Secondary frequencies in the wake of a circular cylinder with vortex shedding

A detailed numerical study of two-dimensional flow past a circular cylinder at moderately low Reynolds numbers was conducted using three different numerical algorithms for solving the time-dependent compressible Navier-Stokes equations. It was found that if the algorithm and associated boundary conditions were consistent and stable, then the major features of the unsteady wake were well-predicted. However, it was also found that even stable and consistent boundary conditions could introduce additional periodic phenomena reminiscent of the type seen in previous wind-tunnel experiments. However, these additional frequencies were eliminated by formulating the boundary conditions in terms of the characteristic variables. An analysis based on a simplified model provides an explanation for this behavior

Breeding for biofuel production

Tese de doutoramento em Ciências Farmacêuticas, na especialidade de Biologia Celular e Molecular, apresentada à Faculdade de Farmácia da Universidade de CoimbraAs sinapses excitatórias são estruturas dinâmicas e a forma como neurónios vizinhos comunicam entre si é ajustada consoante a actividade neuronal. A esta propriedade chama-se plasticidade sináptica e a nível molecular está correlacionada com a aprendizagem e a memória. A potenciação sináptica de longa duração (LTP) é a forma de plasticidade sináptica mais estudada sendo definida como um fortalecimento duradouro na comunicação entre neurónios vizinhos desencadeado pela actividade neuronal. Pelo contrário, a depressão sináptica de longa duração (LTD) é caracterizada por uma diminuição duradoura da potência sináptica. Alterações moleculares nos mecanismos de plasticidade sináptica estão na base de muitas doenças neurológicas e psiquiátricas. Algumas das modificações sinápticas ao nível estrutural, bioquímico e funcional associadas com a plasticidade sináptica requerem a traducão de mRNAs (RNA mensageiros) localizados nas dendrites, resultando em alterações no proteoma sináptico. Várias evidências mostram que a síntese proteica em dendrites desempenha um papel fundamental em várias formas de plasticidade sináptica, incluindo a LTP mediada pelo BDNF (factor neurotrófico derivado do cérebro). Contudo, pouco se sabe sobre a identidade dos mRNA que são traduzidos ao nível da sinapse em resposta ao BDNF e sobre os mecanismos de regulação envolvidos. Além disso, também está ainda por esclarecer de que modo muitas das alterações no proteoma sináptico contribuem para os fenómenos de plasticidade sináptica. Neste trabalho investigámos o papel da Pyk2 (cinase de resíduos de tirosina rica em prolina do tipo 2) na mediação dos efeitos do BDNF na sinapse. A Pyk2 é uma cinase de resíduos de tirosina pertencente à família das FAK (cinases de adesão focal), que desempenha uma grande variedade de funções no sistema nervoso central, incluindo o control da LTP e da LTD por mecanismos que envolvem a regulação dos receptores NMDA (N-metil-D-aspartato). Além disso, pensa-se que esta cinase desempenha um papel importante na remodelação da arquitectura das espículas sinápticas e da arborização dendritica, induzidas pela actividade neuronal. Observámos que a Pyk2 é traduzida ao nível da sinapse e acumulada nas densidades pós-sinápticas de neurónios do hipocampo após a estimulação com BDNF. A acumulação dendritica da Pyk2 em resposta à estimulação com BDNF requer a participação da RBP (proteína que liga RNA), hnRNPK (ribonucleoproteína nuclear heterogénea do tipo K). Estas observações estão de acordo com os resultados anteriores do nosso laboratório mostrando que: (i) a hnRNPK é acumulada nas dendrites dos neurónios do hipocampo após o estimulação com BDNF; (ii) a ligação do mRNA da Pyk2 à hnRNPK é regulada por BDNF. Usando um protocolo químico para aumentar a actividade neuronal e induzir LTP também observámos que a Pyk2 se acumula na sinapse por um mecanismo dependente de BDNF. A principal função da Pyk2 ao nível da densidade pós-sináptica tem sido associada à regulação das correntes mediadas pelos recetores NMDA através da interação direta com a Src, outra cinase de resíduos de tirosina. Neste estudo, observámos que o tratamento com BDNF aumenta a expressão superficial dos receptores NMDA que contêm a subunidade GluN2B, ao nível da sinapse, por um mecanismo dependente da síntese proteica. De acordo com estas observações, observou-se que a estimulação com BDNF aumenta os níveis de Pyk2 fosforilada/activada de forma específica ao nível da sinapse, o que sugere uma regulação diferencial da atividade da cinase. O aumento dos níveis sinápticos dos recetores NMDA induzido pelo BDNF também depende da Pyk2 e da sua actividade de cinase. Por