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Atmospheric-pressure microplasma-assisted electrochemistry was used to synthesize Ag nanoparticles (NPs) for plasmonic applications. It is shown that the size and dispersion of the nanoparticles can be controlled by variation of the microplasma-assisted electrochemical process parameters such as electrolyte concentration and temperature. Moreover, Ag NP synthesis is also achieved in the absence of a stabilizer, with additional control over the dispersion and NP formation possible. As the microplasma directly reduces Ag ions in solution, the incorporation of toxic reducing agents into the electrolytic solution is unnecessary, making this an environmentally friendly fabrication technique with strong potential for the design and growth of plasmonic nanostructures for a variety of applications. These experiments therefore link microplasma-assisted electrochemical synthesis parameters with plasmonic characteristics.

During development, the hematopoietic lineage transits through hemogenic endothelium, but the signaling pathways effecting this transition are incompletely characterized. Although the Hedgehog (Hh) pathway is hypothesized to play a role in patterning blood formation, early embryonic lethality of mice lacking Hh signaling precludes such analysis. To determine a role for Hh signaling in patterning of hemogenic endothelium, we assessed the effect of altered Hh signaling in differentiating mouse ES cells, cultured mouse embryos, and developing zebrafish embryos. In differentiating mouse ES cells and mouse yolk sac cultures, addition of Indian Hh ligand increased hematopoietic progenitors, whereas chemical inhibition of Hh signaling reduced hematopoietic progenitors without affecting primitive streak mesoderm formation. In the setting of Hh inhibition, induction of either Notch signaling or overexpression of Stem cell leukemia (Scl)/T-cell acute lymphocytic leukemia protein 1 rescued hemogenic vascular-endothelial cadherin + cells and hematopoietic progenitor formation. Together, our results reveal that Scl overexpression is sufficient to rescue the developmental defects caused by blocking the Hh and Notch pathways, and inform our understanding of the embryonic endothelial-to-hematopoietic transition.

Tunable synthesis of bimetallic Au(x)Ag(1-x) alloyed nanoparticles and in situ monitoring of their plasmonic responses is presented. This is a new conceptual approach based on green and energy efficient, reactive, and highly-non-equilibrium microplasma chemistry.

Key Points Notch1 induction promotes specification of hemogenic endothelial cells during embryonic stem cell differentiation. Foxc2 functions downstream of Notch in specification of hemogenic endothelium in mouse and zebrafish embryos.

• The type III TGF-b receptor is a marker that distinguishes "early" and "late" BFU-Es.• TGF-b inhibitors increase early BFU-E cell self-renewal and total erythroblast production.Burst-forming unit erythroid progenitors (BFU-Es) are so named based on their ability to generate in methylcellulose culture large colonies of erythroid cells that consist of "bursts" of smaller erythroid colonies derived from the later colony-forming unit erythroid progenitor erythropoietin (Epo)-dependent progenitors. "Early" BFU-E cells forming large BFU-E colonies presumably have higher capacities for self-renewal than do "late" BFU-Es forming small colonies, but the mechanism underlying this heterogeneity remains unknown. We show that the type III transforming growth factor b (TGF-b) receptor (TbRIII) is a marker that distinguishes early and late BFU-Es. Transient elevation of TbRIII expression promotes TGF-b signaling during the early BFU-E to late BFU-E transition. Blocking TGF-b signaling using a receptor kinase inhibitor increases early BFU-E cell self-renewal and total erythroblast production, suggesting the usefulness of this type of drug in treating

Nobel metal can be used to form a category of nanoparticles, termed noble metal nanoparticles (NMNPs), which are inert (resistant to oxidation/corrosion) and have unique physical and optical properties. NMNPs, particularly gold and silver nanoparticles (AuNPs and AgNPs), are highly accurate and sensitive visual biosensors for the analytical detection of a wide range of inorganic and organic compounds. The interaction between noble metal nanoparticles (NMNPs) and inorganic/organic molecules produces colorimetric shifts that enable the accurate and sensitive detection of toxins, heavy metal ions, nucleic acids, lipids, proteins, antibodies, and other molecules. Hydrogen bonding, electrostatic interactions, and steric effects of inorganic/organic molecules with NMNPs surface can react or displacing capping agents, inducing crosslinking and non-crosslinking, broadening, or shifting local surface plasmon resonance absorption. NMNPs-based biosensors have been widely applied to a series of simple, rapid, and low-cost diagnostic products using colorimetric readout or simple visual assessment. In this mini review, we introduce the concepts and properties of NMNPs with chemical reduction synthesis, tunable optical property, and surface modification technique that benefit the development of NMNPs-based colorimetric biosensors, especially for the visual quantification. The “aggregation strategy” based detection principle of NMNPs colorimetric biosensors with the mechanism of crosslinking and non-crosslinking have been discussed, particularly, the critical coagulation concentration-based salt titration methodology have been exhibited by derived equations to explain non-crosslinking strategy be applied to NMNPs based visual quantification. Among the broad categories of NMNPs based biosensor detection analyses, we typically focused on four types of molecules (melamine, single/double strand DNA, mercury ions, and proteins) with discussion from the standpoint of the interaction between NMNPs surface with molecules, and DNA engineered NMNPs-based biosensor applications. Taken together, NMNPs-based colorimetric biosensors have the potential to serve as a simple yet reliable technique to enable visual quantification.

Hepatocyte transplantation (HCTx) has been considered as an alternative to orthotopic liver transplantation for the treatment of acute and chronic liver failure and metabolic liver diseases. One of the factors that mainly limit its application is the significant cellular loss after HCTx. Although liver has been considered as an immunologically privileged organ, transplanted hepatocytes can only survive for 7 to 10 days without immunosuppression. In fact, both innate and adaptive immune system are implicated in the destruction to allografts, which is a particular type of rejection. This article has reviewed the progress in the mechanisms of cellular loss after allogenic HCTx.