Nickel affects gill and muscle development in oriental fire-bellied toad (Bombina orientalis) embryos.

The developmental toxicity of nickel was examined in the embryos of Bombina orientalis, a common amphibian in Korea. Based on a standard frog embryo teratogenesis assay, the LC50 and EC50 for malformation of nickel after 168h of treatment were 33.8µM and 5.4µM, respectively. At a lethal concentration (100µM), nickel treatment decreased the space between gill filaments and caused epithelial swelling and abnormal fusion of gill filaments. These findings suggest that nickel affects the functional development of gills, leading to embryonic death. At sublethal concentrations (1-10µM), nickel produced multiple embryonic abnormalities, including bent tail and tail dysplasia. At 10µM, nickel significantly decreased tail length and tail muscle fiber density in tadpoles, indicating inhibition of myogenic differentiation. Before hatching, the pre-muscular response to muscular response stages (stages 26-31) were the most sensitive period to nickel with respect to tail muscle development. During these stages, MyoD mRNA was upregulated, whereas myogenic regulatory factor 4 mRNA was downregulated by 0.1µM nickel. Calcium-dependent kinase activities in muscular response stage embryos were significantly decreased by nickel, whereas these activities were restored by exogenous calcium. In tadpoles, 10µM nickel significantly decreased the expression of the myosin heavy chain and the 12/101 muscle marker protein in the tail. Expression was restored by exogenous calcium. Our results indicate that nickel affects muscle development by disrupting calcium-dependent myogenesis in developing B. orientalis embryos.

Developmental and acute toxicity of cetylpyridinium chloride in Bombina orientalis (Amphibia: Anura).

In an effort to evaluate the toxicity of cetylpyridinium chloride (CPC), a cationic surfactant in amphibians, we examined the developmental and acute toxicity of CPC in Bombina orientalis embryos and tadpoles. Embryonic exposure to 2.0µM (0.72mg/l) CPC for 7 days significantly decreased the survival rates and increased DNA damage in the intestine of developed tadpoles. Exposure to 1.5µM (0.54mg/l) CPC significantly decreased the growth of embryos and increased developmental abnormalities. The 168-h LC50 and EC50 values of CPC were 1.95µM (0.697mg/l) and 1.48µM (0.531mg/l) in embryos, respectively. In an extended acute toxicity test using tadpoles, the 168-h LC50 value of CPC was 5.07µM (1.82mg/l). In terms of survival and growth rates, the lowest observed effective concentration of CPC was 1.5µM. At sub-lethal concentrations (1.0 and 2.0µM) CPC treatment to embryos increased lipid peroxidation in the intestine and gills of developed tadpoles, indicating that CPC can impose oxidative stress. At 2.0µM CPC, pro-apoptotic Bax and Bak mRNA levels were significantly increased together with DNA fragmentation, indicative of apoptotic cell death. CPC in freshwater system may threaten the normal development of amphibian embryos.

Oxidation behavior of P3HT layers on bare and TiO2-covered ZnO ripple structures evaluated by photoelectron spectroscopy.

P3HT layers with a thickness of ∼5 nm were deposited on bare and TiO2-covered ZnO ripple structures. The ZnO ripples were prepared wet-chemically and a TiO2 layer with a thickness less than 5 nm was prepared by atomic layer deposition. Under humid air and visible light illumination, the oxidation behaviors of P3HT on these surfaces were studied using photoelectron spectroscopy. It was found that P3HT on TiO2/ZnO oxidizes more easily than that on bare ZnO ripples. Using a model substrate of a flat ZnO surface in combination with angle-resolved photoelectron spectroscopy, we found that oxidation of P3HT occurs at the surface of the topmost layer of P3HT, not at the P3HT/oxide interfaces, even though P3HT oxidation is strongly influenced by the interface structure. It is suggested that the lifetime of electron-hole pairs can be strongly influenced by the interface structure, which can also affect the oxidation behavior of P3HT.

Hydrophobic polydimethylsiloxane (PDMS) coating of mesoporous silica and its use as a preconcentrating agent of gas analytes.

Mesoporous silica with mean pore size of ∼14 nm was coated by polydimethylsiloxane (PDMS) using a thermal deposition method. We showed that the inner walls of pores larger than ∼8 nm can be coated by thin layers of PDMS, and the surfaces consisting of PDMS-coated silica were superhydrophobic, with water contact angles close to 170°. We used the PDMS-coated silica as adsorbents of various gas-phase chemical warfare agent (CWA) simulants. PDMS-coated silica allowed molecular desorption of various CWA simulants even after exposure under highly humid conditions and, therefore, is applicable as an agent for the preconcentration of gas-phase analytes to enhance the sensitivities of various sensors.

