Gekeimte Samen als Futtermittel - Analytik

Bis August 2005 dürfen im ökologischen Landbau, wenn eine ausschließliche Versorgung mit ökologischen Futtermitteln nicht möglich ist, im begrenzten Umfang konventionelle zugesetzt werden. Für den Zeitraum danach ist zu klären, ob eine ausreichende Nährstoff- und Eiweißversorgung über den Einsatz von Getreidekeimlingen gewährleistet werden kann. Die während des Keimprozesses bei Getreide auftretenden Veränderungen der für die Fütterung relevanten Inhaltsstoffe wurden untersucht. Die Keimung erfolgte sowohl unter optimierten Bedingungen in Feuchtekammern als auch unter praxisrelevanten Bedingungen in Schalen und im Keimautomat. Dabei zeigte sich, dass mit beginnender Keimung sprunghafte Veränderungen im Enzymstatus nachweisbar sind, während stoffliche Veränderungen später einsetzen und langsamer verlaufen. Das stärkeabbauende Enzym a-Amylase konnte als sensibler Indikator für den Keimungsfortschritt verwendet werden. Während der Keimung stiegen die Aktivitäten der stärkeabbauenden Enzyme und der Stärkegehalt wurde reduziert. Erwartungsgemäß stiegen die Zuckergehalte. Bei unverändertem Rohstickstoffgehalt kam es zu einer Abnahme des Proteinstickstoffgehaltes zu Gunsten der freien Aminosäuren. Der Rohfettgehalt stieg und es erhöhte sich der Gehalt an mehrfach ungesättigten Fettsäuren. Von den Aminosäuren erhöhte sich während der Keimung besonders der Gehalt von Lysin. Die deutlichsten Veränderungen durch die Keimung wurden bei den Vitaminen beobachtet. Von den 8 untersuchten Vitaminen A, B1, B2, B6, C, D3, E und K1 stiegen 6 deutlich an. Bemerkenswert war die Verringerung der Viskosität in Roggenkeimlingen, wodurch der Einsatz dieser Getreideart in der Fütterung interessant wird. Erwähnenswert ist, dass die Phytinsäure, die die Verdaulichkeit des Futters beeinträchtigt, während der Keimung stark abnimmt. Aus ernährungsphysiologischer Sicht treten vorteilhafte Veränderungen während der Keimung auf, die zu einer Verbesserung des Futterwertes beitragen

Einsatz von gekeimtem Getreide als Futtermittel

Die EU-Verordnung 1804/1999 regelt die Einbeziehung der tierischen Erzeugung in den Geltungsbereich der Verordnung (EWG) Nr. 2092/91 über den ökologischen Landbau und die entsprechende Kennzeichnung der landwirtschaftlichen Erzeugnisse und Lebensmittel. Danach müssen im ökologischen Landbau alle Tiere nach den Grundregeln dieser Verordnung gehalten werden. Das Futter soll den ernährungsphysiologischen Bedarf der Tiere decken und aus dem ökologischen Anbau stammen. Dafür dürfen bis August 2005 im begrenzten Umfang konventionelle Futtermittel zugesetzt werden, wenn eine ausschließliche Versorgung mit Futtermitteln aus dem ökologischen Anbau nicht möglich ist. Für die Geflügelfütterung bedeutet das einen zulässigen Höchstanteil an konventionellem Futter von 20% im Jahr (max. 25% Trockenmasse am Tag). Bislang werden dafür besonders die konventionellen Komponenten Maiskleber und Kartoffeleiweiß, die als Nebenprodukte bei der Stärkegewinnung anfallen, eingesetzt. Vergleichbare ökologische Produkte sind z. Z. nicht verfügbar. Unter diesem Aspekt ist zu klären, ob eine ausreichende Nährstoff- und Eiweißversorgung über den Einsatz von 20% Getreidekeimlingen in der Futterration gewährleistet werden kann, die damit zu 100% ökologischer Herkunft ist. In einem, im Rahmen des Bundesprogramms ökologischer Landbau, geförderten Projekt werden alle nachfolgend aufgeführten Parameter analysiert. Proteine, Stärken, Nichtstärkepolysaccharide, Zucker und Fette als wertgebende Inhaltsstoffe sowie Auswuchs, Pilzbefall und Mykotoxine als dominierende Schadfaktoren in Getreide stehen dabei im Mittelpunkt des Interesses. Ziel ist es, Kriterien für die optimale Prozessführung der Keimung und eine hohe Produktqualität der Keimlinge zu sichern, um eine hochwertige Futterkomponente aus dem ökologischen Landbau für die Tierernährung bereitzustellen

