Degradation or excretion of quantum dots in mouse embryonic stem cells.

BACKGROUND: Quantum dots (QDs) have been considered as a new and efficient probe for labeling cells non-invasively in vitro and in vivo, but fairly little is known about how QDs are eliminated from cells after labeling. The purpose of this study is to investigate the metabolism of QDs in different type of cells. RESULTS: Mouse embryonic stem cells (ESCs) and mouse embryonic fibroblasts (MEFs) were labeled with QD 655. QD-labeling was monitored by fluorescence microscopy and flow cytometry for 72 hours. Both types of cells were labeled efficiently, but a quick loss of QD-labeling in ESCs was observed within 48 hours, which was not prevented by inhibiting cell proliferation. Transmission electron microscope analysis showed a dramatic decrease of QD number in vesicles of ESCs at 24 hours post-labeling, suggesting that QDs might be degraded. In addition, supernatants collected from labeled ESCs in culture were used to label cells again, indicating that some QDs were excreted from cells. CONCLUSION: This is the first study to demonstrate that the metabolism of QDs in different type of cells is different. QDs were quickly degraded or excreted from ESCs after labeling.

A smart multi-functional coating based on anti-pathogen micelles tethered with copper nanoparticles via a biosynthesis method using l-vitamin C.

A multi-functional anti-pathogen coating with "release-killing", "contact-killing" and "anti-adhesion" properties was prepared from biocompatible polymer encapsulated chlorine dioxide (ClO2) which protected the active ingredient from the outside environment. A slow sustained-release of ClO2 from micelles over fifteen days was detected for long-term release-killing. Micelles only release ClO2 on demand in minimum inhibitory concentrations. We prepared nanoparticles which were covalently clustered on micelle surfaces to improve contact-killing as well as to improve the stability of the micelle. Copper nanoparticles were generated using the biosynthesis method including l-vitamin C, which avoids the toxicity and allows for the preparation of copper nanoparticles in a green environment. Synergistic anti-pathogen activity could be generated by a combination of micelle released ClO2 and ascorbic acid. In addition to release-killing and contact-killing, a pluronic polymer coated surface also provides an additional "anti-adhesion" property through its protein-repelling ability. In this research, the designed coating demonstrated a broad-spectrum of activity to kill drug-resistant bacteria, viruses and spores in short period of time. Based on scanning electron microscopy (SEM), transmission electron microscopy (TEM) and anti-oxidase assays, we found that the designed coatings killed the pathogens via bio-oxidation. We also carried out acute respiratory toxicity tests in this research. Analysis of blood samples, lung function and histopathological slices indicated that the synthesized micelles allowed a controlled and sustained release of ClO2 to kill pathogens while maintaining an overall ClO2 concentration in the air within a safe range.

Correction: Functional human 3D microvascular networks on a chip to study the procoagulant effects of ambient fine particulate matter.

[This corrects the article DOI: 10.1039/C7RA11357A.].

Platelet endothelial cell adhesion molecule-1, stage-specific embryonic antigen-1, and Flk-1 mark distinct populations of mouse embryonic stem cells during differentiation toward hematopoietic/endothelial cells.

Vascular endothelial cells (ECs) and most hematopoietic cells express platelet endothelial cell adhesion molecule-1 (PECAM-1), which is the cell surface protein also expressed in mouse embryonic stem (ES) cells. To better understand how PECAM-1(+) ES cells differentiate into PECAM-1(+) hematopoietic cells/ECs, 3 cell surface markers, PECAM-1, stage-specific embryonic antigen-1 (SSEA-1), and Flk-1, were utilized to dissect the developmental process during ES cell differentiation in vitro. Undifferentiated ES cells expressed PECAM-1, with a majority of them coexpressing SSEA-1. During ES cell differentiation, expression of PECAM-1 decreased to give rise to PECAM-1⁻/SSEA-1(+) cells, which represented epiblast stem cells. Subsequently, Flk-1-expressing cells developed from PECAM-1⁻/SSEA-1(+) cells, becoming SSEA-1⁻/Flk-1(+) through the downregulation of SSEA-1 expression. Following this, a second wave of PECAM-1 expression, which represented the mature hematopoietic cells/ECs, developed from Flk-1(+) cells. Also, a small portion of PECAM-1(+)/SSEA-1(+) cells, which represented the residual undifferentiated ES cells, were consistently observed in long-term differentiated embryoid bodies. This work revealed a sequential change in PECAM-1, SSEA-1, and Flk-1 expression during ES cell differentiation; therefore, they could be valuable cell surface markers for isolating cells at distinct developmental stages in ES cell differentiation.