Search

The chemical reaction process of high temperature proton exchange membrane fuel cell stack (HT-PEMFC stack) results in poor membrane material durability and nonuniform fuel distribution and influences the fuel cell stack performance and life. The local temperature, voltage and flow inside the high temperature fuel cell stack are three major factors, so this study aims at the three physical phenomena. This study used micro-electro-mechanical systems (MEMS) technology to develop a high temperature electrochemical environment resistant integrated (temperature, voltage and flow) microsensor on a 40 μm thick stainless steel substrate, the protective layer was made of polyimide (PI) with better temperature tolerance. This study also captured the internal information of local temperature and voltage and flow inside the high temperature fuel cell stack instantly. The 100-h persistent effect test at operating temperature of 160 °C and current 6.28 A validated the reliability of the high temperature electrochemical environment resistant integrated microsensor. The experimental results showed the nonuniform temperature and flow distributions in the high temperature fuel cell stack resulted in high temperature contrast and nonuniform voltage distribution, and there was hot stack.

During the chemical reaction process of high-temperature proton exchange membrane fuel cell (HT-PEMFC) stack, the non-uniformity of internal local temperature, voltage, pressure, flow rate and current would result in poor membrane durability, fuel distribution non-uniformity and adverse impact on the fuel cell stack performance and service life. This study applies the micro-electromechanical systems (MEMS) technology to develop a flexible five-in-one micro sensor resistant to the high-temperature electrochemical environment. Six integrated micro sensors are embedded in the cathode field plate of HT-PEMFC stack. At the operational temperature of 160 °C, current (5, 13, 20 A) and long term testing results suggest that the trends of the curves of the internal local temperature, voltage, pressure, flow rate and current density of the fuel cell stack are considerably consistent, and the embedded flexible five-in-one micro sensors for in-situ diagnosis of fuel cell stack have impact of about 1.3% on fuel cell stack performance. The upstream temperature is higher than the downstream. The test result also shows that the heat distribution in the fuel cell stack is nonuniform.

Information signaling is regarded as an important motivating factor in corporate payout decisions, particularly with regard to cash dividends and the costly information signaling which they provide. Although Loderer and Mauer (1992) find little evidence to suggest that the announcements of firms’ equity offers are timed to arrive just after dividend declarations as a means of supporting the offer price. Using updated data, we determine that the dividend declaration does have a positive effect on the market reaction to equity offering announcements. We find that the abnormal returns from the announcement of seasoned equity offerings (SEOs) were −1.45 per cent for those SEO firms which had already made dividend declarations, whereas the returns for those SEO firms where the equity issue did not immediately follow a dividend declaration were −1.83 per cent. In this study, we interpret the changes in the impact of the dividend declaration on the equity offering announcement using the ‘tax regulation hypothesis’ and the ‘information asymmetry hypothesis’, and find that while our empirical results provide strong support for the latter, they provide only weak support for the former.

To determine the incidence and epidemiology of emergency department (ED)-attended mild traumatic brain injury (mTBI) in the US.Secondary analysis of ED visits for mTBI in the National Hospital Ambulatory Medical Care Survey for 1998--2000.MTBI defined by International Classification of Diseases, 9th Revision, Clinical Modification (ICD9-CM) codes for 'skull fracture', 'concussion', 'intracranial injury of unspecified nature' and 'head injury, unspecified'.The average incidence of mTBI was 503.1/100000, with peaks among males (590/100000), American Indians/Alaska Natives (1,026/100000) and those5 years of age (1,115.2/100000). MTBI incidence was highest in the Midwest region (578.4/10000) and in non-urban areas (530.9/100000) of the US. Bicycles and sports accounted for 26.4% of mTBI in the 5-14 age group.The national burden of mTBI is significant and the incidence higher than that reported by others. Possible explanations are discussed. Bicycle and sports-related injuries are an important and highly preventable cause of mTBI underscoring the need to promote prevention programmes on a national level.

