The scientific debate around the installation of a massive underwater curtain to protect Antarctic ice sheets from melting lacks its vital political perspective. A Kobe University research team argues that the serious questions around authority, sovereignty and security should be addressed proactively by the scientific community to avoid the protected seventh continent becoming the scene or object of international discord.

A quick finger prick and a few drops of blood on a card that can be sent in regular mail. This approach could soon make Alzheimer’s testing much more accessible worldwide. A European study led by researchers at the University of Gothenburg, Sweden, is paving the way for this method.

Dr. Hye Jung Chang and Dr. Kyung Joong Yoon (Director) of the Hydrogen Energy Materials Research Center at the Korea Institute of Science and Technology (KIST) have announced that they have elucidated the mechanism of the initial degradation phenomenon that triggers the performance drop of high-temperature solid oxide electrolysis cell systems, using advanced transmission electron microscopy.

Ischemic injury causes dynamic damage to the native extracellular matrix (ECM), which plays a key role in tissue homeostasis and regeneration by providing structural support, facilitating force transmission, and transducing key signals to cells. The main approach aimed at repairing injury to ischemic tissues is restoration of vascular function. Due to their potential to form capillary niches, endothelial cells (ECs) are of greatest interest for vascular regeneration. Integrin binding to ECM is crucial for cell anchorage to the surrounding matrix, spreading, migration, and further activation of intracellular signaling pathways. In this study, we proposed to establish an in-situ engineering strategy to remodel the ECM at the ischemic site to guide EC endogenous binding and establish effective EC/ECM interactions to promote revascularization. We designed and constructed a dual-function molecule (LXW7)₂-SILY, which is comprised of two functional domains: the first one (LXW7) binds to integrin αvβ3 expressed on ECs, and the second one (SILY) binds to collagen. In vitro, we confirmed (LXW7)₂-SILY improved EC adhesion and survival. After in situ injection, (LXW7)₂-SILY showed stable retention at the injured area and promoted revascularization, blood perfusion, and tissue regeneration in a mouse hindlimb ischemia model.