High‐Performance Semitransparent Tandem Solar Cell of 8.02% Conversion Efficiency with Solution‐Processed Graphene Mesh and Laminated Ag Nanowire Top Electrodes

A high‐performance semitransparent tandem solar cell that uses solution‐processed graphene mesh and laminated Ag NW as a transparent anode and cathode, respectively, is demonstrated. The laminated top electrode can be deposited without causing any damage to the underneath organic solar cells. Power conversion efficiencies of 8.02% and 6.47% are obtained when the light is projected from the solution‐processed graphene mesh and laminated AgNW, respectively. The performance of the tandem cell is found to be comparable to a tandem solar cell fabricated using commercially available indium tin oxide. These findings offer a high‐performance device and open a new pathway in searching for a potential replacement to the frequently used transparent conducting electrodes.     

Inhibition of nitric oxide production in LPS-stimulated RAW 264.7 cells by stem bark of Ulmus pumila L.

This study was designed to isolate and identify a potent inhibitory compound against nitric oxide (NO) production from the stem bark of Ulmus pumila L. Ethyl acetate fraction of hot water extract registered a higher level of total phenolics (756.93 mg GAE/g) and also showed strong DPPH (IC₅₀ at 5.6 μg/mL) and ABTS (TEAC value 0.9703) radical scavenging activities than other fractions. Crude extract and its fractions significantly decreased nitrite accumulation in LPS-stimulated RAW 264.7 cells indicating that they potentially inhibited the NO production in a concentration dependent manner. Based on higher inhibitory activity, the ethyl acetate fraction was subjected to Sephadex LH-20 column chromatography and yielded seven fractions and all these fractions registered appreciable levels of inhibitory activity on NO production. The most effective fraction F1 was further purified and subjected to ¹H, ¹³C-NMR and mass spectrometry analysis and the compound was identified as icariside E₄. The results suggest that the U. pumila extract and the isolated compound icariside E₄ effectively inhibited the NO production and may be useful in preventing inflammatory diseases mediated by excessive production of NO.     

On tradeoff between the two compromise factors in assigning tasks on a cluster computing

This paper deals with the static task-assignment problem in a cluster computing system as follows: Given a task composed of a number of interacting modules, assign the task modules to the processors in the system to minimize the communication cost while balancing the processors’ loads. Because these two optimization criteria conflict with each other, a compromise needs to be made between them according to the given task type. This paper proposes a new cost function to evaluate the static task assignments and a heuristic algorithm for solving the transformed problem explicitly describing the tradeoff between the two goals. The simulation results showed that this approach outperforms the existing representative approach for a range of tasks and processing systems.     

Dynamic kinetic resolutions and asymmetric transformations by enzymes coupled with metal catalysis

The combination of enzyme and metal catalysis is described as a useful method for the synthesis of optically active compounds. A key feature of this new methodology is the use of metal catalysts for the in situ racemization of enzymatically unreactive enantiomers in the enzymatic resolution of racemic substrates. So far, two combinations - lipase-ruthenium and lipase-palladium - have been developed for the efficient dynamic kinetic resolution of alcohols and amines. The use of these combinations has also been extended to catalysis of the asymmetric transformation of ketones, their enol acetates, and ketoximes. In most cases, enzyme-metal combination catalysis has provided good yields and high optical purities.     

Dynamic changes in blood immune cell composition and function in Holstein and Jersey steers in response to heat stress

Heat stress has detrimental effects on livestock via diverse immune and physiological changes; heat-stressed animals are rendered susceptible to diverse diseases. However, there is relatively little information available regarding the altered immune responses of domestic animals in heat stress environments, particularly in cattle steers. This study aimed to determine the changes in the immune responses of Holstein and Jersey steers under heat stress. We assessed blood immune cells and their functions in the steers of two breeds under normal and heat stress conditions and found that immune cell proportions and functions were altered in response to different environmental conditions. Heat stress notably reduced the proportions of CD21⁺MHCII⁺ B cell populations in both breeds. We also observed breed-specific differences. Under heat stress, in Holstein steers, the expression of myeloperoxidase was reduced in the polymorphonuclear cells, whereas heat stress reduced the WC1⁺ γδ T cell populations in Jersey steers. Breed-specific changes were also detected based on gene expression. In response to heat stress, the expression of IL-10 and IL-17A increased in Holstein steers alone, whereas that of IL-6 increased in Jersey steers. Moreover, the mRNA expression pattern of heat shock protein genes such as Hsp70 and Hsp90 was significantly increased in only Holstein steers. Collectively, these results indicate that altered blood immunological profiles may provide a potential explanation for the enhanced susceptibility of heat-stressed steers to disease. The findings of this study provide important information that will contribute to developing new strategies to alleviate the detrimental effects of heat stress on steers.     

