Using Near-Infrared Spectroscopy in Agricultural Systems

This chapter provides a review on the state of art of the use of the visible near-infrared (vis-NIR) spectroscopy technique to determine mineral nutrients, organic compounds, and other physical and chemical characteristics in samples from agricultural systems—such as plant tissues, soils, fruits, cocomposted sewage sludge and wastes, cereals, and forage and silage. Currently, all this information is needed to be able to carry out the appropriate fertilization of crops, to handle agricultural soils, determine the organoleptic characteristics of fruit and vegetable products, discover the characteristics of the various substrates obtained in composting processes, and characterize byproducts from the industrial sector. All this needs a large number of samples that must be analyzed; this is a time-consuming work, leading to high economic costs and, obviously, having a negative environmental impact owing to the production of noxious chemicals during the analyses. Therefore, the development of a fast, environmentally friendly, and cheaper method of analysis like vis-NIR is highly desirable. Our intention here is to introduce the main fundamentals of infrared reflectance spectroscopy, and to show that procedures like calibration and validation of data from vis-NIR spectra must be performed, and describe the parameters most commonly measured in the agricultural sector

Inflammatory correlated response in two lines of rabbit selected divergently for litter size environmental variability

[EN] Animal welfare is a priority objective for the livestock industry. Litter size environmental variability has been related to environmental sensitivity. A divergent selection experiment for environmental variance of litter size variance was carried out successfully in rabbits over thirteen generations. The low line showed a lower inflammatory response and susceptibility to infectious disorders than the high line. In conclusion, the decrease of environmental sensitivity seems to increase the adaptation of the animal to the environment, and thus, its welfare.This research was supported by Projects AGL2017-86083, C2-1-P and C2-2-P, funded by Ministerio de Ciencia e Innovacion (MIC)-Agencia Estatal de Investigacion (AEI) and el Fondo Europeo de Desarrollo Regional (FEDER) "Una manera de hacer Europa" and Project AICO/2019/169 funded by Valencia Regional Government.Beloumi, D.; Blasco Mateu, A.; Muelas, R.; Santacreu Jerez, MA.; García, MDLL.; Argente, M. (2020). 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PLOS ONE, 13(8), e0202555. doi:10.1371/journal.pone.0202555Chen, W., Zheng, K. I., Liu, S., Yan, Z., Xu, C., & Qiao, Z. (2020). Plasma CRP level is positively associated with the severity of COVID-19. Annals of Clinical Microbiology and Antimicrobials, 19(1). doi:10.1186/s12941-020-00362-2Stoner, L., Lucero, A. A., Palmer, B. R., Jones, L. M., Young, J. M., & Faulkner, J. (2013). Inflammatory biomarkers for predicting cardiovascular disease. Clinical Biochemistry, 46(15), 1353-1371. doi:10.1016/j.clinbiochem.2013.05.070Iung, L. H. de S., Carvalheiro, R., Neves, H. H. de R., & Mulder, H. A. (2019). Genetics and genomics of uniformity and resilience in livestock and aquaculture species: A review. Journal of Animal Breeding and Genetics, 137(3), 263-280. doi:10.1111/jbg.12454Blasco, A., Martínez-Álvaro, M., García, M.-L., Ibáñez-Escriche, N., & Argente, M.-J. (2017). Selection for environmental variance of litter size in rabbits. 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Oxidative Stress and NLRP3-Inflammasome Activity as Significant Drivers of Diabetic Cardiovascular Complications: Therapeutic Implications. Frontiers in Physiology, 9. doi:10.3389/fphys.2018.00114Fan, J., Kitajima, S., Watanabe, T., Xu, J., Zhang, J., Liu, E., & Chen, Y. E. (2015). Rabbit models for the study of human atherosclerosis: From pathophysiological mechanisms to translational medicine. Pharmacology & Therapeutics, 146, 104-119. doi:10.1016/j.pharmthera.2014.09.009Zhao, X., Li, L., Li, X., Li, J., Wang, D., & Zhang, H. (2019). The Relationship between Serum Bilirubin and Inflammatory Bowel Disease. Mediators of Inflammation, 2019, 1-7. doi:10.1155/2019/5256460Inoguchi, T., Sonoda, N., & Maeda, Y. (2016). Bilirubin as an important physiological modulator of oxidative stress and chronic inflammation in metabolic syndrome and diabetes: a new aspect on old molecule. Diabetology International, 7(4), 338-341. doi:10.1007/s13340-016-0288-5Koenig, G., & Seneff, S. (2015). 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p38MAPK and Chemotherapy: We always need to hear both Sides of the Story