The influence of a fibrous carbon envelope on the formation of CoFe nanoparticles for durable electrocatalytic oxygen evolution.

Co oxides are known to be active and stable alternative anode electrocatalysts possessing the potential to replace the best performing but most expensive Ir and Ru oxides in alkaline water electrolysis. Of late, Co oxides loaded on various carbon supports have been reported as a way to outperform Ir or Ru catalysts by improving the utilization efficiency. In this study, we introduce Co and Fe nanoparticles embedded carbon nanofibers (CoFe-CNFs), fabricated through electrospinning and pyrolysis of a polymer mixed with Co and Fe precursors. This method is a facile route for simultaneously making Co and Fe nanoparticles as well as the stable accommodation of the CoFe nanoparticles in the carbon support. We demonstrate the potential of the CoFe-CNFs as active and stable electrocatalysts for the oxygen evolution reaction (OER) in alkaline media. We conducted detailed physico-chemical characterizations to elucidate the effect of the CNFs on the OER activity and stability of the CoFe-CNFs. It is suggested that the CNFs are a medium in which OER-active CoFe alloy nanoparticles are formed homogeneously, and that carbon layers surrounding the nanoparticles are beneficial to the stability of the CoFe-CNFs in the OER.

Deficiency of C-C chemokine receptor 5 suppresses tumor development via inactivation of NF-κB and inhibition of monocyte chemoattractant protein-1 in urethane-induced lung tumor model.

To evaluate the significance of C-C chemokine receptor type 5 (CCR5) in lung tumor development, we compared carcinogen-induced tumor growth in CCR5 knockout (CCR5(-/-)) mice and wild-type (CCR5(+/+)) mice. CCR5(-/-) mice showed reduced urethane (1g/kg)-induced tumor incidence when compared with those of CCR5(+/+) mice. We investigated the activation of nuclear factor-kappaB/STAT3 since these are implicated transcription factors in the regulation of genes involving tumor growth. Significant inhibition of DNA-binding activity of nuclear factor-kappaB and STAT3, and the translocation of p50 and p65 into the nucleus and the phosphorylation of IĸB were found in the lungs of CCR5(-/-) mice compared with the lungs of CCR5(+/+) mice. Expression of apoptotic protein such as cleaved caspase-3, cleaved PARP and Bax was elevated, whereas the expression levels of survival protein such as Bcl-2 and cIAP1 was decreased in the lungs of CCR5(-/-) mice. Interestingly, we found that the level of monocyte chemoattractant protein-1 (MCP-1), a tumor growth-promoting cytokine, was significantly reduced in the lung tumor tissue and blood of CCR5(-/-) mice compared with the level in CCR5(+/+) mice. In addition, CCR5 small interfering RNA (siRNA) and inhibitor of MCP-1 blocked lung cancer cell growth, which was abolished by the addition of MCP-1 protein in cultured lung cancer cells. Moreover, inactivation of CD8(+) cytotoxic T cell and dendritic cells was significantly increased in the blood, lung tumors and spleens of CCR5(-/-) mice compared with that of CCR5(+/+) mice. Therefore, these results showed that CCR5 deficiency suppressed lung tumor development through the inhibition of nuclear factor-kappaB/STAT3 pathways and the downregulation of MCP-1 in the carcinogen-induced lung tumor model.

The usefulness of colonoscopy as a screening test for detecting colorectal polyps.

BACKGROUND/AIMS: Colonic polyps are the most common lesions encountered during screening colonoscopy. The purpose of this study is to evaluate the usefulness of colonoscopy to detect colonic polyps in adults. METHODOLOGY: From January 2003 to September 2005, a total of 4,629 adults underwent colonoscopic screening as a part of a health evaluation program. We analyzed the completed questionnaires, and the colonoscopic and pathologic findings. RESULTS: Complete colonic evaluation was possible in 4,491 (97.0%) subjects, and 804 (17.9%) had adenomatous polyps, including 153 subjects (3.4%) with advanced adenomas. There were no significant complications such as bowel perforation or massive bleeding requiring transfusion in relation to the procedure. There was a trend toward an increased prevalence of adenomatous polyps with age. Among the subjects with polyps, 72.1% of the subjects had distal polyps and the relative risk for proximal polyp, according to the distal findings, was 5.4 (95% CI: 4.5-6.3) for adenomatous polyp, 5.1 (95% CI 3.6-7.0) for advanced adenoma as compared to the finding of no adenomatous polyp. CONCLUSIONS: Colonoscopy performed by experienced colonoscopists as a screening test is feasible for detecting subjects with colorectal polyps.

