Under the climatic conditions of north-western Europe, silage maize (Zea mays L.) production optimized with respect to nitrogen (N) fertilization and crop rotation is required to reduce N losses. Whether winter catch crops (CC) can serve as a beneficial biological tool in terms of N-loss abatement as well as maize yield also under optimized N management, is unclear. Therefore, a 2-year field experiment was conducted to study the short-term effects of a continuous maize-catch cropping system on maize yield performance, N2O emission and N leaching, as affected by maize harvest/CC sowing date (10, 20, 30 September and 15 October, respectively, hd1–hd4) and CC species (rye, Secale cereale L. and Italian ryegrass, Lolium multiflorum Lam.). Treatments without CC served as control and N fertilization was applied as synthetic N to better adjust to maize N demand. The CC treatment (with or without) had no effect on maize dry matter and N yields, but the N uptake efficiency of maize responded significantly to the N accumulation (Ntot) of CC. Nitrate leaching mostly stayed below the critical load value for EU drinking water and rye significantly reduced nitrate leaching, given that environmental conditions allowed sufficiently high CC biomass accumulation. Annual nitrous oxide emission was unaffected by CC treatment. Restricted N fertilization of maize following CC led to N deficiency, since CC decomposition obviously was not synchronized with maize N demand. Under the given environmental conditions, rye may serve as beneficial CC in continuous maize cropping even in already optimized N management. 相似文献
Monitoring the activity of ATP‐consuming enzymes provides the basis for elucidating their modes of action and regulation. Although a number of ATP analogues have been developed for this, their scope is restricted because of the limited acceptance by respective enzymes. In order to clarify which kind of phosphate‐modified ATP analogues are accepted by the α‐β‐phosphoanhydride‐cleaving ubiquitin‐activating enzyme 1 (UBA1) and the β‐γ‐phosphoanhydride‐cleaving focal adhesion kinase (FAK), we tested phosphoramidate‐ and phosphoester‐modified ATP analogues. UBA1 and FAK were able to convert phosphoramidate‐modified ATP analogues, even with a bulky modification like biotin. In contrast, a phosphoester‐modified analogue was poorly accepted. These results demonstrate that minor variations in the design of ATP analogues for monitoring ATP utilization have a significant impact on enzymatic acceptance. 相似文献
Mobile substations can be defined as completely equipped electrical substations. There is a lack of existing scientific basis in the mechanical design of the structural components of the mobile substation. In concrete there are no capabilities to determine the dynamic behavior during transport and service conditions. Improper dimensioning of the structures results in an important degree of mechanical failures during transport. The dynamic response of structures on a mobile substation to transport motions depends on their strength of construction, ductility, and dynamic properties. Lightly damped structures that have one or more natural modes of oscillation within the frequency band of transport excitations can experience considerable amplification of both the forces and deflections. Thus, items of mobile substation equipment whose natural frequencies lie in the normal frequency range of transport motion are particularly vulnerable to damage and fatigue. Therefore we are interested in analyzing the natural frequencies, damping ratios (modal parameters) and level of accelerations of those components. In this paper it will be shown how above parameters can be retrieved from a road test on a mobile substation and be applied to develop adequate design rules and design tools as well as recommendations in order to guarantee the mechanical integrity of mobile substations during transport and service conditions. Finally the influence of conductor cables on the dynamic behavior of interconnected equipment will briefly be discussed. 相似文献
We propose a novel area/time efficient elliptic curve cryptography (ECC) processor architecture which performs all finite
field arithmetic operations in the discrete Fourier domain. The proposed architecture utilizes a class of optimal extension fields (OEF)GF(qm) where the field characteristic is a Mersenne prime q = 2n − 1 and m = n. The main advantage of our architecture is that it achieves extension field modular multiplication in the discrete Fourier domain with only a linear number of base field GF(q) multiplications in addition to a quadratic number of simpler operations such as addition and bitwise rotation. We achieve
an area between 25k and 50k equivalent gates for the implementations over OEFs of size 169, 289 and 361 bits. With its low
area and high speed, the proposed architecture is well suited for ECC in small device environments such as sensor networks.
