La hojarasca y su descomposición en bosques de castaño de monte alto en el Norte de Portugal

This research aimed to: estimate the inputs of litterfall; model the decomposition process and assess the rates of litter decay and turnover; study the litter decomposition process and dynamics of nutrients in old chestnut high forests. This study aimed to fill a gap in the knowledge of chestnut decomposition process as this type of ecosystems have never been modeled and studied from this point of view in Portugal. The study sites are located in the mountains of Marão, Padrela and Bornes in a west-to-east transect, across northern Portugal, from a more-Atlantic-to-lessmaritime influence. This research was developed on old chestnut high forests for quality timber production submitted to a silviculture management close-to-nature. We collected litterfall using littertraps and studied decomposition of leaf and bur litter by the nylon net bag technique. Simple and double exponential models were used to describe the decomposition of chestnut litterfall incubated in situ during 559 days. The results of the decomposition are discussed in relation to the initial litter quality (C, N, P, K, Ca, Mg) and the decomposition rates. Annually, the mature chestnut high-forest stands (density 360-1,260 tree ha–1, age 55-73 years old) restore 4.9 Mg DM ha–1 of litter and 2.6 Mg ha–1 yr–1 of carbon to the soil. The two-component litter decay model proved to be more biologically realistic, providing a decay rate for the fast initial stage (46-58 yr–1for the leaves and 38-42 yr–1for the burs) and a decay rate related to the recalcitrant pool (0.45-0.60 yr–1for the leaves and 0.22-0.36 yr–1for the burs). This study pointed to some decay patterns and release of bioelements by the litterfall which can be useful for calibrating existing models and indicators of sustainability to improve both silvicultural and environmental approaches for the management of chestnut forests.Esta investigación tuvo como objetivo calcular los aportes de hojarasca; modelar el proceso de descomposición y evaluar las tasas de descomposición de la hojarasca y el turnover; estudiar el proceso de descomposición de la hojarasca y la dinámica de nutrientes en bosques de castaños de monte alto. Asimismo, se quiso llenar un vacío en el conocimiento del proceso de descomposición del castaño ya que este tipo de ecosistemas no han sido modelados y estudiados desde este punto de vista en Portugal. El estudio se realizó en las montañas de Marão, Padrela y Bornes situados en un transepto que va de oeste a este, en el norte de Portugal, de mayor a menor influencia Atlántica. La investigación se desarrolló en bosques de castaños antiguos dedicados a la producción de madera de calidad sometida a una gestión silvícola cercana a la naturaleza. Se emplearon colectores de hojarasca y se estudió la descomposición de hojarasca y erizos mediante el empleo de bolsas de red de nylon. Para describir la descomposición de hojarasca del castaño mediante la incubación in situ durante 559 días se utilizaron modelos exponenciales simple y doble. Los resultados de la descomposición se discuten en relación a la calidad de la hojarasca inicial (C, N, P, K, Ca, Mg) y las tasas de descomposición. Anualmente, las masas de castaño (densidad 360-1.260 árboles ha–1, edad 55-73 años) producen 4,9 Mg DM ha–1 de hojarasca al suelo y 2,6 Mg ha–1 año–1 de carbono. El modelo exponencial doble de descomposición de hojarasca demostró ser biológicamente más realista, con una tasa de descomposición para la fracción lábil (46-58 años–1 para las hojas y 38-42 años–1 para los erizos) y una tasa de descomposición para la fracción recalcitrante (0,45-0,60 años–1 para las hojas y 0,22-0,36 años–1 para los erizos). Los resultados obtenidos mostraron la existencia de patrones de descomposición y liberación de los bioelementos de la hojarasca que pueden ser útiles para la calibración de los modelos existentes y indicadores de sostenibilidad que permitan mejorar los enfoques silvícolas y medioambientales de cara a una gestión sostenible de los bosques de castaño

