Significado de unos potholes modelados en el Mioceno menorquín

In this paper I describe sections of the Miocene in the Menorca Isdand in order to place some strategically potholes belonging possibly to the Miocene

Estudio estratigráfico y sedimentológico de los materiales miocénicos de la isla de Menorca

En esta nota expongo, muy resumidamente, las principales conclusiones a que he llegado después de la memoria que sobre el mismo tema y bajo el mismo título he realizado como tesis de doctorado. Se estudia desde el punto de vista estratigráfico y sedimentológico el Mioceno menorquín, y sellega a la conclusión de que sus materiales corresponden a un medio sedimentario de nearshore

Ambientes sedimentarios en el Mioceno del Baix Camp de Tarragona

In this paper we undertake a synthesis of the sedimentary environments which we have found in the Miocene of the "Baix Camp de Tarragona". At the same time we venture at the possibility of the existence of some pre-miocene arid post-eocene conglomerates which would, nowadays, be disniantled by the erosion

Nuevas localidades con fauna ictiológica para el Neógeno menorquín

New places having ichthyological fauna are described in the Neogene of the island of Menorca (Balearic, Spain) and the Myliobatis sp. is shown to exist for the first time in the island All the referentes are summarized in the chart which is given

Significación sedimentológica y paleogeográfica del nivel arcilloso con corales del Senonuense superior de los alrededores de la Pobla de Segur (Prov. Lérida)

There is in this note a facies description of the upper Cre- taceous clay levels with corals from Pobla de Segur surroundings and á sedimentological interpretation is give regardin, the regional paleogeographic evolution

Significado sedimentológico de los niveles con Assilinas de la Formación Armancies (Eoceno medio) y sus equivalentes laterales

En esta nota exponemos las características sedimentológicas de los niveles con Assilina de la Fm. Armancies y sus equivalentes laterales que permiten precisar algunos aspectos acerca de su génesis.Se llega a la conclusión de que las "barras de Assilinas" de la Fm. Armancies, en su extremo occidental (Bagà-Campdevànol), son canales de "grain flow" depositados originariamente al W de Terrades y deslizados, de E a W, en una cuenca turbidítica sin aportes de clásticos groseros

Distribución y ordenación de Microcodium en la Formación Tremp: anticlinal de Campllong (Pirineos Orientales, provincia de Barcelona)

La abundancia excepcional de Microcodium en los sedimentos continentales de la Formación Tremp en el anticlinal de Campllong (Llinás de Berga, Provincia de Barcelona) es un rasgo característico en este tipo de sedimentos, igual que ocurre en otros puntos de los Pirineos. Diferentes facies litológicas (limos, calizas, areniscas y conglomerados) ricas en Microcodium se asocian en tres secuencias sedimentológicas de: a) somerización lacustre b) paleosuelos calcimorfos y c) relleno de canales fluviales. Los Microcodiums desarrollados in situ aparecen como individuos (colonias) dispersos y como agregados. Los agregados pueden ser masivos, rellenar cavidades ramificadas y formar a techo de capas entramados muy tupidos a modo de tapices. Los prismas disgregados y los fragmentos de individuos de Microcodium se presentan como componentes retrabajados y en ocasiones rellenan cavidades producidas por anélidos. El porcentaje de Microcodium en cada facies y a lo largo de cada secuencia varía considerablemente (5-100%). La abundancia excepcional de Microcodium sugiere una importante exposición sub aérea en la zona más distal de un abanico aluvial, donde tendría lugar el desarrollo de una cubierta vegetal, responsable de un posible proceso de calcitización de raíces

End-stage renal disease preceded by rapid declines in kidney function: a case series