Evaluation of Biased and Balanced Salvinorin A Analogs in Preclinical Models of Pain

This work is licensed under a Creative Commons Attribution 4.0 International License.In the search for safer, non-addictive analgesics, kappa opioid receptor (KOPr) agonists are a potential target, as unlike mu-opioid analgesics, they do not have abuse potential. Salvinorin A (SalA) is a potent and selective KOPr agonist, however, clinical utility is limited by the short duration of action and aversive side effects. Biasing KOPr signaling toward G-protein activation has been highlighted as a key cellular mechanism to reduce the side effects of KOPr agonists. The present study investigated KOPr signaling bias and the acute antinociceptive effects and side effects of two novel analogs of SalA, 16-Bromo SalA and 16-Ethynyl SalA. 16-Bromo SalA showed G-protein signaling bias, whereas 16-Ethynyl SalA displayed balanced signaling properties. In the dose-response tail-withdrawal assay, SalA, 16-Ethynyl SalA and 16-Bromo SalA were more potent than the traditional KOPr agonist U50,488, and 16-Ethynyl SalA was more efficacious. 16-Ethynyl SalA and 16-Bromo SalA both had a longer duration of action in the warm water tail-withdrawal assay, and 16-Ethynyl had greater antinociceptive effect in the hot-plate assay, compared to SalA. In the intraplantar 2% formaldehyde test, 16-Ethynyl SalA and 16-Bromo SalA significantly reduced both nociceptive and inflammatory pain-related behaviors. Moreover, 16-Ethynyl SalA and 16-Bromo SalA had no anxiogenic effects in the marble burying task, and 16-Bromo SalA did not alter behavior in the elevated zero maze. Overall, 16-Ethynyl SalA significantly attenuated acute pain-related behaviors in multiple preclinical models, while the biased KOPr agonist, 16-Bromo SalA, displayed modest antinociceptive effects, and lacked anxiogenic effects.Health Research Council – Explorer grant (16/646)National Institute on Drug Abuse (DA018151)Victoria University of Wellington doctoral scholarshi

Human helminth therapy to treat inflammatory disorders - where do we stand?

Parasitic helminths have evolved together with the mammalian immune system over many millennia and as such they have become remarkably efficient modulators in order to promote their own survival. Their ability to alter and/or suppress immune responses could be beneficial to the host by helping control excessive inflammatory responses and animal models and pre-clinical trials have all suggested a beneficial effect of helminth infections on inflammatory bowel conditions, MS, asthma and atopy. Thus, helminth therapy has been suggested as a possible treatment method for autoimmune and other inflammatory disorders in humans

Copper-dependent activation of hypoxia-inducible factor (HIF)-1: implications for ceruloplasmin regulation

Cellular oxygen partial pressure is sensed by a family of prolyl-4-hydroxylase domain (PHD) enzymes that modify hypoxia-inducible factor (HIF)alpha subunits. Upon hydroxylation under normoxic conditions, HIFalpha is bound by the von Hippel-Lindau tumor suppressor protein and targeted for proteasomal destruction. Since PHD activity is dependent on oxygen and ferrous iron, HIF-1 mediates not only oxygen- but also iron-regulated transcriptional gene expression. Here we show that copper (CuCl(2)) stabilizes nuclear HIF-1alpha under normoxic conditions, resulting in hypoxia-response element (HRE)-dependent reporter gene expression. In in vitro hydroxylation assays CuCl(2) inhibited prolyl-4-hydroxylation independently of the iron concentration. Ceruloplasmin, the main copper transport protein in the plasma and a known HIF-1 target in vitro, was also induced in vivo in the liver of hypoxic mice. Both hypoxia and CuCl(2) increased ceruloplasmin (as well as vascular endothelial growth factor [VEGF] and glucose transporter 1 [Glut-1]) mRNA levels in hepatoma cells, which was due to transcriptional induction of the ceruloplasmin gene (CP) promoter. In conclusion, our data suggest that PHD/HIF/HRE-dependent gene regulation can serve as a sensory system not only for oxygen and iron but also for copper metabolism, regulating the oxygen-, iron- and copper-binding transport proteins hemoglobin, transferrin, and ceruloplasmin, respectively

