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This paper presents a Matlab code for the optimal topology design of materials with extreme properties. For code compactness, an energy-based homogenization approach is adopted rather than the asymptotic approach. The effective constitutive parameters are obtained in terms of element mutual energies. A corresponding solution scheme with periodic boundary conditions is implemented. With a single constraint on material volume fraction, this code allows to maximize or minimize objective functions constituted by homogenized stiffness tensors such as bulk modulus, shear modulus and Poisson's ratio. The complete Matlab code built on top of the 88-line code (Andreassen et al. Struct Multidiscip Optim 43(1):1-16, 2011) is given in the Appendix.

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This study was aimed to investigate the regulatory effects of angiotensin II (Ang II) on the expression of Ang II type 1 (AT1) receptor and to characterize the mechanism underlying AT1 receptor promotion of inflammatory cytokines and reactive oxygen species (ROS). The RAW 264.7 cells were stimulated with various concentrations of Ang II for different times. The mRNA and protein expressions of AT1 receptor in the cells were determined by reverse transcriptase-polymerase chain reaction and Western blot analysis, respectively. The macrophages secretion of proinflammatory cytokines tumor necrosis factor-α, interleukin-1β (IL-1β), IL-6, and anti-inflammatory cytokine IL-10 and generation of ROS (by flow cytometry) were also examined. Nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) activities were determined by electrophoretic mobility shift assay. Ang II resulted in an upregulation of AT1 receptor expression in dose- and time-dependent manners in macrophages. Ang II not only induced the production of tumor necrosis factor-α, IL-1β, IL-6, and IL-10 but also increased the release of ROS. Further, both NF-κB and AP-1 were activated after stimulation with Ang II. However, these events were all abolished by preincubation with ZD7155, a selective competitive antagonist for the AT1 receptor. These results suggest that the AT1 receptor plays an important role in Ang II-induced cytokines production and ROS release via NF-κB and AP-1 pathways in macrophages.

We propose that miR-132 functions as a negative regulator of the inflammatory response in alveolar macrophages by potentiating the cholinergic anti-inflammatory pathway, and represents a potential therapeutic leverage point in modulating inflammatory responses.

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