Experimental Investigation and Large-Eddy Simulation of the Turbulent Flow past a Smooth and Rigid Hemisphere

Computations carried out on the German Federal Top-Level Computer SuperMUC at LRZ Munich under the contract number pr84na.International audienceThe objective of the present paper is to provide a detailed experimental and numerical investigation on the turbulent flow past a hemispherical obstacle (diameter D). For this purpose, the bluff body is exposed to a thick turbulent boundary layer of the thickness δ = D/2 at Re = 50,000. In the experiment this boundary layer thickness is achieved by specific fences placed in the upstream region of the wind tunnel. A detailed measurement of the upstream flow conditions by laser-Doppler and hot-film probes allows to mimic the inflow conditions for the complementary large-eddy simulation of the flow field using a synthetic turbulence inflow generator. These clearly defined boundary and operating conditions are the prerequisites for a combined experimental and numerical investigation of the flow field relying on the laser-Doppler anemometry and a finite-volume Navier-Stokes solver for block-structured curvilinear grids. The results comprise an analysis on the unsteady flow features observed in the vicinity of the hemisphere as well as a detailed discussion of the time-averaged flow field. The latter includes the mean velocity field as well as the Reynolds stresses. Owing to the proper description of the oncoming flow and supplementary numerical studies guaranteeing the choice of an appropriate grid and subgrid-scale model, the results of the measurements and the prediction are found to be in close agreement

Parkin disease: a clinicopathologic entity?

Importance: Mutations in the gene encoding parkin (PARK2) are the most common cause of autosomal recessive juvenile-onset and young-onset parkinsonism. The few available detailed neuropathologic reports suggest that homozygous and compound heterozygous parkin mutations are characterized by severe substantia nigra pars compacta neuronal loss.Objective: To investigate whether parkin-linked parkinsonism is a different clinicopathologic entity to Parkinson disease (PD).Design, Setting, and Participants: We describe the clinical, genetic, and neuropathologic findings of 5 unrelated cases of parkin disease and compare them with 5 pathologically confirmed PD cases and 4 control subjects. The PD control cases and normal control subjects were matched first for age at death then disease duration (PD only) for comparison.Results: Presenting signs in the parkin disease cases were hand or leg tremor often combined with dystonia. Mean age at onset was 34 years; all cases were compound heterozygous for mutations of parkin. Freezing of gait, postural deformity, and motor fluctuations were common late features. No patients had any evidence of cognitive impairment or dementia. Neuronal counts in the substantia nigra pars compacta revealed that neuronal loss in the parkin cases was as severe as that seen in PD, but relative preservation of the dorsal tier was seen in comparison with PD (P=.04). Mild neuronal loss was identified in the locus coeruleus and dorsal motor nucleus of the vagus, but not in the nucleus basalis of Meynert, raphe nucleus, or other brain regions. Sparse Lewy bodies were identified in 2 cases (brainstem and cortex).Conclusions and Relevance: These findings support the notion that parkin disease is characterized by a more restricted morphologic abnormality than is found in PD, with predominantly ventral nigral degeneration and absent or rare Lewy bodies.</br

Parkin Disease A Clinicopathologic Entity?

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Importance: Mutations in the gene encoding parkin (PARK2) are the most common cause of autosomal recessive juvenile-onset and young-onset parkinsonism. The few available detailed neuropathologic reports suggest that homozygous and compound heterozygous parkin mutations are characterized by severe substantia nigra pars compacta neuronal loss. Objective: To investigate whether parkin-linked parkinsonism is a different clinicopathologic entity to Parkinson disease (PD). Design, Setting, and Participants: We describe the clinical, genetic, and neuropathologic findings of 5 unrelated cases of parkin disease and compare them with 5 pathologically confirmed PD cases and 4 control subjects. The PD control cases and normal control subjects were matched first for age at death then disease duration (PD only) for comparison. Results: Presenting signs in the parkin disease cases were hand or leg tremor often combined with dystonia. Mean age at onset was 34 years; all cases were compound heterozygous for mutations of parkin. Freezing of gait, postural deformity, and motor fluctuations were common late features. No patients had any evidence of cognitive impairment or dementia. Neuronal counts in the substantia nigra pars compacta revealed that neuronal loss in the parkin cases was as severe as that seen in PD, but relative preservation of the dorsal tier was seen in comparison with PD (P=.04). Mild neuronal loss was identified in the locus coeruleus and dorsal motor nucleus of the vagus, but not in the nucleus basalis of Meynert, raphe nucleus, or other brain regions. Sparse Lewy bodies were identified in 2 cases (brainstem and cortex). Conclusions and Relevance: These findings support the notion that parkin disease is characterized by a more restricted morphologic abnormality than is found in PD, with predominantly ventral nigral degeneration and absent or rare Lewy bodies.705571579Reta Lila Weston Trust for Medical ResearchParkinson's UKParkinson Disease FoundationReta Lila Weston TrustFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)University of CampinasMonumental Trust Award from Parkinson's UKBayer-ScheringBiogen IdecLundbeckMedtronicIrish Institute of Clinical NeuroscienceMater CollegePRTL1Multiple System Atrophy TrustAlzheimer's Research UKPSP AssociationNational Institute for Health Research Biomedical Research Unit at University College London Hospitals, University College LondonDublin Brain BankWellcome Trust/MRC Joint Call in Neurodegeneration awardFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP