Effect of storage conditions on long-term stability of Ag nanoparticles formed via green synthesis

Spherical Ag nanoparticles (AgNPs) with a diameter of 20 nm or smaller were biologically synthesized using algae Parachlorella kessleri. The effect of storage conditions on the long-term stability of AgNPs was investigated. UV/Vis spectrophotometry, transmission electron microscopy, and dynamic light scattering measurements revealed that the long-term stability of AgNPs was influenced by light and temperature conditions. The most significant loss of stability was observed for the AgNPs stored in daylight at room temperature. The AgNPs stored under these conditions began to lose their stability after approximately 30 d; after 100 d, a substantial amount of agglomerated particles settled to the bottom of the Erlenmeyer flask. The AgNPs stored in the dark at room temperature exhibited better long-term stability. Weak particle agglomeration began at approximately the 100th day. The AgNPs stored in the dark at about 5℃ exhibited the best long-term stability; the AgNPs stored under such conditions remained spherical, with a narrow size distribution, and stable (no agglomeration) even after 6 months. Zeta-potential measurements confirmed better dispersity and stability of AgNPs stored under these conditions.     

Electron Spin Resonance Study of Fuel Cell Polymer Membrane Degradation

1 Introduction The long termstability of the membraneis ani mportant factor li mitingthe fuel cell lifeti me .During ex-tended use the membrane degrades , probably via reaction with hydroxyl and superoxide radicals which areregular intermediates of the oxygenreduction at the cathode .Only extremely stable membranes can withstandthe aggressive chemical and physical environment in an operating fuel cell . Within a given set of operatingconditions,intrinsic chemical and mechanical properties of t…     

SHARP1 suppresses breast cancer metastasis by promoting degradation of hypoxia-inducible factors

The molecular determinants of malignant cell behaviours in breast cancer remain only partially understood. Here we show that SHARP1 (also known as BHLHE41 or DEC2) is a crucial regulator of the invasive and metastatic phenotype in triple-negative breast cancer (TNBC), one of the most aggressive types of breast cancer. SHARP1 is regulated by the p63 metastasis suppressor and inhibits TNBC aggressiveness through inhibition of hypoxia-inducible factor 1α (HIF-1α) and HIF-2α (HIFs). SHARP1 opposes HIF-dependent TNBC cell migration in vitro, and invasive or metastatic behaviours in vivo. SHARP1 is required, and sufficient, to limit expression of HIF-target genes. In primary TNBC, endogenous SHARP1 levels are inversely correlated with those of HIF targets. Mechanistically, SHARP1 binds to HIFs and promotes HIF proteasomal degradation by serving as the HIF-presenting factor to the proteasome. This process is independent of pVHL (von Hippel-Lindau tumour suppressor), hypoxia and the ubiquitination machinery. SHARP1 therefore determines the intrinsic instability of HIF proteins to act in parallel to, and cooperate with, oxygen levels. This work sheds light on the mechanisms and pathways by which TNBC acquires invasiveness and metastatic propensity.     

Mutations in DMRT3 affect locomotion in horses and spinal circuit function in mice

Locomotion in mammals relies on a central pattern-generating circuitry of spinal interneurons established during development that coordinates limb movement. These networks produce left-right alternation of limbs as well as coordinated activation of flexor and extensor muscles. Here we show that a premature stop codon in the DMRT3 gene has a major effect on the pattern of locomotion in horses. The mutation is permissive for the ability to perform alternate gaits and has a favourable effect on harness racing performance. Examination of wild-type and Dmrt3-null mice demonstrates that Dmrt3 is expressed in the dI6 subdivision of spinal cord neurons, takes part in neuronal specification within this subdivision, and is critical for the normal development of a coordinated locomotor network controlling limb movements. Our discovery positions Dmrt3 in a pivotal role for configuring the spinal circuits controlling stride in vertebrates. The DMRT3 mutation has had a major effect on the diversification of the domestic horse, as the altered gait characteristics of a number of breeds apparently require this mutation.     

Crystal structure of the CorA Mg2+ transporter

The magnesium ion, Mg2+, is essential for myriad biochemical processes and remains the only major biological ion whose transport mechanisms remain unknown. The CorA family of magnesium transporters is the primary Mg2+ uptake system of most prokaryotes and a functional homologue of the eukaryotic mitochondrial magnesium transporter. Here we determine crystal structures of the full-length Thermotoga maritima CorA in an apparent closed state and its isolated cytoplasmic domain at 3.9 A and 1.85 A resolution, respectively. The transporter is a funnel-shaped homopentamer with two transmembrane helices per monomer. The channel is formed by an inner group of five helices and putatively gated by bulky hydrophobic residues. The large cytoplasmic domain forms a funnel whose wide mouth points into the cell and whose walls are formed by five long helices that are extensions of the transmembrane helices. The cytoplasmic neck of the pore is surrounded, on the outside of the funnel, by a ring of highly conserved positively charged residues. Two negatively charged helices in the cytoplasmic domain extend back towards the membrane on the outside of the funnel and abut the ring of positive charge. An apparent Mg2+ ion was bound between monomers at a conserved site in the cytoplasmic domain, suggesting a mechanism to link gating of the pore to the intracellular concentration of Mg2+.     

Interaction of chloramphenicol and 181-1181-1181-1in barbital-anesthetized mice

Résumé L'augmentation de l'anesthésie produite par le barbital chez la souris traitée au ¹-tétrahydrocannabinol ( ¹-THC) à 10 ou 20 mg/kg par voie i.p. est accentuée d'une manière significative par le traitement préalable au chloramphénicol (CHPC) à 100 mg/kg, mais non pas par 50 mg/kg de ce composé injecté par voie i.p. Le CHPC seul n'a aucun effet. Le CHPC étant un inhibiteur des systèmes enzymatiques des microsomes hépatiques, on en a conclu que l'effet du ¹-THC sur le prolongement de la durée du sommeil au barbital est dû au composé parent plutôt qu'à l'un des produits de transformation biologique.     

Fraser syndrome and mouse blebbed phenotype caused by mutations in FRAS1/Fras1 encoding a putative extracellular matrix protein

Fraser syndrome (OMIM 219000) is a multisystem malformation usually comprising cryptophthalmos, syndactyly and renal defects. Here we report autozygosity mapping and show that the locus FS1 at chromosome 4q21 is associated with Fraser syndrome, although the condition is genetically heterogeneous. Mutation analysis identified five frameshift mutations in FRAS1, which encodes one member of a family of novel proteins related to an extracellular matrix (ECM) blastocoelar protein found in sea urchin. The FRAS1 protein contains a series of N-terminal cysteine-rich repeat motifs previously implicated in BMP metabolism, suggesting that it has a role in both structure and signal propagation in the ECM. It has been speculated that Fraser syndrome is a human equivalent of the blebbed phenotype in the mouse, which has been associated with mutations in at least five loci including bl. As mapping data were consistent with homology of FRAS1 and bl, we screened DNA from bl/bl mice and identified a premature termination of mouse Fras1. Thus, the bl mouse is a model for Fraser syndrome in humans, a disorder caused by disrupted epithelial integrity in utero.