Room-Temperature Pressure Synthesis of Layered Black Phosphorus–Graphene Composite for Sodium-Ion Battery Anodes

Sodium-ion batteries offer an attractive option for grid-level energy storage due to the high natural abundance of sodium and low material cost of sodium compounds. Phosphorus (P) is a promising anode material for sodium-ion batteries, with a theoretical capacity of 2596 mAh/g. The red phosphorus (RP) form has worse electronic conductivity and lower initial Coulombic efficiency than black phosphorus (BP), but high material cost and limited production capacity have slowed the development of BP anodes. To address these challenges, we have developed a simple and scalable method to synthesize layered BP/graphene composite (BP/rGO) by pressurization at room temperature. A carbon-black-free and binder-free BP/rGO anode prepared with this method achieved specific charge capacities of 1460.1, 1401.2, 1377.6, 1339.7, 1277.8, 1123.78, and 720.8 mAh/g in a rate capability test at charge and discharge current densities of 0.1, 0.5, 1, 5, 10, 20, and 40 A/g, respectively. In a cycling performance test, after 500 deep cycles, the capacity of BP/rGO anodes stabilized at 1250 and 640 mAh/g at 1 and 40 A/g, respectively, which marks a significant performance improvement for sodium-ion battery anodes

Western Pacific atmospheric nutrient deposition fluxes, their impact on surface ocean productivity

The atmospheric deposition of both macronutrients and micronutrients plays an important role in driving primary productivity, particularly in the low-latitude ocean. We report aerosol major ion measurements for five ship-based sampling campaigns in the western Pacific from similar to 25 degrees N to 20 degrees S and compare the results with those from Atlantic meridional transects (similar to 50 degrees N to 50 degrees S) with aerosols collected and analyzed in the same laboratory, allowing full incomparability. We discuss sources of the main nutrient species (nitrogen (N), phosphorus (P), and iron (Fe)) in the aerosols and their stoichiometry. Striking north-south gradients are evident over both basins with the Northern Hemisphere more impacted by terrestrial dust sources and anthropogenic emissions and the North Atlantic apparently more impacted than the North Pacific. We estimate the atmospheric supply rates of these nutrients and the potential impact of the atmospheric deposition on the tropical western Pacific. Our results suggest that the atmospheric deposition is P deficient relative to the needs of the resident phytoplankton. These findings suggest that atmospheric supply of N, Fe, and P increases primary productivity utilizing some of the residual excess phosphorus (P*) in the surface waters to compensate for aerosol P deficiency. Regional primary productivity is further enhanced via the stimulation of nitrogen fixation fuelled by the residual atmospheric iron and P*. Our stoichiometric calculations reveal that a P* of 0.1 mu mol L-1 can offset the P deficiency in atmospheric supply for many months. This study suggests that atmospheric deposition may sustain similar to 10% of primary production in both the western tropical Pacific

The molecular basis of beta-thalassemia intermedia in southern China: genotypic heterogeneity and phenotypic diversity

<p>Abstract</p> <p>Background</p> <p>The clinical syndrome of thalassemia intermedia (TI) results from the β-globin genotypes in combination with factors to produce fetal haemoglobin (HbF) and/or co-inheritance of α-thalassemia. However, very little is currently known of the molecular basis of Chinese TI patients.</p> <p>Methods</p> <p>We systematically analyzed and characterized β-globin genotypes, α-thalassemia determinants, and known primary genetic modifiers linked to the production of HbF and the aggravation of α/β imbalance in 117 Chinese TI patients. Genotype-phenotype correlations were analyzed based on retrospective clinical observations.</p> <p>Results</p> <p>A total of 117 TI patients were divided into two major groups, namely heterozygous β-thalassemia (n = 20) in which 14 were characterized as having a mild TI with the Hb levels of 68-95 g/L except for five co-inherited ααα^anti-3.7triplication and one carried a dominant mutation; and β-thalassemia homozygotes or compound heterozygotes for β-thalassemia and other β-globin defects in which the β⁺-thalassemia mutation was the most common (49/97), hemoglobin E (HbE) variants was second (27/97), and deletional hereditary persistence of fetal hemoglobin (HPFH) or δβ-thalassemia was third (11/97). Two novel mutations, Term CD+32(A→C) and Cap+39(C→T), have been detected.</p> <p>Conclusions</p> <p>Chinese TI patients showed considerable heterogeneity, both phenotypically and genotypically. The clinical outcomes of our TI patients were mostly explained by the genotypes linked to the β- and α-globin gene cluster. However, for a group of 14 patients (13 β⁰/β^Nand 1 β⁺/β^N) with known heterozygous mutations of β-thalassemia and three with homozygous β-thalassemia (β⁰/β⁰), the existence of other causative genetic determinants is remaining to be molecularly defined.</p

TRAPPC4-ERK2 Interaction Activates ERK1/2, Modulates Its Nuclear Localization and Regulates Proliferation and Apoptosis of Colorectal Cancer Cells

