Design of an Unknown Input Observer to Enhance Driver Experience of Electric Power Steering Systems

Electric power steering (EPS) systems assist the driver during manoeuvres by applying an additional steering torque generated by an electric motor. Although there are many advantages for electric actuated steering systems including fuel efficiency, they are known to deteriorate the feel of the steering as experienced by the driver. This paper presents a sliding mode observer based estimation concept which provides signals to evaluate and improve perception and feel of the steering as experienced by the driver. The proposed strategy is based on a physically motivated dynamic model of a power steering system and the measurements considered are typically available in any modern vehicle. The performance of the estimator is investigated using numerical simulation as well as experimental results obtained using a laboratory steering testbed

Differing molecular pathology of pancreatic adenocarcinoma in Egyptian and United States patients

Variations in genetic mutations in pancreatic carcinoma between different populations have not been studied extensively, especially in developing countries where pancreatic cancer is rare. We studied the molecular pathology of 44 pancreatic carcinomas from patients residing in a heavily polluted region in the Nile River delta and compared the findings with tumors from 44 United States (US) patients. We evaluated K-ras mutations in codon 12, p53 mutations in exons 5–8, and Gadd45a mutations in exons 1 and 4. Overall, rates of K-ras , p53 and Gadd45 mutations were not statistically different in tumors of patients from Egypt and the US (67.4 vs. 63.4%; 27.3 vs. 36.4% and 9.1 vs. 4.5%, respectively). However, there were distinct differences in the specific types of K-ras and p53 mutations between the 2 groups. In K-ras , G → T transversion mutation was more frequent in the tumors from Egypt than from the US (58.6 vs. 26.9%), whereas G → C transversion was detected in 26.9% of US tumors but none from Egypt ( p = 0.003). We also found a trend toward differences in the p53 exons in which mutations occurred, with higher frequency of exon 5 mutation and lower frequency of exon 6 mutation in Egyptian tumors. Logistic regression showed that K-ras G → T transversion mutations and p53 exon 6 mutations were predicted by the country of residence of the patients. Our study identifies that there are differences in the types of mutations found in tumors from pancreatic carcinoma patients in Egypt and the US, and suggests that environmental factors may explain these differences. © 2006 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/55779/1/21986_ftp.pd

Neuroactive substances specifically modulate rhythmic body contractions in the nerveless metazoon Tethya wilhelma (Demospongiae, Porifera)

BACKGROUND: Sponges (Porifera) are nerve- and muscleless metazoa, but display coordinated motor reactions. Therefore, they represent a valuable phylum to investigate coordination systems, which evolved in a hypothetical Urmetazoon prior to the central nervous system (CNS) of later metazoa. We have chosen the contractile and locomotive species Tethya wilhelma (Demospongiae, Hadromerida) as a model system for our research, using quantitative analysis based on digital time lapse imaging. In order to evaluate candidate coordination pathways, we extracorporeally tested a number of chemical messengers, agonists and antagonists known from chemical signalling pathways in animals with CNS. RESULTS: Sponge body contraction of T. wilhelma was induced by caffeine, glycine, serotonine, nitric oxide (NO) and extracellular cyclic adenosine monophosphate (cAMP). The induction by glycine and cAMP followed patterns varying from other substances. Induction by cAMP was delayed, while glycine lead to a bi-phasic contraction response. The frequency of the endogenous contraction rhythm of T. wilhelma was significantly decreased by adrenaline and NO, with the same tendency for cAMP and acetylcholine. In contrast, caffeine and glycine increased the contraction frequency. The endogenous rhythm appeared irregular during application of caffeine, adrenaline, NO and cAMP. Caffeine, glycine and NO attenuated the contraction amplitude. All effects on the endogenous rhythm were neutralised by the washout of the substances from the experimental reactor system. CONCLUSION: Our study demonstrates that a number of chemical messengers, agonists and antagonists induce contraction and/or modulate the endogenous contraction rhythm and amplitude of our nerveless model metazoon T. wilhelma. We conclude that a relatively complex system of chemical messengers regulates the contraction behaviour through auto- and paracrine signalling, which is presented in a hypothetical model. We assume that adrenergic, adenosynergic and glycinergic pathways, as well as pathways based on NO and extracellular cAMP are candidates for the regulation and timing of the endogenous contraction rhythm within pacemaker cells, while GABA, glutamate and serotonine are candidates for the direct coordination of the contractile cells

