4 results about "Endometriosis" patented technology

This disclosure belongs to the field of pharmaceutical technology, and specifically relates to the application of targeted proline metabolic enzymes in the treatment of endometriosis. This disclosure, through in vitro experiments and EMS animal models, verifies that the proline content in ectopic endometrial stromal cells increases, the expression of proline synthesis metabolic enzymes is elevated, and fibrosis is significantly activated. This disclosure creatively repurposes proline metabolic enzyme inhibitors for EMS treatment. Proline metabolic enzyme inhibitors specifically inhibit the enzyme activity of key proline metabolism enzymes, blocking the synthesis pathway from glutamate to proline, and directly reducing intracellular proline content. Since proline is a major component amino acid of collagen, the inhibition of proline synthesis directly inhibits collagen synthesis and the expression of fibrosis markers in endometrial stromal cells, ultimately achieving the therapeutic effect of inhibiting fibrosis in EMS ectopic lesions and reducing ectopic lesion growth.

The present disclosure relates to a chemogenetic system and method treating endometriosis using a gene therapy vector to deliver a therapeutic payload to specific cells (nociceptive neurons). Overexpression of the payload increases the sensitivity of the cells to an activator, thereby enabling lower doses of activator drugs to be administered. The disclosure also related to vectors to deliver a nucleotide sequence to the target cells to enable overexpression thereof.

The application relates to an endometriosis organoid intelligent monitoring method, system, device and medium method and system. The method comprises the following steps: acquiring bright field images of an experimental culture cavity and a reference culture cavity in a microfluidic double-chamber, acquiring temperature sensing data and pH sensing data of the two chambers; inputting a lightweight convolutional neural network for foreground segmentation to obtain organoid segmentation masks of the two chambers; extracting morphological features based on the segmentation masks to identify invasive phenotypes, and obtaining invasive indexes and invasive phenotype labels of the two chambers; combining the segmentation masks and the pH sensing data to calculate a target perfusion rate; driving a microfluidic perfusion system to regulate the flow rate, performing temperature proportional integral differential control according to the temperature sensing data to generate temperature regulation state data; and integrating the above data to generate an endometriosis organoid intelligent monitoring result. The method can realize intelligent monitoring and closed-loop regulation of the culture environment of endometriosis organoids, and improve the accuracy and experimental efficiency of organoid invasiveness evaluation.

This invention provides a triptolide sustained-release hydrogel targeting the FOSB and TGFB1 axes and its applications, belonging to the field of biomedical materials and drug delivery technology. The sustained-release hydrogel is a core-shell structured sequential release hydrogel. The outer layer is a 40 mg / mL low-concentration gelatin methacrylamide hydrogel loaded with stromal cell-derived factor-1α (SDF-1α), and the inner layer is a 60 mg / mL high-concentration GelMA hydrogel loaded with triptolide. This invention is the first to clearly demonstrate that the transcription factor FOSB constitutes a core driving pathway for endometriosis fibrosis by transcribing and activating TGFB1. Triptolide can directly bind to FOSB and promote its ubiquitination-mediated degradation, thereby blocking the TGF-β / Smad signaling pathway and mesenchymal-myofibroblast transformation. Through a synergistic recruitment-targeted inhibition strategy using core-shell hydrogels, SDF-1α rapidly recruits myofibroblasts in the lesion area, and tripterygium wilfordii achieves local sustained release over 14 days. While significantly inhibiting fibrosis and reducing the size of endometriosis lesions, it avoids the hepatotoxicity and off-target damage of free drugs.