<p>Abstract</p> <p>Background</p> <p>Few studies have defined alternate pathways by which chronic kidney disease (CKD) patients transition into end-stage renal disease (ESRD).</p> <p>Methods</p> <p>We studied all consecutive patients initiated on maintenance hemodialysis or peritoneal dialysis over several years at two dialysis units in Northern California. Rapid decline in kidney function was considered to have occurred if a patient was documented to have estimated GFR > 30 ml/min/1.73 m²within three months prior to the initiation of chronic dialysis.</p> <p>Results</p> <p>We found that 8 out of 105 incident chronic dialysis patients one dialysis unit (7.6%; 95% confidence interval 3.4-14.5%) and 9 out of 71 incident patients at another (12.7%, 95% CI 6.0%-22.7%) suffered rapid decline in kidney function that was the immediate precipitant for the need for permanent renal replacement therapy. All these patients started hemodialysis and all relied on catheters for vascular access. Documentation submitted to United States Renal Data System did not fully reflect the health status of these patients during their "pre-ESRD" period.</p> <p>Conclusions</p> <p>A sizeable minority of ESRD cases are preceded by rapid declines in kidney function. The importance of these periods of rapid decline may have been under-appreciated in prior studies of the natural history of CKD and ESRD.</p

Occupational and Environmental Risks from Mancozeb in Aviation Facilities in the Banana Producing Area of Teapa, Tabasco, Mexico

Purpose: To identify occupational risks and practices in the four aerial fumigation facilities in the Sierra banana growing region and to evaluate environmental impacts from Mancozeb use.Methods: Occupational health risks were identified and practices in the four aerial fumigation facilities in the Sierra banana growing region were documented. Semi-structured interviews were conducted with installation managers. To evaluate environmental impact, samples of water and soil were collected and analysed in an acute toxicity bioassay with Vibrio fischeri, using uncontaminated soil and water to establish background levels.Results: Even in the largest and best-equipped facility, serious risks to workers’ health were encountered from inadequate use of protective equipment by workers. Furthermore, excessive use of pesticide, lack of re-use of unused product, poor facility design and poor use of wash-water were observed, resulting in  maximum toxicity of &gt; 5 times background in discharged water. Parallel soil samples were &gt; 20 times  more toxic than background, being most toxic at &gt; 0.5 km from the discharge point.Conclusion: Areas of opportunity to improve worker health and the environment include proper and  consistent use of protective equipment, re-use of unused product, wastewater reduction and appropriate wastewater treatment.Keywords: Black Sigatoka, Ethylene thiourea, Fumigation, Pesticide, Mancozeb, Airports, Microtox, Vibrio fischeri, Occupational health risks, Toxicit

Stress hormones promote growth of B16-F10 melanoma metastases: an interleukin 6-and glutathione-dependent mechanism

