Entwicklung von Maissorten für den Ökologischen Anbau

Mais wird im ökologischen Landbau bisher wenig angebaut, obwohl er sowohl als Futterpflanze als auch als Marktfrucht von großem Nutzen sein könnte. Ein Grund hierfür ist, dass der Anbau unter ökologischen Bedingungen höhere und teilweise andere Ansprüche an dem Mais stellt als der unter konventionellen Bedingungen. Die Konkurrenzfähigkeit gegenüber Unkraut ist dabei das am stärksten ökospezifische Merkmal. Dazu wurden pflanzenbauliche und pflanzenzüchterische Untersuchungen durchgeführt. In dreijährigen pflanzenbaulichen Versuchen an zwei ökologisch bewirtschafteten Standorten im südlichen Niedersachsen (Reinshof, Wiebrechtshausen) wurden bei verschiedenen Maissorten acht Untersaat-Varianten geprüft. Mit allen UntersaatVarianten konnte die Sprossmasse der Unkräuter zwischen den Maisreihen verringert werden. Effektiv waren dabei Welsches Weidelgras (61 % weniger Unkraut-Sprossmasse als in der Kontrollvariante), Erdklee (57 % Reduktion) und Wegwarte (im Mittel 53 % Reduktion). Roggen war dagegen nicht effektiv. Die Unterssaaten haben das Wachstum des Maises kaum negativ beeinflusst. In den an den gleichen Standorten durchgeführten züchterischen Versuchen wurde der Unkrautdruck durch eine Untersaat simuliert. Es wurden 180 Testkreuzungen mit und ohne Untersaat geprüft und in zwei Jahren die jeweils leistungsstärksten Genotypen selektiert. Im dritten Versuchsjahr wurden aus den selektierten Linien Hybriden hergestellt und vergleichend mit und ohne Untersaat getestet. Es wurden keine signifikanten Unterschiede zwischen den Selektionsgruppen festgestellt. Die Entwicklung von Maissorten mit spezifischer Unkrauttoleranz erscheint daher wenig aussichtsreich. In einem weiteren Projektteil konnte gezeigt werden, dass auch die Entwicklung von Populationssorten bei Mais möglich ist, da die spontane Selbstbefruchtung in Populationen vernachlässigt werden kann

Konzept einer agentenbasierten Transportsteuerung für komplexe, dynamische und multimodale Logistiknetzwerke

Transports within industrial logistics networks are planned strategically. Due to the existence of uncertainties an operational control of transports is necessary. Thereby, dispatchers are today not supported adequately. A control approach for dynamic, complex and multimodal transports is developed, which intends to support or automate the operational control. The approach has a decentral and heterarchical organization, in which the goods and means of transports are modeled as agents

Gamification as a Means to Improve Stakeholder Management in Urban Planning Participation

As cities and urban areas grow, the stakeholders involved in urban planning processes increase and diversify. Communication between these different stakeholders is paramount to successful architectural and urban planning. Public participation has gained on significance over the last 60 years as a means to incorporate their local knowledge in planning processes. Public participation forms an essential part as a form of democratic decision-making and in building trust between stakeholders. However, public participation offers do not meet the needs of all stakeholder groups at different planning stages. This is most evident when projects provoke resistance from the general population. This research investigated the misalignment of expert offers and public needs in urban planning public participation at early planning phases as well as the possibility and user acceptance of gamification in addressing these

Microsatellite instability, KRAS mutations and cellular distribution of TRAIL-receptors in early stage colorectal cancer.