Catalposide protects Neuro 2A cells from hydrogen peroxide-induced cytotoxicity via the expression of heme oxygenase-1.

Catalposide, the major iridoid glycoside isolated from the stem bark of Catalpa ovata G. Don (Bignoniaceae) has been shown to possess anti-microbial, anti-tumoral, and anti-inflammatory properties. Heme oxygenase-1 (HO-1) is a stress response protein and is known to play a protective role against the oxidative injury. In this study, we examined whether catalposide could protect Neuro 2A cells, a kind of neuronal cell lines, from oxidative damage through the induction of HO-1 protein expression and HO activity. The treatment of the cells with catalposide resulted in dose- and time-dependent up-regulations of both HO-1 protein expression and HO activity. Catalposide protected the cells from hydrogen peroxide-induced cell death. The protective effect of catalposide on hydrogen peroxide-induced cell death was abrogated by zinc protoporphyrin IX (ZnPP IX), a HO inhibitor. Additional experiments revealed the involvement of CO in the cytoprotective effect of catalposide-induced HO-1. These results indicate that catalposide is a potent inducer of HO-1 and HO-1 induction is responsible for the catalposide-mediated cytoprotection against oxidative damage.

The Effect of Intensified Induction Using Vanderbilt Regimen in Patients with an Intermediate Grade Non-Hodgkin's Lymphoma Having 2 or 3 Adverse Factors on the Age-adjusted International Prognostic Index.

PURPOSE: The purpose of our study was to evaluate the outcome of intensified induction therapy using the Vanderbilt regimen in patients with a poor prognosis non-Hodgkin's lymphoma (NHL). MATERIALS AND METHODS: We retrospectively analyzed the results of two pilot studies, which enrolled the patients aged 60 years or less, with a previously untreated NHL of intermediate grade on the Working formulation, having 2 or 3 adverse prognostic factors on the age- adjusted International Prognostic Index. Patients received an intensified induction, with the regimen described by the Vanderbilt group. RESULTS: Thirty-five patients were analyzed. After induction, 29 patients (83%) achieved more than partial response (PR): 22 (63%) complete response (CR) and 7 (20%) PR. Three of the PRs were subsequently converted to CR following consolidation therapy. The overall CR rate, following the completion of treatment, was 71%. The 3-year overall survival (OS) rate of all patients was 53%. In the univariate analysis, age (50 years) was the only factor affecting the OS. The 3-year disease-free survival (DFS) rate of patients with CR was 68%. In the univariate analysis, age and bone marrow involvement were the factors affecting the DFS. Two patients died from the treatment-related toxicity of the induction therapy: one due to sepsis and the other due to congestive heart failure. CONCLUSION: Although the CR rate was relatively high, the OS or DFS of patients with a poor prognosis NHL, who had received the intensified induction using the Vanderbilt regimen, were no different from those that had received the conventional chemotherapy, as reported by the International Prognostic Index Project. However, the OS or DFS in the young patient groups were encouraging. To test the hypothesized benefits of our approach in the young patient groups, a larger cohort of patients aged 50 years or less should be studied.

A Case of Extraskeletal Ewing's Sarcoma Arising from Duodenum.

Extraskeletal Ewing's sarcomas (EES) are rare. Recently, Ewing's sarcoma of the bone, primitive neuroectodermal tumor (PNET), Askin tumor and EES have been included into the family of Ewing's tumors, due to the overlapping features relating to their clinico-pathological and cytogenetic appearance. We experienced a case of an EES arising from the duodenum in a 14-year-old girl who presented with hematemesis and epigastric discomfort. A duodenal biopsy specimen revealed the infiltration of small round cells and rich vasculatures, with immunohistochemical finding of MIC-2 (CD99) (+), vimentin (+), CD56 (NCAM) (+), LCA (-), T-cell (-), B-cell (-), CD43 (-) and CD68 (-). She was treated with several cycles of multiagent chemotherapy, and achieved an initial partial response, but rapid progression of tumor followed, so she was treated with surgical excision. This is the first case report of an EES arising from the duodenum in the literature.