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Most wooden remains from archaeological sites in waterlogged burial environments are found to be intact without shrinkage despite centuries of storage. However, waterlogged wooden remains are subject to shrinkage damage and some even lose up to 80% of their original volume when exposed to air. The shrinkage of archaeological waterlogged wood with the loss of a large part of the initial volume of the wooden remains has been considered irreversible. Here we show that “active alkali-urea”, serving as a re-swelling chemical agent, can almost fully restore the collapsed archaeological wood to its original shape. The restoration experiment showed that the main reason for the restoration of collapsed wood is that the collapsed cell cavity almost completely recovered its original shape during active alkali-urea treatment. We suggest that the shape of collapsed archaeological wood remains can be fully recovered, and that the collapsed archaeological wood can thereby recover its valuable cultural properties.

The nonpeptide AVE0991 is an agonist of the angiotensin-(1–7) (Ang-(1–7)) Mas receptor and is expected to be a putative new drug for treatment of cardiovascular disease. However, the mechanisms involved in the antiproliferative effects of AVE0991 are not fully understood. We saw that the compound attenuated proliferation in an angiotensin II-induced rat vascular smooth muscle cells (VSMC) proliferation model. Moreover, treatment with AVE0991 (10−5 mol/L or10−7 mol/L) significantly attenuated reactive oxygen species (ROS) production, phosphorylation of p38 MAPK, and dose-dependently (10−8to10−5 mol/L) inhibited Ang II-induced VSMC proliferation. Meanwhile, heme oxygenase-1 (HO-1) expression increased in the AVE0991 + Ang II group (10−5 mol/L or10−6 mol/L). However, the beneficial effects of AVE0991 were completely abolished when the VSMC were pretreated with A-779 (10−6 mol/L). Furthermore, treatment with the HO-1 inhibitor ZnPPIX attenuated the inhibitory effect of AVE0991 on Ang II-induced p38MAPK phosphorylation. These results suggest that AVE0991 attenuates Ang II-induced VSMC proliferation in a dose-dependent fashion and that this effect is associated with the Mas/HO-1/p38 MAPK signaling pathway.