Estimates of nonequilibrium ionization phenomena in the inviscid Apollo plasma sheath

Nonequilibrium ionization in asymmetric plasma sheath determined for Apollo spacecraft at superorbital velocity reentr

Design opportunities for wearable devices in learning to climb

In this paper, we present a field study on the learning of climbing aimed at defining the design space of wearable devices to support beginners. Three main findings have emerged from our study. First, climbing has a strong emotional impact on beginners; therefore, learning to climb requires mastering new motor patterns as well as negative emotions, such as stress and fear. Second, the feeling of danger that climbers often experience can be mitigated by trust in the climbing partner and the perception of her active presence. Finally, a big problem in climbing is the communication difficulty between the climbing partners and between climber and instructor. We conclude the paper presenting four design considerations for the design of wearable devices meant to support the learning of climbing by providing the actors involved with augmented communication. Such augmented communication should address both the physical and the emotional difficulties of this sport

One-loop corrections to the instanton transition in the two-dimensional Abelian Higgs model

We present an evaluation of the fluctuation determinant which appears as a prefactor in the instanton transition rate for the two-dimensional Abelian Higgs model. The corrections are found to change the rate at most by a factor of 2 for 0.4 < M_W/M_H < 2.0.Comment: DO-TH-94/17, 20 pages, 4 figures appended as uucompressed .eps files, LaTeX, needs epsfig.st

Paradoxical roles of antioxidant enzymes:Basic mechanisms and health implications

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated from aerobic metabolism, as a result of accidental electron leakage as well as regulated enzymatic processes. Because ROS/RNS can induce oxidative injury and act in redox signaling, enzymes metabolizing them will inherently promote either health or disease, depending on the physiological context. It is thus misleading to consider conventionally called antioxidant enzymes to be largely, if not exclusively, health protective. Because such a notion is nonetheless common, we herein attempt to rationalize why this simplistic view should be avoided. First we give an updated summary of physiological phenotypes triggered in mouse models of overexpression or knockout of major antioxidant enzymes. Subsequently, we focus on a series of striking cases that demonstrate “paradoxical” outcomes, i.e., increased fitness upon deletion of antioxidant enzymes or disease triggered by their overexpression. We elaborate mechanisms by which these phenotypes are mediated via chemical, biological, and metabolic interactions of the antioxidant enzymes with their substrates, downstream events, and cellular context. Furthermore, we propose that novel treatments of antioxidant enzyme-related human diseases may be enabled by deliberate targeting of dual roles of the pertaining enzymes. We also discuss the potential of “antioxidant” nutrients and phytochemicals, via regulating the expression or function of antioxidant enzymes, in preventing, treating, or aggravating chronic diseases. We conclude that “paradoxical” roles of antioxidant enzymes in physiology, health, and disease derive from sophisticated molecular mechanisms of redox biology and metabolic homeostasis. Simply viewing antioxidant enzymes as always being beneficial is not only conceptually misleading but also clinically hazardous if such notions underpin medical treatment protocols based on modulation of redox pathways

Visual ecology of aphids – a critical review on the role of colours in host finding

We review the rich literature on behavioural responses of aphids (Hemiptera: Aphididae) to stimuli of different colours. Only in one species there are adequate physiological data on spectral sensitivity to explain behaviour crisply in mechanistic terms. Because of the great interest in aphid responses to coloured targets from an evolutionary, ecological and applied perspective, there is a substantial need to expand these studies to more species of aphids, and to quantify spectral properties of stimuli rigorously. We show that aphid responses to colours, at least for some species, are likely based on a specific colour opponency mechanism, with positive input from the green domain of the spectrum and negative input from the blue and/or UV region. We further demonstrate that the usual yellow preference of aphids encountered in field experiments is not a true colour preference but involves additional brightness effects. We discuss the implications for agriculture and sensory ecology, with special respect to the recent debate on autumn leaf colouration. We illustrate that recent evolutionary theories concerning aphid–tree interactions imply far-reaching assumptions on aphid responses to colours that are not likely to hold. Finally we also discuss the implications for developing and optimising strategies of aphid control and monitoring

Nachtlärminduzierte Schlafstörungen und Herz-Kreislauf-Risiko

Impairment of sleep in the sense of insomnias, i.e. difficulties falling asleep and staying asleep, early morning awakening and chronical unrestful sleep is widespread in the population and are associated with a variety of physical and mental health disorders. The environmental causes of insomnia include a number of factors, with nighttime noise being an important cause. Recent data from the European Environment Agency shows that environmental noise (road traffic, railway, aircraft and industrial noise) causes severe sleep disorders among 6.5 million people in Europe. New epidemiological and mechanistic field studies show that in particular night traffic noise can lead, among other things, to impaired vascular function, thrombo-inflammatory changes, an increase in stress hormones and increased blood pressure, representing significant risk factors for cardiovascular diseases. According to the European Environment Agency, environmental noise causes 48000 additional cases of ischemic heart disease and 12000 premature deaths each year

Lärm und Herz-Kreislauf-Erkrankungen

Environmental noise is a significant environmental risk factor for public health. The European Environment Agency states that at least 20% of the European population are exposed to harmful day-evening-night noise levels of 55 decibels (dB), whereas the World Health Organization recommends up to 10 dB lower limit values, depending on the noise source, for the protection of the population. Chronic noise can interfere with daily activities and sleep and trigger mental and physiological stress reactions that can increase the risk of cardiovascular disease in the long term. Therefore, preventive measures at the source including noise-reducing structural changes are essential to ensure compliance with noise limits and to protect the population from the negative health effects of noise

Discovery of new therapeutic redox targets for cardioprotection against ischemia/reperfusion injury and heart failure

Global epidemiological studies reported a shift from maternal/infectious communicable diseases to chronic non-communicable diseases and a major part is attributable to atherosclerosis and metabolic disorders. Accordingly, ischemic heart disease was identified as a leading risk factor for global mortality and morbidity with a prevalence of 128 million people. Almost 9 million premature deaths can be attributed to ischemic heart disease and subsequent acute myocardial infarction and heart failure, also representing a substantial socioeconomic burden. As evidenced by typical oxidative stress markers such as lipid peroxidation products or oxidized DNA/RNA bases, the formation of reactive oxygen species by various sources (NADPH oxidases, xanthine oxidase and mitochondrial resperatory chain) plays a central role for the severity of ischemia/reperfusion damage. The underlying mechanisms comprise direct oxidative damage but also adverse redox-regulation of kinase and calcium signaling, inflammation and cardiac remodeling among others. These processes and the role of reactive oxygen species are discussed in the present review. We also present and discuss potential targets for redox-based therapies that are either already established in the clinics (e.g. guanylyl cyclase activators and stimulators) or at least successfully tested in preclinical models of myocardial infarction and heart failure (mitochondria-targeted antioxidants). However, reactive oxygen species have not only detrimental effects but are also involved in essential cellular signaling and may even act protective as seen by ischemic pre- and post-conditioning or eustress – which makes redox therapy quite challenging

Therapeutic effects of the mitochondrial ROS-redox modulator KH176 in a mammalian model of Leigh Disease

Leigh Disease is a progressive neurometabolic disorder for which a clinical effective treatment is currently still lacking. Here, we report on the therapeutic efficacy of KH176, a new chemical entity derivative of Trolox, in Ndufs4 (-/-) mice, a mammalian model for Leigh Disease. Using in vivo brain diffusion tensor imaging, we show a loss of brain microstructural coherence in Ndufs4 (-/-) mice in the cerebral cortex, external capsule and cerebral peduncle. These findings are in line with the white matter diffusivity changes described in mitochondrial disease patients. Long-term KH176 treatment retained brain microstructural coherence in the external capsule in Ndufs4 (-/-) mice and normalized the increased lipid peroxidation in this area and the cerebral cortex. Furthermore, KH176 treatment was able to significantly improve rotarod and gait performance and reduced the degeneration of retinal ganglion cells in Ndufs4 (-/-) mice. These in vivo findings show that further development of KH176 as a potential treatment for mitochondrial disorders is worthwhile to pursue. Clinical trial studies to explore the potency, safety and efficacy of KH176 are ongoing