The p38MAPK signaling pathway was initially described as a stress response mechanism. In fact, during previous decades, it was considered a pathway with little interest in oncology especially in comparison with other MAPKs such as ERK1/2, known to be target of oncogenes like Ras. However, its involvement in apoptotic cell death phenomena makes this signaling pathway more attractive for many cancer research laboratories. This apoptotic role allows to establish a link between p38MAPK and regular chemotherapeutic agents such as Cisplatin or base analogs (Cytarabine, Gemcitabine or 5-Fluorouracil) which are currently used in hospitals across the world. In fact, and more recently, p38MAPK has also been connected with targeted therapies like tyrosine kinase inhibitors (vg. Imatinib, Sorafenib) and, to a lesser extent, with monoclonal antibodies. In addition, the oncogenic or tumor suppressor potential of this signaling pathway has aroused the interest of the scientific community in evaluating p38MAPK as a novel target for cancer therapy. In this review, we will summarize the role of p38MAPK in chemotherapy as well as the potential that p38MAPK inhibition can bring to cancer therapy. All the evidences suggest that p38MAPK could be a double-edged sword and that the search for the most appropriate candidate patients, depending on their pathology and treatment, will lead to a more rational use of this new therapeutic tool

ERK5 signalling pathway is a novel target of sorafenib: Implication in EGF biology

© 2021 The Authors.Sorafenib is a multikinase inhibitor widely used in cancer therapy with an antitumour effect related to biological processes as proliferation, migration or invasion, among others. Initially designed as a Raf inhibitor, Sorafenib was later shown to also block key molecules in tumour progression such as VEGFR and PDGFR. In addition, sorafenib has been connected with key signalling pathways in cancer such as EGFR/EGF. However, no definitive clue about the molecular mechanism linking sorafenib and EGF signalling pathway has been established so far. Our data in HeLa, U2OS, A549 and HEK293T cells, based on in silico, chemical and genetic approaches demonstrate that the MEK5/ERK5 signalling pathway is a novel target of sorafenib. In addition, our data show how sorafenib is able to block MEK5-dependent phosphorylation of ERK5 in the Ser218/Tyr220, affecting the transcriptional activation associated with ERK5. Moreover, we demonstrate that some of the effects of this kinase inhibitor onto EGF biological responses, such as progression through cell cycle or migration, are mediated through the effect exerted onto ERK5 signalling pathway. Therefore, our observations describe a novel target of sorafenib, the ERK5 signalling pathway, and establish new mechanistic insights for the antitumour effect of this multikinase inhibitor.This work was supported by grants from Fundación Leticia Castillejo Castillo, Ministerio de Ciencia, Innovación y Universidades (MCIU), Agencia Estatal de Investigación (AEI) and Fondo Europeo de Desarrollo Regional (FEDER) (RTI2018-094093-B-I00) to RSP and MJRH. OR holds a contract for accessing the Spanish System of Science, Technology, and Innovation (SECTI) funded by the University of Castilla-La Mancha (UCLM) and received partial support from the European Social Fund (FSE) through its Operative Program for Castilla-La Mancha (2007–2013). RSP and MJRH's Research Institute, and the work carried out in their laboratory, received partial support from the European Community through the FEDER. RPS and EAL hold a research predoctoral contract cofounded by the European Social Fund and UCLM. The Spanish Ministry of Economy and Competitiveness (MINECO, Project RTI2018-096724-B-C21) and the Generalitat Valenciana (PROMETEO/2016/006) support work in the Encinar´s laboratory. Authors are grateful to Dr.G- Ferrer Mayorga for her assistance in the transwell assays, and to the ‘Centro de Computación Científica’ (CCC-UAM) for letting us to take advantage of the computer cluster Cibeles (https://www.ccc.uam.es/) and for providing computing facilities

Exploiting the potential of autophagy in cisplatin therapy: a new strategy to overcome resistance

Resistance to cisplatin is a major challenge in the current cancer therapy. In order to explore new therapeutic strategies to cisplatin resistance, we evaluated, in a model of lung cancer (H1299 and H460 cell lines), the nature of the pathways leading to cell death. We observed that H1299 displayed a natural resistance to cisplatin due to an inability to trigger an apoptotic response that correlates with the induction of autophagy. However, pharmacological and genetic approaches showed how autophagy was a mechanism associated to cell death rather than to resistance. Indeed, pro-autophagic stimuli such as mTOR or Akt inhibition mediate cell death in both cell lines to a similar extent. We next evaluated the response to a novel platinum compound, monoplatin, able to promote cell death in an exclusive autophagy-dependent manner. In this case, no differences were observed between both cell lines. Furthermore, in response to monoplatin, two molecular hallmarks of cisplatin response (p53 and MAPKs) were not implicated, indicating the ability of this pro-autophagic compound to overcome cisplatin resistance. In summary, our data highlight how induction of autophagy could be used in cisplatin resistant tumours and an alternative treatment for p53 mutated patient in a synthetic lethally approach

Can Sustained Deficit Irrigation Save Water and Meet the Quality Characteristics of Mango?

