701 research outputs found
Chronic Ethanol Intake Promotes Double Gluthatione S-transferase/transforming Growth Factor-α-positive Hepatocellular Lesions In Male Wistar Rats
The chronic ethanol intake influence on the gluthatione S-transferase (GST-P) and transforming growth factor α (TGF-α) expression in remodeling/persistent preneoplastic lesions (PNLs) was evaluated in the resistant hepatocyte model. Male Wistar rats were allocated into five groups: G1, non-treated, fed water and chow ad libitum; G2, non-treated and pair-fed chow (restricted to match that of G3 group) and a maltodextrin (MD) solution in tap water (matched ethanol-derived calories); G3, fed 5% ethanol in drinking water and chow ad libitum; G4, diethylnitrosamine (DEN, 200 mg/kg, body weight) plus 200 parts per million of 2-acetylaminofluorene (2-AAF) for 3 weeks and pair-fed chow (restricted to match that of G5 group) and an MD solution in tap water (matched ethanol-derived calories); G5, DEN/2-AAF treatment, fed ethanol 5% and chow ad libitum. All animals were subjected to 70% partial hepatectomy at week 3 and sacrificed at weeks 12 or 22, respectively. Liver samples were collected for histological analysis or immunohistochemical expression of GST-P, TGF-α and proliferating cell nuclear antigen or zymography for matrix metalloproteinases-2 and-9. At the end of ethanol treatment, there was a significant increase in the percentage of liver area occupied by persistent GST-P-positive PNLs, the number of TGF-α-positive PNLs and the development of liver tumors in ethanol-fed and DEN/2-AAF-treated groups (G5 versus G4, P < 0.001). In addition, ethanol feeding led to a significant increase in cell proliferation mainly in remodeling and persistent PNLs with immunoreactivity for TGF-α at week 22 (P < 0.001). Gelatinase activities were not altered by ethanol treatment. The results demonstrated that ethanol enhances the selective growth of PNL with double expression of TGF-α and GST-P markers. © 2008 Japanese Cancer Association.992221228Pöschl, G., Seitz, H.K., Alcohol and cancer (2004) Alcohol Alcohol, 39, pp. 155-165Bofetta, P., Hashibe, M., Alcohol and cancer (2006) Lancet Oncol, 7, pp. 149-156Brown, L.M., Epidemiology of alcohol-associated cancers (2005) Alcohol, 35, pp. 161-168Voight, M.D., Alcohol in hepatocellular cancer (2005) Clin Liver Dis, 9, pp. 151-169Vidal, F., Toda, R., Gutiérrez, C., Influence of chronic alcohol abuse and liver disease on hepatic aldehyde dehydrogenase activity (1998) Alcohol, 15, pp. 3-8Lieber, C.S., Abittan, C.S., Pharmacology and metabolism of alcohol, including its metabolics effects and interactions with other drugs (1999) Clin Dermatol, 17, pp. 365-379Bunout, D., Nutritional and metabolic effects of alcoholism: Their relationship with alcoholic liver disease (1999) Nutrition, 15, pp. 583-589Niemellä, O., Distribution of ethanol-induced protein adducts in vivo: Relationship to tissue injury (2001) Free Rad Biol Med, 31, pp. 1533-1538Brooks, T.J., Theruvathu, J.A., DNA adducts from acetaldehyde: Implications for alcohol-related carcinogenesis (2005) Alcohol, 35, pp. 187-193Verna, L., Whysner, J., Williams, G.M., N-Nitrosodiethylamine mechanistic data and risk assessment: Bioactivation, DNA-Adduct formation, mutagenicity and tumor initiation (1996) Pharmacol Ther, 71, pp. 57-81Friedman, S.L., Mechanisms of disease: Mechanisms of hepatic fibrosis and therapeutic implication (2004) Nat Clin Pract Gastroenterol Hepatol, 1, pp. 98-105Purohit, V., Brenner, D.A., Mechanisms of alcohol-induced hepatic fibrosis: A summary of the Ron Thurman symposium (2006) Hepatology, 43, pp. 872-878Arthur, M.J.P., Fibrogenesis: Metalloproteinases and their inhibitors in liver fibrosis (2000) Am J Physiol Gastrointest Liver Phisiol, 279, pp. 245-249Tatsuta, M., Iishi, H., Baba, M., Enhancement by ethyl alcohol experimental hepatocarcinogenesis induced by N-nitrosomorpholine (1997) Int J Cancer, 71, pp. 1045-1048Karim, M.R., Wanibuchi, H., Wei, M., Morimura, K., Salim, E., Fukushima, S., Enhancing risk of ethanol on MeIQx-induced rat hepatocarcinogenesis is accompanied with increased levels of cellular proliferation and oxidative stress (2003) Cancer Lett, 192, pp. 37-47Kushida, M., Wanibuchi, H., Morimura, K., Dose-dependence of promotion of 2-amino-dimethylimidazo[4,5-f]quinoxaline-induced rat hepatocarcinogenesis by ethanol: Evidence for a threshold (2005) Cancer Sci, 96, pp. 747-757Stickel, F., Schuppan, D., Hahn, E.G., Seitz, H.K., Cocarcinogenic