Von J. v. Liebig bis E. A. Mitscherlich. Die Grundlage ressourceneffizienter Pflanzenernährung - Langfassung

We share the visions of the originator of the modern soil science VV Dokuchaev and the great innovators of agrochemistry J v. Liebig, EA Mitscherlich, DN Pryanishnikov, UU Uspanov and others. Their visions were to eliminate hunger and poverty of the population by stable crop yields based on innovative site-adapted soil management and farming

ASSESSMENT OF CROP YIELDS IN MODERN AGRICULTURE ON THE BASIS OF GIS-TECHNOLOGIES - Langfasssung

The uneven distribution of natural properties- for example, soil quality, topography, microclimate - on the territory of any size determined a different degree of their suitability for growing different groups of crops. Information-analytical system of ensuring agricultural technologies was developed on the base of several GIS and models of crop yield. The system included creation of maps of potential yield (function of the natural factors) and possible (function of the real level of the field fertility) yield of various crops. These dates were received in the field experiments with fertilizers and in available modern bases of agro-chemical, landscape, climatic parameters

Effective organic matter stock management in agricultural practices: modeling and observation - Langfassung

RothC soil carbon dynamic model was used for simulation SOC stocks in 6 Russian long-term fertilization experiments for estimation which agricultural practices lead to soil C accumulation. For all the treatments tested above ground NPP input is sufficient for maintaining constant SOM stocks and additional C gain

Monitoring of Soil Fertility (Agroecological Monitoring) Langfassung

Monitoring the ecological status of agricultural land in trials with different inputs of fertilizers is focused on analyzing soil fertility indicators and their impact on productivity. Some of these experiments are long-term and part of international networks. Their results are of fundamental importance for monitoring, modeling, and controlling the status of soils. In a regular survey, we found tendencies toward decreasing soil fertility in some regions

Einsatz von Mikrogranulaten in Kombination mit Mikroorganismen zur Steigerung der Nährstoffeffizienz im Maisanbau - Langfassung

Im Rahmen der strategischen Ausrichtung des Nährstoffmanagements stellt der Einsatz von Mikrogranulaten durch das Applikationsverfahren der Saatbanddüngung eine mögliche Alternative zur konventionellen Phosphat-Unterfußdüngung dar

A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome

Down syndrome, caused by an extra copy of chromosome 21, is associated with a greatly increased risk of early onset Alzheimer disease. It is thought that this risk is conferred by the presence of three copies of the gene encoding amyloid precursor protein (APP), an Alzheimer risk factor, although the possession of extra copies of other chromosome 21 genes may also play a role. Further study of the mechanisms underlying the development of Alzheimer disease in Down syndrome could provide insights into the mechanisms that cause dementia in the general population

Alimentary Treatment with Trehalose in a Pharmacological Model of Alzheimer’s Disease in Mice: Effects of Different Dosages and Treatment Regimens

In the treatment of experimental neurodegeneration with disaccharide trehalose, various regimens are used, predominantly a 2% solution, drunk for several weeks. We studied the effects of different regimens of dietary trehalose treatment in an amyloid-β (Aβ) 25–35-induced murine model of Alzheimer’s disease (AD). Aβ-treated mice received 2% trehalose solution daily, 4% trehalose solution daily (continuous mode) or every other day (intermittent mode), to drink for two weeks. We revealed the dose-dependent effects on autophagy activation in the frontal cortex and hippocampus, and the restoration of behavioral disturbances. A continuous intake of 4% trehalose solution caused the greatest activation of autophagy and the complete recovery of step-through latency in the passive avoidance test that corresponds to associative long-term memory and learning. This regimen also produced an anxiolytic effect in the open field. The effects of all the regimens studied were similar in Aβ load, neuroinflammatory response, and neuronal density in the frontal cortex and hippocampus. Trehalose successfully restored these parameters to the levels of the control group. Thus, high doses of trehalose had increased efficacy towards cognitive impairment in a model of early AD-like pathology. These findings could be taken into account for translational studies and the development of clinical approaches for AD therapy using trehalose

Hippocampal circuit dysfunction in the Tc1 mouse model of Down syndrome

Hippocampal pathology is likely to contribute to cognitive disability in Down syndrome, yet the neural network basis of this pathology and its contributions to different facets of cognitive impairment remain unclear. Here we report dysfunctional connectivity between dentate gyrus and CA3 networks in the transchromosomic Tc1 mouse model of Down syndrome, demonstrating that ultrastructural abnormalities and impaired short-term plasticity at dentate gyrus–CA3 excitatory synapses culminate in impaired coding of new spatial information in CA3 and CA1 and disrupted behavior in vivo. These results highlight the vulnerability of dentate gyrus–CA3 networks to aberrant human chromosome 21 gene expression and delineate hippocampal circuit abnormalities likely to contribute to distinct cognitive phenotypes in Down syndrome

Modulation of the expression of genes related to the system of amyloid-beta metabolism in the brain as a novel mechanism of ceftriaxone neuroprotective properties

