Summary
The critical pathway of deceased donation provides a systematic approach to the organ donation process, considering both donation after cardiac death than donation after brain death. The pathway provides a tool for assessing the potential of deceased donation and for the prospective identification and referral of possible deceased donors.
Mesenchymal stromal cells (MSCs) have shown a high potential for cartilage repair. Collagen-based scaffolds are used to deliver and retain cells at the site of cartilage damage. The aim of the work was a comparative analysis of the capacity of the MSCs from human adipose tissue to differentiate into chondrocytes in vitro and to stimulate the regeneration of articular cartilage in an experimental model of rabbit knee osteoarthrosis when cultured on microheterogenic collagen-based hydrogel (MCH) and the microparticles of decellularized porcine articular cartilage (DPC). The morphology of samples was evaluated using scanning electron microscopy and histological staining methods. On the surface of the DPC, the cells were distributed more uniformly than on the MCH surface. On day 28, the cells cultured on the DPC produced glycosaminoglycans more intensely compared to the MCH with the synthesis of collagen type II. However, in the experimental model of osteoarthrosis, the stimulation of the cartilage regeneration was more effective when the MSCs were administered to the MCH carrier. The present study demonstrates the way to regulate the action of the MSCs in the area of cartilage regeneration: the MCH is more conducive to stimulating cartilage repair by the MSCs, while the DPC is an inducer for a formation of a cartilage-like tissue by the MSCs in vitro.
Background: Impairment of hepatic arterial flow including hepatic arterial thrombosis (HAT), hepatic arterial stenosis (HAS), and splenic artery steal syndrome (SASS) is potentially life-threatening complications. The proposed early diagnosis and urgent treatment strategy of graft arterial flow reduction aim to decrease morbidity and mortality. Methods: Pediatric patients with known hepatic arterial flow impairment were retrospectively reviewed. Patients were grouped by occlusive (HAT) and non-occlusive (HAS/SASS) arterial flow reduction. Patients with HAT were further divided in two groups based on the estimated maximal hepatic artery occlusion time ≤8 and >8 hours. Results: Impairment of hepatic arterial flow developed in 32 of 416 pediatric liver transplant recipients. HAT, HAS, and SASS incidences were 4.1% (n = 17), 2.2%(n = 9), and 1.4% (n = 6), respectively. Neither graft loss nor death occurred in the non-occlusive group. The probabilities of sepsis (OR, 1.7; 95% CI, 1.14-2.53; P=.008) and graft loss or death (OR, 1.42; 95% CI, 1.04-1.92; P=.046) were higher in the occlusive group. Patients with estimated maximal duration of hepatic artery occlusion ≤ 8 hours (n = 7; 41.2%) did not have ischemic-type biliary lesions and sepsis (P=.044 and 0.010, respectively) but had excellent 3-year graft survival compared with > 8 hours group (100% vs 40%; P=.037). Multivariate analysis revealed HAT manifestation by fever was associated with increased chances of graft loss or death.
Conclusion:Occlusive arterial complications impose higher risks of graft loss and death. Thorough arterial supply monitoring by Doppler ultrasonography and urgent endovascular arterial flow restoration may salvage both graft and the recipient.
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