effects of alcohol in hepatocarcinogenesis (2002) Gut, 51, pp. 132-139Croager, E.J., Smith, P.G.J., Yeoh, G.C.T., Ethanol interactions with a choline-deficient, ethionine-supplemented feeding regime potentiate pre-neoplastic cellular alterations in rat liver (2002) Carcinogenesis, 23, pp. 1685-1693Wanibuchi, H., Wei, M., Karim, R., Existence of no hepatocarcinogenic effect levels of 2-amino-dimethylimidazo[4,5-f]quinoxaline with or without coadministration with ethanol (2006) Toxicol Pathol, 34, pp. 232-236Yanagi, S., Yamashita, M., Hiasa, Y., Kamiya, T., Effect of ethanol on hepatocarcinogenesis initiated in rats with 3′-methyl-4-dimethylaminoazobenzene in the absence of liver injuries (1989) Int J Cancer, 44, pp. 681-684Cho, K.J., Jang, J.J., Effects of carbon tetrachloride, ethanol, and acetaldehyde on diethylnitrosamine-induced hepatocarcinogenesis in rats (1993) Cancer Lett, 70, pp. 33-39Holmberg, B., Ekstrom, T., The effects of long-term oral administration of ethanol on Sprague-Dawley rats - A condensed report (1995) Toxicology, 96, pp. 133-145Solt, D., Farber, E., New principles for the analysis of chemical carcinogenesis (1976) Nature, 263, pp. 701-703Semple-Roberts, E., Hayes, M.A., Armstrong, D., Becker, R.A., Racz, W.J., Farber, E., Alternative methods of selecting hepatocellular nodules resistant to 2-acetylaminefluorene (1987) Int J Cancer, 40, pp. 643-645Tatematsu, M., Nagamine, Y., Farber, E., Redifferentiation as a basis for remodeling of carcinogen-induced hepatocyte nodules to normal appearing liver (1983) Cancer Res, 43, pp. 5049-5058Wood, G.A., Sarma, D.S.R., Archer, M.C., Resistance to the promotion of glutathione S-transferase 7-7-positive liver lesions in Copenhagen rats (1999) Carcinogenesis, 20, pp. 1169-1175Bannasch, P., Zerban, H., Predictive value of hepatic preneoplastic lesions as indicators of carcinogenic response (1992) Mechanism of Carcinogenesis in Risk Identification, pp. 389-427. , In: Vainio H, Magee PN, McGregor DB, McMichal AJ, eds. Lyon: IARC. Sci Publications, no. 116Pinheiro, F., Faria, R.R., de Camargo, J.L., Spinardi-Barbisan, A.L., da Eira, E.F., Barbisan, L.F., Chemoprevention of preneoplastic liver foci development by dietary mushroom Agaricus blazei Murrill in the rat (2003) Food Chem Toxicol, 41, pp. 1543-1550Schulte-Hermann, R., Kraupp-Grasl, B., Bursch, W., Gerbracht, U., Timmermann-Trosiener, I., Effects of non-genotoxic hepatocarcinogens phenobarbital and nafenopin on phenotype and growth of different populations of altered foci in rat liver (1989) Toxicol Pathol, 17, pp. 642-649Levin, S., Bucci, T.J., Cohen, S.M., The nomenclature of cell death: Recommendations of an ad hoc Committee of the Society of Toxicologic Pathologists (1999) Toxicol Pathol, 27, pp. 484-490Bradford, M.M., A rapid and sensitive method for the quantification of microgram quantities of protein utilizing the principle of protein-dye binding (1976) Anal Biochem, 72, pp. 248-254Bitsch, A., Hadjiolov, N., Klöhn, P.-C., Bergmann, O., Zwwirner-Baier, I., Neumann, H.-G., Dose-response of early effects related to tumor promotion of 2-acetylaminofluorene (2000) Toxicol Sci, 55, pp. 44-51Imai, T., Masui, T., Ichinose, M., Reduction of glutathione S-transferase P-form mRNA expression in remodeling nodules in rat liver revealed by in situ hybridization (1997) Carcinogenesis, 18, pp. 545-551De Miglio, M.R., Simile, M.M., Muroni, M.R., Phenotypic reversion of rat neoplastic liver nodules is under genetic control (2003) Int J Cancer, 105, pp. 70-75Kaufmann, W.K., Zhang, Y., Kaufmann, D.G., Association between expression of transforming growth factor-alpha and progression of hepatocellular foci to neoplasms (1992) Carcinogenesis, 13, pp. 1481-1483Tamano, S., Merlino, G.T., Ward, J.M., Rapid development of hepatic tumors in transforming growth factor alpha transgenic mice associated with increased cell proliferation in precancerous hepatocellular lesions initiated by N-nitrosodiethylamine and promoted by phenobarbital (1994) Carcinogenesis, 15, pp. 1791-1798Burr, A.W., Toole, K., Mathew, J., Hines, J.E., Chapman, C., Burt, A.D., Transforming growth factor-α expression is altered during experimental hepatocarcinogenesis (1996) J Pathol, 179, pp. 276-282Kitano, M., Wada, J., Ariki, Y., Possible tumour development from double positive foci for TGF-alpha and GST-P observed in early stages on rat hepatocarcinogenesis (2006) Cancer Sci, 97, pp. 478-483Sandgren, E.P., Luetteke, N.C., Qiu, T.H., Palmiter, R.D., Brinster, R.L., Lee, D.C., Transforming