Thus, we evaluated the immunofluorescence pattern of TRAIL-receptors and E-cadherin to assess the fraction of membrane-bound TRAIL-receptors in 231 selected patients with early-stage CRC undergoing surgical treatment only. Moreover, we investigated whether membrane staining for TRAIL-receptors as well as the presence of KRAS mutations or of microsatellite instability (MSI) had an effect on survival and thus a prognostic effect. The fact that the receptors for the TNF-related apoptosis inducing ligand (TRAIL) are almost invariably expressed in colorectal cancer (CRC) represents the rationale for the employment of TRAIL-receptors targeting compounds for the therapy of patients affected by this tumor. Yet, first reports on the use of these bioactive agents provided disappointing results. We therefore hypothesized that loss of membrane-bound TRAIL-R might be a feature of some CRC and that the evaluation of membrane staining rather than that of the overall expression of TRAIL-R might predict the response to TRAIL-R targeting compounds in this tumor. As expected, almost all CRC samples stained positive for TRAIL-R1 and 2. Instead, membrane staining for these receptors was positive in only 71% and 16% of samples respectively. No correlation between KRAS mutation status or MSI-phenotype and prognosis could be detected. TRAIL-R1 staining intensity correlated with survival in univariate analysis, but only membranous staining of TRAIL-R1 and TRAIL-R2 on cell membranes was an independent predictor of survival (cox multivariate analysis: TRAIL-R1: p = 0.019, RR 2.06[1.12-3.77]; TRAIL-R2: p = 0.033, RR 3.63[1.11-11.84]). In contrast to the current assumptions, loss of membrane staining for TRAIL-receptors is a common feature of early stage CRC which supersedes the prognostic significance of their staining intensity. Failure to achieve therapeutic effects in recent clinical trials using TRAIL-receptors targeting compounds might be due to insufficient selection of patients bearing tumors with membrane-bound TRAIL-receptors

Anti-tetherin activities in Vpu-expressing primate lentiviruses

<p>Abstract</p> <p>Background</p> <p>The anti-viral activity of the cellular restriction factor, BST-2/tetherin, was first observed as an ability to block the release of Vpu-minus HIV-1 from the surface of infected cells. However, tetherin restriction is also counteracted by primate lentiviruses that do not express a Vpu protein, where anti-tetherin functions are provided by either the Env protein (HIV-2, SIVtan) or the Nef protein (SIVsm/mac and SIVagm). Within the primate lentiviruses, Vpu is also present in the genomes of SIVcpz and certain SIVsyk viruses. We asked whether, in these viruses, anti-tetherin activity was always a property of Vpu, or if it had selectively evolved in HIV-1 to perform this function.</p> <p>Results</p> <p>We found that despite the close relatedness of HIV-1 and SIVcpz, the chimpanzee viruses use Nef instead of Vpu to counteract tetherin. Furthermore, SIVcpz Nef proteins had activity against chimpanzee but not human tetherin. This specificity mapped to a short sequence that is present in the cytoplasmic tail of primate but not human tetherins, and this also accounts for the specificity of SIVsm/mac Nef for primate but not human tetherins. In contrast, Vpu proteins from four diverse members of the SIVsyk lineage all displayed an anti-tetherin activity that was active against macaque tetherin. Interestingly, Vpu from a SIVgsn isolate was also found to have activity against human tetherin.</p> <p>Conclusions</p> <p>Primate lentiviruses show a high degree of flexibility in their use of anti-tetherin factors, indicating a strong selective pressure to counteract tetherin restriction. The identification of an activity against human tetherin in SIVgsn Vpu suggests that the presence of Vpu in the ancestral SIVmus/mon/gsn virus believed to have contributed the 3' half of the HIV-1 genome may have played a role in the evolution of viruses that could counteract human tetherin and infect humans.</p

Colorectal Cancers Mimic Structural Organization of Normal Colonic Crypts

Colonic crypts are stereotypical structures with distinct stem cell, proliferating, and differentiating compartments. Colorectal cancers derive from colonic crypt epithelia but, in contrast, form morphologically disarrayed glands. In this study, we investigated to which extent colorectal cancers phenocopy colonic crypt architecture and thus preserve structural organization of the normal intestinal epithelium. A subset of colon cancers showed crypt-like compartments with high WNT activity and nuclear beta-Catenin at the leading tumor edge, adjacent proliferation, and enhanced Cytokeratin 20 expression in most differentiated tumor epithelia of the tumor center. This architecture strongly depended on growth conditions, and was fully reproducible in mouse xenografts of cultured and primary colon cancer cells. Full crypt-like organization was associated with low tumor grade and was an independent prognostic marker of better survival in a collection of 221 colorectal cancers. Our findings suggest that full activation of preserved intestinal morphogenetic programs in colon cancer requires in vivo growth environments. Furthermore, crypt-like architecture was linked with less aggressive tumor biology, and may be useful to improve current colon cancer grading schemes

