Surface modification of graphite encapsulated iron nanoparticles by plasma processing☆

The graphite encapsulated iron nanoparticles were fabricated by using arc dischargemethod. The synthesized nanoparticles were pre-treated by an inductively-coupled RF Ar plasma and then post-treated by NH3 plasma under various gas pressures and treatment times. Analyses of XPS spectra have been carried out to study the effect of the plasma treatment on the surface modification of nitrogen-containing groups. The morphological changes of the particles surface by plasma treatment have also been analyzed by using HR-TEM. Present results show that the highest values of N/C atomic ratio of 5.4 % is obtained by applying 10 min of Ar plasma pre-treatment and 2 min of NH3 plasma post-treatment conducted in RF power of 80W and gas pressure of 50 Pa

Pre-Treatment of Recombinant Mouse MFG-E8 Downregulates LPS-Induced TNF-α Production in Macrophages via STAT3-Mediated SOCS3 Activation

Milk fat globule-epidermal growth factor factor 8 (MFG-E8) regulates innate immune function by modulating cellular signaling, which is less understood. Herein, we aimed to investigate the direct anti-inflammatory role of MFG-E8 in macrophages by pre-treatment with recombinant murine MFG-E8 (rmMFG-E8) followed by stimulation with LPS in RAW264.7 cells and in peritoneal macrophages, isolated from wild-type (WT) or MFG-E8−/− mice. RAW264.7 cells and mouse peritoneal macrophages treated with rmMFG-E8 significantly downregulated LPS-induced TNF-α mRNA by 25% and 24%, and protein levels by 29% and 23%, respectively (P<0.05). Conversely, peritoneal macrophages isolated from MFG-E8−/− mice produced 28% higher levels of TNF-α, as compared to WT mice when treated with LPS. In in vivo, endotoxemia induced by intraperitoneal injection of LPS (5 mg/kg BW), at 4 h after induction, serum level of TNF-α was significantly higher in MFG-E8−/− mice (837 pg/mL) than that of WT (570 pg/mL, P<0.05). To elucidate the direct anti-inflammatory effect of MFG-E8, we examined STAT3 and its target gene, SOCS3. Treatment with rmMGF-E8 significantly induced pSTAT3 and SOCS3 in macrophages. Similar results were observed in in vivo treatment of rmMFG-E8 in peritoneal cells and splenic tissues. Pre-treatment with rmMFG-E8 significantly reduced LPS-induced NF-κB p65 contents. These data clearly indicated that rmMFG-E8 upregulated SOCS3 which in turn interacted with NF-κB p65, facilitating negative regulation of TLR4 signaling for LPS-induced TNF-α production. Our findings strongly suggest that MFG-E8 is a direct anti-inflammatory molecule, and that it could be developed as a therapy in attenuating inflammation and tissue injury

Animals exhibit consistent individual differences in their movement: a case study on location trajectories of Japanese macaques

Researching individual recognition (IR) is essential to understand the life history and adaptive behavior of social animals. Investigation of possible IR clues may also help us build new hypotheses about how social animals distinguish between different individuals. This study investigates behavioral individuality in Japanese macaques (Macaca fuscata), focusing on one specific trait that is movement. Using a recently developed tracking system based on Bluetooth® Low Energy beacons, we collected three-dimensional (3D) location data from five Japanese macaques living in a group cage. A non-parametric, neural network-based analysis of the data revealed the existence of consistent individual differences in extremely limited aspects of the movement data (2-min trajectory of 3D location). Our results support the validity of multimodal approaches in studying IR, beyond the typical single-frame face recognition method, both for researchers and animal agents

Polycomb-Mediated Loss of miR-31 Activates NIK-Dependent NF-κB Pathway in Adult T Cell Leukemia and Other Cancers

SummaryConstitutive NF-κB activation has causative roles in adult T cell leukemia (ATL) caused by HTLV-1 and other cancers. Here, we report a pathway involving Polycomb-mediated miRNA silencing and NF-κB activation. We determine the miRNA signatures and reveal miR-31 loss in primary ATL cells. MiR-31 negatively regulates the noncanonical NF-κB pathway by targeting NF-κB inducing kinase (NIK). Loss of miR-31 therefore triggers oncogenic signaling. In ATL cells, miR-31 level is epigenetically regulated, and aberrant upregulation of Polycomb proteins contribute to miR-31 downregulation in an epigenetic fashion, leading to activation of NF-κB and apoptosis resistance. Furthermore, this emerging circuit operates in other cancers and receptor-initiated NF-κB cascade. Our findings provide a perspective involving the epigenetic program, inflammatory responses, and oncogenic signaling

On the Dominance of Trivial Knots among SAPs on a Cubic Lattice

The knotting probability is defined by the probability with which an $N$-step self-avoiding polygon (SAP) with a fixed type of knot appears in the configuration space. We evaluate these probabilities for some knot types on a simple cubic lattice. For the trivial knot, we find that the knotting probability decays much slower for the SAP on the cubic lattice than for continuum models of the SAP as a function of $N$. In particular the characteristic length of the trivial knot that corresponds to a `half-life' of the knotting probability is estimated to be $2.5 \times 10^5$ on the cubic lattice.Comment: LaTeX2e, 21 pages, 8 figur

Multiple early gastric cancer with duodenal invasion

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Evolutionary loss of complexity in human vocal anatomy as an adaptation for speech

Human speech production obeys the same acoustic principles as vocal production in other animals but has distinctive features: A stable vocal source is filtered by rapidly changing formant frequencies. To understand speech evolution, we examined a wide range of primates, combining observations of phonation with mathematical modeling. We found that source stability relies upon simplifications in laryngeal anatomy, specifically the loss of air sacs and vocal membranes. We conclude that the evolutionary loss of vocal membranes allows human speech to mostly avoid the spontaneous nonlinear phenomena and acoustic chaos common in other primate vocalizations. This loss allows our larynx to produce stable, harmonic-rich phonation, ideally highlighting formant changes that convey most phonetic information. Paradoxically, the increased complexity of human spoken language thus followed simplification of our laryngeal anatomy.</jats:p