Search

The effect of Li3PO4 coating was investigated for LiNi0.5Mn1.5O4 epitaxial thin film electrodes synthesized on SrTiO3 substrates by pulsed laser deposition (PLD). Amorphous Li3PO4 with a thickness of 1-4 nm was coated at room temperature onto 30 nm thick epitaxial LiNi0.5Mn1.5O4 thin films with (111), (110) and (100) lattice orientations. Electrodes with the surface coating exhibit high charge-discharge capacities and small capacity degradation during cycling experiments in the high voltage region. X-ray absorption near edge structure (XANES) and hard X-ray photoelectron spectroscopy (HAXPES) analyses indicate a higher manganese valence for the electrode surface of the Li3PO4 stacked LiNi0.5Mn1.5O4 film than that for the surface of a pristine LiNi0.5Mn1.5O4 film. Thus, surface coating affects the manganese valence near the electrode surface and improves the cycling characteristics. [ABSTRACT FROM AUTHOR]

Virulent microorganisms, such as pathogenic bacteria and viruses, are recognized by pattern recognition receptors (PRRs), including toll-like receptors (TLRs) and nucleotide-binding oligomerization-domain proteins (NODs), and induce inflammatory responses in mammalian hosts. Conversely, commensal bacteria and probiotics, which symbiotically confer health benefits on the host organisms, can lodge in the host intestinal tract without inducing intestinal inflammation. Recent advances in investigations concerning host-microbial interactions have shown that some effector molecules secreted from beneficial bacteria activate cell survival pathways, such as those mediated by p38 MAPK and Akt, and bring health benefits to mammalian hosts. It is noteworthy that such bacteria-derived molecules are taken into the intestinal epithelia through a transport or endocytosis system, thereafter exhibiting their beneficial effects. Understanding this traffic control process can aid in the comprehension of host and microbe interactions and may provide new insight to clarify the pathogenesis of intestinal disorders. This paper highlights the intestinal trafficking systems of bacteria-derived molecules that affect the bacterial functions and modulate epithelial signaling cascades. The latter mechanism may contribute to the maintenance of intestinal homeostasis by improving the host damage induced by virulence factors and various disease states. [ABSTRACT FROM AUTHOR]

Focuses on a study conducted where the response of COS-7 cells treated with H2O2 was examine in the activation of protein kinase C (PKC) by tyrosine phosphorylation. Reference to the activation of PKC in cells exposed to H2O2; Identification of tyrosine phosphorylation sites in PKC induced by H2O2 treatment; Results of the study; Discussion of the results of the study.

Presents a response by Tomio Okada, Hiroaki Konishi, Masafumi Ito, J. Asai, and H. Nagura to a letter to the editor about their article "Identification of Secretory Immunoglobulin in Human Sweat and Sweat Glands," published in the 1988 issue of "The Journal of Investigative Dermatology."

Objectives: To evaluate the 'One Stretch' exercise's effect on improvements in low back pain (LBP), psychological factors, and fear avoidance in a large number of nurses. Methods: Between July 2015 and June 2016, we performed a prospective, randomized, parallel-group, multi-center study with central evaluations. Eligible patients were randomly assigned (1:1:1 ratio) to either the control group (Group A) or an intervention group (Group B: 30-min seminar about the 'One Stretch' exercise, Group C: Bþphysical and psychological approaches to LBP treatment). The primary outcome was subjective improvement from baseline to 6 months (improved/unchanged/worsened) and overall exercise habits (good/poor). Results: There were 4767 participants: 1799, 1430, and 1548 in Groups A, B, and C, respectively. We collected data on 3439 participants (949, 706, and 751 in Groups A, B, and C, respectively) at the 6-month follow-up. The improvement rates in Groups A, B, and C were 13.3%, 23.5%, and 22.6%, respectively. The worsened pain rates were 13.0%, 9.6%, and 8.1%, which decreased as the intervention degree increased (the Cochran-Armitage trend test: p<.0001). In Groups A, B, and C, 15.6%, 64.9%, 48.8% of the patients, respectively, exhibited exercise habits. Conclusion: The 'One Stretch' exercise is useful for improving LBP. [ABSTRACT FROM AUTHOR]