J/ψJ/\psi production in PHENIX

Heavy quarkonia production is expected to be sensitive to the formation of a quark gluon plasma (QGP). The PHENIX experiment has measured $J/\psi$ production at $\sqrt{s_{NN}}=$~200 GeV in Au+Au and Cu+Cu collisions, as well as in reference p+p and d+Au runs. $J/\psi$'s were measured both at mid ($|y|<0.35$) and forward ($1.2<|y|<2.2$) rapidity. In this letter, we present the A+A preliminary results and compare them to normal cold nuclear matter expectations derived from PHENIX d+Au and p+p measurements as well as to theoretical models including various effects (color screening, recombination, sequential melting...).Comment: 5 pages, 7 figures. To appear in the proceedings of Hot Quarks 2006: Workshop for Young Scientists on the Physics of Ultrarelativistic Nucleus-Nucleus Collisions, Villasimius, Italy, 15-20 May 200

Association Of Inflammation, Dyslipidemia, Obesity And Physical Activity Status In Children

The aim of this study was to verify the association between inflammatory biomarkers, dyslipidemia, obesity and physical activity status in 10-years old children. Ninety-four children participated in this study and were classified into eutrophic (n=36), overweight (n=34) or obese (n=24) according to their body mass index (BMI). The genic expression of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and chemokine C-C motif ligand 2 (CCL-2) mRNA; the serum concentration of high-density lipoprotein cholesterol (HDL-c) and triglycerides; BMI, percentage of body fat (% BF) and waist circumference; and the number of steps per day were determined. The expression of IL-6, TNF-α and CCL-2 were associated (p 0.05) between pro-inflammatory biomarkers and number of steps per day was found.222182