outro lado, também se observou que em condições de repouso a manutenção na membrana celular dos recetores NMDA contendo subunidades GluN2B depende da atividade de cinase da Pyk2. Finalmente, a sobreexpressão da Pyk2 em neurónios do hipocampo foi suficente para mimetizar os efeitos do BDNF na expressão superficial dos receptores NMDA que contêm a subunidade GluN2B. No seu conjunto, os resultados mostram que o BDNF induz a activação/acumulação da Pyk2 por um mecanismo que envolve a hnRNPK e a síntese dendritica da Pyk2, resultando num aumento da expressão superfical dos receptores NMDA que contêm a subunidade GluN2B. Este mecanismo pode mediar os efeitos do BDNF nos défices cognitivos que são característicos de certas doenças do cérebro.Excitatory synapses are dynamic entities and adjust their strength depending on the activity. This property is named synaptic plasticity and is considered the cellular correlate of learning and memory. Long-term potentiation (LTP) is the best studied form of synaptic plasticity and by definition it is considered as an activity-induced sustained increase in synaptic strength. Long-term depression (LTD) is the opposite form of plasticity, and is characterized by an activity-induced sustained decrease in synaptic strength. Alterations in the molecular basis of synaptic plasticity events underlie several neurological and psychiatric disorders. Some of the structural, biochemical and functional modifications of the synapse associated with synaptic plasticity require translation of dendritic-localized mRNAs, with concomitant alterations in the synaptic proteome. Multiple lines of evidence show that dendritic protein synthesis plays a key role in several forms of synaptic plasticity, including in brain-derived neurotrophic factor (BDNF)-mediated LTP. However, the identity of the mRNAs that are synaptically translated in response to BDNF and the regulatory mechanisms involved are poorly understood. Furthermore, how these changes in the proteome contribute to the plastic alterations of the synapse also remains to be uncovered. In this work, we investigated a role for Pyk2 (proline-rich tyrosine kinase 2) as a mediator of the effects of BDNF at the synapse. Pyk2 is a non-receptor tyrosine kinase, belonging to the FAK (focal adhesion kinase) family of proteins, which plays a wide range of functions in the central nervous system (CNS), including the control of LTP and LTD by mechanisms involving the regulation of NMDA (N-methyl-D-aspartate) receptors. Furthermore, this kinase is thought to play an important role in the activity-induced remodeling of spine architecture and dendritic arborization. We found that the protein kinase Pyk2 is synaptically translated in hippocampal neurons and accumulates at post-synaptic density following BDNF treatment. The dendritic accumulation of Pyk2 upon stimulation with BDNF requires the participation of the RNA-binding protein hnRNPK (heterogeneous nuclear ribonucleoprotein K). This is in accordance with previous results from our laboratory showing that (i) hnRNPK is accumulated in dendrites of hippocampal neurons upon BDNF treatment and (ii) the binding of Pyk2 mRNA to hnRNPK is regulated by BDNF. Using a chemical protocol to increase neuronal activity and to induce LTP, we also observed that Pyk2 accumulates at the synapse by a mechanism requiring BDNF. The main function of Pyk2 at the post-synaptic compartment has been attributed to the regulation of NMDA receptor currents through a direct interaction with a different tyrosine kinase, Src. Herein we found that BDNF treatment increases the surface expression of GluN2B-containing NMDA receptors (NMDAR) at synapses, by a mechanism dependent on protein synthesis. In agreement with these observations, the levels of phosphorylated/activated Pyk2 were specifically enhanced at the synapse upon BDNF treatment, suggesting a compartment-specific regulation of Pyk2 activity by BDNF. The BDNF-induced increase on surface NMDARs also requires Pyk2 and its kinase activity. The maintenance of basal levels of GluN2B-containing NMDAR at the cell surface was also dependent on Pyk2 kinase activity. Finally, overexpression of Pyk2 in hippocampal neurons was sufficient, per se, to mimic the BDNF-induced increase in GluN2B-NMDAR surface expression. Taken together, the results show that BDNF induces synaptic activation/accumulation of Pyk2 by a mechanism involving hnRNPK and dendritic Pyk2 synthesis, resulting in an enhancement in the surface levels of GluN2B-containing NMDAR. This mechanism may mediate the effects of BDNF on synaptic plasticity and may constitute a novel therapeutic target to restore the cognitive deficits characteristic of some brain disorders.FCT - SFRH/BD/80332/201