Mango is one of the most cultivated tropical fruits worldwide and one of few drought-tolerant plants. Thus, in this study the effect of a sustained deficit irrigation (SDI) strategy on mango yield and quality was assessed with the aim of reducing irrigation water in mango crop. A randomized block design with four treatments was developed: (i) full irrigation (FI), assuring the crop’s water needs, and three levels of SDI receiving 75%, 50%, and 33% of irrigation water (SDI75, SDI50, and SDI33). Yield, morphology, color, titratable acidity (TA), total soluble solids (TSS), organic acids (OA), sugars, minerals, fiber, antioxidant activity (AA), and total phenolic content (TPC) were analyzed. The yield was reduced in SDI conditions (8%, 11%, and 20% for SDI75, SDI50, and SDI33, respectively), but the irrigation water productivity was higher in all SDI regimes. SDI significantly reduced the mango size, with SDI33 generating the smallest mangoes. Peel color significantly changed after 13 days of ripening, with SDI75 being the least ripe. The TA, AA, and citric acid were higher in SDI75, while the TPC and fiber increased in all SDI levels. Consequently, SDI reduced the mango size but increased the functionality of samples, without a severe detrimental effect on the yield

Exploiting the potential of autophagy in cisplatin therapy: A new strategy to overcome resistance

Resistance to cisplatin is a major challenge in the current cancer therapy. In order to explore new therapeutic strategies to cisplatin resistance, we evaluated, in a model of lung cancer (H1299 and H460 cell lines), the nature of the pathways leading to cell death. We observed that H1299 displayed a natural resistance to cisplatin due to an inability to trigger an apoptotic response that correlates with the induction of autophagy. However, pharmacological and genetic approaches showed how autophagy was a mechanism associated to cell death rather than to resistance. Indeed, pro-autophagic stimuli such as mTOR or Akt inhibition mediate cell death in both cell lines to a similar extent. We next evaluated the response to a novel platinum compound, monoplatin, able to promote cell death in an exclusive autophagy-dependent manner. In this case, no differences were observed between both cell lines. Furthermore, in response to monoplatin, two molecular hallmarks of cisplatin response (p53 and MAPKs) were not implicated, indicating the ability of this pro-autophagic compound to overcome cisplatin resistance. In summary, our data highlight how induction of autophagy could be used in cisplatin resistant tumours and an alternative treatment for p53 mutated patient in a synthetic lethally approach.This work was supported by grants from Fundación Leticia Castillejo Castillo and Ministerio de Economía y Competitividad (grant SAF2012-30862 to RSP and grant CTQ2011-24434 to FAJ). RSP Research Institute, and the work carried out in his laboratory receive support from the European Community through the regional development funding program (FEDER). JGC received funding from the Regional Ministry of Education and Science of Castilla–La Mancha (FPI-JCCM) and from Fundación Leticia Castillejo Castillo. MCC and RSP have a contract from the INCRECYT progra

Blockage of autophagic ux is associated with lymphocytosis and higher percentage of tumoral cells in chronic lymphocytic leukemia of B-cells

Póster presentado al 42nd Congress of the Spanish Society of Biochemistry and Molecular Biology (SEBBM), celebrado en Madrid del 16 al 19 de julio de 2019.[Objective] Autophagy has lately emerged as an important biological process with implications in several hematological pathologies. Recently, a growing body of evidence supports a putative role of autophagy in chronic lymphocytic leukemia, however no definitive clue has been established so far. To elucidate this issue, we have developed a pilot study to measure autophagic flux in peripheral blood mononuclear cells from chronic lymphocytic leukemia patients, and explored its correlation with classical clinical/analytical parameters. [Methods/Patients] Thirty-three chronic lymphocytic leukemia patients participated in the study. Autophagic flux in peripheral blood mononuclear cells was determined by western blot measuring the levels of the proteins p62 and lipidated LC3. Moreover, p62 mRNA levels were studied by RT-qPCR. [Results] Lymphocytosis and the percentage of tumoral lymphocytes in chronic lymphocityc leukemia patients statistically correlates with a blocked autophagic flux. [Conclusion] Alterations in autophagic flux could play an important role in the physiopathology of chronic lymphocytic leukemia.Fundación Leticia Castillejo Castillo, Ministerio de Economía y Competitividad. Sociedad Castellano Manchega de Hematología y Hemoterapia. RSP and MJRH Research Institutes, and the work carried out in their laboratories received support from the European Community through the Regional Development Funding Program (FEDER).Peer reviewe