Correlation Between Audiometric Data And The 35delg Mutation In Ten Patients

Mutations in the connexin 26 gene seem to be extremely common in non-syndromic hereditary deafness genesis, especially the 35delG, but there are still only a few studies that describe the audiometric characteristics of patients with these mutations. Aim: to analyze the audiometric characteristics of patients with mutations in the connexin 26 gene in order to outline genotype-phenotype correlation. Materials and Methods: Tonal audiometries of 33 index cases of non-syndromic sensorineural hearing loss were evaluated and eight affected relatives. Specific molecular tests were carried out to analyze mutations in the connexin 26 gene. Experiment Design: Retrospective, cross-sectional study. Results: A 27.3% prevalence of mutation 35delG was found in the index cases and 12.5% among the relatives affected. In relation to hearing loss degree, 41.5% of the patients were found with profound hearing loss, 39% with severe HL and 19.5% with moderate HL with homozygote and heterozygote patients for the 35delG predominating in the severe-moderate hearing losses. Conclusion: Our results suggest that the audiometric data associated with the molecular diagnose of hearing loss helped us to outline a genotype-phenotype correlation in ten patients with 35delG mutation. However, it is still necessary to run multicentric studies to verify the real phenotypic expression in the Brazilian population, as far as the 35delG mutation is concerned. © Revista Brasileira de Otorrinolaringologia. All Rights reserved.736777783Morton, N.E., Genetic epidemiology of hearing impairment (1991) Ann N Y Acad Sci, 630, pp. 16-31Mustafa, T., Arnos, K.S., Pandya, A., Advances in hereditary deafness (2001) Lancet, 358, pp. 1082-1090Skvorak Giersch, A.B., Morton, C.C., Genetic causes of nonsyndromic hearing loss (1999) Curr Opin Pediatr, 11 (6), pp. 551-557Petit, C., Genes responsible for human hereditary deafness: Symphony of a thousand (1996) Nature Genet, 14, pp. 385-391Van Camp, G., Willems, P.J., Smith, R.J.H., Nonsyndromic hearing impairment: Unparalleled heterogeneity (1997) Am J Hum Genet, 60, pp. 758-764Kelsell, D.P., Dunlop, J., Stevens, H.P., Lench, N.J., Liang, J.N., Parry, G., Mueller, R.F., Leigh, I.M., Connexin 26 mutations in hereditary non-syndromic sensorineural deafness (1997) Nature, 387, pp. 80-83Kelley, P.M., Harris, D.J., Comer, B.C., Askew, J.W., Fowler, T., Smith, S.D., Kimberling, W.J., Novel mutations in the connexin 26 gene (GJB2) that cause autossomal recessive (DFNB1) hearing loss (1998) Am J Hum Genet, 62, pp. 792-799Scott, D.A., Kraft, M.L., Carmi, R., Ramesh, A., Elbedour, K., Yari, Y., Srisailapathy, C.R.S., Identification of mutation on the connexin 26 gene that cause autossomal recessive nonsyndromic hearing loss (1998) Hum Mutat, 11, pp. 387-394Gabriel H, Kupsch P, Sudendey Jr, Winterhager E, Jahnke K, et al. Mutations in the connexin 26/GJB2 gene are the most common event in non-syndromic hearing loss among the German population. Hum Mutat 2001;17:521-2Van Camp G, Smith RJH. Na Hereditary Hearing Loss Homepage [Site na Internet]. Disponível em: http://webhost.ua.ac.be/hhh/. Acessado em 2006Zelante, L., Gasparini, P., Estivill, X., Melchionda, S., D'Agruma, L., Govea, N., Mila, M., Della Monica, M., Connexin 26 mutations associated with the most common form of non-syndromic neurosensory autossomal recessive deafness (DFNB1) in Mediterraneans (1997) Hum Molec Genet, 6, pp. 1605-1609Estivill, X., Fortina, P., Surrey, S., Rabionet, R., Melchionda, S., D'Agruma, L., Mansfield, E., Rappaport, E., Connexin 26 mutations in sporadic and inherited sensorineural deafness (1998) Lancet, 351, pp. 394-398Antoniadi, T., Gronskov, K., Sand, A., Pampanos, A., Brondum-Nielsen, K., Petersen, M.B., Mutation analysis of the GJB2 (connexin 26) gene by DGGE in greek patients with sensorineural deafness (2000) Hum Mutat, 16, pp. 7-12Oliveira, C.A., Maciel-Guerra, A.T., Sartorato, E.L., Deafness