Doxorubicin (DOXO) is widely used to treat solid tumors. However, its clinical use is limited by side effects including serious cardiotoxicity due to cardiomyocyte damage. Resident cardiac progenitor cells (hCPCs) act as key regulators of homeostasis in myocardial cells. However, little is known about the function of hCPCs in DOXO-induced cardiotoxicity. In this study, we found that DOXO-mediated hCPC toxicity is closely related to calcium-related autophagy signaling and was significantly attenuated by blocking mTOR signaling in human hCPCs. DOXO induced hCPC apoptosis with reduction of SMP30 (regucalcin) and autophagosome marker LC3, as well as remarkable induction of the autophagy-related markers, Beclin-1, APG7, and P62/SQSTM1 and induction of calcium-related molecules, CaM (Calmodulin) and CaMKII (Calmodulin kinase II). The results of an LC3 puncta assay further indicated that DOXO reduced autophagosome formation via accumulation of cytosolic Ca²⁺. Additionally, DOXO significantly induced mTOR expression in hCPCs, and inhibition of mTOR signaling by rapamycin, a specific inhibitor, rescued DOXO-mediated autophagosome depletion in hCPCs with significant reduction of DOXO-mediated cytosolic Ca²⁺ accumulation in hCPCs, and restored SMP30 and mTOR expression. Thus, DOXO-mediated hCPC toxicity is linked to Ca²⁺-related autophagy signaling, and inhibition of mTOR signaling may provide a cardio-protective effect against DOXO-mediated hCPC toxicity.

Cardiac progenitor cells (CPCs) are resident stem cells present in a small portion of ischemic hearts and function in repairing the damaged heart tissue. Intense oxidative stress impairs cell metabolism thereby decreasing cell viability. Protecting CPCs from undergoing cellular apoptosis during oxidative stress is crucial in optimizing CPC-based therapy. Histochrome (sodium salt of echinochrome A—a common sea urchin pigment) is an antioxidant drug that has been clinically used as a pharmacologic agent for ischemia/reperfusion injury in Russia. However, the mechanistic effect of histochrome on CPCs has never been reported. We investigated the protective effect of histochrome pretreatment on human CPCs (hCPCs) against hydrogen peroxide (H₂O₂)-induced oxidative stress. Annexin V/7-aminoactinomycin D (7-AAD) assay revealed that histochrome-treated CPCs showed significant protective effects against H₂O₂-induced cell death. The anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and Bcl-xL were significantly upregulated, whereas the pro-apoptotic proteins BCL2-associated X (Bax), H₂O₂-induced cleaved caspase-3, and the DNA damage marker, phosphorylated histone (γH2A.X) foci, were significantly downregulated upon histochrome treatment of hCPCs in vitro. Further, prolonged incubation with histochrome alleviated the replicative cellular senescence of hCPCs. In conclusion, we report the protective effect of histochrome against oxidative stress and present the use of a potent and bio-safe cell priming agent as a potential therapeutic strategy in patient-derived hCPCs to treat heart disease.

Direct hemoperfusion therapy with a polymyxin B-immobilized fiber column (PMX-HP) has been introduced as a therapeutic option for gram negative bacterial septic shock in adults. However, its use in neonates and children has not yet been established. We successfully performed hemoperfusion therapy using an adult polymyxin B-immobilized fiber column in a neonate with carbapenem resistant Acinetobacter baumannii septic shock. The application was technically feasible because the neonate was on extracorporeal membrane oxygenation (ECMO). Although it did not rescue the patient, there was significant short-lasting improvement in pulmonary oxygenation and hemodynamics, leading to wean the patient from ECMO. PMX-HP could be used as an adjunctive treatment for selected neonatal and pediatric patients with gram negative bacterial septic shock.

Objectives: To evaluate early- and long-term outcomes of the surgical treatment for coarctation of the aorta based on a new classification system.Methods: A retrospective clinical review of 111 patients with coarctation of the aorta who underwent surgery (March 2011 to August 2020) was performed. We categorised coarctation of the aorta into type I, with all three head vessels tightly packed; type II, with the left subclavian artery separated from the two other head vessels; and type III, with all three head vessels separated from one another. Each type included subtype a, with a short isthmic portion, and subtype b, with a long isthmic portion.Results: The median patient age and weight at operation were 8 (range, 1–1490) days and 3.2 (range, 1.9–18.5) kg, respectively. Extended end-to-end anastomosis was performed via sternotomy in 54, via thoracotomy in 12, end-to-side anastomosis in 31, autologous main pulmonary artery patch augmentation in 12, and modified end-to-end anastomosis combined with subclavian artery flap aortoplasty in two patients. There was one (0.9%) case of early mortality and 12 (10.8%) cases of post-operative complications. Two (1.8%) late deaths occurred during follow-up. Five (4.5%) patients underwent balloon dilatation and three (2.7%) underwent reoperation for restenosis of coarctation of the aorta. All patients with type Ia (21 patients, 18.9%) underwent extended end-to-end anastomosis via sternotomy or thoracotomy.Conclusions: According to the early and late outcomes observed in this study, surgical treatment of coarctation of the aorta using the new classification system could be safe and low risk.

Background: Persistent fifth aortic arch (PFAA) is a rare anomaly often associated with aortic coarctation or interruption, and various surgical techniques for this anomaly have been reported. Herein, we show a case of an infant with PFAA and severe aortic coarctation. Case presentation: A 41-day-old female infant was admitted for sustained fever. Initially, the patient was diagnosed with bacterial meningitis, and echocardiography showed PFAA with severe aortic coarctation. Because the patient presented progressive oliguria and metabolic acidosis, she was transferred for emergency cardiac surgical intervention. The aortic arch was reconstructed using end-to-side anastomosis between the fifth aortic arch and the descending aorta without any artificial conduit or patching material. Conclusions: PFAA with aortic coarctation can be repaired by various surgical methods. Among them, our surgical approach is easy and effective, has growth potential, and an additional surgery is not needed.