OBJECTIVES: The aim of this study was to investigate the effect of the timing of valve surgery on the clinical outcomes of patients with active infective endocarditis (IE) accompanied by cerebral complications. METHODS: We retrospectively analysed a cohort of 568 patients, comprising 118 with non-haemorrhagic cerebral infarction (CI), 54 with intracranial haemorrhage (ICH) and 396 without cerebral events (C; control), who underwent surgery for left-sided active IE in 15 Japanese institutes from 2000 to 2011. The mean age was 58.4 ± 16.9 years in the CI group; 54.5 ± 17.4 years in the ICH group and 56.9 ± 16.0 years in the C group. Clinical outcomes were analysed according to the timing of surgery after the diagnosis of CI or ICH was made. RESULTS: In the CI group, there were 9 (7.6%) hospital deaths, 13 (11%) new cerebral events and 1 (0.8%) redo valve surgery. In the ICH group, there were 3 (5.6%) hospital deaths, 8 (14.8%) new cerebral events and 2 (3.7%) redo valve surgeries. In the C group, there were 36 (9.1%) hospital deaths, 23 (5.8%) new cerebral events and 9 (2.3%) redo valve surgeries. Risk factors for hospital death were prosthetic valve endocarditis (P = 0.045), high C-reactive protein (CRP; P < 0.001) and the elderly (P < 0.001) in the CI group. Delayed surgery (2 weeks after CI) seemed result in a higher incidence of hospital death in the CI group. Patients who had surgery between 15 and 28 days or after 29 days from the onset of CI had higher incidences of hospital death [odds ratio 5.90 (P = 0.107) and 4.92 (P = 0.137), respectively] compared with those who had surgery within 7 days. In the ICH group, risk factors for hospital death were high CRP (P = 0.002) and elderly (P < 0.001). Contrary to CI patients, patients who had surgery between 8 and 21 days or after 22 days after the onset of ICH had lower incidences of hospital death [odds ratio 0.79 (P = 0.843) and 0.12 (P = 0.200), respectively] compared with those who had surgery within 7 days. CONCLUSIONS: Although statistically insignificant, early surgery in active IE patients with CI is safe, but very early surgery (within 7 days) should be avoided in patients with ICH. [ABSTRACT FROM AUTHOR]

Grb2-associated regulator of Erk/MAPK1 (GAREM) is an adaptor molecule in the EGF-mediated signaling pathway. GAREM is expressed ubiquitously in human organs and cultured cells. Two GAREM homologues are encoded by the human genome. Therefore, previously identified GAREM is named GAREM1. Here we characterized a new subtype of GAREM, GAREM2, that is specifically expressed in the mouse, rat, and human brain. Three GAREM2 tyrosines (Tyr-102, Tyr-429, and Tyr-551) are phosphorylated upon EGF stimulation and are necessary for binding to Grb2. Furthermore, GAREM2 and Shp2 regulate Erk activity in EGF-stimulated cells. These characteristics are similar to those of GAREM1. GAREM2 is expressed in some neuroblastoma cell lines and is also tyrosine-phosphorylated and bound to Grb2 after treatment with EGF. Eventually, GAREM2 regulates Erk activation in the presence of EGF or insulin like growth factor 1. GAREM2 also regulates insulin-like growth factor 1-induced neuronal differentiation of the SH-SY5Y neuroblastoma cell line. Although the structure and function of both GAREM subtypes are similar, GAREM1 is recruited into the nucleus and GAREM2 is not. Nuclear localization of GAREM1 might be controlled by a GAREM1-specific nuclear localization sequence and 14-3-3∈ binding. The N-terminal 20 amino acids of GAREM1 make up its nuclear localization sequence that is also a 14-3-3∈ binding site. The GAREM family is a new class of adaptor molecules with subtype-specific biological functions. [ABSTRACT FROM AUTHOR]

In acute and chronic neurodegeneration, Ca2+ mishandling and disruption of the cytoskeleton compromise neuronal integrity, yet abnormalities in the signaling roles of cytoskeletal proteins remain largely unexplored. We now report that the microtubule-associated protein p600 (also known as UBR4) promotes neuronal survival. Following depletion of p600, glutamate-induced Ca2+ influx through NMD A receptors, but not AMP A receptors, initiates a degenerative process characterized by endoplasmic reticulum fragmentation and endoplasmic reticu-lum Ca2+ release via inositol 1,4,5-trisphosphate receptors. Downstream of NMDA receptors, p600 associates with the calmodulin-calmodulin-dependent protein kinase IIα complex. A direct and atypical p600/calmodulin interaction is required for neuronal survival. Thus, p600 counteracts specific Ca2+-induced death pathways through regulation of Ca2+ homeostasis and signaling. [ABSTRACT FROM AUTHOR]