Upcycling of Spent Tea Leaves and Spent Coffee Grounds into Sustainable 3D-Printing Materials: Natural Plasticization and Low-Energy Fabrication

Food processing byproducts are potential filling materials for fabricating sustainable composites with broad applications. We herein report the use of spent coffee grounds (SCG) and spent tea leaves (STL) to prepare biomass/poly(lactic acid) (PLA) composites as novel 3D-printing inks. The results show that the 3D-printability can be upheld at a high biomass loading of 40 wt %. As for strength performance, the biomass addition disrupted the PLA structure and reduced the tensile strength of the 3D-printed specimens. However, elongation at break was enhanced 5-fold at 20 wt % SCG, which could be attributed to the plasticizing effect of the naturally occurring oil in SCG. The SCG oil can be added to STL/PLA for improved ductility. With little oil (<30 mg/g composite) at ∼20 wt % biomass loading, samples prepared from 155 °C-filament showed higher tensile strength than those at 185 °C. Microscopic imaging evidenced more significant pore formation in the latter, rendering the structure delicate. These findings reveal the complex effects of filler properties on the biomass-PLA interface that determines the composite performance

Bayesian Skyline Plot and dated phylogeny of the the Hong Kong MSM HIV-1 subtype B viruses.

<p>Nonparametric reconstruction of the epidemic history with appropiate confidence limits and time-scaled phylogenies of the <i>pol</i> gene are shown. The demographic history of the subtype B virus among Hong Kong MSM represented in black, and the 95% confidence limits of the estimate are represented in grey. The tree represents the phylogenetic relationships of the sequences has the same time scale as the skyline plot.</p

Population dynamics estimates of the subtype B epidemic among MSM in Hong Kong.

<p>Population dynamics estimates of the subtype B epidemic among MSM in Hong Kong.</p

Synergistic Induction of Apoptosis by Methylseleninic Acid and Cisplatin, The Role of ROS-ERK/AKT-p53 Pathway

Cisplatin-based therapy is one of the most important chemotherapy treatments for cancers. However, its efficacy is greatly limited by drug resistance and undesirable side effects. Therefore, it is of great importance to develop chemosensitizing agents to cisplatin. In the present study, we demonstrated the strategy to use methylseleninic acid (MeSe) as a synergistic agent of cisplatin and elucidated their action mechanisms. The combination of MeSe and cisplatin exhibited synergistic anticancer efficacy and achieved greater selectivity between cancer cell and normal cell. By inducing intracellular oxidative stress, MeSe potentiated cisplatin-induced DNA damage and led to enhanced p53 phosphorylation, followed by increased activation of both mitochondrial and death receptor pathway. Down-regulation of phosphorylated AKT and ERK also played important roles in the synergistic effects of MeSe and cisplatin. Our results suggested that the strategy to apply MeSe as a synergistic agent to cisplatin could be a highly efficient way to achieve anticancer synergism by targeting the intracellular redox system. MeSe might be a candidate for clinical application as a chemosensitizer to cisplatin-based therapy for cancer treatments, especially for hepatocellular carcinoma

The <i>pol</i> and <i>env</i> genotype of the 34 unassigned genotype samples.

<p>N/A represents PCR amplification or DNA sequencing failed.</p

Phylogenetic relationships of 34 unassigned <i>pol</i> gene sequences (1a) and 31 unassigned <i>env</i> gene C2V3 region sequences (1b).

<p>Genotype unassigned sequences were highlighted in blue and all reference sequences were in black. Bootstrap values >70 were shown at the nodes of the trees.</p

Bootscanning plots of the unassigned <i>pol</i> gene variants.

<p>The bootstrap values are plotted for a window of 300–400bp moving in increments of 50 bps along the alignment.</p

The epidemiological background of the 33 genotype unassigned recombinants.

<p>The epidemiological background of the 33 genotype unassigned recombinants.</p