[EN] Background: Interleukin (IL)-6 (mainly of tumor origin) activates glutathione (GSH) release from hepatocytes and its interorgan transport to B16-F10 melanoma metastatic foci. We studied if this capacity to overproduce IL-6 is regulated by cancer cell-independent mechanisms. Methods: Murine B16-F10 melanoma cells were cultured, transfected with red fluorescent protein, injected i.v. into syngenic C57BL/6J mice to generate lung and liver metastases, and isolated from metastatic foci using high-performance cell sorting. Stress hormones and IL-6 levels were measured by ELISA, and CRH expression in the brain by in situ hybridization. DNA binding activity of NF-kappa B, CREB, AP-1, and NF-IL-6 was measured using specific transcription factor assay kits. IL-6 expression was measured by RT-PCR, and silencing was achieved by transfection of anti-IL-6 small interfering RNA. GSH was determined by HPLC. Cell death analysis was distinguished using fluorescence microscopy, TUNEL labeling, and flow cytometry techniques. Statistical analyses were performed using Student's t test. Results: Plasma levels of stress-related hormones (adrenocorticotropin hormone, corticosterone, and noradrenaline) increased, following a circadian pattern and as compared to non-tumor controls, in mice bearing B16-F10 lung or liver metastases. Corticosterone and noradrenaline, at pathophysiological levels, increased expression and secretion of IL-6 in B16-F10 cells in vitro. Corticosterone- and noradrenaline-induced transcriptional up-regulation of IL-6 gene involves changes in the DNA binding activity of nuclear factor-kappa B, cAMP response element-binding protein, activator protein-1, and nuclear factor for IL-6. In vivo inoculation of B16-F10 cells transfected with anti-IL-6-siRNA, treatment with a glucocorticoid receptor blocker (RU-486) or with a beta-adrenoceptor blocker (propranolol), increased hepatic GSH whereas decreased plasma IL-6 levels and metastatic growth. Corticosterone, but not NORA, also induced apoptotic cell death in metastatic cells with low GSH content. Conclusions: Our results describe an interorgan system where stress-related hormones, IL-6, and GSH coordinately regulate metastases growthThis research was supported by grant (SAF2009-07729 and IPT-010000-2010-21) from the Ministerio de Economia y Competitividad (http://www.idi.mineco.gob.es), Spain.Valles, SL.; Benlloch, M.; Rodriguez, ML.; Mena-Mollá, S.; Pellicer, JA.; Asensi-Miralles, MÁ.; Obrador, E.... (2013). Stress hormones promote growth of B16-F10 melanoma metastases: an interleukin 6-and glutathione-dependent mechanism. Journal of Translational Medicine. 11:1-14. https://doi.org/10.1186/1479-5876-11-72S11411Meister, A. (1983). Selective modification of glutathione metabolism. Science, 220(4596), 472-477. doi:10.1126/science.6836290Estrela, J. M., Ortega, A., & Obrador, E. (2006). Glutathione in Cancer Biology and Therapy. Critical Reviews in Clinical Laboratory Sciences, 43(2), 143-181. doi:10.1080/10408360500523878Obrador, E., Benlloch, M., Pellicer, J. A., Asensi, M., & Estrela, J. M. (2011). Intertissue Flow of Glutathione (GSH) as a Tumor Growth-promoting Mechanism. Journal of Biological Chemistry, 286(18), 15716-15727. doi:10.1074/jbc.m110.196261Meister, A. (1991). Glutathione deficiency produced by inhibition of its synthesis, and its reversal; Applications in research and therapy. Pharmacology & Therapeutics, 51(2), 155-194. doi:10.1016/0163-7258(91)90076-xHanigan, M. H. (1995). Expression of gamma-glutamyl transpeptidase provides tumor cells with a selective growth advantage at physiologic concentrations