28 research outputs found
Nanoscale Contacts between Carbon Nanotubes and Metallic Pads
It is well-known that the electrical properties and performance of carbon nanotube field-effect transistors (CNTFETs) are largely dominated by their nanotube/metal contacts. Such nanometer-scaled contacts are typically different from traditional bulk semiconductor/metal contacts, as a thin layer of molecules could be unintentionally introduced between the CNTs and metal electrodes through either adsorption of environmental molecules or device fabrication processes. Here, we present a nanocontact model, in which the energy band bending in the CNTs near the contacts is quantitatively characterized through establishment of electrostatic charge balance between the CNTs and metallic pads under the influences of environmental oxygen. The concept of dipole polarization along the CNT channel in the FET geometry is, for the first time, introduced in order to interpret puzzling findings from several CNT Schottky transistors with asymmetric source and drain contacts
Additional file 1 of Deciphering the effect of phytosterols on Alzheimer’s disease and Parkinson’s disease: the mediating role of lipid profiles
Supplementary Material 1
Lanthanide-Polyoxometalate-Based Film with Reversible Photochromism and Luminescent Switching Properties for Erasable Inkless Security Printing
Security printing is of the utmost importance in the
information
era. However, the excessive use of inks and paper still faces many
economic and environmental issues. Thus, developing erasable inkless
security printing materials is a remarkable strategy to save resources,
protect the environment, and improve information security. To this
endeavor, a photoresponsive lanthanide-polyoxometalate-doped gelatin
film with high transparency was developed through the solution casting
method. Attenuated total reflection Fourier-transform infrared spectroscopy
confirmed the electrostatic and hydrogen bond interactions between
gelatin and lanthanide-polyoxometalate. Absorption spectra, luminescent
spectra, and digital images indicated that the film displayed reversible
photochromism behavior and was accompanied by luminescent switching
property upon exposure to UV irradiation and oxygen (in the dark)
alternately, which allowed its potential application as a reprintable
medium for inkless security printing. The printed information can
be erased upon exposure to oxygen in the dark, and the film can be
reused for printing again. The film exhibited excellent erasability,
reprintability, renewability, and low toxicity. In addition, multiple
encryption strategies were designed to improve information security.
This work offers an attractive alternative strategy for constructing
a reprintable film for inkless security printing in terms of simplifying
the preparation process, saving resources, and protecting the environment
Sensing Mechanisms for Carbon Nanotube Based NH<sub>3</sub> Gas Detection
There has been an argument on carbon nanotube (CNT) based gas detectors with a field-effect transistor (FET) geometry: do the response signals result from charge transfer between adsorbed gas molecules and the CNT channel and/or from the gas species induced Schottky barrier modulation at the CNT/metal contacts? To differentiate the sensing mechanisms, we employed three CNTFET structures, i.e., (1) the entire CNT channel and CNT/electrode contacts are accessible to NH3 gas; (2) the CNT/electrode contacts are passivated with a Si3N4 thin film, leaving the CNT channel open to the gas and, in contrast, (3) the CNT channel is covered with the film, while the contacts are open to the gas. We suggest that the Schottky barrier modulation at the contacts is the dominant mechanism from room temperature to 150 °C. At higher temperatures, the charge transfer process contributes to the response signals. There is a clear evidence that the adsorption of NH3 on the CNT channel is facilitated by environmental oxygen
Spinophilin is required for maintaining the sustained ERK1/2 activation induced by the Del301-303 α<sub>2B</sub>AR in MEFs.
<p>(A) Sp<sup>+/+</sup> MEFs expressing the WT or Del301-303 α<sub>2B</sub>AR were stimulated with 1μM clonidine for indicated time points. Representative blots show phospho- and total-ERK1/2. (B) Quantitation of ERK1/2 activation in Sp<sup>+/+</sup> MEFs. The relative ERK1/2 activation at each time point was expressed as a ratio to the peak level of ERK1/2 activation in the same experiment, which was arbitrarily defined as 1.0. n = 7 for the WT α<sub>2B</sub> group and n = 6 for the Del301-303 α<sub>2B</sub> group. *, <i>p</i><0.05; ***, <i>p</i><0.001, WT α<sub>2B</sub><i>vs</i>. Del301-303 α<sub>2B</sub>. (C) Sp<sup>-/-</sup> MEFs expressing the WT or Del301-303 α<sub>2B</sub>AR were stimulated with 1μM clonidine for indicated time points. Representative blots show phospho- and total-ERK1/2. (D) Quantitation of ERK1/2 activation in Sp<sup>-/-</sup> MEFs. n = 4 for the WT α<sub>2B</sub> group and n = 3 for the Del301-303 α<sub>2B</sub> group.</p
Spinophilin and arrestin reciprocally regulate α<sub>2B</sub>AR-induced ERK1/2 activation kinetics in MEFs.
