Application of biostimulant products and biological control agents in sustainable viticulture: A review

Current and continuing climate change in the Anthropocene epoch requires sustainable agricultural practices. Additionally, due to changing consumer preferences, organic approaches to cultivation are gaining popularity. The global market for organic grapes, grape products, and wine is growing. Biostimulant and biocontrol products are often applied in organic vineyards and can reduce the synthetic fertilizer, pesticide, and fungicide requirements of a vineyard. Plant growth promotion following application is also observed under a variety of challenging conditions associated with global warming. This paper reviews different groups of biostimulants and their effects on viticulture, including microorganisms, protein hydrolysates, humic acids, pyrogenic materials, and seaweed extracts. Of special interest are biostimulants with utility in protecting plants against the effects of climate change, including drought and heat stress. While many beneficial effects have been reported following the application of these materials, most studies lack a mechanistic explanation, and important parameters are often undefined (e.g., soil characteristics and nutrient availability). We recommend an increased study of the underlying mechanisms of these products to enable the selection of proper biostimulants, application methods, and dosage in viticulture. A detailed understanding of processes dictating beneficial effects in vineyards following application may allow for biostimulants with increased efficacy, uptake, and sustainability.KJ wishes to acknowledge financial support (3710473400); MS-M thanks to RTI2018-099417-B-I00 (Spanish Ministry of Science, Innovation and Universities cofunded with EU FEDER funds); JB wish to acknowledge the Conselho Nacional de Desenvolvimento Científico e Tecnológico/Brasil (CNPQ process number 309477/2021-2); RO-H is supported by the Ramón y Cajal program from the MICINN (RYC-2017 22032), PAIDI 2020 (Ref. 20_00323), AEI GGOO 2020 (GOPC-CA-20-0001), “José Castillejo” program from the “Ministerio de Universidades” (CAS21/00125) and PID2019-106004RA-I00/AEI/10.13039/501100011033. SM and GT thanks to Ministerio de Ciencia e Innovación (grant PID2020-114330GB-100). PAIDI2020 from Junta de Andalucía, grant P18-RT-1401 to SM, MD, and GT is also acknowledged. GT acknowledge the support of the publication fee by the CSIC Open Access Publication Support Initiative through its Unit of Information Resources for Research (URICI)

Repositioning of the global epicentre of non-optimal cholesterol

High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world3 and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol—which is a marker of cardiovascular risk—changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95% credible interval 3.7 million–4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world.</p

Repositioning of the global epicentre of non-optimal cholesterol

High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world3 and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol�which is a marker of cardiovascular risk�changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95 credible interval 3.7 million�4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world. © 2020, The Author(s), under exclusive licence to Springer Nature Limited

Decomposition patterns of surface leaf of six plant species along a Chihuahua desert watershed

Mass losses from litter bags of surface creosote bush litter placed along a Chihuahuan Desert watershed were measured to answer the following questions: (1) Do edaphic factors affect organic matter losses? (2) Are there differences in mass losses between the litter of the site-dominant plant species and creosote bush leaf litter? We hypothesized that (1) mass losses of all litter types would be higher at the base of the watershed and lower on the upper portions of the watershed and (2) mass losses of the litter of the site-dominant plants would be higher than those of creosote bush leaf litter in the same site. Mass losses from creosote bush leaf litter did not follow the moisture-organic matter gradient present in the watershed. Mass losses were higher at mid-slope run-on areas than in upper-slope erosional sites and the dry lake basin. Mass losses were highest where subterranean termite activity was the highest. There were differences between losses from the litter of the site-dominant and creosote bush leaf litter in some instances, but these differences were not attributable to differences in lignin content nor C:N ratio. Mass losses of litter of site-dominant species were not always higher than that of creosote bush leaf litter in the same site. Mass losses were best described by the double exponential model

Effects of MPP+ on the molecular pathways involved in cell cycle control in B65 neuroblastoma cells

The toxicity caused by cell exposure to 1-methyl-4-phenylpyridinium ion (MPP+) is a useful model in the study of Parkinson's disease (PD). However, the exact molecular mechanisms triggered by MPP+ in cell death are currently unclear. In the present research, we show that exposure to MPP+ induce the cell death of neuroblastoma-derived dopaminergic B65 cells, which is not reversed by the widely known caspase inhibitor Z-VADfmk or by calpain inhibition. Likewise, when B65 cells were treated with MPP+, the DNA damage pathway that involves p53 was activated, and cells were arrested in the G2/M phase of the cell cycle. Interestingly, MPP+ has two effects on the expression of cell cycle-related proteins. It increases the content of cyclins A, E, cdk2 and the phosphorylated form of pRb (serine 780). However, MPP+ 5mM decreased the expression of cyclin D1, B1 and cdk4. The decrease in the expression of cyclin B1 may be related to the arrest of cells observed in the G2/M phase of cell cycle. The increase in S phase cell cycle proteins and retinoblastoma protein phosphorylation was an unexpected result. As the antioxidant trolox attenuated the process of cell loss and changes in the cell cycle, as measured by flow cytometry, we concluded that oxidative stress was involved in the effects of MPP+ in this cell line. In summary, the present work characterizes the molecular changes involved in damage caused by MPP+ in B65 cells, and highlights the effects of MPP+ on molecules involved in the control of cell cycle progression. © 2010 Elsevier Ltd

Antiapoptotic effects of roscovitine on camptothecin-induced DNA damage in neuroblastoma cells

In the present study dopaminergic neuroblastoma B65 cells were exposed to Camptothecin (CPT) (0.5-10 μM), either alone or in the presence of roscovitine (ROSC). The results show that CPT induces apoptosis through the activation of ataxia telangiectasia mutated (ATM)-induced cell-cycle alteration in neuroblastoma B65 cells. The apoptotic process is mediated through the activation of cystein proteases, namely calpain/caspases. However, whereas a pan-caspase inhibitor, zVADfmk, inhibited CPT-mediated apoptosis, a calpain inhibitor, calpeptin, did not prevent cell death. Interestingly, CPT also induces CDK5 activation and ROSC (25 μM) blocked CDK5, ATM activation and apoptosis (as measured by caspase-3 activation). By contrast, selective inhibition of ATM, by KU55933, and non-selective inhibition, by caffeine, did not prevent CPT-mediated apoptosis. Thus, we conclude that CDK5 is activated in response to DNA damage and that CDK5 inhibition prevents ATM and p53ser15 activation. However, pharmacological inhibition of ATM using KU55933 and caffeine suggests that ATM inhibition by ROSC is not the only mechanism that might explain the anti-apoptotic effects of this drug in this apoptosis model. Our findings have a potential clinical implication, suggesting that combinatory drugs in the treatment of cancer activation should be administered with caution. © 2011 Springer Science+Business Media, LLC