234 research outputs found
An Experimental-Numerical Investigation of the Wake Structure of a Hovering Rotor by PIV Combined with a Γ2 Vortex Detection Criterion
The rotor wake aerodynamic characterization is a fundamental aspect for the development
and optimization of future rotary-wing aircraft. The paper is aimed at experimentally and
numerically characterizing the blade tip vortices of a small-scale four-bladed isolated rotor in hover
conditions. The investigation of the vortex decay process during the downstream convection of
the wake is addressed. Two-component PIV measurements were carried out below the rotor disk
down to a distance of one rotor radius. The numerical simulations were aimed at assessing the
modelling capabilities and the accuracy of a free-wake Boundary Element Methodology (BEM). The
experimental and numerical results were investigated by the G2 criterion to detect the vortex location.
The rotor wake mean velocity field and the instantaneous vortex characteristics were investigated.
The experimental/numerical comparisons show a reasonable agreement in the estimation of the
mean velocity inside the rotor wake, whereas the BEM predictions underestimate the diffusion effects.
The numerical simulations provide a clear picture of the filament vortex trajectory interested in
complex interactions starting at about a distance of z/R = 0.5. The time evolution of the tip vortices
was investigated in terms of net circulation and swirl velocity. The PIV tip vortex characteristics
show a linear mild decay up to the region interested by vortex pairing and coalescence, where a
sudden decrease, characterised by a large data scattering, occurs. The numerical modelling predicts
a hyperbolic decay of the swirl velocity down to z/R = 0.4 followed by an almost constant decay.
Instead, the calculated net circulation shows a gradual decrease throughout the whole wake development.
The comparisons show discrepancies in the region immediately downstream the rotor disk but
significant similarities beyond z/R = 0.5
An assessment of vortex detection criteria for 2C-2D PIV data
The aim of the article is to propose a robust and reliable engineering method for identifying and characterizing vortical structures within a flow field measured with a classic twocomponent PIV measurement system. Some of the most popular vortex-detection criteria are briefly presented for comparison purposes. Many of these fail if spurious vectors are present within the flow field due to poor PIV image quality. The proposed method was tested both on synthetic images of ideal vortices, having different spatial resolutions and different noise levels in order to perform a parametric assessment, and on real PIV images of a four-bladed rotor wake
Ultrastructural analysis reveals abnormal mitochondria in cloned blastocysts
Somatic cell nuclear transfer (SCNT) is a powerful technique, but still very inefficient despite 20 years passed by since the cloned mammal was born. We have recently shown that the major cause of abnormalities observed in cloned fetuses are mitochondrial dysfunctions in placenta collected from cloned sheep. Investigations on mitochondria in SCNT are limited to the mtDNA hetero/homoplasmy in cloned offspring, whereas no data is available for an eventual role of mitochondria dysfunction on the developmental failure of cloned animals. Here we wanted to know whether mitochondrial abnormalities are observed already in cloned blastocysts since mitochondrial replication does not occur after the hatched blastocysts stage. SCNT and in vitro processed (IVP) blastocysts were produced and analysed for mitochondrial structure and functionality. First, embryos were analysed using transmission electron microscope (TEM). Drastic differences in mitochondrial structure between SCNT and IVP blastocysts were observed. Decrease density of mature mitochondria, very high degree of cytoplasmic vacuolisation, numerous cytoplasmic vesicle and autophagosomes were observed in SCNT blastocysts. Moreover, statistically lower expression of major mitochondrial, autophagic and apoptotic proteins were observed in SCNT embryos. Obtained results clearly shown that mitochondrial abnormalities are already observed in blastocysts stage embryos. It is important to point out that activity of mitochondria are strictly control by nuclear signals, thus, obtained results may suggest that incomplete nuclear reprogramming in cloned nucleus might be responsible also for the impaired mitochondrial function in cloned embryos/fetuses
Polychlorinated biphenyls (PCBs) alter DNA methylation and genomic integrity of sheep fetal cells in a simplified in vitro model of pregnancy exposure
Polychlorinated biphenyls (PCBs) are persistent organic pollutants ubiquitously detectable in the environment
and in the food chain. Prenatal exposure to PCBs negatively affects fetal development and produces long-term
detrimental effects on child health. The present study sought to evaluate the cytotoxic and genotoxic effects of
chronic PCB exposure on fetal cells during pregnancy. To this aim, sheep embryonic fibroblasts (SEF) and
amniocytes (SA) were cultured in vitro in the presence of low doses of PCBs for a period of 120 days, comparable
to the full term of ovine pregnancy. Cellular proliferation rates, global DNA methylation, chromosome integrity,
and markers of DNA damage were evaluated at different time points. Moreover, SEF treated with PCBs for
60 days were left untreated for one further month and then examined in order to evaluate the reversibility of
PCB-induced epigenetic defects. PCB-treated SEF were more sensitive than SA treated with PCBs, in terms of low
cell proliferation, and increased DNA damage and global DNA methylation, which were still detectable after
interruption of PCB treatment. These data indicate that chronic exposure of fetal cells to PCBs causes permanent
genomic and epigenetic instability, which may influence both prenatal and post-natal growth up to adulthood.