Finite-Size Scaling of the Domain Wall Entropy Distributions for the 2D ±J\pm J Ising Spin Glass

The statistics of domain walls for ground states of the 2D Ising spin glass with +1 and -1 bonds are studied for $L \times L$ square lattices with $L \le 48$, and $p$ = 0.5, where $p$ is the fraction of negative bonds, using periodic and/or antiperiodic boundary conditions. When $L$ is even, almost all domain walls have energy $E_{dw}$ = 0 or 4. When $L$ is odd, most domain walls have $E_{dw}$ = 2. The probability distribution of the entropy, $S_{dw}$, is found to depend strongly on $E_{dw}$. When $E_{dw} = 0$, the probability distribution of $|S_{dw}|$ is approximately exponential. The variance of this distribution is proportional to $L$, in agreement with the results of Saul and Kardar. For $E_{dw} = k > 0$ the distribution of $S_{dw}$ is not symmetric about zero. In these cases the variance still appears to be linear in $L$, but the average of $S_{dw}$ grows faster than $\sqrt{L}$. This suggests a one-parameter scaling form for the $L$-dependence of the distributions of $S_{dw}$ for $k > 0$.Comment: 13 page

Finite-Size Scaling in the Energy-Entropy Plane for the 2D +- J Ising Spin Glass

For $L \times L$ square lattices with $L \le 20$ the 2D Ising spin glass with +1 and -1 bonds is found to have a strong correlation between the energy and the entropy of its ground states. A fit to the data gives the result that each additional broken bond in the ground state of a particular sample of random bonds increases the ground state degeneracy by approximately a factor of 10/3. For $x = 0.5$ (where $x$ is the fraction of negative bonds), over this range of $L$, the characteristic entropy defined by the energy-entropy correlation scales with size as $L^{1.78(2)}$. Anomalous scaling is not found for the characteristic energy, which essentially scales as $L^2$. When $x= 0.25$, a crossover to $L^2$ scaling of the entropy is seen near $L = 12$. The results found here suggest a natural mechanism for the unusual behavior of the low temperature specific heat of this model, and illustrate the dangers of extrapolating from small $L$.Comment: 9 pages, two-column format; to appear in J. Statistical Physic