HIV-1 Vpu and HIV-2 Env counteract BST-2/tetherin by sequestration in a perinuclear compartment

<p>Abstract</p> <p>Background</p> <p>In the absence of the Vpu protein, newly formed HIV-1 particles can remain attached to the surface of human cells due to the action of an interferon-inducible cellular restriction factor, BST-2/tetherin. Tetherin also restricts the release of other enveloped viral particles and is counteracted by a several viral anti-tetherin factors including the HIV-2 Env, SIV Nef and KSHV K5 proteins.</p> <p>Results</p> <p>We observed that a fraction of tetherin is located at the surface of restricting cells, and that co-expression of both HIV-1 Vpu and HIV-2 Env reduced this population. In addition, Vpu, but not the HIV-2 Env, reduced total cellular levels of tetherin. An additional effect observed for both Vpu and the HIV-2 Env was to redirect tetherin to an intracellular perinuclear compartment that overlapped with markers for the TGN (<it>trans</it>-Golgi network). Sequestration of tetherin in this compartment was independent of tetherin's normal endocytosis trafficking pathway.</p> <p>Conclusions</p> <p>Both HIV-1 Vpu and HIV-2 Env redirect tetherin away from the cell surface and sequester the protein in a perinuclear compartment, which likely blocks the action of this cellular restriction factor. Vpu also promotes the degradation of tetherin, suggesting that it uses more than one mechanism to counteract tetherin restriction.</p

Succinic semialdehyde dehydrogenase deficiency: in vitro and in silico characterization of a novel pathogenic missense variant and analysis of the mutational spectrum of ALDH5A1

Succinic semialdehyde dehydrogenase deficiency (SSADHD) is a rare, monogenic disorder affecting the degradation of the main inhibitory neurotransmitter \u3b3-amino butyric acid (GABA). Pathogenic variants in the ALDH5A1 gene that cause an enzymatic dysfunction of succinic semialdehyde dehydrogenase (SSADH) lead to an accumulation of potentially toxic metabolites, including \u3b3-hydroxybutyrate (GHB). Here, we present a patient with a severe phenotype of SSADHD caused by a novel genetic variant c.728T &gt; C that leads to an exchange of leucine to proline at residue 243, located within the highly conserved nicotinamide adenine dinucleotide (NAD)+ binding domain of SSADH. Proline harbors a pyrrolidine within its side chain known for its conformational rigidity and disruption of protein secondary structures. We investigate the effect of this novel variant in vivo, in vitro, and in silico. We furthermore examine the mutational spectrum of all previously described disease-causing variants and computationally assess all biologically possible missense variants of ALDH5A1 to identify mutational hotspots

Two Different Forms of Arousal in Drosophila Are Oppositely Regulated by the Dopamine D1 Receptor Ortholog DopR via Distinct Neural Circuits

Arousal is fundamental to many behaviors, but whether it is unitary or whether there are different types of behavior-specific arousal has not been clear. In Drosophila, dopamine promotes sleep-wake arousal. However, there is conflicting evidence regarding its influence on environmentally stimulated arousal. Here we show that loss-of-function mutations in the D1 dopamine receptor DopR enhance repetitive startle-induced arousal while decreasing sleep-wake arousal (i.e., increasing sleep). These two types of arousal are also inversely influenced by cocaine, whose effects in each case are opposite to, and abrogated by, the DopR mutation. Selective restoration of DopR function in the central complex rescues the enhanced stimulated arousal but not the increased sleep phenotype of DopR mutants. These data provide evidence for at least two different forms of arousal, which are independently regulated by dopamine in opposite directions, via distinct neural circuits