Currently, four-dimensional (4D) printing programming methods are mainly structure-based, which usually requires more than one material to endow products with site-specific attributes. Here, we propose a new 4D printing programming approach that enables site-specific shape-morphing behaviors in a single material by regulating the printing parameters. Specifically, a direct ink writing three-dimensional (3D) printer with the ability to change printing parameters (e.g., deposition speed) on the fly is reported. By site-specifically adjusting print speed and print path to control the local nematic arrangements of printed liquid crystal elastomers (LCEs), the shape-morphing behaviors of the LCEs can be successfully programmed. In this way, locally programmed popping-up, self-assembling, and oscillating behaviors can be designed by varying the print speed in specific regions. Snake-like curling is realized by uniformly boosting the print speed in a single line. Furthermore, two theories and an ultrasound image diagnostic apparatus are employed to reveal the mechanism behind this behavior. This work provides a feasible way to realize the gradient transition of material properties through a single material. It broadens the design space and pushes the envelope of 4D printing, which is expected to be helpful in the fabrication of soft robotics and flexible electronics.
We have demonstrated that mesenchymal cells from spontaneously hypertensive rats genetically express complement 3 (C3). Mature tubular epithelial cells can undergo epithelial-to-mesenchymal transition (EMT) that is linked to the pathogenesis of renal fibrosis and injury. In this study, we investigated the contribution of C3 in EMT and in the renal renin-angiotensin (RA) systems associated with hypertension. C3a induced EMT in mouse TCMK-1 epithelial cells, which displayed increased expression of renin and Krüppel-like factor 5 (KLF5) and nuclear localization of liver X receptor α (LXRα). C3 and renin were strongly stained in the degenerated nephrotubulus and colocalized with LXRα and prorenin receptor in unilateral ureteral obstruction (UUO) kidneys from wild-type mice. In C3-deficient mice, hydronephrus and EMT were suppressed, with no expression of renin and C3. After UUO, systolic blood pressure was increased in wild-type but not C3-deficient mice. In wild-type mice, intrarenal angiotensin II (ANG II) levels were markedly higher in UUO kidneys than normal kidneys and decreased with aliskiren. There were no increases in intrarenal ANG II levels after UUO in C3-deficient mice. Thus C3 induces EMT and dedifferentiation of epithelial cells, which produce renin through induction of LXRα. These data indicate for the first time that C3 may be a primary factor to activate the renal RA systems to induce hypertension.
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