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Boron (B) deficiency influences sugar beet development and productivity. A hydroponic set up of experiment was conducted by utilizing different B concentrations to study the impact of different morphological and physiological responses of sugar beet seedlings under B deficiency. The results showed that B deficiency (14 days of stress) inhibited the growth of different plant parts of sugar beet. The B deficiency significantly increased the leaf specific weight (SLW) and the root-shoot ratio of sugar beet seedlings. The activities of peroxidase (POD), catalase (CAT), and superoxide dismutase (SOD) showed a decreasing tendency under B deficiency, while the contents of hydrogen peroxide (H 2 O 2 ) and superoxide (O 2 -) increased with B concentration. Malonaldehyde (MDA) and proline contents were induced at B deficiency.In conclusion, B deficiency significantly reduced dry weight and leaf area, resulting in stunted sugar beet seedlings. It was manifested by a significant decrease in antioxidant enzyme activities and accumulation of ROS in the plant cells, inducing oxidative stress. The current study revealed that B deficiency affects plant growth and various morpho-physiological processes.

Liver metastasis is common in patients with pancreatic cancer (PC) and is the leading cause of death associated with PC. Liver fibrosis induced by activated hepatic stellate cells (HSCs) creates a favorable metastatic microenvironment that promotes metastasis growth. B7-33, a therapeutic peptide (relaxin analog) that targets relaxin family peptide receptors on activated HSCs, inhibits the pSMAD2/3 signaling pathway and weakens the fibrogenic properties of activated HSCs. However, the short half-life and highly conserved nature of the B7-33 sequence limit its application in vivo. Here, B7-33 is modified with the cRGD sequence, which does not affect the efficacy of B7-33 and allows B7-33 to assemble into vascular endothelial cell membrane-derived vesicles by specifically interacting with integrin α v β 3 . These rationally designed vesicles (B7-33-HNPs) are able to prolong the half-life of B7-33 in vivo and accumulate in the liver to reverse HSCs activation. Moreover, B7-33-HNPs prevent the formation and growth of liver metastases in a mouse model of metastatic PC. This study proposes a feasible strategy for building a therapeutic peptide delivery system through specific interactions, serving as a reference for preventing liver metastasis of PC through the regulation of HSCs.