Magnetic field effects on the density of states of orthorhombic superconductors

The quasiparticle density of states in a two-dimensional d-wave superconductor depends on the orientation of the in-plane external magnetic field H. This is because. in the region of the gap nodes, the Doppler shift due to the circulating supercurrents around a vortex depend on the direction of H. For a tetragonal system the induced pattern is four-fold symmetric and, at zero energy, the density of states exhibits minima along the node directions. But YBa_2C_3O_{6.95} is orthorhombic because of the chains and the pattern becomes two-fold symmetric with the position of the minima occuring when H is oriented along the Fermi velocity at a node on the Fermi surface. The effect of impurity scattering in the Born and unitary limit is discussed.Comment: 24 pages, 11 Figure

Phenomenological description of the microwave surface impedance and complex conductivity of high-TcT_c single crystals

Measurements of the microwave surface impedance $Z_s(T)=R_s(T)+iX_s(T)$ and of the complex conductivity $\sigma_s(T)$ of high-quality, high-$T_c$ single crystals of YBCO, BSCCO, TBCCO, and TBCO are analyzed. Experimental data of $Z_s(T)$ and $\sigma_s(T)$ are compared with calculations based on a modified two-fluid model which includes temperature-dependent quasiparticle scattering and a unique temperature variation of the density of superconducting carriers. We elucidate agreement as well as disagreement of our analysis with the salient features of the experimental data. Existing microscopic models are reviewed which are based on unconventional symmetry types of the order parameter and on novel mechanisms of quasiparticle relaxation.Comment: 15 pages, 17 figures, 1 tabl

Dynamic simulations on the mitochondrial fatty acid Beta-oxidation network

<p>Abstract</p> <p>Background</p> <p>The oxidation of fatty acids in mitochondria plays an important role in energy metabolism and genetic disorders of this pathway may cause metabolic diseases. Enzyme deficiencies can block the metabolism at defined reactions in the mitochondrion and lead to accumulation of specific substrates causing severe clinical manifestations. Ten of the disorders directly affecting mitochondrial fatty acid oxidation have been well-defined, implicating episodic hypoketotic hypoglycemia provoked by catabolic stress, multiple organ failure, muscle weakness, or hypertrophic cardiomyopathy. Additionally, syndromes of severe maternal illness (HELLP syndrome and AFLP) have been associated with pregnancies carrying a fetus affected by fatty acid oxidation deficiencies. However, little is known about fatty acids kinetics, especially during fasting or exercise when the demand for fatty acid oxidation is increased (catabolic stress).</p> <p>Results</p> <p>A computational kinetic network of 64 reactions with 91 compounds and 301 parameters was constructed to study dynamic properties of mitochondrial fatty acid β-oxidation. Various deficiencies of acyl-CoA dehydrogenase were simulated and verified with measured concentrations of indicative metabolites of screened newborns in Middle Europe and South Australia. The simulated accumulation of specific acyl-CoAs according to the investigated enzyme deficiencies are in agreement with experimental data and findings in literature. Investigation of the dynamic properties of the fatty acid β-oxidation reveals that the formation of acetyl-CoA – substrate for energy production – is highly impaired within the first hours of fasting corresponding to the rapid progress to coma within 1–2 hours. LCAD deficiency exhibits the highest accumulation of fatty acids along with marked increase of these substrates during catabolic stress and the lowest production rate of acetyl-CoA. These findings might confirm gestational loss to be the explanation that no human cases of LCAD deficiency have been described.</p> <p>Conclusion</p> <p>In summary, this work provides a detailed kinetic model of mitochondrial metabolism with specific focus on fatty acid β-oxidation to simulate and predict the dynamic response of that metabolic network in the context of human disease. Our findings offer insight into the disease process (e.g. rapid progress to coma) and might confirm new explanations (no human cases of LCAD deficiency), which can hardly be obtained from experimental data alone.</p

Mathematical Modeling and Simulation of Ventricular Activation Sequences: Implications for Cardiac Resynchronization Therapy

Next to clinical and experimental research, mathematical modeling plays a crucial role in medicine. Biomedical research takes place on many different levels, from molecules to the whole organism. Due to the complexity of biological systems, the interactions between components are often difficult or impossible to understand without the help of mathematical models. Mathematical models of cardiac electrophysiology have made a tremendous progress since the first numerical ECG simulations in the 1960s. This paper briefly reviews the development of this field and discusses some example cases where models have helped us forward, emphasizing applications that are relevant for the study of heart failure and cardiac resynchronization therapy