growth factor alpha dramatically enhances oncogene-induced carcinogenesis in transgenic mouse pancreas and liver (1993) Mol Cell Biol, 13, pp. 320-330Thorgeirsson, S.S., Santoni-Rugiu, E., Transgenic mouse models in carcinogenesis: Interaction of c-myc with transforming growth factor alpha and hepatocyte growth factor in hepatocarcinogenesis (1996) Br J Clin Pharmacol, 42, pp. 43-52Kato, J., Sato, Y., Inui, N., Ethanol induces transforming-growth factor-α expression in hepatocytes, leading to a stimulation of collagen synthesis by hepatic stellate cells (2003) Alcohol Clin Exp Res, 27, pp. 58S-63SZerban, H., Radig, S., Kopp-Schneider, A., Bannasch, P., Cell proliferation and cell death (apoptosis) in hepatic preneoplasia and neoplasia are closely related to phenotypic cellular diversity and instability (1994) Carcinogenesis, 15, pp. 2467-2473Grasl-Kraupp, B., Ruttkay-Nedecky, B., Müllauer, H., Taper, H., Huber, W., Bursch, W., Schulte-Hermann R Inherent increase of apoptosis in liver tumors: Implications for carcinogenesis and tumor regression (1997) Hepatology, 25, pp. 906-912Tanaka, T., Hirota, Y., Kuriyama, M., Nishiguchi, S., Otani, S., Time course of change in glutathione s-transferase positive foci and ornithine decarboxylase activity after cessation of long-term alcohol administration in rats (2001) Asian Pac J Cancer Prev, 2, pp. 131-134Mazzantini, R.P., de Conti, A., Moreno, F.S., Persistent and remodeling hepatic preneoplastic lesions present differences in cell proliferation and apoptosis, as well as in p53, Bcl-2 and NF-kappaB pathways (2007) J Cell BiochemFoda, H.D., Zucker, S., Matrix metalloproteinases in cancer invasion, metastasis and angiogenesis (2001) Drug Discov Today, 6, pp. 478-482Aye, M.M., Cuiling, M.A., Lin, H., Bower, K.A., Wiggins, R.C., Luo, J., Ethanol-induced in vitro invasion of breast cancer cells. the contribution of MMP-2 by fibroblasts (2004) Int J Cancer, 112, pp. 738-746Ke, Z., Lin, H., Fan, Z., MMP-2 mediates ethanol-induced invasion of mammary epithelial cells over-expressing ErbB2 (2006) Int J Cancer, 119, pp. 8-1
BPS Operators in N=4 SYM: Calogero Models and 2D Fermions
A connection between the gauge fixed dynamics of protected operators in
superconformal Yang-Mills theory in four dimensions and Calogero systems is
established. This connection generalizes the free Fermion description of the
chiral primary operators of the gauge theory formed out of a single complex
scalar to more general operators. In particular, a detailed analysis of
protected operators charged under an su(1|1)contained in psu(2,2|4) is carried
out and a class of operators is identified, whose dynamics is described by the
rational super-Calogero model. These results are generalized to arbitrary BPS
operators charged under an su(2|3) of the superconformal algebra. Analysis of
the non-local symmetries of the super-Calogero model is also carried out, and
it is shown that symmetry for a large class of protected operators is a
contraction of the corresponding Yangian algebra to a loop algebra.Comment: 29 pages, 3 figure
Discrete symmetries, invisible axion and lepton number symmetry in an economic 3-3-1 model
We show that Peccei-Quinn and lepton number symmetries can be a natural
outcome in a 3-3-1 model with right-handed neutrinos after imposing a Z_11 x
Z_2 symmetry. This symmetry is suitably accommodated in this model when we
augmented its spectrum by including merely one singlet scalar field. We work
out the breaking of the Peccei-Quinn symmetry, yielding the axion, and study
the phenomenological consequences. The main result of this work is that the
solution to the strong CP problem can be implemented in a natural way, implying
an invisible axion phenomenologically unconstrained, free of domain wall
formation and constituting a good candidate for the cold dark matter.Comment: 17 pages, Revtex
Prevalence of anti-Neospora caninum antibodies in cattle from the state of Mato Grosso do Sul, Brazil
