Procurement of Abdominal Organs in Multi-Organ Donation in Deceased Donor

Organ procurement is an essential step for organ transplantation, from which a quality organ is received for subsequent transplantation. As the demand for organ transplantation continues to grow, multi-organ donation including the heart, lung, live, pancreas, kidneys, and small intestine from one potential donor is always a priority to meet the demand. The donor is generally rigorously assessed for suitability of organ donation prior to proceeding to organ procurement. The quality of the organ from multi-organ procurement is usually satisfactory without jeopardizing its transplantation. In this chapter, the surgical technique for procurement of the organs from the abdomen is described. Some alternative techniques have also been discussed. Some pictures are inserted to facilitate understanding of the surgical procedure

A comparative study on the efficacy of a retrograde perfusion technique and an antegrade perfusion technique for donor kidney recovery in transplantation in pigs

Abstract Background Donor organ shortage is a significant problem in kidney transplantation. Improvement of perfusion techniques can increase the number of available organs. The aim of this study is to investigate the efficiency and safety of retrograde perfusion (RP) of kidney grafts during organ recovery after transplantation in pigs. Methods Ten pigs were divided into two groups, six in the study group for the RP technique and four in the control group for standard antegrade perfusion (AP). The left kidney was removed and perfused by the RP or AP method according to the study group. The perfused left kidney was auto-transplanted to the right groin location. The right kidney was removed and perfused in the same manner and then stored at 4 °C for 24 h prior to histopathological analysis. Data in both groups were observed and recorded. Results All kidneys perfused by both the RP and AP methods were satisfactory in appearance. All grafts showed diuresis from the first postoperative day onward. On postoperative day 7, the mean serum creatinine (Scr) and blood urea nitrogen (BUN) levels were 174 ± 9.7 ìmol/L and 27.7 ± 2.5 mg/dL in the RP group, and they were 168 ± 13.7 ìmol/L and 26.5 ± 4.3 mg/dL, respectively, in the AP group (p = 0.483 for Scr and p = 0.646 for BUN). The mean peak Scr levels in the RP group (570 ìmol/L) and the AP group (530 ìmol/L) were similar. All pigs survived with adequate renal function throughout the study period. There was minimal interstitial and tubular edema, and there was endothelial cell swelling in some specimens before revascularization in both groups. At postoperative day 7, the auto-transplanted kidneys showed normal glomerular and tubular structure with little interstitial edema and inflammatory cell infiltration in the grafts. No differences were identified between the two groups. Under electron microscopy, the tubular epithelial cells, glomeruli, and glomerular capillary endothelium of the grafts appeared normal in both groups after 24 h in cold storage. Conclusions Kidney grafts in pigs perfused by RP had normal function after transplantation compared with the AP control group. Therefore,retrograde perfusion is potentially an efficient, safe kidney perfusion method for organ recovery

Nanoparticles transfected with plasmid-encoded lncRNA-OIP5-AS1 inhibit renal ischemia-reperfusion injury in mice via the miR-410-3p/Nrf2 axis

Nanostructures composed of liposomes and polydopamine (PDA) have demonstrated efficacy as carriers for delivering plasmids, effectively alleviating renal cell carcinoma. However, their role in acute kidney injury (AKI) remains unclear. This study aimed to investigate the effects of the plasmid-encoded lncRNA-OIP5-AS1@PDA nanoparticles (POP-NPs) on renal ischemia/reperfusion (RI/R) injury and explore the underlying mechanisms. RI/R or OGD/R models were established in mice and HK-2 cells, respectively. In vivo, vector or POP-NPs were administered (10 nmol, IV) 48 h after RI/R treatment. In the RI/R mouse model, the OIP5-AS1 and Nrf2/HO-1 expressions were down-regulated, while miR-410-3p expression was upregulated. POP-NPs treatment effectively reversed RI/R-induced renal tissue injury, restoring altered levels of blood urea nitrogen, creatinine, malondialdehyde, inflammatory factors (IL-8, IL-6, TNF-α), ROS, apoptosis, miR-410-3p, as well as the suppressed expression of SOD and Nrf2/HO-1 in the model mice. Similar results were obtained in cell models treated with POP-NPs. Additionally, miR-410-3p mimics could reverse the effects of POP-NPs on cellular models, partially counteracted by Nrf2 agonists. The binding relationship between OIP5-AS1 and miR-410-3p, alongside miR-410-3p and Nrf2, has been substantiated by dual-luciferase reporter and RNA pull-down assays. The study revealed that POP-NPs can attenuate RI/R-induced injury through miR-410-3p/Nrf2 axis. These findings lay the groundwork for future targeted therapeutic approaches utilizing nanoparticles for RI/R-induced AKI

