Manipulating Electron Transfer between Single-Walled Carbon Nanotubes and Diazonium Salts for High Purity Separation by Electronic Type

Diazonium salts preferentially react with metallic single-walled carbon nanotubes (SWNT) over semiconducting SWNT, enabling the separation of SWNT by electronic type. Therefore, the reaction selectivity of diazonium salts for metallic SWNT is crucial for high purity separation of both metallic and semiconducting SWNT. Herein, we developed an efficient method of increasing the reaction selectivity by manipulating the redox potential of diazonium salts. The electron affinity of diazonium salts is effectively lowered when the para-substituent of the diazonium salts is an electron-donating group, (i.e., 4-hydroxy and 4-propargyloxy) rather than an electron-withdrawing group (i.e., 4-nitro, 4-carboxy, and 4-cholro). The reduction potential of 4-hydroxyphenyl and 4-propargyloxyphenyl diazonium salt was greater than the oxidation potential of semiconducting SWNT; therefore, the electron transfer reaction between these two reagents was effectively suppressed, leading to a highly selective reaction for metallic SWNT. We confirmed that this highly selective reaction scheme can be used to separate SWNT, and high purity semiconducting SWNT can be obtained via density-induced separation

Design of a Polymer–Carbon Nanohybrid Junction by Interface Modeling for Efficient Printed Transistors

Molecularly hybridized materials composed of polymer semiconductors (PSCs) and single-walled carbon nanotubes (SWNTs) may provide a new way to exploit an advantageous combination of semiconductors, which yields electrical properties that are not available in a single-component system. We demonstrate for the first time high-performance inkjet-printed hybrid thin film transistors with an electrically engineered heterostructure by using specially designed PSCs and semiconducting SWNTs (sc-SWNTs) whose system achieved a high mobility of 0.23 cm² V^–1 s^–1, no <i>V</i>_on shift, and a low off-current. PSCs were designed by calculation of the density of states of the backbone structure, which was related to charge transfer. The sc-SWNTs were prepared by a single cascade of the density-induced separation method. We also revealed that the binding energy between PSCs and sc-SWNTs was strongly affected by the side-chain length of PSCs, leading to the formation of a homogeneous nanohybrid film. The understanding of electrostatic interactions in the heterostructure and experimental results suggests criteria for the design of nanohybrid heterostructures

ACA dose-dependently suppressed expression of several Th1/2 cytokines in OVA-induced asthma.

<p>(a) IL-4 mRNA levels. (b) IL-6 mRNA levels. (c) IL-12α mRNA levels. (d) IL-13 mRNA levels. Results are expressed as mean ± SD (n = 6 per group). *<i>p</i><0.05 and **<i>p</i><0.01 vs. OVA group.</p

ACA reduced eosinophil numbers in bronchoalveolar lavage fluid recovered from mice with OVA-induced asthma.

<p>Results are expressed as mean ± SD (n = 7). NEU, neutrophils; LYMs, lymphocytes; EOSs, eosinophils; BASs, basophils; LUCs, large unstained cells.</p>a<p><i>p</i><0.01 vs. CON (vehicle control); ^b<i>p</i><0.01 vs. OVA (OVA-induced asthma model); ^c<i>p</i><0.01 vs. DEX (dexamethasone treatment); ^d<i>p</i><0.01 vs. ACA-25 mg (25 mg/kg/day ACA treatment).</p

ACA dose-dependently inhibited histopathological changes in the lungs of mice with OVA-induced asthma.

<p>(a) ACA dose-dependently reduced inflammatory cell infiltration around vessels and bronchioles, mucus secretion and cell debris in bronchioles, and goblet cell hyperplasia in the lungs. Bar size, 50 μm; hematoxylin and eosin stain. (b) ACA dose-dependently decreased bronchial secretion of glycoproteins in OVA-induced asthma. Bar size, 50 μm; PAS stain. Arrow: inflammatory cell infiltration. Br, bronchiole; Gc, goblet cell; M, mucus secretion; V, vessel. A, vehicle control; B, OVA-induced asthma model; C, dexamethasone; D, 25 mg/kg/day ACA; E, 50 mg/kg/day ACA.</p

ACA suppressed T cells but not B cells in mice with OVA-induced asthma.

<p>(a) ACA dose-dependently suppressed the upregulation of CD8+ cytotoxic T cells in the lungs. (b) ACA suppressed the upregulation of CD4+ Th cells as effectively as dexamethasone. (c) ACA did not affect CD79α+ B cells in the lungs of mice with OVA-induced asthma. Immunopositive cells were counted in five randomly selected nonoverlapping fields (×200 magnification) of three separately immunostained lung sections per animal. A, vehicle control; B, OVA-induced asthma model; C, dexamethasone; D, 25 mg/kg/day ACA; E 50 mg/kg/day ACA.</p

ACA reduced expression of Th2 and Th1 cytokines in OVA-induced asthma.

<p>Treatment with ACA reduced (a) IL-13 expression and (b) almost completely blocked IL-4 expression in the lungs. (c) ACA also decreased IL-5 expression but to a lesser extent. (d) ACA almost completely blocked IL-12α expression and (e) downregulated IFN-γ expression. Immunopositive cells were counted in five randomly selected nonoverlapping fields (×200 magnification) of three separately immunostained lung sections per each animal. A, vehicle control; B, OVA-induced asthma model; C, dexamethasone; D, 25 mg/kg/day ACA; E, 50 mg/kg/day ACA. Results are expressed as mean ± SD (n = 7 per group);*<i>p</i><0.05 and **<i>p</i><0.01 vs. OVA group.</p

Chemical structure of 1′-acetoxychavicol acetate.

<p>Chemical structure of 1′-acetoxychavicol acetate.</p