Nonlinear buckling and symmetry breaking of a soft elastic sheet sliding on a cylindrical substrate

We consider the axial compression of a thin sheet wrapped around a rigid cylindrical substrate. In contrast to the wrinkling-to-fold transitions exhibited in similar systems, we find that the sheet always buckles into a single symmetric fold, while periodic solutions are unstable. Upon further compression, the solution breaks symmetry and stabilizes into a recumbent fold. Using linear analysis and numerics, we theoretically predict the buckling force and energy as a function of the compressive displacement. We compare our theory to experiments employing cylindrical neoprene sheets and find remarkably good agreement.Comment: 20 pages, 5 figure

Making big steps in trajectories

We consider the solution of initial value problems within the context of hybrid systems and emphasise the use of high precision approximations (in software for exact real arithmetic). We propose a novel algorithm for the computation of trajectories up to the area where discontinuous jumps appear, applicable for holomorphic flow functions. Examples with a prototypical implementation illustrate that the algorithm might provide results with higher precision than well-known ODE solvers at a similar computation time

Immunology of schizophrenia

Increased proinflammatory markers like cytokines have been described in the blood and cerebrospinal fluid of patients suffering from schizophrenia. Animal models have shown that a hit in early life to the immune system might trigger a lifelong increased immune reactivity. Many epidemiological and clinical studies show the role of various infectious agents as risk factors for schizophrenia with overlap to other psychoses. The first large-scale epidemiological study in psychiatry from Denmark clearly demonstrates severe infections and autoimmune disorders during lifetime to be risk factors for schizophrenia. Genetic studies have shown the strongest signal for schizophrenia on chromosome 6p22.1, in a region related to the major histocompatibility complex and other immune functions. The vulnerability-stress-inflammation model is important as stress may increase proinflammatory cytokines and even contribute to a lasting proinflammatory state. The immune system itself is considered an important further piece in the puzzle, as in autoimmune disorders in general, which are always linked to three factors: genes, the environment and the immune system. Alterations of dopaminergic, serotonergic, noradrenergic and glutamatergic neurotransmission have been shown with low-level neuroinflammation and may directly be involved in the generation of schizophrenic symptoms. Loss of central nervous system volume and microglial activation has been demonstrated in schizophrenia in neuroimaging studies, which supports the assumption of a low-level neuroinflammatory process. Further support comes from the therapeutic benefit of anti-inflammatory medications in specific studies and the anti-inflammatory and immunomodulatory intrinsic effects of antipsychotics

Immunology of major depression

High levels of several proinflammatory components of the immune system, such as interleukin-6, C-reactive protein, tumor necrosis factor (TNF)-\textgreeka, or neopterin in patients suffering from major depression (MD) point to the involvement of an inflammatory process in the pathophysiology of MD. The direct and indirect effects of cytokines on neurotransmitter storage and release - mediated by microglia cells and astrocytes - are discussed. The tryptophan/kynurenine metabolism is one of the indirect mechanisms because the enzyme indoleamine 2,3-dioxygenase - a key enzyme of this metabolism in the central nervous system - is driven by pro- and anti-inflammatory cytokines and degrades serotonin. Moreover, neuroactive kynurenines such as kynurenic acid and quinolinic acid act on the glutamatergic neurotransmission as N-methyl-D-aspartate antagonists and agonists, respectively. Alterations of the serotonergic, noradrenergic and glutamatergic neurotransmission have been shown with low-level neuroinflammation and may be involved in symptom generation. Epidemiological and clinical studies show a role for inflammation as a risk factor for MD. A large-scale epidemiological study in MD clearly demonstrates that severe infections and autoimmune disorders are lifetime risk factors for MD. The vulnerability-stress-inflammation model matches with this view as stress may increase proinflammatory cytokines and even contribute to a lasting proinflammatory state. Further support comes from the therapeutic benefit of anti-inflammatory medications such as the cyclo-oxygenase-2 inhibitors, TNF-\textgreeka antagonists and others, and the anti-inflammatory and immunomodulatory intrinsic effects of antidepressants

The Role of Intercellular Adhesion Molecule-1 in the Pathogenesis of Psychiatric Disorders