Nanoparticles transfected with plasmid-encoded lncRNA-OIP5-AS1 inhibit renal ischemia-reperfusion injury in mice via the miR-410-3p/Nrf2 axis

Nanostructures composed of liposomes and polydopamine (PDA) have demonstrated efficacy as carriers for delivering plasmids, effectively alleviating renal cell carcinoma. However, their role in acute kidney injury (AKI) remains unclear. This study aimed to investigate the effects of the plasmid-encoded lncRNA-OIP5-AS1@PDA nanoparticles (POP-NPs) on renal ischemia/reperfusion (RI/R) injury and explore the underlying mechanisms. RI/R or OGD/R models were established in mice and HK-2 cells, respectively. In vivo, vector or POP-NPs were administered (10 nmol, IV) 48 h after RI/R treatment. In the RI/R mouse model, the OIP5-AS1 and Nrf2/HO-1 expressions were down-regulated, while miR-410-3p expression was upregulated. POP-NPs treatment effectively reversed RI/R-induced renal tissue injury, restoring altered levels of blood urea nitrogen, creatinine, malondialdehyde, inflammatory factors (IL-8, IL-6, TNF-α), ROS, apoptosis, miR-410-3p, as well as the suppressed expression of SOD and Nrf2/HO-1 in the model mice. Similar results were obtained in cell models treated with POP-NPs. Additionally, miR-410-3p mimics could reverse the effects of POP-NPs on cellular models, partially counteracted by Nrf2 agonists. The binding relationship between OIP5-AS1 and miR-410-3p, alongside miR-410-3p and Nrf2, has been substantiated by dual-luciferase reporter and RNA pull-down assays. The study revealed that POP-NPs can attenuate RI/R-induced injury through miR-410-3p/Nrf2 axis. These findings lay the groundwork for future targeted therapeutic approaches utilizing nanoparticles for RI/R-induced AKI.</p

Novel insight into the underlying dysregulation mechanisms of immune cell-to-cell communication by analyzing multitissue single-cell atlas of two COVID-19 patients

Abstract How does SARS-CoV-2 cause lung microenvironment disturbance and inflammatory storm is still obscure. We here performed the single-cell transcriptome sequencing from lung, blood, and bone marrow of two dead COVID-19 patients and detected the cellular communication among them. Our results demonstrated that SARS-CoV-2 infection increase the frequency of cellular communication between alveolar type I cells (AT1) or alveolar type II cells (AT2) and myeloid cells triggering immune activation and inflammation microenvironment and then induce the disorder of fibroblasts, club, and ciliated cells, which may cause increased pulmonary fibrosis and mucus accumulation. Further study showed that the increase of T cells in the lungs may be mainly recruited by myeloid cells through ligands/receptors (e.g., ANXA1/FPR1, C5AR1/RPS19, and CCL5/CCR1). Interestingly, we also found that certain ligands/receptors (e.g., ANXA1/FPR1, CD74/COPA, CXCLs/CXCRs, ALOX5/ALOX5AP, CCL5/CCR1) are significantly activated and shared among lungs, blood and bone marrow of COVID-19 patients, implying that the dysregulation of ligands/receptors may lead to immune cell’s activation, migration, and the inflammatory storm in different tissues of COVID-19 patients. Collectively, our study revealed a possible mechanism by which the disorder of cell communication caused by SARS-CoV-2 infection results in the lung inflammatory microenvironment and systemic immune responses across tissues in COVID-19 patients