CONJUGATE MIXED CONVECTION IN AIR-COOLED HEAT SINKS USING A NON-BOUSSINESQ APPROACH

This work reports a numerical study of the mixed convection in finned duct flow that occurs in heat sinks devices. The laminar flow is considered fully developed and the convection-conduction coupling is treated by a conjugated approach. The mathematical formulation of this problem is constituted by the mass, momentum and energy equations. The partial differential equations system is solved by the Galerkin finite element method, adopting a pressure Poisson equation to establish the pressure-velocity coupling and to obtain a mass conserving flow. The results using the classical Boussinesq approximation (density varies linearly with the temperature in the buoyancy-term) are compared with the non-Boussinesq approach (density variation in all terms of the governing equations) showing that both the heat transfer and friction factor are affected by the new considerations. The duct aspect ratio and the solid to fluid thermal conductivity ratio influences on the heat transfer rate are also analyzed. This analysis tool was also shown appropriate for the optimization of electronic components air-cooled heat sinks

Specific Heat of Ce(1-x)La(x)RhIn(5) in Zero and Applied Magnetic Field: A Very Rich Phase Diagram

Specific heat and magnetization results as a function of field on single- and poly-crystalline samples of Ce(1-x)La(x)RhIn(5) show 1.) a specific heat gamma of about 100 mJ/moleK^2 (in agreement with recent dHvA results of Alvers et al.); 2.) upturns at low temperatures in C/T and chi that fit a power law behavior ( Griffiths phase non-Fermi liquid behavior); 3.) a field induced anomaly in C/T as well as M vs H behavior in good agreement with the recent Griffiths phase theory of Castro Neto and Jones, where M~H at low field, M ~ H^lambda above a crossover field, C/T ~ T^(-1+lambda) at low field, and C/T ~ (H^(2+lambda/2)/T^(3-lambda/2))*exp(-mu(eff)H/T) above the same crossover field as determined in the magnetization and where lambda is independently determined from the temperature dependence of chi at low temperatures, chi ~ T^(-1+lambda) and low fields.Comment: 13 pages, 9 figures, to be published in Physical Review

Altered Dendritic Morphology of Purkinje cells in Dyt1 ΔGAG Knock-In and Purkinje Cell-Specific Dyt1 Conditional Knockout Mice

BACKGROUND: DYT1 early-onset generalized dystonia is a neurological movement disorder characterized by involuntary muscle contractions. It is caused by a trinucleotide deletion of a GAG (ΔGAG) in the DYT1 (TOR1A) gene encoding torsinA; the mouse homolog of this gene is Dyt1 (Tor1a). Although structural and functional alterations in the cerebellum have been reported in DYT1 dystonia, neuronal morphology has not been examined in vivo. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we examined the morphology of the cerebellum in Dyt1 ΔGAG knock-in (KI) mice. Golgi staining of the cerebellum revealed a reduction in the length of primary dendrites and a decrease in the number of spines on the distal dendrites of Purkinje cells. To determine if this phenomenon was cell autonomous and mediated by a loss of torsinA function in Purkinje cells, we created a knockout of the Dyt1 gene only in Purkinje cells of mice. We found the Purkinje-cell specific Dyt1 conditional knockout (Dyt1 pKO) mice have similar alterations in Purkinje cell morphology, with shortened primary dendrites and decreased spines on the distal dendrites. CONCLUSION/SIGNIFICANCE: These results suggest that the torsinA is important for the proper development of the cerebellum and a loss of this function in the Purkinje cells results in an alteration in dendritic structure

Enhanced Hippocampal Long-Term Potentiation and Fear Memory in Btbd9 Mutant Mice

Polymorphisms in BTBD9 have recently been associated with higher risk of restless legs syndrome (RLS), a neurological disorder characterized by uncomfortable sensations in the legs at rest that are relieved by movement. The BTBD9 protein contains a BTB/POZ domain and a BACK domain, but its function is unknown. To elucidate its function and potential role in the pathophysiology of RLS, we generated a line of mutant Btbd9 mice derived from a commercial gene-trap embryonic stem cell clone. Btbd9 is the mouse homolog of the human BTBD9. Proteins that contain a BTB/POZ domain have been reported to be associated with synaptic transmission and plasticity. We found that Btbd9 is naturally expressed in the hippocampus of our mutant mice, a region critical for learning and memory. As electrophysiological characteristics of CA3-CA1 synapses of the hippocampus are well characterized, we performed electrophysiological recordings in this region. The mutant mice showed normal input-output relationship, a significant impairment in pre-synaptic activity, and an enhanced long-term potentiation. We further performed an analysis of fear memory and found the mutant mice had an enhanced cued and contextual fear memory. To elucidate a possible molecular basis for these enhancements, we analyzed proteins that have been associated with synaptic plasticity. We found an elevated level of dynamin 1, an enzyme associated with endocytosis, in the mutant mice. These results suggest the first identified function of Btbd9 as being involved in regulating synaptic plasticity and memory. Recent studies have suggested that enhanced synaptic plasticity, analogous to what we have observed, in other regions of the brain could enhance sensory perception similar to what is seen in RLS patients. Further analyses of the mutant mice will help shine light on the function of BTBD9 and its role in RLS

Alternating Hemiplegia of Childhood-Related Neural and Behavioural Phenotypes in Na+,K+-ATPase α3 Missense Mutant Mice

Missense mutations in ATP1A3 encoding Na(+),K(+)-ATPase α3 have been identified as the primary cause of alternating hemiplegia of childhood (AHC), a motor disorder with onset typically before the age of 6 months. Affected children tend to be of short stature and can also have epilepsy, ataxia and learning disability. The Na(+),K(+)-ATPase has a well-known role in maintaining electrochemical gradients across cell membranes, but our understanding of how the mutations cause AHC is limited. Myshkin mutant mice carry an amino acid change (I810N) that affects the same position in Na(+),K(+)-ATPase α3 as I810S found in AHC. Using molecular modelling, we show that the Myshkin and AHC mutations display similarly severe structural impacts on Na(+),K(+)-ATPase α3, including upon the K(+) pore and predicted K(+) binding sites. Behavioural analysis of Myshkin mice revealed phenotypic abnormalities similar to symptoms of AHC, including motor dysfunction and cognitive impairment. 2-DG imaging of Myshkin mice identified compromised thalamocortical functioning that includes a deficit in frontal cortex functioning (hypofrontality), directly mirroring that reported in AHC, along with reduced thalamocortical functional connectivity. Our results thus provide validation for missense mutations in Na(+),K(+)-ATPase α3 as a cause of AHC, and highlight Myshkin mice as a starting point for the exploration of disease mechanisms and novel treatments in AHC