Recent evidence suggests that the majority of cholesterol-laden cells found in atherosclerotic lesions are vascular smooth muscle cells (VSMC) that have transdifferentiated into macrophage-like cells (MLC). Furthermore, cholesterol-laden MLC of VSMC origin have demonstrated impaired ABCA1-dependent cholesterol efflux, but it is poorly understood why this occurs. A possible mechanism which may at least partially be attributed to cholesterol-laden MLC demonstrating attenuated ABCA1-dependent cholesterol efflux is a miR-33a expression, as a primary function of this microRNA is to silence ABCA1 expression, but this has yet to be rigorously investigated. Therefore, the VSMC line MOVAS cells were used to generate miR-33a knockout (KO) MOVAS cells, and we used KO and wild-type (WT) MOVAS cells to delineate any possible proatherogenic role of miR-33a expression in VSMC. When WT and KO MOVAS cells were cholesterol-loaded to convert into MLC, this resulted in the WT MOVAS cells to exhibit impaired ABCA1-dependent cholesterol efflux. In the cholesterol-loaded WT MOVAS MLC, we also observed a delayed restoration of the VSMC phenotype when these cells were exposed to the ABCA1 cholesterol acceptor, apoAI. These results imply that miR-33a expression in VSMC drives atherosclerosis by triggering MLC transdifferentiation via attenuated ABCA1-dependent cholesterol efflux.

Human infection by either Trypanosoma brucei gambiense (Tbg) or Trypanosoma brucei rhodesiense (Tbr) and the establishment of disease is made possible by the intermittent switching of their variant surface glycoprotein (VSG) and expression of serum resistance associated (SRA) protein (by Tbr) which nullifies the lytic action of the normal human serum. The ability to switch expression from one VSG to the other is recognized to be the major mechanism that permits the parasite to evade the otherwise efficient host antibody, hence preventing parasite elimination and allowing the establishment of a chronic infection. These changes were reported to: disable the host's capacity to mount a protective anti-parasite antibody response and prevent the development of effective B-cell memory against encountered variant antigenic parasite types (VATs). Both B cell-mediated antibody response and the Th1 cell responses leading to the production of interferon-gamma (IFN-) are required for maximum host resistance to trypanosomes, with IFN-acting to induce macrophage trypanolytic and trypanostatic activities. High levels of both tumor necrosis factor alpha (TNF) and interleukin 10 (IL-10) have been associated with trypanosomal infection. Trypanosomal genetics (including the parasite's intrinsic characteristics), human immune response polymorphisms and geographical locations are important elements that describe the severity or mildness of HAT. As the parasite devices ways to evade the human immune system, and in the absence of a suitable vaccine, surveillance, prompt diagnosis and treatment with available drugs and vector control efforts will go along way in reducing the incidence of HAT.

The brittle nature of ceramic reinforcement in metal matrixes has initiated a gap in the utilization of metal-based particles as supplementary reinforcement. This present study investigated the influence of adding FeTi as supplementary reinforcement to B4C and FeTi in an aluminum-silicon (Al-12Si) matrix for automobile applications. The FeTi alloy was introduced at 3, 6, and 9 wt.% alongside the 5 wt.% B4C particles. The effect of such an addition on the morphology, physical, and mechanical properties was examined. The X-ray diffraction pattern identified the presence of B4C and FeTi reinforcing phases alongside Al3Fe and Ti5Si3 phases. The examined morphology revealed that the particles were well dispersed in the matrix, with consequent effects on their properties. Porosity was reported to reduce linearly with a rise in FeTi dosage, consequently engendering a linear rise in density and relatively high density. Inclusive of the hardness, the yield and ultimate strength were enhanced progressively upon a progressive rise in FeTi dosage, with a contrary reduction in ductility. The result revealed that the inclusion of FeTi reinforcing fillers in the matrix is capable of causing an appreciable improvement in the mechanical properties of the composite.