Abstract Background The dominant hypothesis about the pathogenesis of Alzheimer’s disease (AD) is the “amyloid cascade” concept and modulating the expression of proteins involved in the metabolism of amyloid-beta (Aβ) is proposed as an effective strategy for the prevention and therapy of AD. Recently, we found that an antibiotic ceftriaxone (CEF), which possesses neuroprotective activity, reduced cognitive deficits and neurodegenerative changes in OXYS rats, a model of sporadic AD. The molecular mechanisms of this effect are not completely clear, we suggested that the drug might serve as the regulator of the expression of the genes involved in the metabolism of Aβ and the pathogenesis of AD. The study was aimed to determine the effects of CEF on mRNA levels of Bace1 (encoding β-secretase BACE1 involved in Aβ production), Mme, Ide, Ece1, Ace2 (encoding enzymes involved in Aβ degradation), Epo (encoding erythropoietin related to endothelial function and clearance of Aβ across the blood brain barrier) in the frontal cortex, hippocampus, striatum, hypothalamus, and amygdala of OXYS and Wistar (control strain) male rats. Starting from the age of 14 weeks, animals received CEF (100 mg/kg/day, i.p., 36 days) or saline. mRNA levels were evaluated with RT-qPCR method. Biochemical parameters of plasma were measured for control of system effects of the treatment. Results To better understand strain variations studied here, we compared the gene expression between untreated OXYS and Wistar rats. This comparison showed a significant decrease in mRNA levels of Ace2 in the frontal cortex and hypothalamus, and of Actb in the amygdala of untreated OXYS rats. Analysis of potential effects of CEF revealed its novel targets. In the compound-treated OXYS cohort, CEF diminished mRNA levels of Bace1 and Ace2 in the hypothalamus, and Aktb in the frontal cortex. Furthermore, CEF augmented Mme, Ide, and Epo mRNA levels in the amygdala as well as the levels of Ece1 and Aktb in the striatum. Finally, CEF also attenuated the activity of ALT and AST in plasma of OXYS rats. Conclusion Those findings disclosed novel targets for CEF action that might be involved into neuroprotective mechanisms at early, pre-plaque stages of AD-like pathology development

A syntenic cross species aneuploidy genetic screen links RCAN1 expression to β-cell mitochondrial dysfunction in type 2 diabetes

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Type 2 diabetes (T2D) is a complex metabolic disease associated with obesity, insulin resistance and hypoinsulinemia due to pancreatic β-cell dysfunction. Reduced mitochondrial function is thought to be central to β-cell dysfunction. Mitochondrial dysfunction and reduced insulin secretion are also observed in β-cells of humans with the most common human genetic disorder, Down syndrome (DS, Trisomy 21). To identify regions of chromosome 21 that may be associated with perturbed glucose homeostasis we profiled the glycaemic status of different DS mouse models. The Ts65Dn and Dp16 DS mouse lines were hyperglycemic, while Tc1 and Ts1Rhr mice were not, providing us with a region of chromosome 21 containing genes that cause hyperglycemia. We then examined whether any of these genes were upregulated in a set of ~5,000 gene expression changes we had identified in a large gene expression analysis of human T2D β-cells. This approach produced a single gene, RCAN1, as a candidate gene linking hyperglycemia and functional changes in T2D β-cells. Further investigations demonstrated that RCAN1 methylation is reduced in human T2D islets at multiple sites, correlating with increased expression. RCAN1 protein expression was also increased in db/db mouse islets and in human and mouse islets exposed to high glucose. Mice overexpressing RCAN1 had reduced in vivo glucose-stimulated insulin secretion and their β-cells displayed mitochondrial dysfunction including hyperpolarised membrane potential, reduced oxidative phosphorylation and low ATP production. This lack of β-cell ATP had functional consequences by negatively affecting both glucosestimulated membrane depolarisation and ATP-dependent insulin granule exocytosis. Thus, from amongst the myriad of gene expression changes occurring in T2D β-cells where we had little knowledge of which changes cause β-cell dysfunction, we applied a trisomy 21 screening approach which linked RCAN1 to β-cell mitochondrial dysfunction in T2D. Author Summary Mitochondrial dysfunction and reduced insulin secretion are key features of β-cell dysfunction in Type 2 diabetes (T2D). Down syndrome (DS) is a genetic disorder caused by trisomy of chromosome 21 that also displays β-cell mitochondrial dysfunction and reduced insulin secretion in humans. Given these similarities in β-cell dysfunction in T2D and DS, we developed a trisomy 21 screening method to identify genes that may be important in T2D. This approach used different DS mouse models combined with human gene expression data from T2D β-cells. From this we identified a single candidate, Regulator of calcineurin 1 (RCAN1). High RCAN1 expression occurs in human and mouse T2D islets. Increased RCAN1 expression in mice reduced β-cell mitochondrial function and ATP availability, and this has negative implications for multiple ATP-dependent steps in glucose- stimulated insulin secretion