Strong, anti-swelling, and biodegradable seaweed-based straws with surface mineralized CaCO3 armor.

While the extensive utilization of disposable plastic straws has resulted in significant environmental issues such as microplastics and soil and ocean pollution, the quest for alternative straws for versatile use remains a formidable challenge. Here, drawing inspiration from naturally water-resistant materials such as bones and sea urchins, we have developed seaweed-based straws with significantly improved water resistance and mechanical strength via in-situ mineralization of CaCO3 on their surfaces. Specifically, the COO- groups on the G (α-L-guluronate) blocks of alginate were employed to establish a robust cross-linked network, while the COO- groups on the M (ß-D-mannuronate) blocks attracted free Ca2+ through electrostatic forces, thereby promoting CaCO3 nucleation. This effectively prevents COOH groups from hydrating, reducing swelling, and results in the fabrication of nano- to micron-sized CaCO3 particles that reinforce the structure without compromising the cross-linked network. Compared with the control group, the S5% sample (prepared with 5 % Na2CO3 solution) exhibited a 102 % increase in water contact angle, a 35 % decrease in swelling degree, and a 35.5 % and 37.5 % increase in ultimate flexural and tensile stress, respectively. Furthermore, the potential use of these straws as a waste for heavy metal adsorption was investigated, addressing environmental concerns while demonstrating economic feasibility.

Insulin Receptor Substrate 1 Is Involved in the Phycocyanin-Mediated Antineoplastic Function of Non-Small Cell Lung Cancer Cells.

Phycocyanin, derived from marine algae, is known to have noteworthy antineoplastic properties. However, the underlying mechanism involved in phycocyanin-mediated anti-growth function on non-small cell lung cancer (NSCLC) cells is still ambiguous. Here, we investigated the mechanism of action of phycocyanin on H1299, A549, and LTEP-a2 cells. According to the results obtained, insulin receptor substrate 1 (IRS-1) expression was reduced by phycocyanin. Cell phenotype tests showed that siRNA knockdown of IRS-1 expression significantly inhibited the growth, migration, colony formation, but promoted the apoptosis of NSCLC cells. Meanwhile, phycocyanin and IRS-1 siRNA treatment both reduced the PI3K-AKT activities in NSCLC cells. Moreover, overexpression of IRS-1 accelerated the proliferation, colony formation, and migration rate of H1299, A549, and LTEP-a2 cells, which was contradicting to the knockdown results. Overall, this study uncovered a regulatory mechanism by which phycocyanin inhibited the growth of NSCLC cells via IRS-1/AKT pathway, laying the foundation for the potential target treatment of NSCLC.