resulting from mutations in the GJB2 (connexin 26) gene on Brazilian patients (2002) Clin Genet, 61, pp. 354-358Kammen-Jolly, K., Ichiki, H., Scholtz, A.W., Gsenger, M., Kreczy, A., Schrott-Fischer, A., Connexin 26 in human fetal development of the inner ear (2001) Hear Res, 160 (1-2), pp. 15-21Denoyelle, F., Marlin, S., Weil, D., Moatti, L., Chauvin, P., Garabedian, E.N., Petit, C., Clinical features of the prevalent form of childhood deafness, DFNB1, due to a connexin 26 gene defect: Implications for genetic counselling (1999) Lancet, 17 (9161), pp. 1298-1303Cryns, K., Orzan, E., Murgia, A., Huygen, P.L.M., Moreno, F., del Castilo, I., A genotype-phenotype correlation for GJB2 (connexin 26) deafness) (2004) J Med Genet, 41, pp. 147-154(1991) Report of the informal working group on prevention of deafness and hearing impairment programme planning, , World Health Organization, Geneva: WHO, 22pAntoniadi, T., Gronskov, K., Sand, A., Pampanos, A., Brondum-Nielsen, K., Petersen, M.B., Mutation analysis of the GJB2 (connexin 26) gene by DGGE in Greek patients with sensorineural deafness (2000) Hum Mutat, 16, pp. 7-12del Castillo, I., Villamar, M., Moreno-Pelayo, M.A., del Castillo, F.J., Alvarez, A., Telleria, D., A deletion involving the connexin 30 gene in nonsyndromic hearing impairment (2002) N Engl J Med, 346, pp. 243-249Kelley, P.M., Harris, D.J., Comer, B.C., Askew, J.W., Fowler, T., Smith, S.D., Kimberling, W.J., Novel mutations in the connexin 26 gene (GJB2) that cause autossomal recessive (DFNB1) hearing loss (1998) Am J Hum Genet, 62, pp. 792-799Sobe, T., Vreugde, S., Shahin, H., Berlin, M., Davis, N., The prevalence and expression of inherited connexin 26 mutations associated with non-syndromic hearing loss in the Israeli population (2000) Hum Genet, 106, pp. 50-57Wilcox, S.A., Saunders, K., Osborn, A.H., Arnold, A., Wunderlich, J., High frequency hearing loss correlated with mutations in the GJB2 gene (2000) Hum Genet, 106, pp. 399-405del Castillo, I., Villamar, M., Moreno-Pelayo, M.A., del Castillo, F.J., Alvarez, A., Telleria, D., A deletion involving the connexin 30 gene in nonsyndromic hearing impairment (2002) N Engl J Med, 346, pp. 243-249Frei, K., Szuhai, K., Lucas, T., Weipoltshammer, K., Schofer, C., Ramsebner, R., Connexin 26 mutations in cases of sensorineural deafness in eastern Austria (2002) Eur J Hum Genet, 10, pp. 427-432Pampanos, A., Economides, J., Iliadou, V., Neou, P., Leotsakos, P., Voyiatzis, Prevalence of GJB2 mutations in prelingual deafness in the Greek population (2002) Int J Pediatr Otorhinolaryngol, 65, pp. 101-108Gasparini, P., Estivill, X., Volpini, V., Totaro, A., Castellvi-Bel, S., Linkage of DFNB1 to non-syndromic neurosensory autosomal-recessive deafness in Mediterranean families (1997) Eur J Hum Genet, 5, pp. 83-88Estivill, X., Fortina, P., Surrey, S., Rabionet, R., Melchionda, S., D'Agruma, L., Mansfield, E., Rappaport, E., Connexin 26 mutations in sporadic and inherited sensorineural deafness (1998) Lancet, 351, pp. 394-398Kenna, M.A., Wu, B.-L., Cotanche, D.A., Korf, B.R., Rehm, H.L., Connexin 26 studies in patientes with sensorineural hearing loss (2001) Arch Otolaryngol Head Neck Surg, 127, pp. 1037-1042Simsek, M., Al-Wardy, N., Al-Khayat, A., Shanmugakonar, M., Al-Bulushi, T., Al-Khabory, M., Absence of deafness associated connexin 26 (GJB2) gene mutations in the Omani population (2001) Hum Mutat, 18, pp. 545-546Nance, W.E., The genetics of deafness (2003) Ment Retard Disabil Res Rev, 9, pp. 109-119del Castillo, I., Moreno-Pelayo, M.A., del Castillo, F.J., Brownstein, Z., Marlin, S., Adina, Q., Prevalence and Evolutionary Origins of the del(GJB6-D13S1830) Mutation in the DFNB1 Locus in Hearing Impaired Subjects: A Multicenter Study (2003) Am J Hum Genet, 73, pp. 1452-1458Piatto, V.B., Oliveira, C.A., Alexandrino, F., Pimpinati, C.J., Sartorato, E.L., Perspectivas para triagem auditiva genética: Rastreamento da mutação 35delG em neonatos. (2005) J Pediatr, 81, pp. 