High frequency Scanning Gate Microscopy and local memory effect of carbon nanotube transistors

We use impedance spectroscopy to measure the high frequency properties of single-walled carbon nanotube field effect transistors (swCN-FETs). Furthermore, we extend Scanning Gate Microscopy (SGM) to frequencies up to 15MHz, and use it to image changes in the impedance of swCN-FET circuits induced by the SGM-tip gate. In contrast to earlier reports, the results of both experiments are consistent with a simple RC parallel circuit model of the swCN-FET, with a time constant of 0.3 ms. We also use the SGM tip to show the local nature of the memory effect normally observed in swCN-FETs, implying that nanotube-based memory cells can be miniaturized to dimensions of the order of tens of nm.Comment: 7 pages, 3 figures, to appear in Nano Letter

Dissociation of ssDNA - Single-Walled Carbon Nanotube Hybrids by Watson-Crick Base Pairing

The unwrapping event of ssDNA from the SWNT during the Watson-Crick base paring is investigated through electrical and optical methods, and binding energy calculations. While the ssDNA-metallic SWNT hybrid shows the p-type semiconducting property, the hybridization product recovered metallic properties. The gel electrophoresis directly verifies the result of wrapping and unwrapping events which was also reflected to the Raman shifts. Our molecular dynamics simulations and binding energy calculations provide atomistic description for the pathway to this phenomenon. This nano-physical phenomenon will open up a new approach for nano-bio sensing of specific sequences with the advantages of efficient particle-based recognition, no labeling, and direct electrical detection which can be easily realized into a microfluidic chip format.Comment: 4 pages, 4 figure

A pH sensor based on electric properties of nanotubes on a glass substrate

We fabricated a pH-sensitive device on a glass substrate based on properties of carbon nanotubes. Nanotubes were immobilized specifically on chemically modified areas on a substrate followed by deposition of metallic source and drain electrodes on the area. Some nanotubes connected the source and drain electrodes. A top gate electrode was fabricated on an insulating layer of silane coupling agent on the nanotube. The device showed properties of ann-type field effect transistor when a potential was applied to the nanotube from the top gate electrode. Before fabrication of the insulating layer, the device showed that thep-type field effect transistor and the current through the source and drain electrodes depend on the buffer pH. The current increases with decreasing pH of the CNT solution. This device, which can detect pH, is applicable for use as a biosensor through modification of the CNT surface

Extracellular matrix nano-mechanics determine megakaryocyte function.

The iron hormone hepcidin is inhibited by matriptase-2 (MT2), a liver serine protease encoded by the TMPRSS6 gene. Cleaving the bone morphogenetic protein (BMP) coreceptor hemojuvelin (HJV), MT2 impairs the BMP/son of mothers against decapentaplegic homologs (SMAD) signaling pathway, down-regulates hepcidin, and facilitates iron absorption. TMPRSS6 inactivation causes iron-deficiency anemia refractory to iron administration both in humans and mice. Genome-wide association studies have shown that the SNP rs855791, which causes the MT2 V736A amino acid substitution, is associated with variations of serum iron, transferrin saturation, hemoglobin, and erythrocyte traits. In the present study, we show that, in vitro, MT2 736(A) inhibits hepcidin more efficiently than 736(V). Moreover, in a genotyped population, after exclusion of samples with iron deficiency and inflammation, hepcidin, hepcidin/transferrin saturation, and hepcidin/ferritin ratios were significantly lower and iron parameters were consistently higher in homozygotes 736(A) than in 736(V). Our results indicate that rs855791 is a TMPRSS6 functional variant and strengthen the idea that even a partial inability to modulate hepcidin influences iron parameters and, indirectly, erythropoiesis

Extracellular matrix structure and nano-mechanics determine megakaryocyte function.

The iron hormone hepcidin is inhibited by matriptase-2 (MT2), a liver serine protease encoded by the TMPRSS6 gene. Cleaving the bone morphogenetic protein (BMP) coreceptor hemojuvelin (HJV), MT2 impairs the BMP/son of mothers against decapentaplegic homologs (SMAD) signaling pathway, down-regulates hepcidin, and facilitates iron absorption. TMPRSS6 inactivation causes iron-deficiency anemia refractory to iron administration both in humans and mice. Genome-wide association studies have shown that the SNP rs855791, which causes the MT2 V736A amino acid substitution, is associated with variations of serum iron, transferrin saturation, hemoglobin, and erythrocyte traits. In the present study, we show that, in vitro, MT2 736(A) inhibits hepcidin more efficiently than 736(V). Moreover, in a genotyped population, after exclusion of samples with iron deficiency and inflammation, hepcidin, hepcidin/transferrin saturation, and hepcidin/ferritin ratios were significantly lower and iron parameters were consistently higher in homozygotes 736(A) than in 736(V). Our results indicate that rs855791 is a TMPRSS6 functional variant and strengthen the idea that even a partial inability to modulate hepcidin influences iron parameters and, indirectly, erythropoiesis

Extracellular matrix nano-mechanics determines megakaryocyte function

Cell contact with extracellular matrix proteins (ECMs) leads to activation of specific biochemical signaling pathways and to cyto-skeletal modifications that regulate processes such as cell differentiation, migration and apoptosis. Mechanical properties of ECMs play an important role in determining cells behavior during these processes. In the bone marrow, ECMs concur to the generation of cues that are important for hemopoietic stem cells maturation and differentiation. Sites around the endosteal bone and vascular districts have been proposed as critical niches for stem cell differentiation into megakaryocytes (Mks). In this scenario, fibrillar type I collagen seems to be a key regulator of platelet release, as in vitro adhesion of Mks to this protein inhibits platelet release through the generation of a bulk cell contraction mediated by mechano-sensitive proteins, such as fibronectin, Rho-GTPase and myosin, that lead to cell spreading overtime. In this work we have used a chemical modified collagen that completely override in vitro collagen ligand pathways in directing Mks response in term of cell spreading, migration, platelet release and fibronectin assembly. This different behavior seems to be related to the different nano-mechanical properties of modified collagen with respect to native protein. In particular, N-acetylation of lysine side chains of collagen blocks the formation of banded fibrils and self-aggregation leading to differences in the in vitro sopramolecular organization. Atomic force microscopy analysis of Mks interaction with collagens clearly demonstrated that absence of fibrils, despite similar integrin engagement, and different mechanical properties of these proteins, regulate Mks behaviour and fate. New insights into signaling pathways and in mechano-sensing systems of cells need to be addressed but nanoscale mechanical properties of ECMs seem to have an important role in regulating megakaryocyte behavior in vitro and probably in vivo