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Abstract. A total of 25 flexural and 55 uniaxial compressive strength tests were conducted in laboratory using landfast sea ice samples collected in the Prydz Bay. Three-point bending tests were performed at ice temperatures of −12 to −3 ∘C with force applied vertically to original ice surface, and compressive strength tests were performed at −3 ∘C with a strain-rate level of 10−6–10−2 s−1 in the directions vertical and horizontal to ice surface. Judging from crystal structure, the ice samples were divided into congelation ice, snow ice, and a mixture of the two. The results of congelation ice showed that the flexural strength had a decreasing trend depending on porosity rather than brine volume, based on which a mathematical equation was established to estimate flexural strength. Both flexural strength and effective modulus of elasticity increased with increasing platelet spacing. The uniaxial compressive strength increased and decreased with strain rate below and above the critical regime, respectively, which is 8.0 × 10−4–1.5 × 10−3 s−1 for vertically loaded samples and 2.0 × 10−3–3.0 × 10−3 s−1 for horizontally loaded samples. A drop-off in compressive strength was shown with increasing sea ice porosity. Consequently, a model was developed to depict the combined effects of porosity and strain rate on compressive strength in both ductile and brittle regimes. The mechanical strength of mixed ice was lower than congelation ice, and that of snow ice was much weaker. To provide a safe guide for the transportation of goods on landfast sea ice in the Prydz Bay, the bearing capacity of the ice cover is estimated with the lower and upper envelopes of flexural strength and effective elastic modulus, respectively, which turned out to be a function of sea ice porosity.

Novel anthraquinone compounds that induce ER stress and paraptosis-like cell death were designed and synthesized. Compound 4a is the first organic micromolecule to kill tumor cells by only paraptosis, and its mechanism of action has been further explored. Paraptosis does not appear to involve either phosphatidylserine translocation associated with apoptosis or cell cycle arrest. The bisbenzyloxy and N-(2hydroxyethyl)formamide structures may be two critical pharmacophores for paraptosis. Bisbenzyloxy can induce ER stress, and the N-(2-hydroxyethyl)formamide structure can increase the ratio of LC3II/I and cytoplasmic vacuolization and facilitates paraptosis. Some antitumor drugs fail to eradicate malignant cell lines with impaired apoptotic pathways; paraptosis may be a route to kill such cells and provides a new potential strategy for cancer chemotherapy.

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