kidney in Experimental Diabetes

Abstract Oxidative phosphorylation drives ATP production by mitochondria, which are dynamic organelles, constantly fusing and dividing to maintain kidney homeostasis. In diabetic kidney disease, mitochondria appear dysfunctional, but the temporal development of diabetes-induced adaptations in mitochondrial structure and bioenergetics, have not been previously documented. Here, we map the changes in mitochondrial dynamics and function in rat kidney mitochondria at 4, 8, 16 and 32 weeks of diabetes. Our data reveal that changes in mitochondrial bioenergetics and dynamics precede the development of albuminuria and renal histological changes. Specifically, in early diabetes (4 weeks) a decrease in ATP content and mitochondrial fragmentation within proximal tubule epithelial cells of diabetic kidneys were clearly apparent, but no change urinary albumin excretion or glomerular morphology were evident at this time. By 8 weeks of diabetes, there was increased capacity for mitochondrial permeability transition (mPT) by pore opening, which persisted over time and correlated with mitochondrial hydrogen peroxide generation and glomerular damage. Late in diabetes, by week 16, tubular damage was evident with increased urinary Kidney injury molecule (Kim)-1 excretion, where an increase in Complex I-linked oxygen consumption rate, in the context of a decrease in kidney ATP, indicated mitochondrial uncoupling. Taken together, these data show that changes in mitochondrial bioenergetics and dynamics may precede the development of the renal lesion in diabetes, and this supports the hypothesis that mitochondrial dysfunction is a primary cause of diabetic kidney disease. Summary statement We identified that dysfunction of cellular power stations, mitochondria, may precede the development of kidney disease in diabetes. This suggests that mitochondrial dysfunction is a primary cause of diabetic nephropathy, which could be targeted to improve the burden of this disease. Short title: Mitochondrial adaptations in diabetic nephropath

Mapping time-course mitochondrial adaptations in the kidney in experimental diabetes

Abstract Oxidative phosphorylation (OXPHOS) drives ATP production by mitochondria, which are dynamic organelles, constantly fusing and dividing to maintain kidney homoeostasis. In diabetic kidney disease (DKD), mitochondria appear dysfunctional, but the temporal development of diabetes-induced adaptations in mitochondrial structure and bioenergetics have not been previously documented. In the present study, we map the changes in mitochondrial dynamics and function in rat kidney mitochondria at 4, 8, 16 and 32 weeks of diabetes. Our data reveal that changes in mitochondrial bioenergetics and dynamics precede the development of albuminuria and renal histological changes. Specifically, in early diabetes (4 weeks), a decrease in ATP content and mitochondrial fragmentation within proximal tubule epithelial cells (PTECs) of diabetic kidneys were clearly apparent, but no changes in urinary albumin excretion or glomerular morphology were evident at this time. By 8 weeks of diabetes, there was increased capacity for mitochondrial permeability transition (mPT) by pore opening, which persisted over time and correlated with mitochondrial hydrogen peroxide (H 2 O 2 ) generation and glomerular damage. Late in diabetes, by week 16, tubular damage was evident with increased urinary kidney injury molecule-1 (KIM-1) excretion, where an increase in the Complex I-linked oxygen consumption rate (OCR), in the context of a decrease in kidney ATP , indicated mitochondrial uncoupling. Taken together, these data show that changes in mitochondrial bioenergetics and dynamics may precede the development of the renal lesion in diabetes, and this supports the hypothesis that mitochondrial dysfunction is a primary cause of DKD

Surface Deposition and Phase Behavior of Oppositely Charged Polyion–Surfactant Ion Complexes. Delivery of Silicone Oil Emulsions to Hydrophobic and Hydrophilic Surfaces

The adsorption from mixed polyelectrolyte-surfactant solutions at hydrophobized silica surfaces was investigated by in situ null-ellipsometry, and compared to similar measurements for hydrophilic silica surfaces. Three synthetic cationic copolymers of varying hydrophobicity and one cationic hydroxyethyl cellulose were compared in mixtures with the anionic surfactant sodium dodecylsulfate (SDS) in the absence or presence of a dilute silicone oil emulsion. The adsorption behavior was mapped while stepwise increasing the concentration of SDS to a polyelectrolyte solution of constant concentration. The effect on the deposition of dilution of the bulk solution in contact with the surface was also investigated by gradual replacement of the bulk solution with 1 mM aqueous NaCl. An adsorbed layer remained after complete exchange of the polyelectrolyte/surfactant solution for aqueous NaCl. In most cases, there was a codeposition of silicone oil droplets, if such droplets were present in the formulation before dilution. The overall features of the deposition were similar at hydrophobic and hydrophilic surfaces, but there were also notable differences. SDS molecules adsorbed selectively at the hydrophobized silica surface, but not at the hydrophilic silica, which influenced the coadsorption of the cationic polymers. The largest amount of deposited material after dilution was found for hydrophilic silica and for the least-hydrophobic cationic polymers. For the least-hydrophobic polyions, no significant codeposition of silicone oil was detected at hydrophobized silica after dilution if the initial SDS concentration was high

