4D Printing of High-Performance Thermal-Responsive Liquid Metal Elastomers Driven by Embedded Microliquid Chambers.

Four-dimensional (4D) printing of swellable materials have been viewed as an ideal approach to build shape morphing architectures. However, there is less variety in high-performance swellable materials, limiting its development. To address this challenge, we proposed a new strategy for designing high-performance thermal-responsive swellable materials. The reversible liquid-vapor phase change of embedded low boiling point liquid chambers and functional liquid metal fillers endows the designed elastomer with the reversible thermal-responsive swellable property with high stability, fast response speed, and large equilibrium deformation. Notably, liquid metal fillers play a crucial role in improving the thermal-responsive property via improving the thermal conductivity and fracture toughness and decreasing the stiffness. To demonstrate the feasibility of constructing shape morphing architectures with proposed thermal-responsive liquid metal elastomers, typical bilayer structures were printed and investigated. By altering the key design parameters, the response speed and equilibrium deformation can be adjusted as needed. Therefore, complex shape morphing architectures can be printed. This study could provide a new avenue to design swellable material systems for 4D printing of shape morphing architectures.

Inhibition of Lung Carcinoma A549 Cell Growth by Knockdown of Hexokinase 2 In Situ and In Vivo.

Hexokinase 2 (HK2) has been identified as an oncogene in some malignant diseases such as breast cancer and ovarian cancer. However, the role of HK2 in lung cancer remains unclear. In this study, we explored the functional role of HK2 in lung cancer cell proliferation and tumorigenesis and determine its expression profile in lung cancer. HK2 expression was increased in primary lung cancer tissues of patients. Knocking down HK2 expression by small interfering RNA (siRNA) inhibited cell proliferation in lung cancer cells and nude mice. Thus, HK2 is required for sustained proliferation and survival of tumor cells in vitro and in vivo, and its aberrant expression may contribute to the pathogenesis of lung cancer. Thus, our study provided evidence that HK2 functions as a novel oncogene in lung cancer and may be a potential therapeutic target for lung cancer.

Benzylpenicillin inhibits the renal excretion of acyclovir by OAT1 and OAT3.

BACKGROUND: Acyclovir is acyclic guanosine derivative. Benzylpenicillin (PCG) is a ß-lactam antibiotic. The purpose of this study was to investigate the pharmacokinetic drug-drug interaction (DDI) between PCG and acyclovir. METHOD: When acyclovir and PCG were co-administered, plasma concentration of acyclovir, urinary excretion of acyclovir in vivo, uptake of acyclovir in kidney slices and uptake of acyclovir in human (h) OAT1/hOAT3- HEK293 cells were determined to examine the effect of PCG on urinary excretion of acyclovir. RESULTS: The plasma concentration of acyclovir was increased markedly and accumulative renal excretion and renal clearance of acyclovir were decreased significantly after intravenous administration of acyclovir in combination with PCG. PCG could decrease the uptake of acyclovir in kidney slices and in hOAT1-/hOAT3-human embryonic kidney (HEK293) cells. CONCLUSIONS: It indicates that acyclovir is a substrate for OAT1 and OAT3. PCG inhibits the renal excretion of acyclovir by inhibiting renal transporters OAT1 and OAT3 in vivo and in vitro. These results suggest important information for DDI between PCG and acyclovir in kidney.

Inhibitory effect of JBP485 on renal excretion of acyclovir by the inhibition of OAT1 and OAT3.

The purpose is to investigate whether the targets of drug-drug interactions (DDIs) between JBP485 and acyclovir are OAT1 and OAT3 in kidney. Plasma concentration and accumulative urinary excretion of acyclovir in vivo, uptake of acyclovir in kidney slices and uptake of acyclovir in human (h) OAT1/ hOAT3-human embryonic kidney (HEK) 293 cells in vitro were performed to examine the effect of JBP485 on urinary excretion of acyclovir. The plasma concentration of acyclovir was increased markedly and accumulative urinary excretion and renal clearance of acyclovir were decreased significantly after intravenous administration of acyclovir in combination with JBP485. JBP485 (a substrate for OAT1 and OAT3), p-aminohippurate (PAH) (a substrate for OAT1) and benzylpenicillin (PCG) (a substrate for OAT3) could decrease the uptake of acyclovir in kidney slices and in hOAT1-/hOAT3-HEK293 cells. These results suggest that JBP485 inhibits the renal excretion of acyclovir by inhibiting renal transporters OAT1 and OAT3 in vivo and in vitro. Our results indicate the possibility of DDI between dipeptide and acyclovir.