Recently, the first commercial dye solar cell (DSC) products based on the mesoscopic principle were successfully launched. Introduction to the market has been accompanied by a strong increase in patent applications in the field during the last four years, which is a good indication of further commercialization activity. Materials and cell concepts have been developed to such extent that easy uptake by industrial manufacturers is possible. The critical phase for broad market acceptance has therefore been reached, which implies focusing on standardization-related research topics. In parallel the number of scientific publications on DSC is growing further (>3500 since 2012), and the range of new or renewed fundamental topics is broadening. A recent example is the introduction of the perovskite mesoscopic cell, for which an efficiency of 14.1% has been certified. Thus, a growing divergence between market introduction and research could be the consequence. Herein, an attempt is made to show that such an unwanted divergence can be prevented, for example, by developing suitable reference-type cell and module concepts as well as manufacturing routes. An in situ cell manufacturing concept that can be applied to mesoscopic-based solar cells in a broader sense is proposed. As a guideline for future module concepts, recent results for large-area, glass-frit-sealed DSC modules from efficiency studies (6.6% active-area efficiency) and outdoor analysis are discussed. Electroluminescence measurements are introduced as a quality tool. Another important point that is addressed is sustainability, which affects both market introduction and the direction of fundamental research.

Although microdisk electrode arrays (MEAs) have been extensively used for more than three decades, the existing rules do not provide an unambiguous formula for the calculation of the minimum interelectrode distance (d) necessary for steady-state current response. With the aim of formulating generally applicable guidelines for design and experiment with MEAs, cyclic voltammograms were simulated for coplanar and shallow recessed microdisk electrode arrays with various interelectrode distances and dimensionless scan rates (V). The dimensionless scan rate (V) is a function of the radius (a) of the individual electrodes in the array, the diffusion coefficient (D) of the analyte, and the potential scan rate (v). The cyclic voltammograms at microdisk electrode arrays are grouped into five categories corresponding to the contributions of linear and radial diffusion to the overall responses. These categories are illustrated in a zone diagram based on the effect of V and d on the shape of cyclic voltammograms. The zone diagram reveals the minimum d and a cluster of linked d and V values that are incident to sigmoidal wave responses. For shallow recessed microdisk electrode arrays, the zones representing hemispherical diffusion are larger than that for coplanar arrays. The minimum d necessary for hemispherical diffusion becomes smaller as recess depth increases. With the zone diagram, one can predict the type of the cyclic voltammograms that can be expected for different microelectrode array geometries and experimental conditions. The fitting between simulation and experimental data validates our conclusions.

p53, a tumor suppressor protein and a transcription factor, is capable of inhibiting the growth of tumor cells by eliciting either cell-cycle arrest or apoptosis through a cascade of events. p53 binds sites within the promoters of several genes that conform to a sequence commonly defined as the consensus site. In more than 50% of cancer cases, the p53 gene has been found to be mutated and the p53 protein loses its ability to bind the consensus DNA. In this work, double-stranded (ds-) oligonucleotides (ODNs) containing the consensus site are immobilized onto gold electrodes to capture wild-type p53. The cysteine residues on the exterior of the p53 molecule were derivatized for the attachment of gold nanoparticle/streptavidin conjugates capped with multiple ferrocene (Fc) groups. Well-defined voltammetric peaks of high signal intensity were obtained, and p53 concentration as low as 2.2 pM was measured. The peak heights were found to be dependent on the surface density of the consensus ds-ODN, the sequence of the immobilized ODNs, and the p53 concentration. With base pair(s) in the full consensus binding sequence altered, the level of p53 binding was found to decrease sharply, and no p53 binding occurred at electrodes covered with nonconsensus ds-ODNs. The amenability of this method to the analyses of p53 from normal and cancer cell lysates was also demonstrated. Owing to the p53 mutation in the cancer cells, the concentration of the wild-type p53 was found to decrease significantly (by about 50-182 times). The sensitivity and amenability for real sample analysis of the method compared well with enzyme-linked immunosorbant assay (ELISA), and complements ELISA in that wild-type p53, instead of total p53 (wild-type and mutant p53) concentration, is measured. The method described herein is simple and selective and does not require the use of p53 antibodies.