CXCR7 Protein Expression in Human Adult Brain and Differentiated Neurons

Background: CXCR7 and CXCR4 are receptors for the chemokine CXCL12, which is involved in essential functions of the immune and nervous systems. Although CXCR7 transcripts are widely expressed throughout the central nervous system, little is known about its protein distribution and function in the adult brain. To evaluate its potential involvement in CXCL12/CXCR4 signaling in differentiated neurons, we studied CXCR7 protein expression in human brain and cultured neurons. Methodology/Principal Findings: Immunohistochemistry and RT-PCR analyses of cortex and hippocampus from control and HIV-positive subjects provided the first evidence of CXCR7 protein expression in human adult neurons, under normal and pathological conditions. Furthermore, confocal microscopy and binding assays in cultured neurons show that CXCR7 protein is mainly located into cytoplasm, while little to no protein expression is found on neuronal plasma membrane. Interestingly, specific CXCR7 ligands that inhibit CXCL12 binding to CXCR7 do not alter CXCR4-activated survival signaling (pERK/pAkt) in rat cortical neurons. Neuronal CXCR7 co-localizes to some extent with the endoplasmic reticulum marker ERp29, but not with early/late endosome markers. Additionally, large areas of overlap are detected in the intracellular pattern of CXCR7 and CXCR4 expression. Conclusions/Significance: Overall, these results implicate CXCR4 as the main CXCL12 signaling receptor on the surface o

An Expanded Evaluation of Protein Function Prediction Methods Shows an Improvement In Accuracy

Background: A major bottleneck in our understanding of the molecular underpinnings of life is the assignment of function to proteins. While molecular experiments provide the most reliable annotation of proteins, their relatively low throughput and restricted purview have led to an increasing role for computational function prediction. However, assessing methods for protein function prediction and tracking progress in the field remain challenging. Results: We conducted the second critical assessment of functional annotation (CAFA), a timed challenge to assess computational methods that automatically assign protein function. We evaluated 126 methods from 56 research groups for their ability to predict biological functions using Gene Ontology and gene-disease associations using Human Phenotype Ontology on a set of 3681 proteins from 18 species. CAFA2 featured expanded analysis compared with CAFA1, with regards to data set size, variety, and assessment metrics. To review progress in the field, the analysis compared the best methods from CAFA1 to those of CAFA2. Conclusions: The top-performing methods in CAFA2 outperformed those from CAFA1. This increased accuracy can be attributed to a combination of the growing number of experimental annotations and improved methods for function prediction. The assessment also revealed that the definition of top-performing algorithms is ontology specific, that different performance metrics can be used to probe the nature of accurate predictions, and the relative diversity of predictions in the biological process and human phenotype ontologies. While there was methodological improvement between CAFA1 and CAFA2, the interpretation of results and usefulness of individual methods remain context-dependent

An expanded evaluation of protein function prediction methods shows an improvement in accuracy

Background: A major bottleneck in our understanding of the molecular underpinnings of life is the assignment of function to proteins. While molecular experiments provide the most reliable annotation of proteins, their relatively low throughput and restricted purview have led to an increasing role for computational function prediction. However, assessing methods for protein function prediction and tracking progress in the field remain challenging. Results: We conducted the second critical assessment of functional annotation (CAFA), a timed challenge to assess computational methods that automatically assign protein function. We evaluated 126 methods from 56 research groups for their ability to predict biological functions using Gene Ontology and gene-disease associations using Human Phenotype Ontology on a set of 3681 proteins from 18 species. CAFA2 featured expanded analysis compared with CAFA1, with regards to data set size, variety, and assessment metrics. To review progress in the field, the analysis compared the best methods from CAFA1 to those of CAFA2. Conclusions: The top-performing methods in CAFA2 outperformed those from CAFA1. This increased accuracy can be attributed to a combination of the growing number of experimental annotations and improved methods for function prediction. The assessment also revealed that the definition of top-performing algorithms is ontology specific, that different performance metrics can be used to probe the nature of accurate predictions, and the relative diversity of predictions in the biological process and human phenotype ontologies. While there was methodological improvement between CAFA1 and CAFA2, the interpretation of results and usefulness of individual methods remain context-dependent. Keywords: Protein function prediction, Disease gene prioritizationpublishedVersio