Subextensive singularity in the 2D ±J\pm J Ising spin glass

The statistics of low energy states of the 2D Ising spin glass with +1 and -1 bonds are studied for $L \times L$ square lattices with $L \le 48$, and $p$ = 0.5, where $p$ is the fraction of negative bonds, using periodic and/or antiperiodic boundary conditions. The behavior of the density of states near the ground state energy is analyzed as a function of $L$, in order to obtain the low temperature behavior of the model. For large finite $L$ there is a range of $T$ in which the heat capacity is proportional to $T^{5.33 \pm 0.12}$. The range of $T$ in which this behavior occurs scales slowly to $T = 0$ as $L$ increases. Similar results are found for $p$ = 0.25. Our results indicate that this model probably obeys the ordinary hyperscaling relation $d \nu = 2 - \alpha$, even though $T_c = 0$. The existence of the subextensive behavior is attributed to long-range correlations between zero-energy domain walls, and evidence of such correlations is presented.Comment: 13 pages, 7 figures; final version, to appear in J. Stat. Phy

High frequency longitudinal and transverse dynamics in water

High-resolution, inelastic x-ray scattering measurements of the dynamic structure factor S(Q,\omega) of liquid water have been performed for wave vectors Q between 4 and 30 nm^-1 in distinctly different thermodynamic conditions (T= 263 - 420 K ; at, or close to, ambient pressure and at P = 2 kbar). In agreement with previous inelastic x-ray and neutron studies, the presence of two inelastic contributions (one dispersing with Q and the other almost non-dispersive) is confirmed. The study of their temperature- and Q-dependence provides strong support for a dynamics of liquid water controlled by the structural relaxation process. A viscoelastic analysis of the Q-dispersing mode, associated with the longitudinal dynamics, reveals that the sound velocity undergoes the complete transition from the adiabatic sound velocity (c_0) (viscous limit) to the infinite frequency sound velocity (c_\infinity) (elastic limit). On decreasing Q, as the transition regime is approached from the elastic side, we observe a decrease of the intensity of the second, weakly dispersing feature, which completely disappears when the viscous regime is reached. These findings unambiguously identify the second excitation to be a signature of the transverse dynamics with a longitudinal symmetry component, which becomes visible in the S(Q,\omega) as soon as the purely viscous regime is left.Comment: 28 pages, 12 figure

Conductance and its universal fluctuations in the directed network model at the crossover to the quasi-one-dimensional regime

The directed network model describing chiral edge states on the surface of a cylindrical 3D quantum Hall system is known to map to a one-dimensional quantum ferromagnetic spin chain. Using the spin wave expansion for this chain, we determine the universal functions for the crossovers between the 2D chiral metallic and 1D metallic regimes in the mean and variance of the conductance along the cylinder, to first nontrivial order.Comment: 10 pages, REVTeX, uses epsf, 2 .eps figures included. Newly written Introduction and small changes to other section

Dynamics and Critical Behaviour of the q-model

The $q$-model, a random walk model rich in behaviour and applications, is investigated. We introduce and motivate the $q$-model via its application proposed by Coppersmith {\em et al.} to the flow of stress through granular matter at rest. For a special value of its parameters the $q$-model has a critical point that we analyse. To characterise the critical point we imagine that a uniform load has been applied to the top of the granular medium and we study the evolution with depth of fluctuations in the distribution of load. Close to the critical point explicit calculation reveals that the evolution of load exhibits scaling behaviour analogous to thermodynamic critical phenomena. The critical behaviour is remarkably tractable: the harvest of analytic results includes scaling functions that describe the evolution of the variance of the load distribution close to the critical point and of the entire load distribution right at the critical point, values of the associated critical exponents, and determination of the upper critical dimension. These results are of intrinsic interest as a tractable example of a random critical point. Of the many applications of the q-model, the critical behaviour is particularly relevant to network models of river basins, as we briefly discuss. Finally we discuss circumstances under which quantum network models that describe the surface electronic states of a quantum Hall multilayer can be mapped onto the classical $q$-model. For mesoscopic multilayers of finite circumference the mapping fails; instead a mapping to a ferromagnetic supersymmetric spin chain has proved fruitful. We discuss aspects of the superspin mapping and give a new elementary derivation of it making use of operator rather than functional methods.Comment: 34 pages, Revtex, typo correcte