No abstract

A new class of oxygen reduction reaction (ORR) catalysts based on graphene quantum dots (GQDs) supported by graphene nanoribbons (GNRs) has been developed through a one-step simultaneous reduction reaction, leading to ultrahigh performance for O reduction with an excellent electrocatalytic activity (higher limiting current density and lower overpotential than those of platinum) and high selectivity and stability in alkaline media comparable to the best C-based ORR catalysts reported so far. Electron microscopy revealed numerous surface/edge defects on the GQD/GNR surfaces and at their interface to act as the active sites. This, coupled with efficient charge transfer between the intimately contacted GQDs and GNRs, rationalized the observed ultrahigh electrocatalytic performance for the resultant GQD-GNR hybrids. Thus, this study opens a new direction for developing low-cost, highly efficient, C-based ORR electrocatalysts.

Aldehyde dehydrogenase (ALDH) activity is used to define normal hematopoietic stem cell (HSC), but its link to leukemic stem cells (LSC) in acute myeloid leukemia (AML) is currently unknown. We hypothesize that ALDH activity in AML might be correlated with the presence of LSC. Fifty-eight bone marrow (BM) samples were collected from AML (n ¼ 43), acute lymphoblastic leukemia (ALL) (n ¼ 8) and normal cases (n ¼ 7). In 14 AML cases, a high SSC lo ALDH br cell population was identified (ALDH þ AML) (median: 14.89%, range: 5.65-48.01%), with the majority of the SSC lo ALDH br cells coexpressing CD34 þ . In another 29 cases, there was undetectable (n ¼ 23) or rare (p5%) (n ¼ 6) SSC lo ALDH br population (ALDH À AML). Among other clinicopathologic variables, ALDH þ AML was significantly associated with adverse cytogenetic abnormalities. CD34 þ BM cells from ALDH þ AML engrafted significantly better in NOD/ SCID mice (ALDH þ AML: injected bone 21.1179.07%; uninjected bone 1.5270.75% vs ALDH À AML: injected bone 1.7771.66% (P ¼ 0.05); uninjected bone 0.2370.23% (P ¼ 0.03)) with the engrafting cells showing molecular and cytogenetic aberrations identical to the original clones. Normal BM contained a small SSC lo ALDH br population (median: 2.92%, range: 0.92-5.79%), but none of the ALL cases showed this fraction. In conclusion, SSC lo ALDH br cells in ALDH þ AML might denote primitive LSC and confer an inferior prognosis in patients.

Cardiac injury in neonatal 1-day-old mice stimulates a regenerative response characterized by reactive cardiomyocyte proliferation, which is distinguished from the fibrotic repair process in adults. Acute inflammation occurs immediately after heart injury and has generally been believed to exert a negative effect on heart regeneration by promoting scar formation in adults; however, little is known about the role of acute inflammation in the cardiac regenerative response in neonatal mice. Here, we show that acute inflammation induced cardiomyocyte proliferation after apical intramyocardial microinjection of immunogenic zymosan A particles into the neonatal mouse heart. We also found that cardiac injury-induced regenerative response was suspended after immunosuppression in neonatal mice, and that cardiomyocytes could not be reactivated to proliferate after neonatal heart injury in the absence of interleukin-6 (IL-6). Furthermore, cardiomyocyte-specific deletion of signal transducer and activator of transcription 3 (STAT3), the major downstream effector of IL-6 signaling, decreased reactive cardiomyocyte proliferation after apical resection. Our results indicate that acute inflammation stimulates the regenerative response in neonatal mouse heart, and suggest that modulation of inflammatory signals might have important implications in cardiac regenerative medicine.