of cyst(e)ine. Carcinogenesis, 16(2), 181-185. doi:10.1093/carcin/16.2.181Obrador, E. (2002). γ-Glutamyl transpeptidase overexpression increases metastatic growth of B16 melanoma cells in the mouse liver. Hepatology, 35(1), 74-81. doi:10.1053/jhep.2002.30277Ballatori, N., & Rebbeor, J. (1998). Roles of MRP2 and oatp1 in Hepatocellular Export of Reduced Glutathione. Seminars in Liver Disease, 18(04), 377-387. doi:10.1055/s-2007-1007171Hodge, D. R., Hurt, E. M., & Farrar, W. L. (2005). The role of IL-6 and STAT3 in inflammation and cancer. European Journal of Cancer, 41(16), 2502-2512. doi:10.1016/j.ejca.2005.08.016Barton, B. E. (2005). Interleukin-6 and new strategies for the treatment of cancer, hyperproliferative diseases and paraneoplastic syndromes. Expert Opinion on Therapeutic Targets, 9(4), 737-752. doi:10.1517/14728222.9.4.737Rose-John, S., Waetzig, G. H., Scheller, J., Grötzinger, J., & Seegert, D. (2007). The IL-6/sIL-6R complex as a novel target for therapeutic approaches. Expert Opinion on Therapeutic Targets, 11(5), 613-624. doi:10.1517/14728222.11.5.613Ara, T., & DeClerck, Y. A. (2010). Interleukin-6 in bone metastasis and cancer progression. European Journal of Cancer, 46(7), 1223-1231. doi:10.1016/j.ejca.2010.02.026Emmenegger, U., & Kerbel, R. S. (2010). Chemotherapy counteracted. Nature, 468(7324), 637-638. doi:10.1038/468637aWang, Y., Niu, X. L., Qu, Y., Wu, J., Zhu, Y. Q., Sun, W. J., & Li, L. Z. (2010). Autocrine production of interleukin-6 confers cisplatin and paclitaxel resistance in ovarian cancer cells. Cancer Letters, 295(1), 110-123. doi:10.1016/j.canlet.2010.02.019Sternberg, E. M. (1997). Neural-immune interactions in health and disease. Journal of Clinical Investigation, 100(11), 2641-2647. doi:10.1172/jci119807Reiche, E. M. V., Nunes, S. O. V., & Morimoto, H. K. (2004). Stress, depression, the immune system, and cancer. The Lancet Oncology, 5(10), 617-625. doi:10.1016/s1470-2045(04)01597-9Besedovsky, H. O., Del Rey, A., Klusman, I., Furukawa, H., Monge Arditi, G., & Kabiersch, A. (1991). Cytokines as modulators of the hypothalamus-pituitary-adrenal axis. The Journal of Steroid Biochemistry and Molecular Biology, 40(4-6), 613-618. doi:10.1016/0960-0760(91)90284-cBethin, K. E., Vogt, S. K., & Muglia, L. J. (2000). Interleukin-6 is an essential, corticotropin-releasing hormone-independent stimulator of the adrenal axis during immune system activation. Proceedings of the National Academy of Sciences, 97(16), 9317-9322. doi:10.1073/pnas.97.16.9317Herr, I., & Pfitzenmaier, J. (2006). Glucocorticoid use in prostate cancer and other solid tumours: implications for effectiveness of cytotoxic treatment and metastases. The Lancet Oncology, 7(5), 425-430. doi:10.1016/s1470-2045(06)70694-5Bernabé, D. G., Tamae, A. C., Biasoli, É. R., & Oliveira, S. H. P. (2011). Stress hormones increase cell proliferation and regulates interleukin-6 secretion in human oral squamous cell carcinoma cells. Brain, Behavior, and Immunity, 25(3), 574-583. doi:10.1016/j.bbi.2010.12.012Antoni, M. H., Lutgendorf, S. K., Cole, S. W., Dhabhar, F. S., Sephton, S. E., McDonald, P. G., … Sood, A. K. (2006). The influence of bio-behavioural factors on tumour biology: pathways and mechanisms. Nature Reviews Cancer, 6(3), 240-248. doi:10.1038/nrc1820Yang, E. V., Kim, S., Donovan, E. L., Chen, M., Gross, A. C., Webster Marketon, J. I., … Glaser, R. (2009). Norepinephrine upregulates VEGF, IL-8, and IL-6 expression in human melanoma tumor cell lines: Implications for stress-related enhancement of tumor progression. Brain, Behavior, and Immunity, 23(2), 