Reformvorschläge zur Lösung der zentralen Probleme des österreichischen Gesundheitswesens

Weyrer SebaldKlagenfurt, Alpen-Adria-Univ., Dipl.-Arb., 2009KB2009 25(VLID)241181

Die interne Konzernkommunikation der Stadtwerke Klagenfurt Gruppe

Weyrer SabineKlagenfurt, Alpen-Adria-Univ., Dipl.-Arb., 2009KB2009 09(VLID)241158

Inbetriebnahme, Modellierung und Regelung eines Prüfstandes für elektrische Lenkunterstützung

Matthias WeyrerZsfassung in engl. SpracheKlagenfurt, Alpen-Adria-Univ., Master-Arb., 2015(VLID)241325

Molecular Mechanisms of Presynaptic Plasticity and Function in the Mammalian Brain

I specifically want to thank all the people of the Paulsen and Regehr labs that helped and supported me.Synaptic plasticity describes efficacy changes in synaptic transmission and ranges in duration from tens to hundreds of milliseconds (short-term), to hours and days (long-term). Short-term plasticity plays crucial roles in synaptic computation, information processing, learning, working and short-term memory as well as its dysfunction in psychiatric and neurodegenerative diseases. The main aim of my PhD thesis was to determine the molecular mechanisms of different forms of presynaptic plasticity. Short-term facilitation increases neurotransmitter release in response to a high-frequency pair (paired-pulse facilitation; PPF) or train (train facilitation; TF) of presynaptic stimuli. Synaptotagmin 7 (Syt7) has been shown to act as residual calcium (Ca$_{res}$) sensor for PPF and TF at various synapses. Syt7 also seems to be involved in recovery from depression, whereas its role in neurotransmission remains controversial. My aim was to express Syt7 in a synapse where it is not normally found and determine how it affects short-term synaptic plasticity. Immunohistochemistry indicated that Syt7 is not localized to cerebellar climbing fibers (CFs). Wild-type (WT) and Syt7 knockout (KO) recordings at CF to Purkinje cell (CF-PC) synapses established that at near-physiological external calcium (Ca$_{ext}$) levels both genotypes displayed similar recovery from paired-pulse depression. In low Ca$_{ext}$,WT CF-PC synapses showed robust PPF, which turned out to be independent of Syt7. All my experiments strongly suggested that WT CFs do not express native Syt7, but display low Ca$_{ext}$ CF-PC PPF and TF. Thus, channelrhodopsin-2 and Syt7 were bicistronically expressed via AAV9 virus in CFs. This ectopic Syt7 expression in CFs led to big increases in low-Ca$_{ext}$ CF-PC facilitation, more than doubling PPF and more than tripling TF. While overexpression of Syt7 might turn out to have an effect on the initial release probability (pr), the observed CF-PC facilitation increase still critically depended on presynaptic Syt7 expression. And when comparing only cells in a defined EPSC1 amplitude range, the Syt7-induced increase in low-Ca$_{ext}$ PPF could not be accounted for by changes in initial pr, suggesting a general role for Syt7 as calcium sensor for facilitation. Another form of short-term plasticity, post-tetanic potentiation (PTP), is believed to be mediated presynaptically by calcium-dependent protein kinase C (PKC) isoforms that phosphorylate Munc18-1 proteins. It is unknown how generally applicable this mechanism is throughout the brain and if other proteins might be able to modulate PTP. Combining genetic (PKCαβy triple knockout [TKO] and Munc18-1SA knock-in [Munc18 KI] mice, in which Munc18- 1 cannot get phosphorylated) with pharmacological tools (PKC inhibitor GF109203), helped us show that PTP at the cerebellar parallel fiber to Purkinje cell (PF-PC) synapse seems to depend on PKCs but seems mostly independent of Munc18-1 phosphorylation. In addition, compared to WT animals, genetic elimination of presynaptic active zone protein Liprin-α3 led to similar PF-PC PTP and paired-pulse ratios (PPRs). At the hippocampal CA3-CA1 synapse previous pharmacological studies suggested that PKC mediates PTP. A genetic approach helped to show that calcium dependent PKCs do not seem to be required for CA3-CA1 PTP. Pharmacologically inhibiting protein kinase A as well as genetically eliminating Syt7 also had no effect on CA3-CA1 PTP. In addition, Ca IM-AA mutant mice, in which Ca$_{v}$2.1 channels have a mutated IQ-like motif (IM) so that it cannot get bound by calcium sensor proteins any more, not only displayed regular PTP, but also normal PPF and TF at CA3-CA1 synapses. In conclusion, my PhD thesis helped further characterize different forms of presynaptic plasticity, underlined that short-term synaptic plasticity can be achieved through diverse mechanisms across the Mammalian brain and supported a potentially general role for synaptotagmin 7 acting as residual calcium sensor for facilitation.Boehringer Ingelheim Fonds PhD Fellowship; B&C Privatstiftun

