Ingestion of multiple magnets: The count does matter

AbstractIngestion of multiple magnets poses a particular risk for various intraabdominal complications in children. We herein report a case of ingestion of multiple magnets, of which 3 were spontaneously expelled, and the remaining magnets were surgically removed. Since the total amount of ingestion was unknown upon presentation and the remaining intraabdominal magnets failed to pass after 24 h, emergency surgery was performed. Two magnets sandwiched the bowel walls and formed a jejunoileal fistula. There was no peritoneal contamination. We found that not all the ingested multiple magnets attracted each other, and multiple magnets could appear as single material on a plain radiograph. Confirming the exact count of ingested magnets is important; if the count is in doubt or two or more attachments are evident, prompt surgical intervention is warranted

Formation of Warped Disks by Galactic Fly-by Encounters. I. Stellar Disks

Warped disks are almost ubiquitous among spiral galaxies. Here we revisit and test the `fly-by scenario' of warp formation, in which impulsive encounters between galaxies are responsible for warped disks. Based on N-body simulations, we investigate the morphological and kinematical evolution of the stellar component of disks when galaxies undergo fly-by interactions with adjacent dark matter halos. We find that the so-called `S'-shaped warps can be excited by fly-bys and sustained for even up to a few billion years, and that this scenario provides a cohesive explanation for several key observations. We show that disk warp properties are governed primarily by the following three parameters; (1) the impact parameter, i.e., the minimum distance between two halos, (2) the mass ratio between two halos, and (3) the incident angle of the fly-by perturber. The warp angle is tied up with all three parameters, yet the warp lifetime is particularly sensitive to the incident angle of the perturber. Interestingly, the modeled S-shaped warps are often non-symmetric depending on the incident angle. We speculate that the puzzling U- and L-shaped warps are geometrically superimposed S-types produced by successive fly-bys with different incident angles, including multiple interactions with a satellite on a highly elongated orbit.Comment: 16 pages, 13 figures, 3 tables. Accepted for publication in Ap

Statistical Models for Hot Electron Degradation in Nano-Scaled MOSFET Devices

In a MOS structure, the generation of hot carrier interface states is a critical feature of the item\u27s reliability. On the nano-scale, there are problems with degradation in transconductance, shift in threshold voltage, and decrease in drain current capability. Quantum mechanics has been used to relate this decrease to degradation, and device failure. Although the lifetime, and degradation of a device are typically used to characterize its reliability, in this paper we model the distribution of hot-electron activation energies, which has appeal because it exhibits a two-point discrete mixture of logistic distributions. The logistic mixture presents computational problems that are addressed in simulation

Light-chain amyloidosis presenting with rapidly progressive submucosal hemorrhage of the stomach

SummaryThe gastrointestinal tract is frequently in involved light-chain (AL) amyloidosis, but significant hemorrhagic complications are rare. A 71-year-old man presented to our hospital with dyspepsia and heartburn for 1 month. Gastroscopy revealed a large submucosal hematoma at the gastric fundus. Two days later, a follow-up gastroscopy indicated extensive expansion of the hematoma throughout the upper half of the stomach. The hematoma displayed ongoing expansion during the endoscopic examination, suggesting that rupture was imminent. Emergency total gastrectomy was performed, and amyloidosis was confirmed after examining the surgical specimen. Bone marrow examination revealed multiple myeloma, and serum immunoglobulin assay confirmed the diagnosis of myeloma-associated AL amyloidosis. At manuscript submission, the patient was doing well and was undergoing chemotherapy

Identification of Gene Expression Signature Modulated by Nicotinamide in a Mouse Bladder Cancer Model

BACKGROUND: Urinary bladder cancer is often a result of exposure to chemical carcinogens such as cigarette smoking. Because of histological similarity, chemically-induced rodent cancer model was largely used for human bladder cancer studies. Previous investigations have suggested that nicotinamide, water-soluble vitamin B3, may play a key role in cancer prevention through its activities in cellular repair. However, to date, evidence towards identifying the genetic alterations of nicotinamide in cancer prevention has not been provided. Here, we search for the molecular signatures of cancer prevention by nicotinamide using a N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN)-induced urinary bladder cancer model in mice. METHODOLOGY/PRINCIPAL FINDINGS: Via microarray gene expression profiling of 20 mice and 233 human bladder samples, we performed various statistical analyses and immunohistochemical staining for validation. The expression patterns of 893 genes associated with nicotinamide activity in cancer prevention were identified by microarray data analysis. Gene network analyses of these 893 genes revealed that the Myc and its associated genes may be the most important regulator of bladder cancer prevention, and the gene expression signature correlated well with protein expression data. Comparison of gene expression between human and mouse revealed that BBN-induced mouse bladder cancers exhibited gene expression profiles that were more similar to those of invasive human bladder cancers than to those of non-invasive human bladder cancers. CONCLUSIONS/SIGNIFICANCE: This study demonstrates that nicotinamide plays an important role as a chemo-preventive and therapeutic agent in bladder cancer through the regulation of the Myc oncogenic signature. Nicotinamide may represent a promising therapeutic modality in patients with muscle-invasive bladder cancer

High glucose induces MCP-1 expression partly via tyrosine kinase–AP-1 pathway in peritoneal mesothelial cells