267-275. doi:10.1016/j.bbi.2008.10.005Carretero, J., Obrador, E., Anasagasti, M. J., Martin, J. J., Vidal-Vanaclocha, F., & Estrela, J. M. (1999). Clinical and Experimental Metastasis, 17(7), 567-574. doi:10.1023/a:1006725226078Lachize, S., Apostolakis, E. M., van der Laan, S., Tijssen, A. M. I., Xu, J., de Kloet, E. R., & Meijer, O. C. (2009). Steroid receptor coactivator-1 is necessary for regulation of corticotropin-releasing hormone by chronic stress and glucocorticoids. Proceedings of the National Academy of Sciences, 106(19), 8038-8042. doi:10.1073/pnas.0812062106Veenema, A. H., Reber, S. O., Selch, S., Obermeier, F., & Neumann, I. D. (2008). Early Life Stress Enhances the Vulnerability to Chronic Psychosocial Stress and Experimental Colitis in Adult Mice. Endocrinology, 149(6), 2727-2736. doi:10.1210/en.2007-1469Asensi, M., Sastre, J., Pallardo, F. V., Delaasuncion, J. G., Estrela, J. M., & Vina, J. (1994). A High-Performance Liquid Chromatography Method for Measurement of Oxidized Glutathione in Biological Samples. Analytical Biochemistry, 217(2), 323-328. doi:10.1006/abio.1994.1126Ortega, A. L., Carretero, J., Obrador, E., Gambini, J., Asensi, M., Rodilla, V., & Estrela, J. M. (2003). Tumor Cytotoxicity by Endothelial Cells. Journal of Biological Chemistry, 278(16), 13888-13897. doi:10.1074/jbc.m207140200SAKAKIBARA, H., KOYANAGI, A., SUZUKI, T., SUZUKI, A., LING, L., & SHIMOI, K. (2010). Effects of Animal Care Procedures on Plasma Corticosterone Levels in Group-Housed Mice during the Nocturnal Active Phase. Experimental Animals, 59(5), 637-642. doi:10.1538/expanim.59.637Lucot, J. B., Jackson, N., Bernatova, I., & Morris, M. (2005). Measurement of plasma catecholamines in small samples from mice. Journal of Pharmacological and Toxicological Methods, 52(2), 274-277. doi:10.1016/j.vascn.2004.11.004Dobos, J., Kenessey, I., Tímár, J., & Ladányi, A. (2011). Glucocorticoid Receptor Expression and Antiproliferative Effect of Dexamethasone on Human Melanoma Cells. Pathology & Oncology Research, 17(3), 729-734. doi:10.1007/s12253-011-9377-8Tsuji, M., Kuno, T., Tanaka, C., Ichihashi, M., & Mishima, Y. (1983). Beta-adrenergic receptors of B16 melanoma cell. Archives of Dermatological Research, 275(6), 415-416. doi:10.1007/bf00417345Im, A., & Appleman, L. J. (2010). Mifepristone: pharmacology and clinical impact in reproductive medicine, endocrinology and oncology. Expert Opinion on Pharmacotherapy, 11(3), 481-488. doi:10.1517/14656560903535880Smoak, K. A., & Cidlowski, J. A. (2004). Mechanisms of glucocorticoid receptor signaling during inflammation. Mechanisms of Ageing and Development, 125(10-11), 697-706. doi:10.1016/j.mad.2004.06.010Cole, S. W., & Sood, A. K. (2011). Molecular Pathways: Beta-Adrenergic Signaling in Cancer: Figure 1. Clinical Cancer Research, 18(5), 1201-1206. doi:10.1158/1078-0432.ccr-11-0641Matsusaka, T., Fujikawa, K., Nishio, Y., Mukaida, N., Matsushima, K., Kishimoto, T., & Akira, S. (1993). Transcription factors NF-IL6 and NF-kappa B synergistically activate transcription of the inflammatory cytokines, interleukin 6 and interleukin 8. Proceedings of the National Academy of Sciences, 90(21), 10193-10197. doi:10.1073/pnas.90.21.10193McEwen, B. S. (2007). Physiology and Neurobiology of Stress and Adaptation: Central Role of the Brain. Physiological Reviews, 87(3), 873-904. doi:10.1152/physrev.00041.2006Lee, J.-H., Yoo, S. B., Kim, N. Y., Cha, M. J., & Jahng, J. W. (2008). Interleukin-6 and the Hypothalamic-Pituitary-Adrenal Activation in a Tumor Bearing Mouse. International Journal of Neuroscience, 118(3), 355-364. doi:10.1080/00207450701592915Li, Y.