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Sporadic Alzheimer’s disease (sAD) represents a serious and growing worldwide economic and healthcare burden. Almost 95% of current AD patients are associated with sAD as opposed to patients presenting with well-characterized genetic mutations that lead to AD predisposition, i.e., familial AD (fAD). Presently, the use of transgenic (Tg) animals overexpressing human versions of these causative fAD genes represents the dominant research model for AD therapeutic development. As significant differences in etiology exist between sAD and fAD, it is perhaps more appropriate to develop novel, more sAD-reminiscent experimental models that would expedite the discovery of effective therapies for the majority of AD patients. Here we present the oDGal mouse model, a novel model of sAD that displays a range of AD-like pathologies as well as multiple cognitive deficits reminiscent of AD symptomology. Hippocampal cognitive impairment and pathology were delayed with N-acetyl-cysteine (NaC) treatment, which strongly suggests that reactive oxygen species (ROS) are the drivers of downstream pathologies such as elevated amyloid beta and hyperphosphorylated tau. These features demonstrate a desired pathophenotype that distinguishes our model from current transgenic rodent AD models. A preclinical model that presents a phenotype of non-genetic AD-like pathologies and cognitive deficits would benefit the sAD field, particularly when translating therapeutics from the preclinical to the clinical phase.

Magnetic fields, spontaneously generated around laser heating nonuniformities, have been found to invert and enhance electron pressure perturbations in the conduction zones of laser-produced plasmas without applied magnetic fields. The application of a sufficiently strong magnetic field is predicted to damp this phenomenon, but may instead result in magneto-thermal instability. Two-dimensional Vlasov–Fokker–Planck simulations of the conduction zone of laser-produced plasmas, subject to externally applied magnetic fields of different field strengths, are performed. The effects of non-locality upon extended collisional transport terms and instability thresholds are investigated. It is found that magnetized transport terms Righi–Leduc heat flow and thermoelectric heat flow are strongly enhanced by non-locality (up to twofold), even at the top of the temperature gradient, due to larger magnetization of the mediating hot electrons (relative to their thermal counterparts). Meanwhile, the Nernst effect efficiently advects magnetic field out of the conduction zone before instability (which requires Hall parameters, χ>0.1) can take hold.

Extended-magnetohydrodynamics (MHD) transports magnetic flux and electron energy in high-energy-density experiments, but individual transport effects remain unobserved experimentally. Two factors are responsible in defining the transport: electron temperature and electron current. Each electron energy transport term has a direct analog in magnetic flux transport. To measure the thermally driven transport of magnetic flux and electron energy, a simple experimental configuration is explored computationally using a laser-heated pre-magnetized under-dense plasma. Changes to the laser heating profile precipitate clear diagnostic signatures from the Nernst, cross-gradient-Nernst, anisotropic conduction, and Righi-Leduc heat-flow. With a wide operating parameter range, this configuration can be used in both small and large scale facilities to benchmark MHD and kinetic transport in collisional/semi-collisional, local/non-local, and magnetized/unmagnetized regimes.

We present kinetic two-dimensional Vlasov-Fokker-Planck simulations, including both self-consistent magnetic fields and ablating ion outflow, of a planar ablating foil subject to nonuniform laser irradiation. Even for small Hall parameters (ωτ_{ei}≲0.05) self-generated magnetic fields are sufficient to invert and enhance pressure perturbations. The mode inversion is caused by a combination of the Nernst advection of the magnetic field and the Righi-Leduc heat flux. Nonlocal effects modify these processes. The mechanism is robust under plasma conditions tested; it is amplitude independent and occurs for a broad spectrum of perturbation wavelengths, λ_{p}=10-100μm. The ablating plasma response to a dynamically evolving speckle pattern perturbation, analogous to an optically smoothed beam, is also simulated. Similar to the single-mode case, self-generated magnetic fields increase the degree of nonuniformity at the ablation surface by up to an order of magnitude and are found to preferentially enhance lower modes due to the resistive damping of high mode number magnetic fields.

Macrophage-derived foam cells are the predominant component of arterial plaques in the early stages of atherosclerosis. One factor that poses a major risk for plaque development is high levels of plasma low-density lipoprotein (LDL) as a result of a high-fat meal. In order to better understand how an individuals' diet affects arterial plaque deposition via the process of foam cell formation, we measured the acute circulating monocyte activity response after consuming a high-fat meal (85% of daily fat allowance).Venous blood samples from 17 participants were acquired on a FlowSight. Samples were analyzed to identify nonclassical (CD14+/16+) and classical (CD14+/16-) monocytes. We measured monocyte concentration, adhesion molecule expression, CD36 expression, and oxidized LDL (oxLDL) endocytosis for preprandial 1, 3, and 5 h postprandial.Consuming a high-fat meal caused increases in oxLDL uptake, adhesion molecule expression, and CD36 expression in both classical and nonclassical monocytes, with the nonclassical monocytes responding with larger increases than the classical monocytes.These results suggest that consumption of a high-fat meal increased the potential of monocytes to become foam cells, and implicates nonclassical monocytes as having greater potential than classical monocytes to become foam cells. © 2016 International Clinical Cytometry Society.