A Stark decelerator on a chip

A microstructured array of 1254 electrodes on a substrate has been configured to generate an array of local minima of electric field strength with a periodicity of 120 $\mu$m about 25 $\mu$m above the substrate. By applying sinusoidally varying potentials to the electrodes, these minima can be made to move smoothly along the array. Polar molecules in low-field seeking quantum states can be trapped in these traveling potential wells. Recently, we experimentally demonstrated this by transporting metastable CO molecules at constant velocities above the substrate [Phys. Rev. Lett. 100 (2008) 153003]. Here, we outline and experimentally demonstrate how this microstructured array can be used to decelerate polar molecules directly from a molecular beam. For this, the sinusoidally varying potentials need to be switched on when the molecules arrive above the chip, their frequency needs to be chirped down in time, and they need to be switched off before the molecules leave the chip again. Deceleration of metastable CO molecules from an initial velocity of 360 m/s to a final velocity as low as 240 m/s is demonstrated in the 15-35 mK deep potential wells above the 5 cm long array of electrodes. This corresponds to a deceleration of almost $10^5$ $g$, and about 85 cm$^{-1}$ of kinetic energy is removed from the metastable CO molecules in this process.Comment: 17 pages, 6 figure

Tunneling calculations for GaAs-Al(x)Ga(1-x) as graded band-gap sawtooth superlattices

Quantum mechanical tunneling calculations for sawtooth (linearly graded band-gap) and step-barrier AlGaAs superlattices were performed by means of a transfer matrix method, within the effective mass approximation. The transmission coefficient and tunneling current versus applied voltage were computed for several representative structures. Particular consideration was given to effective mass variations. The tunneling properties of step and sawtooth superlattices show some qualitative similarities. Both structures exhibit resonant tunneling, however, because they deform differently under applied fields, the J-V curves differ

The Effects of Traffic on Human Health of Local Residents

In this study, a model is proposed to evaluate the local human health damage caused by (changes in) road traffic on a particular road. These damages are due to global health effects occurring due to the traffic life cycle, as assessed in standard life cycle assessments, and to exposure of local residents to noise and outdoor pollutants originating from road traffic on the road considered. The results of this model were compared with the global human health damage occurring in the life cycle of both traffic and dwellings. The fate factor calculation for pollutants is based on the Dutch CAR model, which relates traffic densities to pollutant concentrations at the facade of dwellings, and on an indoor airflow and exposure model. The effect and damage factors for pollutants are derived from the Eco-Indicator 99 methodology. For noise, the calculation of the fate, effect and damage factor is derived from a methodology developed by the Swiss Agency for the Environment, Forests and Landscape SAEFL to integrate the human health effects of noise due to road traffic in life cycle assessments. It appears that for someone living in a dwelling along a street local health damage due to changes in road traffic situations may be of the same order of magnitude as the human health damage associated with the life cycle of dwellings as calculated by standard LCA methodologies. Compared to the human health damage occurring in the life cycle of vehicles as calculated by standard LCA procedures, the local human health damage may be two to three orders of magnitude larger. The local human health effects due to (changes in) road traffic situations thus cannot be neglected when carrying out life cycle assessments of dwellings or complete residential areas. For the road studied, the magnitude of the effect of a decrease in road traffic density on the human health are smaller when the initial number of cars per hour is smaller than 50 or when the distance of the facade to the road axis is more than eight meter. This is because for noise levels there are thresholds to impact. In the future, the improvement of the model, the addition of the effects of other means of transport and the assessment of real neighborhoods might be carried out

The aspartic proteinase family of three Phytophthora species

Background - Phytophthora species are oomycete plant pathogens with such major social and economic impact that genome sequences have been determined for Phytophthora infestans, P. sojae and P. ramorum. Pepsin-like aspartic proteinases (APs) are produced in a wide variety of species (from bacteria to humans) and contain conserved motifs and landmark residues. APs fulfil critical roles in infectious organisms and their host cells. Annotation of Phytophthora APs would provide invaluable information for studies into their roles in the physiology of Phytophthora species and interactions with their hosts. Results - Genomes of Phytophthora infestans, P. sojae and P. ramorum contain 11-12 genes encoding APs. Nine of the original gene models in the P. infestans database and several in P. sojae and P. ramorum (three and four, respectively) were erroneous. Gene models were corrected on the basis of EST data, consistent positioning of introns between orthologues and conservation of hallmark motifs. Phylogenetic analysis resolved the Phytophthora APs into 5 clades. Of the 12 sub-families, several contained an unconventional architecture, as they either lacked a signal peptide or a propart region. Remarkably, almost all APs are predicted to be membrane-bound. Conclusions - One of the twelve Phytophthora APs is an unprecedented fusion protein with a putative G-protein coupled receptor as the C-terminal partner. The others appear to be related to well-documented enzymes from other species, including a vacuolar enzyme that is encoded in every fungal genome sequenced to date. Unexpectedly, however, the oomycetes were found to have both active and probably-inactive forms of an AP similar to vertebrate BACE, the enzyme responsible for initiating the processing cascade that generates the Aß peptide central to Alzheimer's Disease. The oomycetes also encode enzymes similar to plasmepsin V, a membrane-bound AP that cleaves effector proteins of the malaria parasite Plasmodium falciparum during their translocation into the host red blood cell. Since the translocation of Phytophthora effector proteins is currently a topic of intense research activity, the identification in Phytophthora of potential functional homologues of plasmepsin V would appear worthy of investigation. Indeed, elucidation of the physiological roles of the APs identified here offers areas for future study. The significant revision of gene models and detailed annotation presented here should significantly facilitate experimental design

Towards a computational model for stimulation of the Pedunculopontine nucleus

The pedunculopontine nucleus (PPN) has recently been suggested as a new therapeutic target for deep brain stimulation (DBS) in patients suffering from Parkinson's disease, particularly those with severe gait and postural impairment [1]. Stimulation at this site is typically delivered at low frequencies in contrast to the high frequency stimulation required for therapeutic benefit in the subthalamic nucleus (STN) [1]. Despite real therapeutic successes, the fundamental physiological mechanisms underlying the effect of DBS are still not understood. A hypothesis is that DBS masks the pathological synchronized firing patterns of the basal ganglia that characterize the Parkinsonian state with a regularized firing pattern. It remains unclear why stimulation of PPN should be applied with low frequency in contrast to the high frequency stimulation of STN. To get a better understanding of PPN stimulation we construct a computational model for the PPN Type I neurons in a network