Neospora caninum is an obligate intracellular parasite that can infect domestic and wild canids, as well as ruminants and equines. It was described in 1988 and has been known as a major cause of abortion in bovines and neuromuscular alterations and death in dogs. To estimate the prevalence of bovine neosporosis in the 22 municipalities of the so-called Estrato 1 subregion of the Brazilian state of Mato Grosso do Sul, blood samples were collected from cows aged 24 months and older, from December 2003 to March 2004. During sample collection, a questionnaire was used to gather data of epidemiological interest. The samples were subjected to serological diagnosis (indirect fluorescence antibody test - IFAT). Prevalences of 14.9% (449/2488) and 69.8% (143/205) were found for the animals and herds sampled, respectively. The variable found to be associated with seropositivity to N. caninum was abortion (OR 2.52; CI 1.25-5.06). The results revealed the presence of infection by N. caninum in the herds investigated, drawing attention to its role as a potential cause of abortion in cattle in Mato Grosso do Sul.Neospora caninum é um parasita intracelular obrigatório que pode infectar canídeos domésticos e selvagens, ruminantes e eqüídeos. Esse parasita foi descrito em 1988 e, desde sua descoberta, tem emergido como uma das principais causas de aborto em bovinos, além de causar alterações neuromusculares e morte em cães. Para estimar a prevalência da neosporose bovina em 22 municípios que compõem a sub-região denominada Estrato 1 do estado de Mato Grosso do Sul, foram analisados soros obtidos no período de dezembro de 2003 a março de 2004 de fêmeas com idade igual ou superior a 24 meses. Durante a colheita das amostras foi preenchido um questionário com informações de interesse epidemiológico. A determinação da presença de anticorpos anti-N. caninum foi feita pela Reação de Imunofluorescência Indireta, sendo as prevalências encontradas nos animais e nos rebanhos amostrados de 14,9% (449/2488) e 69,8% (143/205), respectivamente. A variável que apresentou associação de soropositividade com N. caninum foi o aborto (OR 2,52; IC 1,25-5,06). Os resultados indicam que a infecção por N. caninum está presente nos rebanhos e que deveria ser considerada como uma potencial causa de aborto em Mato Grosso do Sul
The Brazilian Developments On The Regional Atmospheric Modeling System (brams 5.2): An Integrated Environmental Model Tuned For Tropical Areas
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)We present a new version of the Brazilian developments on the Regional Atmospheric Modeling System (BRAMS), in which different previous versions for weather, chemistry, and carbon cycle were unified in a single integrated modeling system software. This new version also has a new set of state-of-the-art physical parameterizations and greater computational parallel and memory usage efficiency. The description of the main model features includes several examples illustrating the quality of the transport scheme for scalars, radiative fluxes on surface, and model simulation of rainfall systems over South America at different spatial resolutions using a scale aware convective parameterization. Additionally, the simulation of the diurnal cycle of the convection and carbon dioxide concentration over the Amazon Basin, as well as carbon dioxide fluxes from biogenic processes over a large portion of South America, are shown. Atmospheric chemistry examples show the model performance in simulating near-surface carbon monoxide and ozone in the Amazon Basin and the megacity of Rio de Janeiro. For tracer transport and dispersion, the model capabilities to simulate the volcanic ash 3-D redistribution associated with the eruption of a Chilean volcano are demonstrated. The gain of computational efficiency is described in some detail. BRAMS has been applied for research and operational forecasting mainly in South America. Model results from the operational weather forecast of BRAMS on 5km grid spacing in the Center for Weather Forecasting and Climate Studies, INPE/Brazil, since 2013 are used to quantify the model skill of near-surface variables and rainfall. The scores show the reliability of BRAMS for the tropical and subtropical areas of South America. Requirements for keeping this modeling system competitive regarding both its functionalities and skills are discussed. Finally, we highlight the relevant contribution of this work to building a South American community of model developers. © Author(s) 2017.1011892222014/01563-1, FAPESP, Fundação de Amparo à Pesquisa do Estado de São Paulo2014/01564-8, FAPESP, Fundação de Amparo à Pesquisa do Estado de São Paulo2015/10206-0, FAPESP, Fundação de Amparo à Pesquisa do Estado de São Paulo306340/2011-9, Conselho Nacional de Desenvolvimento Científico e TecnológicoFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq
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