139-142Sartorato, E.L., Gottardi, E., Oliveira, C.A., Magna, L.A., Annichio-Bizzacchi, J.M., Seixas, C.A., Maciel-Guerra, A.T., Determination of the frequency of the 35delG in Brazilian neonates (2000) Clin Genet, 58, pp. 339-340Oliveira, C.A., Alexandrino, F., Abe-Sandes, K., Silva Jr, W.A., Maciel-Guerra, A.T., Magna, L.A., Sartorato, E.L., Frequency of 35delG in the GJB2 gene in samples of Caucasians, Asians and African Brazilians (2004) Hum Biol, 76, pp. 313-316Pandya, A., Arnos, K.S., Xia, X.J., Welch, K.O., Blanton, S.H., Friedman, T.B., Frequency and distribution of GJB2 (connexin 26) and GJB6 (connexin 30) mutations in a large North American repository of deaf probands (2003) Genet Med, 5, pp. 295-303Stevenson, V.A., Ito, M., Milunsky, J.M., Connexin-30 deletion analysis in connexin-26 heterozygotes (2003) Genet Test, 7, pp. 151-154Cohn, E.S., Kelley, P.M., Fowler, T.W., Gorga, M.P., Lefkowitz, Clinical studies of families with hearing loss attributable to mutations in the connexin 26 gene (GJB2/DFNB1) (1999) Pediatrics, 103, pp. 546-550Murgia, A., Orzan, E., Polli, R., Martella, M., Vinazi, C., Leonardi, E., Arslan, E., Zacchello, F., Cx26 deafness: Mutation analysis and clinical variability (1999) J Med Genet, 36, pp. 829-832Marlin, S., Garabedian, E.-N., Roger, G., Moatti, L., Matha, N., Lewin, P., Petit, C., Denoyelle, F., Connexin 26 gene mutations in congenitally deaf children (2001) Arch Otolaryngol Head Neck Surg, 127, pp. 927-933Rabionet, R., Zelante, L., Lopez-Bigas, N., DAgruma, L., Melchionda, S., Restagno, G., Molecular basis of childhood deafness resulting from mutations in the GJB2 (connexin 26) gene (2000) Hum Genet, 106, pp. 40-44Cohn, E.S., Kelley, P.M., Clinical phenotype and mutations in connexin 26 (DFNB1/GJB2), the most commom cause of childhood hearing loss (1999) Am J Med Genet, 89, pp. 130-136Denoyelle, F., Marlin, S., Weil, D., Moatti, L., Chauvin, P., Garabedian, E.N., Petit, C., Clinical features of the prevalent form of childhood deafness, DFNB1, due to a connexin 26 gene defect: Implications for genetic counselling (1999) Lancet, 17, pp. 1298-1303Engel-Yeger, B., Zaaroura, S., Zlotogora, J., Shalev, S., Hujeirat, Y., Carrasquilo, M., Barges, S., Pratt, H., The effects of a connexin 26 mutation - 35delG - an oto-acoustic emissions and brainstem evoked potentials: Homozygotes and carriers (2002) Hear Res, 163, pp. 93-100Mustapha, M., Salem, N., Delague, V., Chouery, E., Ghassibeh, M., Rai, M., Loiselet, J., Megarbane, A., Autosomal recessive non-syndromic hearing loss in the Libanese population: Prevalence of the 30delG mutation and report of two novel mutations in the connexin 26 (GJB2) gene (2001) J Med Genet, 38, pp. e36Yoshinaga-Itano, C., Sedey, A.L., Coulter, D.K., Mehl, A.L., Language of early-and later-identified children with hearing loss (1998) Pediatrics, 102, pp. 1161-117

Efeito da adição de uréia e sulfato de amônio sobre o pH e nitrificação em um solo ácido

The variation of pH and the production of nitrate were studied in a Dark Red Latosol, Guamium séries, in function of the addition of 200 and 400 ppm of N, as urea and ammonium sulphate in the presence and absence of Ca(0H)2, for a period of 30 days. The results obtained showed that the pH decreased with ammonium sulphate and increased with urea. The variations were observed even in the presence of Ca(0H)2. The production of nitrate increased with pH considering the same level and source of nitrogen.A variação do pH e a produção de nitrato foram estudados em um Latossolo Vermelho Escuro, Série Guamium, em função da adição de 200 e 400 ppm de N nas formas de uréia e sulfato de amônio, em presença e ausência de Ca(OH)2 por um período de 30 dias. Os resultados obtidos mostraram que o pH decresceu com o sulfato de amônio e aumentou com a uréia. As variações foram observadas mesmo empresença de Ca(0H)2. A produção de nitrato aumentou com o pH, considerando o mesmo nível e fonte de nitrogênio. Não foi observado no conjunto uma relação entre pH e produção de nitrato