OBJECTIVE: To establish the role of the measurement of beta-hydroxybutyrate (beta-OHB) in distinguishing simple hyperglycaemia from ketosis, and as an indicator of adequate resolution of ketoacidosis, using an electrochemical blood ketone meter. The aim of the study is to assess the accuracy and precision of the meter and to develop clinical guidelines for the use of the ketone meter at home and in hospital.
METHODS: Twenty patients with poor glycaemic control (mean HbA1c 10.2%) were recruited from the diabetes clinic and 14 patients admitted with diabetic ketoacidosis (DKA) were recruited from two Accident and Emergency Departments. The blood obtained at each routine fingerprick test for glucose measurement was tested for beta-OHB using the ketone meter. Plasma beta-OHB concentrations were also measured on admission using a laboratory enzymatic method.
RESULTS: Paired glucose and beta-OHB meter readings (n = 1099) in clinic patients demonstrated that, in the absence of intercurrent illness, beta-OHB levels did not exceed 1 mmol/l, irrespective of glucose readings. In the 14 ketoacidotic patients, the mean plasma beta-OHB concentration, measured in the laboratory, on admission was 7.4 mmol/l (range 3.9-12.3 mmol/l). The median half-life of beta-OHB was 1.64 h (1st IQR 2.27 h, 3rd IQR 1.34 h). The median time taken, from the initiation of treatment, for beta-OHB concentrations to fall to below 1 mmol/l was 8.46 h (range 5-58.33 h).
CONCLUSIONS: Near patient blood ketone testing is a useful adjunct to blood glucose monitoring in distinguishing between ketosis and simple hyperglycaemia. The data suggest that beta-OHB levels > or = 1 mmol/l require further action and levels > 3 mmol/l necessitate medical review. In addition, the rate of fall of beta-OHB in DKA can be used as an indicator of the adequacy of treatment.

A synthetic gene encoding a \'consensus\' calmodulin (synCaM) was able to substitute for the Saccharomyces cerevisiae calmodulin gene (CMDI), even though synCaM is only 60% identical in primary amino acid sequence to yeast Cmd1. Twelve different synCaM mutants were also expressed in yeast. Seven of the 12 mutant synCaMs supported germination and growth of Cmd1-deficient spores. Five of the 12 mutant synCaMs were incapable of supporting germination of Cmd1-deficient spores and, of these, four were also incapable of supporting vegetative growth of Cmd1-deficient haploid cells. The five nonfunctional synCaM mutants were expressed at levels equivalent to, or higher than, the seven synCaM mutants that were able to substitute for Cmd1; thus, the inability to function was not simply due to inadequate expression or rapid degradation. All nonfunctional synCaM mutants shared a single charge reversal mutation in the central helix (E84K), which was found to be sufficient to confer the lethal phenotype. The ability of another mutant synCaM (S101F) to support growth of Cmd1-deficient cells was dependent on cell ploidy. Another mutant (K115Y) supported spore germination and vegetative growth, but not meiosis and sporulation. The terminal phenotype of cells lacking a functional calmodulin included a dramatic accumulation of polymerized microtubules.

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A model structure of Naja naja kaouthia cobra venom phospholipase A2 has been constructed by utilizing molecular modeling techniques. Analysis of the model and available biochemical data reveal the presence in this enzyme of a putative recognition site for choline derivatives in loop 57-70 made up of residues Trp-61, Tyr-63, Phe-64, and Lys-65, together with Glu-55. The magnitude and shape of the electrostatic potential in this binding site are approximately 80% similar to that in the McPC603 antibody binding site specifically recognizing phosphocholine. Docking studies indicate that the recognition site we now describe and the phosphocholine head of an n-alkylphosphocholine molecule are complementary both sterically and electronically, mainly due to anion-cation and cation-pi interactions. Moreover, binding enthalpies of n-heptylphosphocholine to this site are found to parallel the catalytic rate of pancreatic, mutant pancreatic, and cobra venom phospholipase A2 enzymes acting on dihexanoylphosphatidylcholine micelles, suggesting that it behaves as an activator site. This proposal is in keeping with the \"dual phospholipid\" model put forward to account for the phenomenon of interfacial activation. This novel site is also shown to be able to discriminate choline derivatives from ethanolamine derivatives, in accord with experimental data. On the basis of the results obtained, two functions are assigned to this putative activator site: (i) desolvation of the lipid-enzyme interface, particularly the surroundings of tyrosine at position 69 (Tyr-63), and (ii) opening of the entrance to the active site by means of a conformational change of Tyr-63 whose chi 2 angle rotates nearly 60 degrees.