Copper complexes with mononucleating tridentate ligands of the N−O−N type, including 1,3-bis(benzimidazol-2-yl)-2-oxapropane (bbmo), 1,3-bis(N-methylbenzimidazol-2-yl)-2-oxapropane (bbMemo), 1,3-bis(N-n-propylbenzimidazol-2-yl)-2-oxapropane (bbPrmo), and 1,3-bis(pyrid-2-yl)-2-oxapropane (bpmo), were tested for the oxygenation of phenols. Mixed ligand copper complexes of [Cu(N−O−N)(N−N)](ClO4)2, where N−N denotes 2,2′-bipyridine (bipy), 1,10-phenanthroline (phen), ethylenediamine (en), and/or N,N,N′,N′-tetramethylethylenediammine (tmen), were prepared and characterized by elemental analyses, and electronic, vibrational, and epr spectroscopic measurements. The molecular structures of fac-[Cu(bbMemo)(bipy)(H2O)](ClO4)2(H2O) (1a), fac-[Cu(bbMemo)(phen)](ClO4)2(CH3CN) (4a), fac-[Cu(bbPrmo)(phen)](ClO4)2 (5a), and fac-[Cu(bpmo)(bipy)(ClO4)](ClO4) (7a) were determined by X-ray diffraction methods. The structures of these complexes are square pyramids or elongated octahedra with the heterocycle nuclei forming the basal or equatorial planes. The terminal heterocycles of the facially coordinated tridentate ligands are nearly perpendicular to the basal or equatorial planes. Similar structures are proposed for the remaining complexes, based on spectroscopic data. Both stoichiometric and catalytic oxidation reactions of 2,4-di-tert-butylphenol and 2,4-di-tert-butylphenolate with dioxygen adducts of [Cu(bbPrmo)]+ at room temperature afforded 3,3′,5,5′-tetra-tert-butyl-2,2′-biphenol and 3,5-di-tert-butyl-o-quinone. Similar reactions with the dioxygen adduct of [Cu(bpmo)]+ yielded only 3,3′,5,5′-tetra-tert-butyl-2,2′-biphenol. In light of the tyrosinase-like reactivity, the possible intermediates, [(bbPrmo)2Cu2(μ-η2:η2-peroxo)]2+, [(bbPrmo)2Cu2(μ-oxo)2]2+, and [(bpmo)2Cu2(μ-oxo)2]2+ are proposed. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)

OBJECTIVES: To identify racial, ethnic, and gender disparities in the emergency department (ED) care for mild traumatic brain injury (mTBI). METHODS: A secondary analysis of ED visits in the National Hospital Ambulatory Medical Care Survey for the years 1998 through 2000 was performed. Cases of mTBI were identified using ICD-9 codes 800.0, 800.5, 850.9, 801.5, 803.0, 803.5, 804.0, 804.5, 850.0, 850.1, 850.5, 850.9, 854.0, and 959.01. ED care variables related to imaging, procedures, treatments, and disposition were analyzed along racial, ethnic, and gender categories. The relationship between race, ethnicity, and selected ED care variables was analyzed using multivariate logistic regression with control for associated injuries, geographic region, and insurance type. RESULTS: The incidence of mTBI was highest among men (590/100,000), Native Americans/Alaska Natives (1026.2/100,000), and non-Hispanics (391.1/100,000). After controlling for important confounders, Hispanics were more likely than non-Hispanics to receive a nasogastric tube (OR, 6.36; 95% CI = 1.2 to 33.6); nonwhites were more likely to receive ED care by a resident (OR, 3.09; 95% CI = 1.9 to 5.0) and less likely to be sent back to the referring physician after ED discharge (OR, 0.47; 95% CI = 0.3 to 0.9). Men and women received equivalent ED care. CONCLUSIONS: There are significant racial and ethnic but not gender disparities in ED care for mTBI. The causes of these disparities and the relationship between these disparities and post-mTBI outcome need to be examined. Language: en

Adlay has long been used in traditional Chinese medicine and as a nourishing food. The acetone extract of adlay hull had previously been demonstrated to possess potent antimutagenic activity. The aims of this study were to identify the antimutagenic constituents from adlay hull by using Ames antimutagenic activity-guide isolation procedures and to investigate their chemopreventive efficacies in cultured cells. The results demonstrated that six compounds showing great antimutagenic activity were identified by spectroscopic methods and by comparison with authentic samples to be p-hydroxybenzaldehyde, vanillin, syringaldehyde, trans-coniferylaldehyde, sinapaldehyde, and coixol. Two of them, trans-coniferylaldehyde and sinapaldehyde, exhibit relatively potent scavenging of DPPH radicals, inhibit TPA stimulated superoxide anion generation in neutrophil-like leukocytes, and induce Nrf2/ARE-driven luciferase activity in HSC-3 cells. Moreover, trans-coniferylaldehyde possesses cytoprotective efficacy against tert-butyl hydroperoxide-induced DNA double-strand breaks in cultured cells, and the chemopreventive potency induced by trans-coniferylaldehyde may be through the activation of kinase signals, including p38, ERK1/2, JNK, MEK1/2, and MSK1/2. In summary, we first identified six antimutagenic constituents from adlay hull. Among them, trans-coniferylaldehyde would be a highly promising agent for cancer chemoprevention and merits further investigation.