High glucose induces MCP-1 expression partly via tyrosine kinase–AP-1 pathway in peritoneal mesothelial cells.BackgroundHigh glucose in peritoneal dialysis solutions has been implicated in the pathogenesis of peritoneal fibrosis in chronic ambulatory peritoneal dialysis (CAPD) patients. However, the mechanisms are not very clear. Peritoneal macrophages seem to participate in the process of peritoneal fibrosis and monocyte chemoattractant protein-1 (MCP-1) plays a key role in the recruitment of monocytes toward the peritoneal cavity. However, little is known about the effect of high glucose on MCP-1 expression and its signal transduction pathway in human peritoneal mesothelial cells.MethodsMesothelial cells were cultured with glucose (5 to 100 mmol/L) or mannitol chronically for up to seven days. MCP-1 expression of mRNA and protein was measured by Northern blot analysis and enzyme-linked immunosorbent assay (ELISA). Chemotactic activity of high-glucose–conditioned culture supernatant was measured by chemotactic assay. To examine the roles of the transcription factors activator protein-1 (AP-1) and nuclear factor-κB (NF-κB), electrophoretic mobility shift assay (EMSA) was performed.ResultsGlucose induced MCP-1 mRNA expression in a time- and dose-dependent manner. MCP-1 protein in cell culture supernant was also increased. Equivalent concentrations of mannitol had no significant effect. High-glucose–conditioned supernatant possessed an increased chemotactic activity for monocytes, which was neutralized by anti–MCP-1 antibody. EMSA revealed that glucose increased the AP-1 binding activity in a time- and dose-dependent manner, but not NF-κB. Curcumin, an inhibitor of AP-1, dose-dependently suppressed the induction of MCP-1 mRNA by high glucose. Tyrosine kinase inhibitors such as genistein (12.5 to 50 μmol/L) and herbimycin A (0.1 to 1 μmol/L) inhibited the high-glucose–induced MCP-1 mRNA expression in a dose-dependent manner, and also suppressed the high-glucose–induced AP-1 binding activity.ConclusionsHigh glucose induced mesothelial MCP-1 expression partly via the tyrosine kinase-AP-1 pathway

TRAIL sensitize MDR cells to MDR-related drugs by down-regulation of P-glycoprotein through inhibition of DNA-PKcs/Akt/GSK-3β pathway and activation of caspases

<p>Abstract</p> <p>Background</p> <p>The development of new modulator possessing high efficacy, low toxicity and high selectivity is a pivotal approach to overcome P-glycoprotein (P-gp) mediated multidrug resistance (MDR) in cancer treatment. In this study, we suggest a new molecular mechanism that TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) down-regulates P-glycoprotein (P-gp) through inhibition of DNA-PKcs/Akt/GSK-3β pathway and activation of caspases and thereby sensitize MDR cells to MDR-related drugs.</p> <p>Results</p> <p>MDR variants, CEM/VLB_10-2, CEM/VLB_55-8and CEM/VLB₁₀₀cells, with gradually increased levels of P-gp derived from human lymphoblastic leukemia CEM cells, were gradually more susceptible to TRAIL-induced apoptosis and cytotoxicity than parental CEM cells. The P-gp level of MDR variants was positively correlated with the levels of DNA-PKcs, pAkt, pGSK-3β and c-Myc as well as DR5 and negatively correlated with the level of c-FLIPs. Hypersensitivity of CEM/VLB₁₀₀cells to TRAIL was accompanied by the activation of mitochondrial apoptotic pathway as well as the activation of initiator caspases. In addition, TRAIL-induced down-regulation of DNA-PKcs/Akt/GSK-3β pathway and c-FLIP and up-regulation of cell surface expression of death receptors were associated with the increased susceptibility to TRAIL of MDR cells. Moreover, TRAIL inhibited P-gp efflux function via caspase-3-dependent degradation of P-gp as well as DNA-PKcs and subsequently sensitized MDR cells to MDR-related drugs such as vinblastine and doxorubicin. We also found that suppression of DNA-PKcs by siRNA enhanced the susceptibility of MDR cells to vincristine as well as TRAIL via down-regulation of c-FLIP and P-gp expression and up-regulation of DR5.</p> <p>Conclusion</p> <p>This study showed for the first time that the MDR variant of CEM cells was hypersensitive to TRAIL due to up-regulation of DR5 and concomitant down-regulation of c-FLIP, and degradation of P-gp and DNA-PKcs by activation of caspase-3 might be important determinants of TRAIL-induced sensitization of MDR cells to MDR-related drugs. Therefore, combination of TRAIL and chemotherapeutic drugs may be a good strategy for treatment of cancer with multidrug resistance.</p

Micro-Segregated Liquid Crystal Haze Films for Photovoltaic Applications: A Novel Strategy to Fabricate Haze Films Employing Liquid Crystal Technology

Herein, a novel strategy to fabricate haze films employing liquid crystal (LC) technology for photovoltaic (PV) applications is reported. We fabricated a high optical haze film composed of low-molecular LCs and polymer and applied the film to improve the energy conversion efficiency of PV module. The technique utilized to fabricate our haze film is based on spontaneous polymerization-induced phase separation between LCs and polymers. With optimized fabrication conditions, the haze film exhibited an optical haze value over 95% at 550 nm. By simply attaching our haze film onto the front surface of a silicon-based PV module, an overall average enhancement of 2.8% in power conversion efficiency was achieved in comparison with a PV module without our haze film