This patented device resolves these clinical challenges by integrating a circular stapler mechanism directly with a suture thread. The system features a tubular sheath containing a stapling head and a separate anvil with a central mast.During the procedure, the anvil is separated from the stapling head to create a working space. A suture thread is looped around the viscus and tightened against the anvil's mast, gathering and folding the tissue. The anvil is then pulled close to the stapling head, compressing the folded tissue, and the stapler is fired. The staples drive through the double-layered tissue and bend securely against the anvil, locking the purse-string fold and thread firmly in place.

Key Advantages & FeaturesSecure & Vascularized Closure: Unlike linear stapling methods, this device creates a uniform, well-vascularized purse-string tissue border that is securely locked by closed staples, reducing the risk of post-operative leaks.Knotless "Pusher Stick" System: The device includes specialized projections and recesses that allow the surgeon to use a pusher stick to tighten the thread without needing to tie a knot.

Incision-Free Specimen Extraction: Because the thread can be tightened without knotting, the purse-string suture can be temporarily opened and closed.

This allows surgeons to extract the resected, diseased portion of the viscus directly through the hollow organ (e.g., transanally), potentially avoiding the need for an additional abdominal incision during laparoscopic procedures.

Versatile Compatibility: The mechanism can be manufactured as a standalone instrument or designed to securely couple with conventional circular anastomosis staplers currently on the market.

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Conductive polyaniline based primer for steel.

Conductive polymer-based redox active, self-healing, scratch/pinhole tolerant, eco-friendly (toxic metal-free), single-component high-performance primer for steel (download the technical specification and safety data sheet below).

Pack Size: 20 Litre
Minimum Order: 500 Liltres
Price: 30 eur / litre

Coverage: ~6 m²/kg
Dry Film Thickness: 20 micrometers

*Conforms to Regulation (EC) No. 453/2010 (REACH), Annex II, as amended by Regulation (EU) No. 2015/830

Demonstrate the robust, specific activation of NRF2 by candidate compounds. ARE-luciferase assays (EC50/IC50). KEAP1/NRF2 protein-protein interaction assays (FP/AlphaScreen). NRF2-dependent gene and protein expression profiling. Promoter occupancy confirmation (TransAM, ChIP-qPCR/ChIP-seq)

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Early de-risking to flag promiscuous compounds and off-target liabilities. ADME/DMPK predictions (permeability, stability, PPB, clearance) AI-based toxicity alerts (hERG, CYP TDI, mitochondrial toxicity, etc.) Compound scoring and go/no-go recommendations.

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Functional proof-of-concept across human and rodent cell systems. Oxidative stress challenges (t-BHP/H₂O₂) in hepatocytes, SH-SY5Y neurons, retinal and cardiac cells. Readouts: viability, ROS, apoptosis via flow cytometry and confocal microscopy. Pharmacodynamics: NRF2-dependent genes and proteins (HMOX1, NQO1).

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Translational in vivo efficacy integrating NRF2 pharmacodynamic biomarkers. Endpoints: NAS (steatosis, inflammation, ballooning), fibrosis, ALT/AST, lipids, hepatic NRF2 biomarkers. Animal models: STAM and choline-deficient variants (in collaboration with IIB “Sols-Morreale” CSIC-UAM). Imaging: MRI for non-invasive hepatic/adipose metabolism assessment.

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Evaluate NRF2 contribution in translational neurodegenerative models. Alzheimer’s: APP/TAU ± NRF2 models; pathology, neuroinflammation, and behavior. Parkinson’s: MPTP and α-synuclein models; motor and nigrostriatal biomarkers. CNS-NRF2 panel: integration of oxidative stress and inflammasome markers.

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Characterize NRF2 modulation across inflammatory processes. In vitro & in vivo LPS activation in cells and mice; cytokine profiling. Key biomarkers: caspase-1, IL-1β, IL-18; tissue-level NRF2 pharmacodynamics. Deliverables: integrated cytokine profiles, mechanistic links to NRF2 activity.

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