The Noise Exposure Structured Interview (NESI): an instrument for the comprehensive estimation of lifetime noise exposure

Lifetime noise exposure is generally quantified by self report. The accuracy of retrospective self report is limited by respondent recall, but is also bound to be influenced by reporting procedures. Such procedures are of variable quality in current measures of lifetime noise exposure, and off-the-shelf instruments are not readily available. The Noise Exposure Structured Interview (NESI) represents an attempt to draw together some of the stronger elements of existing procedures and to provide solutions to their outstanding limitations. Reporting is not restricted to pre-specified exposure activities, and instead encompasses all activities that the respondent has experienced as noisy (defined based on sound level estimated from vocal effort). Changing exposure habits over time are reported by dividing the lifespan into discrete periods in which exposure habits were approximately stable, with life milestones used to aid recall. Exposure duration, sound level, and use of hearing protection are reported for each life period separately. Simple-to-follow methods are provided for the estimation of free-field sound level, the sound level emitted by personal listening devices, and the attenuation provided by hearing protective equipment. An energy-based means of combining the resulting data is supplied, along with a primarily energy-based method for incorporating firearm-noise exposure. Finally, the NESI acknowledges the need of some users to tailor the procedures; this flexibility is afforded and reasonable modifications are described. Competency needs of new users are addressed through detailed interview instructions (including troubleshooting tips) and a demonstration video. Limited evaluation data are available and future efforts at evaluation are proposed

Hybrid Shell Engineering of Animal Cells for Immune Protections and Regulation of Drug Delivery: Towards the Design of “Artificial Organs”

BACKGROUND: With the progress in medicine, the average human life expectancy is continuously increasing. At the same time, the number of patients who require full organ transplantations is augmenting. Consequently, new strategies for cell transplantation are the subject of great interest. METHODOLOGY/PRINCIPAL FINDINGS: This work reports the design, the synthesis and the characterisation of robust and biocompatible mineralised beads composed of two layers: an alginate-silica composite core and a Ca-alginate layer. The adequate choice of materials was achieved through cytotoxicity LDH release measurement and in vitro inflammatory assay (IL-8) to meet the biocompatibility requirements for medical purpose. The results obtained following this strategy provide a direct proof of the total innocuity of silica and alginate networks for human cells as underscored by the non-activation of immune defenders (THP-1 monocytes). The accessible pore size diameter of the mineralised beads synthesized was estimated between 22 and 30 nm, as required for efficient immuno-isolation without preventing the diffusion of nutrients and metabolites. The model human cells, HepG2, entrapped within these hybrid beads display a high survival rate over more than six weeks according to the measurements of intracellular enzymatic activity, respiration rate, as well as the "de novo" biosynthesis and secretion of albumin out of the beads. CONCLUSIONS/SIGNIFICANCE: The current study shows that active mammalian cells can be protected by a silica-alginate hybrid shell-like system. The functionality of the cell strain can be maintained. Consequently, cells coated with an artificial and a biocompatible mineral shell could respond physiologically within the human body in order to deliver therapeutic agents in a controlled fashion (i.e. insulin), substituting the declining organ functions of the patient

Retinoic Acid Mediates Regulation of Network Formation by COUP-TFII and VE-Cadherin Expression by TGFβ Receptor Kinase in Breast Cancer Cells

Tumor development, growth, and metastasis depend on the provision of an adequate vascular supply. This can be due to regulated angiogenesis, recruitment of circulating endothelial progenitors, and/or vascular transdifferentiation. Our previous studies showed that retinoic acid (RA) treatment converts a subset of breast cancer cells into cells with significant endothelial genotypic and phenotypic elements including marked induction of VE-cadherin, which was responsible for some but not all morphological changes. The present study demonstrates that of the endothelial-related genes induced by RA treatment, only a few were affected by knockdown of VE-cadherin, ruling it out as a regulator of the RA-induced endothelial genotypic switch. In contrast, knockdown of the RA-induced gene COUP-TFII prevented the formation of networks in Matrigel but had no effect on VE-cadherin induction or cell fusion. Two pan-kinase inhibitors markedly blocked RA-induced VE-cadherin expression and cell fusion. However, RA treatment resulted in a marked and broad reduction in tyrosine kinase activity. Several genes in the TGFβ signaling pathway were induced by RA, and specific inhibition of the TGFβ type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Together these data indicate a role for the TGFβ pathway and COUP-TFII in mediating the endothelial transdifferentiating properties of RA