The work at hand presents the first hardware implementation of a frequency domain multiplier suitable for ECC and the first
hardware implementation of ECC in the frequency domain.
The solid and thermally instable azoinitiators V‐65 and VR‐110 were embedded within a polymer particle by using the miniemulsion process and afterwards quickly decomposed by thermal treatment below the glass temperature of the polymer. The resulting nitrogen gas overpressure inside the particles leads to a disruption of the polymer particle and a possible sudden release of encapsulated substances. It is shown, by electron microscopic measurements, that the number of burst particles correlates with the applied temperatures as well as the heating time. The surface deformation could be verified by scanning electron microscope analyses.
Improving field performance of telecommunication systems is the key objective of both telecom suppliers and operators, as
an increasing amount of business critical systems worldwide are relying on dependable telecommunication. Early defect detection
improves field performance in terms of reduced field failure rates and reduced intrinsic downtime. This paper describes an
integrated approach to improve early defect detection and thus field reliability of telecommunication switching systems. The
assumptions at the start of the projects discussed in this paper are: Wide application of code inspections and thorough module
testing must lead to a lower fault detection density in subsequent phases. At the same time criteria for selecting the most
critical components for code reviews, code inspections and module test are provided in order to optimize efficiency. The primary
goal is to identify critical components and to make failure predictions as early as possible during the life cycle and hence
reduce managerial risk combined with too early or too late release of such a system to the field. During test release time
prediction and field performance prediction are both based on tailored and superposed ENHPP reliability models. Experiences
from projects of Alcatel’s Switching and Routing Division are included to show practical impacts.
This revised version was published online in June 2006 with corrections to the Cover Date. 相似文献
In a cellular mobile radio system an SDMA (Space Division Multiple Access) component can be implemented for the reuse of radio channels physically incorporated by time, frequency or code slots. Since SDMA is based on the spatial separation of different users operating in the same channel, a DOA (Direction of arrival) sensitive channel allocation scheme is essential for maximizing system capacity. In this paper we present the Eigenvector method, a computationally efficient algorithm to do this job. We also present simulation results on the Eigenvector method operating in a typical urban mobile radio cell. The simulated blocking probabilities are then used to predict the capacity increase which can be expected after adding an SDMA component to a conventional mobile radio system. 相似文献
Neurodegenerative diseases such as Alzheimer’s disease (AD) have long been acknowledged as mere disorders of the central nervous system (CNS). However, in recent years the gut with its autonomous nervous system and the multitude of microbial commensals has come into focus. Changes in gut properties have been described in patients and animal disease models such as altered enzyme secretion or architecture of the enteric nervous system. The underlying cellular mechanisms have so far only been poorly investigated. An important organelle for integrating potentially toxic signals such as the AD characteristic A-beta peptide is the primary cilium. This microtubule-based signaling organelle regulates numerous cellular processes. Even though the role of primary cilia in a variety of developmental and disease processes has recently been recognized, the contribution of defective ciliary signaling to neurodegenerative diseases such as AD, however, has not been investigated in detail so far. The AD mouse model 5xFAD was used to analyze possible changes in gut functionality by organ bath measurement of peristalsis movement. Subsequently, we cultured primary enteric neurons from mutant mice and wild type littermate controls and assessed for cellular pathomechanisms. Neurite mass was quantified within transwell culturing experiments. Using a combination of different markers for the primary cilium, cilia number and length were determined using fluorescence microscopy. 5xFAD mice showed altered gut anatomy, motility, and neurite mass of enteric neurons. Moreover, primary cilia could be demonstrated on the surface of enteric neurons and exhibited an elongated phenotype in 5xFAD mice. In parallel, we observed reduced β-Catenin expression, a key signaling molecule that regulates Wnt signaling, which is regulated in part via ciliary associated mechanisms. Both results could be recapitulated via in vitro treatments of enteric neurons from wild type mice with A-beta. So far, only a few reports on the probable role of primary cilia in AD can be found. Here, we reveal for the first time an architectural altered phenotype of primary cilia in the enteric nervous system of AD model mice, elicited potentially by neurotoxic A-beta. Potential changes on the sub-organelle level—also in CNS-derived neurons—require further investigations. 相似文献