A Robust Test for Two‐Stage Design in Genome‐Wide Association Studies

Summary A two‐stage design is cost‐effective for genome‐wide association studies (GWAS) testing hundreds of thousands of single nucleotide polymorphisms (SNPs). In this design, each SNP is genotyped in stage 1 using a fraction of case–control samples. Top‐ranked SNPs are selected and genotyped in stage 2 using additional samples. A joint analysis, combining statistics from both stages, is applied in the second stage. Follow‐up studies can be regarded as a two‐stage design. Once some potential SNPs are identified, independent samples are further genotyped and analyzed separately or jointly with previous data to confirm the findings. When the underlying genetic model is known, an asymptotically optimal trend test (TT) can be used at each analysis. In practice, however, genetic models for SNPs with true associations are usually unknown. In this case, the existing methods for analysis of the two‐stage design and follow‐up studies are not robust across different genetic models. We propose a simple robust procedure with genetic model selection to the two‐stage GWAS. Our results show that, if the optimal TT has about 80% power when the genetic model is known, then the existing methods for analysis of the two‐stage design have minimum powers about 20% across the four common genetic models (when the true model is unknown), while our robust procedure has minimum powers about 70% across the same genetic models. The results can be also applied to follow‐up and replication studies with a joint analysis.     

Abrogating Munc18-1-SNARE Complex Interaction Has Limited Impact on Exocytosis in PC12 Cells

Neuronal communication relies on the fusion of neurotransmitter-containing vesicles with the plasma membrane. The soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE) proteins initiate membrane fusion through the formation of the SNARE complex, a process tightly regulated by Sec1/Munc18-1 (SM) proteins. The emerging trend is that SM proteins promote SNARE-mediated membrane fusion by binding to a Syntaxin N-terminal motif. Here we report that mutations in the hydrophobic pocket of Munc18-1 (F115E and E132A), predicted to disrupt the N-terminal Sx1a interaction have a modest effect on binding to Sx1a in its free state, but abolish binding to the SNARE complex. Overexpression of the Munc18-1 mutant in PC12 cells lacking Munc18-1 rescues both neuroexocytosis and the plasma membrane localization of Syntaxin. However, total internal reflection fluorescence microscopy analysis reveals that expression of a Munc18-1 double mutant reduces the rate of vesicle fusion, an effect only detectable at the onset of stimulation. The Munc18-1 hydrophobic pocket is therefore critical for SNARE complex binding. However, mutations abrogating this interaction have a limited impact on Ca²⁺-dependent exocytosis in PC12 cells.Following stimulation of neurons, a number of well orchestrated protein/protein (1) and protein/lipid (2) interactions underpin the fusion of secretory vesicles with the presynaptic plasma membrane. In this sequence of interactions, vesicles approach the plasma membrane (tethering and docking), undergo priming and, upon Ca²⁺ influx, fuse with the plasma membrane, thereby releasing neurotransmitter into the synaptic cleft (1). Vesicular exocytosis relies on the function of soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE)² proteins as demonstrated by the blockade of neuroexocytosis following SNARE protein cleavage by clostridial neurotoxins (3). One of the key players in SNARE regulation is the cytosolic regulatory protein, Munc18-1 (Munc18a, nsec-1) (4–7). Although the function of SNARE proteins in mediating exocytosis is well established (2, 8), the precise role of Munc18-1 in exocytosis is still a subject of heated debate (6, 7, 9, 10).Munc18-1 belongs to the Sec1/Munc18 (SM) family of proteins that are involved in mediating membrane trafficking events (11–13). Mutations in these proteins have recently been associated with infantile epileptic encephalopathy (14). Although the function of Munc18-1 and its interaction with SNAREs have been studied for over 10 years, the molecular mechanism of Munc18-1 regulation of membrane fusion is still not clear. Munc18-1 was originally characterized as a negative regulator of exocytosis as it binds to the target membrane SNARE, Syntaxin 1a (Sx1a) (5) in a conformation that sequesters the Sx1a SNARE helix and inhibits SNARE complex formation (7, 15). Other SM proteins have been shown to bind to their cognate syntaxins via an N-terminal motif (16–19), allowing interactions that are associated with a positive role for SM proteins in SNARE-mediated membrane fusion (20). Despite biochemical evidence supporting a negative regulatory role for Munc18-1, there is strong genetic evidence for a critical positive role for Munc18-1 in exocytosis, as demonstrated by a Munc18-1 knock-out mouse that exhibits a complete blockage of neurotransmission (21).Recently, a short N-terminal peptide from Sx1a was also shown to bind to Munc18-1 via a novel interaction that promotes SNARE-mediated fusion of liposomes in vitro (6). Moreover, the N-terminal truncation of Sx1a only affects the binding of the open conformation of Sx1a to Munc18-1 occurring near the plasma membrane (10). Oddly, the Munc18-1-Sx1a interaction in solution predominantly involves the closed conformation (10), which raises the question of the relative contribution of the Sx1a N terminus to the overall Munc18-1-Sx1a interaction.To address the functional significance of the N-terminal interaction, we took a reverse strategy and investigated the molecular nature of the binding of Munc18-1 to the Sx1a N terminus and to the SNARE complex. We mutated Munc18-1:Phe¹¹⁵ and Glu¹³², which are located in an evolutionarily conserved surface pocket of Munc18-1 (17, 22). We found that whereas these mutations have only a mild effect on the binding of Munc18-1 to Sx1a in its free state, they completely abrogate Munc18-1 binding to the SNARE complex. Expression of these mutants in PC12 cells lacking Munc18-1 rescues exocytosis to a similar extent to that obtained with Munc18-1-WT. Total internal reflection fluorescence (TIRF) microscopy of vesicle docking at the cell surface reveals that these mutations support exocytosis. However, the rate of vesicle fusion is markedly reduced at the onset of stimulation, arguing for a role of Munc18-1 in regulating the dynamics of SNARE-mediated vesicle fusion during exocytosis.