Yaron, J. R. | bioRxiv Science

bioRxiv2025

Tissue-Adhesive Endoscopic Tattoo Inks for Precise Marking and Surveillance of Gastrointestinal Lesions

Accurate marking of lesions and polyps is essential for effective management of gastrointestinal (GI) diseases, including colorectal cancer. Existing FDA-approved endoscopic carbon suspensions diffuse extensively within tissue and can extravasate intraperitoneally, compromising lesion localization, increasing fibrosis risk, and triggering inflammatory responses. These limitations reduce surgical precision and adversely affect patient outcomes. Here, we developed Tissue Adhesive Tattoos, generation 2 (TAT2) inks, composed of iron oxide nanoparticles encapsulated in bioadhesive polymers to improve spatial accuracy while maintaining high endoscopic contrast. TAT2 inks exhibit easy injectability, long-term stability, low macrophage inflammation, and strong spatial localization in ex vivo porcine intestinal tissue. Compared to clinical carbon ink, which spreads widely, TAT2 inks remained sharply localized with excellent contrast after submucosal injection in live mice and pigs. TAT2 also enabled visualization from both luminal and serosal surfaces and supported precise quadrant marking. Additionally, TAT2 inks were MR-compatible, expanding multimodality. Overall, TAT2 inks are biocompatible, non-inflammatory, precisely localized, and improve endoscopic marking for GI disease. TeaserEngineered bioadhesive tattoo inks deliver precise, durable GI marking with minimal spread and compatibility across imaging modalities.

bioengineering↗

bioRxiv2019

Prolonged inflammation leads to ongoing damage after spinal cord injury.

The pathogenesis of spinal cord injury (SCI) remains poorly understood and treatment remains limited. Emerging evidence indicates the severity of post-SCI inflammation and an ongoing controversy in the roles of astrocytes with studies identifying astrocytes as associated both with ongoing inflammation and damage as well as potentially having a protective role. We have completed an extensive systematic study with MRI, histopathology, proteomics and ELISA analyses designed to further define the severe protracted and damaging inflammation after SCI in a rat model. We have identified 3 distinct phases of SCI: acute (first 2 days), inflammatory (starting day 3) and resolution (>3 months) in 16 weeks follow up. Actively phagocytizing, CD68+/CD163- macrophages infiltrate myelin-rich necrotic areas converting them into cavities of injury (COI) when deep in the spinal cord. Alternatively, superficial SCI areas are infiltrated by granulomatous tissue, or arachnoiditis where glial cells are obliterated. In the COI, CD68+/CD163- macrophage numbers reach a maximum in the first 4 weeks and then decline. Myelin phagocytosis is present at 16 weeks indicating ongoing inflammatory damage. The COI and arachnoiditis are defined by a wall of progressively hypertrophied astrocytes. MR imaging indicates persistent spinal cord edema that is linked to the severity of inflammation. Microhemorrhages in the spinal cord around the lesion are eliminated, presumably by reactive astrocytes within the first week post-injury. Acutely increased levels of TNF-, IL-1{beta}, IFN-{gamma} and other pro-inflammatory cytokines, chemokines and proteases decrease and anti-inflammatory cytokines increase in later phases. In this study we elucidated a number of fundamental mechanisms in pathogenesis of SCI and have demonstrated a close association between progressive astrogliosis and reduction in the severity of inflammation.

pathology↗