-F., He, R.-R., Tsoi, B., Li, X.-D., Li, W.-X., Abe, K., & Kurihara, H. (2012). Anti-Stress Effects of Carnosine on Restraint-Evoked Immunocompromise in Mice through Spleen Lymphocyte Number Maintenance. PLoS ONE, 7(4), e33190. doi:10.1371/journal.pone.0033190Sarabdjitsingh, R. A., Kofink, D., Karst, H., de Kloet, E. R., & Joëls, M. (2012). Stress-Induced Enhancement of Mouse Amygdalar Synaptic Plasticity Depends on Glucocorticoid and ß-Adrenergic Activity. PLoS ONE, 7(8), e42143. doi:10.1371/journal.pone.0042143Moreno-Smith, M., Lutgendorf, S. K., & Sood, A. K. (2010). Impact of stress on cancer metastasis. Future Oncology, 6(12), 1863-1881. doi:10.2217/fon.10.142Tissing, W. J. E., Meijerink, J. P. P., den Boer, M. L., & Pieters, R. (2003). Molecular determinants of glucocorticoid sensitivity and resistance in acute lymphoblastic leukemia. Leukemia, 17(1), 17-25. doi:10.1038/sj.leu.2402733Anderer, G., Schrappe, M., Brechlin, A. M., Lauten, M., Muti, P., Welte, K., & Stanulla, M. (2000). Polymorphisms within glutathione S-transferase genes and initial response to glucocorticoids in childhood acute lymphoblastic leukaemia. Pharmacogenetics, 10(8), 715-726. doi:10.1097/00008571-200011000-00006Thaker, P. H., & Sood, A. K. (2008). Neuroendocrine influences on cancer biology. Seminars in Cancer Biology, 18(3), 164-170. doi:10.1016/j.semcancer.2007.12.005Takeda, T., Kurachi, H., Yamamoto, T., Nishio, Y., Nakatsuji, Y., Morishige, K., … Murata, Y. (1998). Crosstalk between the interleukin-6 (IL-6)-JAK-STAT and the glucocorticoid-nuclear receptor pathway: synergistic activation of IL-6 response element by IL-6 and glucocorticoid. Journal of Endocrinology, 159(2), 323-330. doi:10.1677/joe.0.1590323Rodriguez-Rocha, H., Garcia Garcia, A., Zavala-Flores, L., Li, S., Madayiputhiya, N., & Franco, R. (2012). Glutaredoxin 1 Protects Dopaminergic Cells by Increased Protein Glutathionylation in Experimental Parkinson’s Disease. Antioxidants & Redox Signaling, 17(12), 1676-1693. doi:10.1089/ars.2011.4474Tome, M. E., Jaramillo, M. C., & Briehl, M. M. (2011). Hydrogen peroxide signaling is required for glucocorticoid-induced apoptosis in lymphoma cells. Free Radical Biology and Medicine, 51(11), 2048-2059. doi:10.1016/j.freeradbiomed.2011.09.002Lázár-Molnár, E., Hegyesi, H., Tóth, S., & Falus, A. (2000). AUTOCRINE AND PARACRINE REGULATION BY CYTOKINES AND GROWTH FACTORS IN MELANOMA. Cytokine, 12(6), 547-554. doi:10.1006/cyto.1999.0614Sansone, P., & Bromberg, J. (2012). Targeting the Interleukin-6/Jak/Stat Pathway in Human Malignancies. Journal of Clinical Oncology, 30(9), 1005-1014. doi:10.1200/jco.2010.31.8907Arrigo, A.-P. (1999). Gene expression and the thiol redox state. Free Radical Biology and Medicine, 27(9-10), 936-944. doi:10.1016/s0891-5849(99)00175-6Antelmann, H., & Helmann, J. D. (2011). Thiol-Based Redox Switches and Gene Regulation. Antioxidants & Redox Signaling, 14(6), 1049-1063. doi:10.1089/ars.2010.3400Leibowitz, B., & Yu, J. (2010). Mitochondrial signaling in cell death via the Bcl-2 family. Cancer Biology & Therapy, 9(6), 417-422. doi:10.4161/cbt.9.6.11392Powe, D. G., Voss, M. J., Habashy, H. O., Zänker, K. S., Green, A. R., Ellis, I. O., & Entschladen, F. (2011). Alpha- and beta-adrenergic receptor (AR) protein expression is associated with poor clinical outcome in breast cancer: an immunohistochemical study. Breast Cancer Research and Treatment, 130(2), 457-463. doi:10.1007/s10549-011-1371-zPowe, D. G., & Entschladen, F. (2011). Using β-blockers to inhibit breast cancer progression. Nature Reviews Clinical Oncology, 8(9), 511-512. doi:10.1038/nrclinonc.2011.12