Our in vitro model offer a simple and controlled means of studying the effects of different contaminants on fetal
cells - one that could set the stage for targeted in vivo studies
Experimental testing of a horizontal-axis wind turbine to assess its performance
This paper describes a test procedure to investigate the performance of a micro wind turbine with horizontal-axis. A 3D model of a rotor with five blades has been designed by a MATLAB software; its airfoil is optimized to efficiently work at low wind speed. The rotor is coupled to an electric generator and this equipment is tested in a wind tunnel. An anemometer is used to measure and set the desired wind speeds. Electric quantities, i.e., voltage, current and power, are acquired by a digital multimeter. A variable resistance is used to change the operating point of the generator. Preliminary results are reported that refer to the application of the proposed test procedures to a wind turbine with a 0.2 m2 swept area
Identification of Autophagy as a Functional Target Suitable for the Pharmacological Treatment of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) In Vitro
Mitochondrial membrane protein-associated neurodegeneration (MPAN) is a relentlessly progressive neurodegenerative disorder caused by mutations in the C19orf12 gene. C19orf12 has been implicated in playing a role in lipid metabolism, mitochondrial function, and autophagy, however, the precise functions remain unknown. To identify new robust cellular targets for small compound treatments, we evaluated reported mitochondrial function alterations, cellular signaling, and autophagy in a large cohort of MPAN patients and control fibroblasts. We found no consistent alteration of mitochondrial functions or cellular signaling messengers in MPAN fibroblasts. In contrast, we found that autophagy initiation is consistently impaired in MPAN fibroblasts and show that C19orf12 expression correlates with the amount of LC3 puncta, an autophagy marker. Finally, we screened 14 different autophagy modulators to test which can restore this autophagy defect. Amongst these compounds, carbamazepine, ABT-737, LY294002, oridonin, and paroxetine could restore LC3 puncta in the MPAN fibroblasts, identifying them as novel potential therapeutic compounds to treat MPAN. In summary, our study confirms a role for C19orf12 in autophagy, proposes LC3 puncta as a functionally robust and consistent readout for testing compounds, and pinpoints potential therapeutic compounds for MPAN.</p
Identification of Autophagy as a Functional Target Suitable for the Pharmacological Treatment of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) In Vitro
Mitochondrial membrane protein-associated neurodegeneration (MPAN) is a relentlessly progressive neurodegenerative disorder caused by mutations in the C19orf12 gene. C19orf12 has been implicated in playing a role in lipid metabolism, mitochondrial function, and autophagy, however, the precise functions remain unknown. To identify new robust cellular targets for small compound treatments, we evaluated reported mitochondrial function alterations, cellular signaling, and autophagy in a large cohort of MPAN patients and control fibroblasts. We found no consistent alteration of mitochondrial functions or cellular signaling messengers in MPAN fibroblasts. In contrast, we found that autophagy initiation is consistently impaired in MPAN fibroblasts and show that C19orf12 expression correlates with the amount of LC3 puncta, an autophagy marker. Finally, we screened 14 different autophagy modulators to test which can restore this autophagy defect. Amongst these compounds, carbamazepine, ABT-737, LY294002, oridonin, and paroxetine could restore LC3 puncta in the MPAN fibroblasts, identifying them as novel potential therapeutic compounds to treat MPAN. In summary, our study confirms a role for C19orf12 in autophagy, proposes LC3 puncta as a functionally robust and consistent readout for testing compounds, and pinpoints potential therapeutic compounds for MPAN
Identification of Autophagy as a Functional Target Suitable for the Pharmacological Treatment of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) In Vitro
Mitochondrial membrane protein-associated neurodegeneration (MPAN) is a relentlessly progressive neurodegenerative disorder caused by mutations in the C19orf12 gene. C19orf12 has been implicated in playing a role in lipid metabolism, mitochondrial function, and autophagy, however, the precise functions remain unknown. To identify new robust cellular targets for small compound treatments, we evaluated reported mitochondrial function alterations, cellular signaling, and autophagy in a large cohort of MPAN patients and control fibroblasts. We found no consistent alteration of mitochondrial functions or cellular signaling messengers in MPAN fibroblasts. In contrast, we found that autophagy initiation is consistently impaired in MPAN fibroblasts and show that C19orf12 expression correlates with the amount of LC3 puncta, an autophagy marker. Finally, we screened 14 different autophagy modulators to test which can restore this autophagy defect. Amongst these compounds, carbamazepine, ABT-737, LY294002, oridonin, and paroxetine could restore LC3 puncta in the MPAN fibroblasts, identifying them as novel potential therapeutic compounds to treat MPAN. In summary, our study confirms a role for C19orf12 in autophagy, proposes LC3 puncta as a functionally robust and consistent readout for testing compounds, and pinpoints potential therapeutic compounds for MPAN.</p
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