Arsenic trioxide (As(2)O(3)) is an effective treatment for relapsed or refractory acute promyelocytic leukemia (APL). After the discovery of As(2)O(3) as a promising treatment for APL, several studies investigated the use of As(2)O(3) as a single agent in the treatment of solid tumors; however, its therapeutic efficacy is limited. Thus, the systematic study of the combination of As(2)O(3) with other clinically used chemotherapeutic drugs to improve its therapeutic efficacy in treating human solid tumors is merited. In this study, we demonstrate for the first time, using isobologram analysis, that As(2)O(3) exhibits a synergistic interaction with N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU). The synergistic augmentation of the cytotoxicity of As(2)O(3) with BCNU is in part through the autophagic cell death machinery in human solid tumor cells. As(2)O(3) and BCNU in combination produce enhanced cytotoxicity via the depletion of reduced glutathione (GSH) and augmentation of reaction oxygen species (ROS) production. Further analysis indicated that the extension of GSH depletion by this combined regimen occurs through the inhibition of the catalytic activity of glutathione reductase. Blocking ROS production with antioxidants or ROS scavengers effectively inhibits cell death and autophagy formation, indicating that redox-mediated autophagic cell death involves the synergism of As(2)O(3) with BCNU. Taken together, this is the first evidence that BCNU could help to extend the therapeutic spectrum of As(2)O(3). These findings will be useful in designing future clinical trials of combination chemotherapy with As(2)O(3) and BCNU, with the potential for broad use against a variety of solid tumors.

Nasopharyngeal carcinoma (NPC) is one of the predominant cancers found in Southeastern China and Taiwan. Chemotherapy is one of the major treatment modalities, and the cisplatin-based regimen is the front-line treatment. However, NPC patients failing to cisplatin treatment will have a compromised survival. To explore the resistance spectrum and mechanisms of cisplatin resistance in NPC, two cisplatin-resistant sublines (cis6 and cis15) derived from the parental NPC cell line HONE-1 were obtained. Compared with HONE-1 cells, cis6 and cis15 cells showed upto 18-fold resistance to cisplatin in each, and also possessed a cross-resistance to oxaliplatin and arsenic trioxide. The level of platinum-DNA-adduct and γH2AX were significantly decreased in cis6 and cis15 cells. To unravel the behind details, the systems of DNA repair and cisplatin detoxification were examined and found to be more active in both resistant cells. In terms of the DNA repair proteins, the levels of p-DNA-PK and XRCC1 were increased; in terms of cellular localization of cisplatin, the level of copper transporter ATP7A was upregulated; in terms of Nrf2/antioxidant/detoxifizing enzyme, the resistant cells had a higher Nrf2 activity and an increased intracellular level of GSH, GR, NQO1, AKR1C1 and AKR1C2. Moreover, as compared with HONE-1 cells, our results showed that the resistant cells spared the cisplatin-induced cell death via the suppression of pro-apoptotic proteins and the enhancement of anti-apoptotic proteins. Since the members of ErbB family could be overexpressed in NPC and the ErbB/Akt/FoxO axis could involve in the actions of apoptosis, DNA damage repair and detoxification of reactive oxygen species, the ErB/Akt/FoxO were investigated. Indeed, the phosphorylations of Akt, FoxO1, and FoxO3 were upregulated in cis6 and cis15 cells. Thus, the resistance to cisplatin in cis6 and cis15 cells was partially explained by the Akt/FoxO pathway. Surprisingly, EGFR was downregulated in the resistant cells, whereas ErbB2 was upregulated. The elevations of the negative regulators of EGFR, including c-Cbl, GCF and LRIG1, were observed in cis6 and cis15 cells, indicating that the negative regulation of EGFR could be at the levels of transcription and protein degradation. Since LRIG1 could be upregulated and negatively feedback to control the level of ErbB after the ErbB was activated, it was plausible that the overexpression of ErbB2 upregulated the expression of LRIG1 and subsequently, caused the downregulation of EGFR. Nevertheless, the hypothesis which both overexpression of ErbB2 and LRIG1 contributes to the resistance to cisplatin in our cell model awaits experimental verification. Taken together, our results suggested that the mechanism responsible for cisplatin resistance in NPC, at least in part, through Akt/FoxO pathway. (The study was supported by grants of Department of Health DOH99-TD-C-111-004, Taiwan, R.O.C.) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1701. doi:10.1158/1538-7445.AM2011-1701