Numerical simulation on drying process of an inkjet droplet using lagrangian FEM

Paper presented to the 10th International Conference on Heat Transfer, Fluid Mechanics and Thermodynamics, Florida, 14-16 July 2014.A mathematical model is proposed to describe the fluid dynamics, mass and heat transfer in a solution droplet evaporating on a flat surface during drying process. A decrease of droplet volume due to evaporation of a solvent, evaporation latent heat generated on the free surface, and an increase of a solute on the free surface are considered in the model. Governing equations are numerical solved using a finite element method. A Lagrangian method is applied to predict the deformation of an evaporating droplet. Firstly, the outward flow caused during selfpinning of the contact line are examined under an ideal condition. The calculated velocities agree well with calculated results using a one-dimensional model. Secondly, the drying process of a polystyrene/anisole solution droplet with the equivalent diameter of 20 µm are estimated. The migration of the solute at the contact line is found to be finished by the instant when a thin liquid film with a low solute concentration are still remained at the center part. As a result, a ring structure develops on the periphery of the dried film. Lastly, the effect of fluid viscosity is investigated. A high viscosity essentially decreases the fluid velocity, resulting in vanishing the ring structure. The effect of viscosity on the configuration of the film agrees with empirical results.cf201

Breakpoint mapping of 13 large parkin deletions/duplications reveals an exon 4 deletion and an exon 7 duplication as founder mutations

Early-onset Parkinson’s disease (EOPD) has been associated with recessive mutations in parkin (PARK2). About half of the mutations found in parkin are genomic rearrangements, i.e., large deletions or duplications. Although many different rearrangements have been found in parkin before, the exact breakpoints involving these rearrangements are rarely mapped. In the present study, the exact breakpoints of 13 different parkin deletions/duplications, detected in 13 patients out of a total screened sample of 116 EOPD patients using Multiple Ligation Probe Amplification (MLPA) analysis, were mapped using real time quantitative polymerase chain reaction (PCR), long-range PCR and sequence analysis. Deletion/duplication-specific PCR tests were developed as a rapid and low cost tool to confirm MLPA results and to test family members or patients with similar parkin deletions/duplications. Besides several different deletions, an exon 3 deletion, an exon 4 deletion and an exon 7 duplication were found in multiple families. Haplotype analysis in four families showed that a common haplotype of 1.2 Mb could be distinguished for the exon 7 duplication and a common haplotype of 6.3 Mb for the deletion of exon 4. These findings suggest common founder effects for distinct large rearrangements in parkin

Molecular Basis for Vulnerability to Mitochondrial and Oxidative Stress in a Neuroendocrine CRI-G1 Cell Line

Many age-associated disorders (including diabetes, cancer, and neurodegenerative diseases) are linked to mitochondrial dysfunction, which leads to impaired cellular bioenergetics and increased oxidative stress. However, it is not known what genetic and molecular pathways underlie differential vulnerability to mitochondrial dysfunction observed among different cell types.Starting with an insulinoma cell line as a model for a neuronal/endocrine cell type, we isolated a novel subclonal line (named CRI-G1-RS) that was more susceptible to cell death induced by mitochondrial respiratory chain inhibitors than the parental CRI-G1 line (renamed CRI-G1-RR for clarity). Compared to parental RR cells, RS cells were also more vulnerable to direct oxidative stress, but equally vulnerable to mitochondrial uncoupling and less vulnerable to protein kinase inhibition-induced apoptosis. Thus, differential vulnerability to mitochondrial toxins between these two cell types likely reflects differences in their ability to handle metabolically generated reactive oxygen species rather than differences in ATP production/utilization or in downstream apoptotic machinery. Genome-wide gene expression analysis and follow-up biochemical studies revealed that, in this experimental system, increased vulnerability to mitochondrial and oxidative stress was associated with (1) inhibition of ARE/Nrf2/Keap1 antioxidant pathway; (2) decreased expression of antioxidant and phase I/II conjugation enzymes, most of which are Nrf2 transcriptional targets; (3) increased expression of molecular chaperones, many of which are also considered Nrf2 transcriptional targets; (4) increased expression of β cell-specific genes and transcription factors that specify/maintain β cell fate; and (5) reconstitution of glucose-stimulated insulin secretion.The molecular profile presented here will enable identification of individual genes or gene clusters that shape vulnerability to mitochondrial dysfunction and thus represent potential therapeutic targets for diabetes and neurodegenerative diseases. In addition, the newly identified CRI-G1-RS cell line represents a new experimental model for investigating how endogenous antioxidants affect glucose sensing and insulin release by pancreatic β cells

