Latex Migration in Battery Slurries during Drying

We used real-time fluorescence microscopy to investigate the migration of latex particles in drying battery slurries. The time evolution of the fluorescence signals revealed that the migration of the latex particles was suppressed above the entanglement concentration of carboxymethyl cellulose (CMC), while it was significantly enhanced when CMC fully covered the surfaces of the graphite particles. In particular, a two-step migration was observed when the graphite particles flocculated by depletion attraction at high CMC/graphite mass ratios. The transient states of the nonadsorbing CMC and graphite particles in a medium were discussed, and the uses of this novel measurement technique to monitor the complex drying processes of films were demonstrated

Latex Migration in Battery Slurries during Drying

We used real-time fluorescence microscopy to investigate the migration of latex particles in drying battery slurries. The time evolution of the fluorescence signals revealed that the migration of the latex particles was suppressed above the entanglement concentration of carboxymethyl cellulose (CMC), while it was significantly enhanced when CMC fully covered the surfaces of the graphite particles. In particular, a two-step migration was observed when the graphite particles flocculated by depletion attraction at high CMC/graphite mass ratios. The transient states of the nonadsorbing CMC and graphite particles in a medium were discussed, and the uses of this novel measurement technique to monitor the complex drying processes of films were demonstrated

Risk Factors for Failure of Initial Intravenous Immunoglobulin Treatment in Kawasaki Disease

The aims of this study were to determine the occurrence and variables associated with the initial intravenous immunoglobulin (IVIG) treatment failure in Kawasaki disease (KD) and to categorize differences in clinical characteristics between responders and nonresponders to initial IVIG treatment. Patients were classified into two groups. Group A included 33 patients who received a single dose of IVIG treatment and responded. Group B included 18 patients who received more than two doses of IVIG due to failure of the initial treatment. The mean duration of fever after initial treatment in group B was significantly longer than it was in group A. In group B, we found that higher bilirubin, aspartate aminotransferase (AST), polymorphonuclear cells (PMN) (%), and lower platelet values at baseline were independent predictors of persistent or recurrent fever in patients with KD. Coronary artery abnormalities were found in 8 patients (44.4%) in group B and in two patients (6.1%) in group A. We found that abnormal liver function tests and a lower platelet count at baseline were possible predictors of nonresponders to IVIG in patients with KD. There is a need for a prospective study focused on baseline hepatobiliary parameters

Diesel exhaust particles increase IL-1β-induced human β-defensin expression via NF-κB-mediated pathway in human lung epithelial cells

BACKGROUND: Human β-defensin (hBD)-2, antimicrobial peptide primarily induced in epithelial cells, is a key factor in the innate immune response of the respiratory tract. Several studies showed increased defensin levels in both inflammatory lung diseases, such as cystic fibrosis, diffuse panbronchiolitis, idiopathic pulmonary fibrosis and acute respiratory distress syndrome, and infectious diseases. Recently, epidemiologic studies have demonstrated acute and serious adverse effects of particulate air pollution on respiratory health, especially in people with pre-existing inflammatory lung disease. To elucidate the effect of diesel exhaust particles (DEP) on pulmonary innate immune response, we investigated the hBD-2 and interleukin-8 (IL-8) expression to DEP exposure in interleukin-1 beta (IL-1β)-stimulated A549 cells. RESULTS: IL-1β markedly up-regulated the hBD-2 promoter activity, and the subsequent DEP exposure increased dose-dependently the expression of hBD-2 and inflammatory cytokine IL-8 at the transcriptional level. In addition, DEP further induced the NF-κB activation in IL-1β-stimulated A549 cells more rapidly than in unstimulated control cells, which was showed by nuclear translocation of p65 NF-κB and degradation of IκB-α. The experiment using two NF-κB inhibitors, PDTC and MG132, confirmed that this increase of hBD-2 expression following DEP exposure was regulated through NF-κB-mediated pathway. CONCLUSION: These results demonstrated that DEP exposure increases the expression of antimicrobial peptide and inflammatory cytokine at the transcriptional level in IL-1β-primed A549 epithelial cells and suggested that the increase is mediated at least partially through NF-κB activation. Therefore, DEP exposure may contribute to enhance the airway-responsiveness especially on the patients suffering from chronic respiratory disease

Notch1 binds and induces degradation of Snail in hepatocellular carcinoma

<p>Abstract</p> <p>Background</p> <p>Hepatocellular carcinoma (HCC) is a common, highly invasive malignant tumor associated with a high mortality rate. We previously reported that the aberrant expression of Snail via activation of reactive oxygen species contributes to the invasive property of HCC, in part by downregulation of E-cadherin through both transcriptional repression and epigenetic modification of the E-cadherin promoter. Having demonstrated the ability of Snail to bind and recruit histone deacetylase 1 and DNA methyltransferase 1 in this context, we set out to look for other interactions that could affect its ability to promote oncogenic transformation and cancer cell invasion.</p> <p>Results</p> <p>Using cells that stably expressed Snail, we characterized Snail protein interactors by tandem affinity purification and mass spectrometry. Immunoprecipitation and subcellular colocalization studies were performed to confirm our identification of the Notch1 intracellular domain (NICD) as a novel Snail-binding partner. NICD interaction with Snail was found to induce ubiquitination and MDM2-dependent degradation of Snail. Interestingly, NICD inhibited Snail-dependent invasive properties in both HCC cells and mouse embryonic fibroblasts.</p> <p>Conclusions</p> <p>Our study demonstrates that NICD can oppose Snail-dependent HCC cell invasion by binding and inducing proteolytic degradation of Snail. Although Notch signaling and Snail are both widely considered tumor-promoting factors, our findings indicate that the individual oncogenic contribution of Notch1 and Snail in malignant systems should be interpreted carefully, particularly when they are conjointly expressed.</p

Lung Metastasis from an Immature Teratoma of the Nasal Cavity Masquerading as Small Cell Carcinoma of the Lung

We report a case of small cell lung cancer that turned out to be a metastatic teratoma from the nasal cavity rather than a new primary cancer. A 54-year-old woman was diagnosed with an immature teratoma of the nasal cavity with a predominant neuroblastomatous component. Small cell lung cancer was detected by bronchoscopic biopsy 21 months later, and it was treated with concurrent radiochemotherapy as if it had been a new primary cancer. Since a recurrent tumor containing fat-like density grew slowly on the serial chest CT scans after achieving complete response, we reached the conclusion that the small undifferentiated cells could be metastatic neuroblastomatous components from the immature teratoma of the nasal cavity

Photospheric Signatures of Granular-scale Flux Emergence and Cancellation at the Penumbral Boundary

We studied flux emergence events of sub-granular scale in a solar active region. New Solar Telescope (NST) of Big Bear Solar Observatory made it possible to clearly observe the photospheric signature of flux emergence with very high spatial (0".11 at 7057{\AA}) and temporal (15 s) resolution. From TiO observations with the pixel scale of 0".0375, we found several elongated granule-like features (GLFs) stretching from the penumbral filaments of a sunspot at a relatively high speed of over 4 km s-1. After a slender arched darkening appeared at a tip of a penumbral filament, a bright point (BP) developed and quickly moved away from the filament forming and stretching a GLF. The size of a GLF was approximately 0.5" wide and 3" long. The moving BP encountered nearby structures after several minutes of stretching, and a well-defined elongated shape of a GLF faded away. Magnetograms from SDO/HMI and NST/IRIM revealed that those GLFs are photospheric indicators of small-scale flux emergence, and their disappearance is related to magnetic cancellation. From two well-observed events, we describe detailed development of the sub-structures of GLFs, and different cancellation processes that each of the two GLFs underwent.Comment: Accepted for publication in The Astrophysical Journa

Crystal structure of peroxiredoxin 3 from Vibrio vulnificus

Peroxiredoxins (Prxs) are ubiquitous cysteine-based peroxidase enzymes. Recently, a new type of Prx, VvPrx3, was identified in the pathogenic bacterium Vibrio vulnificus as being important for survival in macrophages. It employs only one catalytic cysteine residue to decompose peroxides. Here, crystal structures of VvPrx3 representing its reduced and oxidized states have been determined, together with an H2O2-bound structure, at high resolution. The crystal structure representing the reduced Prx3 showed a typical dimeric interface, called the A-type interface. However, VvPrx3 forms an oligomeric interface mediated by a disulfide bond between two catalytic cysteine residues from two adjacent dimers, which differs from the doughnut-like oligomers that appear in most Prxs. Subsequent biochemical studies showed that this disulfide bond was induced by treatment with nitric oxide (NO) as well as with peroxides. Consistently, NO treatment induced expression of the prx3 gene in V. vulnificus, and VvPrx3 was crucial for the survival of bacteria in the presence of NO. Taken together, the function and mechanism of VvPrx3 in scavenging peroxides and NO stress via oligomerization are proposed. These findings contribute to the understanding of the diverse functions of Prxs during pathogenic processes at the molecular level