Singularity Avoidance Control of a Non-Holonomic Mobile Manipulator for Intuitive Hand Guidance

Mobile manipulators are robot systems capable of combining logistics and manipulation tasks. They thus fulfill an important prerequisite for the integration into flexible manufacturing systems. Another essential feature required for modern production facilities is a user-friendly and intuitive human-machine interaction. In this work the goal of code-less programming is addressed and an intuitive and safe approach to physically interact with such robot systems is derived. We present a natural approach for hand guiding a sensitive mobile manipulator in task space using a force torque sensor that is mount close to the end effector. The proposed control structure is capable of handling the kinematic redundancies of the system and avoid singular arm configurations by means of haptic feedback to the user. A detailed analysis of all possible singularities of the UR robot family is given and the functionality of the controller design is shown with laboratory experiments on our mobile manipulator

Calcium-Dependent Protein Kinase C Is Not Required for Post-Tetanic Potentiation at the Hippocampal CA3 to CA1 Synapse

Post-tetanic potentiation (PTP) is a widespread form of short-term synaptic plasticity in which a period of elevated presynaptic activation leads to synaptic enhancement that lasts tens of seconds to minutes. A leading hypothesis for the mechanism of PTP is that tetanic stimulation elevates presynaptic calcium that in turn activates calcium-dependent protein kinase C (PKC) isoforms to phosphorylate targets and enhance neurotransmitter release. Previous pharmacological studies have implicated this mechanism in PTP at hippocampal synapses, but the results are controversial. Here we combine genetic and pharmacological approaches to determine the role of classic PKC isoforms in PTP. We find that PTP is unchanged in PKC triple knock-out (TKO) mice in which all calcium-dependent PKC isoforms have been eliminated (PKCα, PKCβ, and PKCγ). We confirm previous studies and find that in wild-type mice 10 μm of the PKC inhibitor GF109203 eliminates PTP and the PKC activator PDBu enhances neurotransmitter release and occludes PTP. However, we find that the same concentrations of GF109203 and PDBu have similar effects in TKO animals. We also show that 2 μm GF109203 does not abolish PTP even though it inhibits the PDBu-dependent phosphorylation of PKC substrates. We conclude that at the CA3 to CA1 synapse Ca(2+)-dependent PKC isoforms do not serve as calcium sensors to mediate PTP. SIGNIFICANCE STATEMENT Neurons dynamically regulate neurotransmitter release through many processes known collectively as synaptic plasticity. Post-tetanic potentiation (PTP) is a widespread form of synaptic plasticity that lasts for tens of seconds that may have important computational roles and contribute to short-term memory. According to a leading mechanism, presynaptic calcium activates protein kinase C (PKC) to increase neurotransmitter release. Pharmacological studies have also implicated this mechanism at hippocampal CA3 to CA1 synapses, but there are concerns about the specificity of PKC activators and inhibitors. We therefore used a molecular genetic approach and found that PTP was unaffected when all calcium-dependent PKC isozymes were eliminated. We conclude that PKC isozymes are not the calcium sensors that mediate PTP at the CA3 to CA1 synapse