The rise of policy coherence for development: a multi-causal approach

In recent years policy coherence for development (PCD) has become a key principle in international development debates, and it is likely to become even more relevant in the discussions on the post-2015 sustainable development goals. This article addresses the rise of PCD on the Western donors’ aid agenda. While the concept already appeared in the work of Organisation for Economic Co-operation and Development (OECD) in the early 1990s, it took until 2007 before PCD became one of the Organisation’s key priorities. We adopt a complexity-sensitive perspective, involving a process-tracing analysis and a multi-causal explanatory framework. We argue that the rise of PCD is not as contingent as it looks. While actors such as the EU, the DAC and OECD Secretariat were the ‘active causes’ of the rise of PCD, it is equally important to look at the underlying ‘constitutive causes’ which enabled policy coherence to thrive well

A Complete Pathway Model for Lipid A Biosynthesis in Escherichia coli.

Lipid A is a highly conserved component of lipopolysaccharide (LPS), itself a major component of the outer membrane of Gram-negative bacteria. Lipid A is essential to cells and elicits a strong immune response from humans and other animals. We developed a quantitative model of the nine enzyme-catalyzed steps of Escherichia coli lipid A biosynthesis, drawing parameters from the experimental literature. This model accounts for biosynthesis regulation, which occurs through regulated degradation of the LpxC and WaaA (also called KdtA) enzymes. The LpxC degradation signal appears to arise from the lipid A disaccharide concentration, which we deduced from prior results, model results, and new LpxK overexpression results. The model agrees reasonably well with many experimental findings, including the lipid A production rate, the behaviors of mutants with defective LpxA enzymes, correlations between LpxC half-lives and cell generation times, and the effects of LpxK overexpression on LpxC concentrations. Its predictions also differ from some experimental results, which suggest modifications to the current understanding of the lipid A pathway, such as the possibility that LpxD can replace LpxA and that there may be metabolic channeling between LpxH and LpxB. The model shows that WaaA regulation may serve to regulate the lipid A production rate when the 3-deoxy-D-manno-oct-2-ulosonic acid (KDO) concentration is low and/or to control the number of KDO residues that get attached to lipid A. Computation of flux control coefficients showed that LpxC is the rate-limiting enzyme if pathway regulation is ignored, but that LpxK is the rate-limiting enzyme if pathway regulation is present, as it is in real cells. Control also shifts to other enzymes if the pathway substrate concentrations are not in excess. Based on these results, we suggest that LpxK may be a much better drug target than LpxC, which has been pursued most often

Microelectronics Education at Fachhochschulen in Baden-Wuerttemberg

The paper describes the Multi Project Chip Group at Fachhochschulen in Baden-Wuerttemberg, Germany. The activities of this group focuses on microelectronics education. Projekt examples are given, covering digital and analog VLSI design, cell layout and PCB design

Memory effects in the action of ozone on conifers.

Conifers are known to possess relative ozone tolerance in short-term experiments. A scenario for ozone damage of conifers is now derived from the first exposure experiments in which both the initial biochemical response phase and delayed visible symptom development were studied. A number of early biochemical ozone responses could be detected in Norway spruce (Picea abies [L.] Karst.) and Scots pine (Pinus sylvestris L.). The stress metabolite catechin persisted over several months. In the year following ozone treatment of spruce, decreases in pigment content and photosynthetic capacity, as well as development of visible symptoms (chlorosis, banding), were determined in the needle age classes previously exposed to an accumulated hourly ozone dose above 40 ppb (AOT40) of >/=60-80 ppm small middle doth. The visible symptoms developed during spring emergence of the new flush. In the case of Scots pine, an ozone dose (AOT40) of >/=30 ppm small middle doth caused the premature shedding of needles 9 months after treatment. The delayed symptoms of both spruce and pine occurred during known phases of endogenous stress. The symptoms appeared to reflect an ozone "memory" imprinted by the induced early stress reactions. Ambient AOT40 ozone doses in Central Europe are in the range 4 and 50 ppm small middle doth per growing season. Ozone is proposed to potentially damage conifers through memory effects ("abiotic" pathway) or through predisposition for pathogen attack ("biotic" pathway)