<p>(A) Arr2,3<sup>-/-</sup> and corresponding WT (Arr2,3<sup>+/+</sup>) MEFs expressing HA-α<sub>2B</sub>AR were stimulated with 1μM clonidine for indicated time points. Phospho- and total-ERK1/2 were detected by Western blots. Representative blots from multiple independent experiments are shown. (B) Quantitation of ERK1/2 activation in Arr2,3<sup>+/+</sup> or Arr2,3<sup>-/-</sup> MEFs at indicated time points. The relative ERK1/2 activation at each time point was expressed as a ratio to the peak level of ERK1/2 activation in the same experiment, which was arbitrarily defined as 1.0. Data were mean ± SEM. n = 4 for each condition. *, <i>p</i><0.05, Arr2,3<sup>-/-</sup><i>vs</i>. Arr2,3<sup>+/+</sup>. (C) Sp<sup>-/-</sup> and corresponding WT (Sp<sup>+/+</sup>) MEFs expressing HA-α<sub>2B</sub>AR were stimulated. Representative blots for phospho- and total ERK1/2 from multiple independent experiments are shown. (D) Quantitation of ERK1/2 activation in Sp<sup>+/+</sup> or Sp<sup>-/-</sup> MEFs at indicated time points. Data were mean ± SEM. n = 7 for data collected in Sp<sup>+/+</sup> cells and n = 4 for Sp<sup>-/-</sup> cells. *, <i>p</i><0.05; ***, <i>p</i><0.001, Sp<sup>-/-</sup><i>vs</i>. Sp<sup>+/+</sup>.</p
Del301-303 α<sub>2B</sub>AR has a stronger interaction with spinophilin than WT α<sub>2B</sub>AR.
<p>(A) Cells co-expressing Myc-spinophilin together with HA-tagged WT or Del301-303 α<sub>2B</sub>AR were stimulated with 100μM epinephrine (plus 1μM propranolol to block βARs). (B) Quantitation of the agonist-induced fold change of Myc-spinophilin in the IP complex with the WT α<sub>2B</sub> or Del301-303 α<sub>2B</sub>AR. n = 3–5 for each condition. **, <i>p<</i>0.01, WT <i>vs</i>. Del301-303 α<sub>2B</sub>.</p
The endogenous arrestin and spinophilin competes for interaction with the α<sub>2B</sub>AR.
<p>(A) Interaction between α<sub>2B</sub>AR and the endogenous arrestin 3 was enhanced in Sp<sup>-/-</sup> MEFs. Sp<sup>-/-</sup> and corresponding WT (Sp<sup>+/+</sup>) MEFs expressing HA-α<sub>2B</sub>AR were stimulated with 100μM epinephrine (plus 1 μM propranolol to block βARs) for indicated time points. Cell lysates were subjected to IP assays using an HA antibody. (B) Quantitation of the fold change of arrestin 3 in the IP complex isolated from cells with or without stimulation. Data were mean ± SEM. n = 4 for each condition. *, <i>p</i><0.05 by unpaired Student’s <i>t</i> test, Sp<sup>-/-</sup><i>vs</i>. Sp<sup>+/+</sup>. (C) Interaction between α<sub>2B</sub>AR and the endogenous spinophilin was enhanced in Arr2,3<sup>-/-</sup> MEFs. Arr2,3<sup>-/-</sup> and corresponding WT (Arr2,3<sup>+/+</sup>) MEFs expressing HA-α<sub>2B</sub>AR were stimulated with 100μM epinephrine (plus 1μM propranolol to block βARs). Lane C (control) refers to MEFs (Arr2,3<sup>+/+</sup> or Arr2,3<sup>-/-</sup>) without HA-α<sub>2B</sub>AR overexpression. (D) Quantitation of the fold change of spinophilin in the IP complex isolated from cells with or without stimulation. Data were mean ± SEM. n = 4 for each condition. **, <i>p</i><0.01, Arr2,3<sup>-/-</sup><i>vs</i>. Arr2,3<sup>+/+</sup>.</p
TAPI-0 reversed the inhibitory effect of AST on TNF-induced IκBα degradation.
<p>Confluent mAECs were pre-incubated with 4 µM of TAPI-0 for 30 min, then with 250 µg/mL of AST or ASIV for 2 h, and then they were treated with 30 ng/mL TNFα for 30 min. The expression of IκBα was measured by Western blot analysis. Data were representative of three independent experiments with determinations made in triplicate and shown as mean values+S.D. **<i>P</i><0.01 compared with cells treated with TNF+CHX. <sup>## </sup><i>P</i><0.01 compared with cells treated with AST and then TNF+CHX.</p
The α<sub>2B</sub>AR dependent hypertensive response is diminished in spinophilin deficient mice.
<p>(A) Mean arterial pressure (MAP) measured in Sp<sup>+/+</sup> and Sp<sup>-/-</sup> mice in the same genetic background after UK14,304 injection (0.1mg/kg i.v.). (B) Quantitation of agonist-induced changes in MAP(ΔMAP) over the basal level. (C) Quantitation of area under curve of the hypertensive response curve. n = 5 for each group. *, <i>p</i> <0.05, Sp<sup>+/+</sup><i>vs</i>. Sp<sup>-/-</sup>.</p