The trafficking protein particle complex 4 (TRAPPC4) is implicated in vesicle-mediated transport, but its association with disease has rarely been reported. We explored its potential interaction with ERK2, part of the ERK1/2 complex in the Extracellular Signal-regulated Kinase/ Mitogen-activated Protein Kinase (ERK-MAPK) pathway, by a yeast two-hybrid screen and confirmed by co-immunoprecipitation (Co-IP) and glutathione S-transferase (GST) pull-down. Further investigation found that when TRAPPC4 was depleted, activated ERK1/2 specifically decreased in the nucleus, which was accompanied with cell growth suppression and apoptosis in colorectal cancer (CRC) cells. Overexpression of TRAPPC4 promoted cell viability and caused activated ERK1/2 to increase overall, but especially in the nucleus. TRAPPC4 was expressed more highly in the nucleus of CRC cells than in normal colonic epithelium or adenoma which corresponded with nuclear staining of pERK1/2. We demonstrate here that TRAPPC4 may regulate cell proliferation and apoptosis in CRC by interaction with ERK2 and subsequently phosphorylating ERK1/2 as well as modulating the subcellular location of pERK1/2 to activate the relevant signaling pathway

Down-Regulation of GEP100 Causes Increase in E-Cadherin Levels and Inhibits Pancreatic Cancer Cell Invasion

AIMS: Invasion and metastasis are major reasons for pancreatic cancer death and identifying signaling molecules that are specifically used in tumor invasion is of great significance. The purpose of this study was to elucidate the role of GEP100 in pancreatic cancer cell invasion and metastasis and the corresponding molecular mechanism. METHODS: Stable cell lines with GEP100 knocked-down were established by transfecting GEP100 shRNA vector into PaTu8988 cells and selected by puromycin. qRT-PCR and Western blot were performed to detect gene expression. Matrigel-invasion assay was used to detect cancer cell invasion in vitro. Liver metastasis in vivo was determined by splenic injection of indicated cell lines followed by spleen resection. Immunofluorescence study was used to detect the intracellular localization of E-cadherin. RESULTS: We found that the expression level of GEP100 protein was closely related to the invasive ability of a panel of 6 different human pancreatic cancer cell lines. Down-regulation of GEP100 in PaTu8988 cells significantly decreased invasive activity by Matrigel invasion assay, without affecting migration, invasion and viability. The inhibited invasive activity was rescued by over-expression of GEP100 cDNA. In vivo study showed that liver metastasis was significantly decreased in the PaTu8988 cells with GEP100 stably knocked-down. In addition, an epithelial-like morphological change, mimicking a mesenchymal to epithelial transition (MET) was induced by GEP100 down-regulation. The expression of E-cadherin protein was increased 2-3 folds accompanied by its redistribution to the cell-cell contacts, while no obvious changes were observed for E-cadherin mRNA. Unexpectedly, the mRNA of Slug was increased by GEP100 knock-down. CONCLUSION: These findings provided important evidence that GEP100 plays a significant role in pancreatic cancer invasion through regulating the expression of E-cadherin and the process of MET, indicating the possibility of it becoming a potential therapeutic target against pancreatic cancer

Numerical magnitude affects temporal memories but not time encoding

Previous research has suggested that the perception of time is influenced by concurrent magnitude information (e.g., numerical magnitude in digits, spatial distance), but the locus of the effect is unclear, with some findings suggesting that concurrent magnitudes such as space affect temporal memories and others suggesting that numerical magnitudes in digits affect the clock speed during time encoding. The current paper reports 6 experiments in which participants perceived a stimulus duration and then reproduced it. We showed that though a digit of a large magnitude (e.g., 9), relative to a digit of a small magnitude (e.g., 2), led to a longer reproduced duration when the digits were presented during the perception of the stimulus duration, such a magnitude effect disappeared when the digits were presented during the reproduction of the stimulus duration. These findings disconfirm the account that large numerical magnitudes accelerate the speed of an internal clock during time encoding, as such an account incorrectly predicts that a large numerical magnitude should lead to a shorter reproduced duration when presented during reproduction. Instead, the findings suggest that numerical magnitudes, like other magnitudes such as space, affect temporal memories when numerical magnitudes and temporal durations are concurrently held in memory. Under this account, concurrent numerical magnitudes have the chance to influence the memory of the perceived duration when they are presented during perception but not when they are presented at the reproduction stage

Systematic Single-Cell Analysis of Pichia pastoris Reveals Secretory Capacity Limits Productivity

Biopharmaceuticals represent the fastest growing sector of the global pharmaceutical industry. Cost-efficient production of these biologic drugs requires a robust host organism for generating high titers of protein during fermentation. Understanding key cellular processes that limit protein production and secretion is, therefore, essential for rational strain engineering. Here, with single-cell resolution, we systematically analysed the productivity of a series of Pichia pastoris strains that produce different proteins both constitutively and inducibly. We characterized each strain by qPCR, RT-qPCR, microengraving, and imaging cytometry. We then developed a simple mathematical model describing the flux of folded protein through the ER. This combination of single-cell measurements and computational modelling shows that protein trafficking through the secretory machinery is often the rate-limiting step in single-cell production, and strategies to enhance the overall capacity of protein secretion within hosts for the production of heterologous proteins may improve productivity