Sand may seem simple, but for scientists it is one of nature’s trickiest materials to model. At the Institute of Science and Technology Austria (ISTA), researchers are reimagining sand one grain at a time, showing how tiny changes in shape can make sand flow, pile up, resist pressure—or even withstand attacks like a fortified (sand)castle. The findings were presented at a leading computer graphics conference and published in ACM Transactions on Graphics.

Inspired by the sophisticated visual systems found in nature, bioinspired adaptive optical imaging technology is undergoing a profound transformation from static imitation to dynamic intelligence. A review article published online on March 30, 2026, in Volume 2 of Opto-Electronics Plus, titled "Bioinspired adaptive optical imaging technology," systematically outlines the landscape of this field. The review focuses on two core research directions and anticipates future trends. The study is led by Dr. Wang Qionghua, Professor and Doctoral Supervisor at Beihang University, China.

Type 2 diabetes (T2D) develops through the long-term interplay of genetic predisposition, lifestyle, and environmental exposures. Residential greenness is increasingly studied as a measurable environmental exposure that may be related to diabetes risk. However, prospective evidence from Chinese populations remains limited, and whether genetic susceptibility modifies the greenness–T2D association, particularly in terms of absolute risk reduction, has remained unclear.

Metabolic dysfunction-associated steatotic liver disease (MASLD), which affects about 30% of the population worldwide, is driven in part by excessive hepatic de novo lipogenesis (the production of fatty acids within the liver). In mice, the minor intron splicing factors ZRSR1 and ZRSR2 can influence hepatic lipid metabolism by controlling the processing of Insig transcripts. Whether these proteins also regulate metabolism independently of their canonical splicing function has remained unclear.

Chronic kidney disease (CKD) affects millions worldwide, with renal fibrosis representing a final common pathway of chronic renal injury. Defective fatty acid oxidation (FAO) in renal tubular epithelial cells has been shown to promote kidney fibrosis, but whether FAO impairment in kidney vascular endothelial cells contributes to renal pathology has remained unclear.

Perivascular adipose tissue (PVAT), the fat layer surrounding blood vessels, is increasingly recognized as an active regulator of vascular function rather than a passive structural cushion. Yet whether PVAT contains functionally important sympathetic nerves has remained debated, largely because conventional two-dimensional imaging can miss sparse, spatially complex neural structures.

Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of death worldwide. Elevated low-density lipoprotein cholesterol (LDL-C) is a major modifiable driver of ASCVD, and PCSK9 has become an important therapeutic target because it regulates hepatic LDL receptor recycling and circulating LDL-C levels. Although PCSK9-targeting monoclonal antibodies and siRNA therapies can substantially lower LDL-C, their cost and need for repeated administration have motivated efforts to develop longer-lasting and more accessible approaches.

Type 2 diabetes (T2D) is marked by insulin resistance together with the progressive failure of pancreatic β-cells. Increasing evidence suggests that this failure is shaped not only by β-cells themselves, but also by the local islet immune microenvironment, where resident and recruited macrophages can influence inflammation, islet architecture, and insulin secretion. Exercise is a cornerstone of diabetes management, yet how it acts within this islet microenvironment has remained unclear.

The plasma membrane is more than a passive boundary. It is organized into dynamic lipid-rich microdomains, often referred to as lipid rafts, that concentrate receptors and signaling molecules. In glioblastoma (GBM), the most aggressive primary brain tumor in adults, the epidermal growth factor receptor (EGFR) signaling is a major oncogenic driver. Yet how tumor cells maintain the membrane platforms that support such proliferative signaling has remained incompletely understood.