NRF2 Activation Restores Disease Related Metabolic Deficiencies in Olfactory Neurosphere-Derived Cells from Patients with Sporadic Parkinson's Disease

Extent: 14p.Background: Without appropriate cellular models the etiology of idiopathic Parkinson’s disease remains unknown. We recently reported a novel patient-derived cellular model generated from biopsies of the olfactory mucosa (termed olfactory neurosphere-derived (hONS) cells) which express functional and genetic differences in a disease-specific manner. Transcriptomic analysis of Patient and Control hONS cells identified the NRF2 transcription factor signalling pathway as the most differentially expressed in Parkinson’s disease. Results: We tested the robustness of our initial findings by including additional cell lines and confirmed that hONS cells from Patients had 20% reductions in reduced glutathione levels and MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)- 2-(4-sulfophenyl)-2H-tetrazolium, inner salt] metabolism compared to cultures from healthy Control donors. We also confirmed that Patient hONS cells are in a state of oxidative stress due to higher production of H2O2 than Control cultures. siRNA-mediated ablation of NRF2 in Control donor cells decreased both total glutathione content and MTS metabolism to levels detected in cells from Parkinson’s Disease patients. Conversely, and more importantly, we showed that activation of the NRF2 pathway in Parkinson’s disease hONS cultures restored glutathione levels and MTS metabolism to Control levels. Paradoxically, transcriptomic analysis after NRF2 pathway activation revealed an increased number of differentially expressed mRNAs within the NRF2 pathway in L-SUL treated Patient-derived hONS cells compared to L-SUL treated Controls, even though their metabolism was restored to normal. We also identified differential expression of the PI3K/AKT signalling pathway, but only post-treatment. Conclusions: Our results confirmed NRF2 as a potential therapeutic target for Parkinson’s disease and provided the first demonstration that NRF2 function was inducible in Patient-derived cells from donors with uniquely varied genetic backgrounds. However, our results also demonstrated that the response of PD patient-derived cells was not co-ordinated in the same way as in Control cells. This may be an important factor when developing new therapeutics.Anthony L. Cook, Alejandra M. Vitale, Sugandha Ravishankar, Nicholas Matigian, Greg T. Sutherland, Jiangou Shan, Ratneswary Sutharsan, Chris Perry, Peter A. Silburn, George D. Mellick, Murray L. Whitelaw, Christine A. Wells, Alan Mackay-Sim and Stephen A. Woo

Evaluation of the change in the morphology of gold nanoparticles during sintering

Morphological changes of agglomerates consisting of nanometer primary gold particles were studied experimentally and theoretically. Gold aerosol nanoparticles were produced using the evaporation/condensation method, and the change in agglomerate size by reheating was examined experimentally using a tandem DMA setup. Numerical calculations, based on two extreme mechanisms to reshape agglomerates, i.e., subsequent coalescence of primary particles and subsequent rearrangement of primary particles, were carried out. By comparison with the experimental results, the sintering time and the rate constant of restructuring were obtained. Using these values, the change in particle size for different generation conditions could be calculated. The change in morphology of agglomerates can be explained from the comparison of the experimental results with the theoretical calculations: agglomerates with smaller primary particles will compact mainly by the subsequent coalescence of primary particles, while agglomerates with larger primary particles will compact mainly by a rearrangement of primary particles

Unveiling the magic of H2S on the CVD-Al2O3 coating

The role of H2S in the mechanism of CVD-Al2O3 coating was investigated by measuring particles suspended in the gas phase with an optical particle counter. H2S doping of the CVD-Al2O3 process improves the homogeneity of thickness and growth rate of the Al2O3 layer. The number of particles produced in the reactor whose size was larger than 200 nm was dramatically reduced by H2S doping. The effect of H2S doping appears to be a reduction of the size of Al2O3 particles present in the reactor. These smaller particles have a greater mobility, which will allow them to arrive at the surface, regardless of the shape or arrangement of the substrate inside the reactor