Intercellular adhesion molecule-1 (ICAM-1) is a transmembrane glycoprotein that is overexpressed in many pathological states. Although, like many other immune molecules, ICAM-1 plays only a limited role in the abundant concert of the immune response, it may be more important than we realize. In the central nervous system (CNS), ICAM-1 is expressed in microglial cells and astrocytes and in endothelial cells in the white and gray matter of the human forebrain. It is of particular interest in psychiatric disorders for two reasons: It has a key function for the blood-brain barrier, which plays an important role in the biology of psychiatric disorders, and it is a marker for inflammation. Although the blood level of soluble ICAM-1 (sICAM-1) might be lower in acute unmedicated schizophrenia, it has been reported to be increased in many other psychiatric conditions, such as major depression, bipolar disorder, and dementia. In bipolar disorder, high sICAM levels were found during both the depressed and the manic states and also during the euthymic phase (the free interval), possibly indicating that sICAM is a trait marker. High sICAM-1 blood levels have also been found in depression comorbid to a somatic disease state. Interestingly, sICAM-1 levels also increase during aging. Some studies investigated sICAM-1 levels in the cerebrospinal fluid of psychiatric disorders and ICAM-1 expression in postmortem CNS tissue of psychiatric patients and found that the overall duration and duration of the chronic phase of the psychiatric disorder seem to play a role in both. Moreover, confounders, such as antipsychotic and antidepressive medication, have to be considered. sICAM-1 levels seem to be associated with hypopermeability or hyperpermeability of the blood-brain barrier and thus to influence the communication between the CNS immune system, represented by glia cells, and the peripheral immune system. The balance between the influx and efflux of immune molecules into and out of the CNS may be one of the pinpoints in psychiatric disorders, in particular in the chronic phase, e.g., in schizophrenia. This aspect, however, needs further intense research, in particular to enable researchers to develop therapeutic principles based on an immune/inflammatory approach

Parameterized Uniform Complexity in Numerics: from Smooth to Analytic, from NP-hard to Polytime

The synthesis of classical Computational Complexity Theory with Recursive Analysis provides a quantitative foundation to reliable numerics. Here the operators of maximization, integration, and solving ordinary differential equations are known to map (even high-order differentiable) polynomial-time computable functions to instances which are `hard' for classical complexity classes NP, #P, and CH; but, restricted to analytic functions, map polynomial-time computable ones to polynomial-time computable ones -- non-uniformly! We investigate the uniform parameterized complexity of the above operators in the setting of Weihrauch's TTE and its second-order extension due to Kawamura&Cook (2010). That is, we explore which (both continuous and discrete, first and second order) information and parameters on some given f is sufficient to obtain similar data on Max(f) and int(f); and within what running time, in terms of these parameters and the guaranteed output precision 2^(-n). It turns out that Gevrey's hierarchy of functions climbing from analytic to smooth corresponds to the computational complexity of maximization growing from polytime to NP-hard. Proof techniques involve mainly the Theory of (discrete) Computation, Hard Analysis, and Information-Based Complexity

Screening of winter barley varieties (Hordeum vulgare) for resistance against loose smut (Ustilago nuda) and covered smut (Ustilago hordei) in Germany

Up to now organic farmers depend greatly on conventionally bred and produced varieties of barley. A turning point was set in 2004 by EU regulation No. 1452/2003 restricting the use of conventionally propagated seed and planting material for organic agriculture. Concerning smut fungi in barley, conventional seed producer's attention was rarely directed to plant resistance due to the possibility of chemical seed treatment (controlling the diseases completely). A main problem for organic seed producers is that organically produced seeds have to fulfil the same regular phytosanitary requirements like conventionally produced seeds. For the production of certified seeds not more than five ears infected with Ustilago hordei (Uh) and/or U. nuda (Un) are allowed on an area of 150 m² in Germany (RUTZ 1998). Though warm or hot water treatment can give excellent control of Un and Uh in organic farming (WINTER et al. 1996), the effect is not sufficient for seed production. Even biological control agents (for example Tillecur®) cannot reach the demands of the guidelines reliably. As an effective way to keep the restrictions remains the cultivation of resistant varieties. Aim of the presented study was to screen winter barley varieties for their degree of smut resistance in Germany. It started in 2000 (KLAUSE & SPIESS 2003) and is sponsored within the Federal Organic Farming Scheme since 2002

Nitroreductase (GlNR1) increases susceptibility of Giardia lamblia and Escherichia coli to nitro drugs

Objectives The protozoan parasite Giardia lamblia causes the intestinal disease giardiasis, which may lead to acute and chronic diarrhoea in humans and various animal species. For treatment of this disease, several drugs such as the benzimidazole albendazole, the nitroimidazole metronidazole and the nitrothiazolide nitazoxanide are currently in use. Previously, a G. lamblia nitroreductase 1 (GlNR1) was identified as a nitazoxanide-binding protein. The aim of the present project was to elucidate the role of this enzyme in the mode of action of the nitro drugs nitazoxanide and metronidazole. Methods Recombinant GlNR1 was overexpressed in both G. lamblia and Escherichia coli (strain BL21). The susceptibility of the transfected bacterial and giardial cell lines to nitazoxanide and metronidazole was analysed. Results G. lamblia trophozoites overexpressing GlNR1 had a higher susceptibility to both nitro drugs. E. coli were fully resistant to nitazoxanide under both aerobic and semi-aerobic growth conditions. When grown semi-aerobically, bacteria overexpressing GlNR1 became susceptible to nitazoxanide. Conclusions These findings suggest that GlNR1 activates nitro drugs via reduction yielding a cytotoxic produc