6 research outputs found
Effect of TIPE2 Overexpression on LPS-induced iNOS expression.
<p>RAW264.7 cells were stably transfected with TIPE2 plasmid or vector control. TIPE2 expression levels were determined by quantitative RT-PCR (<b>A</b>) and Western blot (<b>B</b>), respectively. For quantitative PCR, the results were presented as folds expression of TIPE2 RNA to that of β-actin. TIPE2 overexpression RAW264.7 cells or control cells were treated with 100 ng/mL LPS for 24 h, and iNOS mRNA (<b>C</b>) and protein (<b>D</b>) levels were detected by quantitative PCR and Western blot, respectively. Data are shown as mean ±SE of one representative experiment. **<i>P</i><0.01; ***<i>P</i><0.001.</p
TIPE2-deficient deficient mice exhibit greater iNOS induction and NO production in response to LPS challenge compared to WT controls.
<p>WT and TIPE2<sup>−/−</sup> mice injected intraperitoneal with phosphate buffered saline (PBS) or with LPS (1.5 mg/kg body weight) and sacrificed 3 or 24 h later. Sera concentration of NO and urea were examined (A and B). Liver and lung tissues of these animals were collected to extract total RNA and protein. The mRNA levels of iNOS, arginase I and arginase II in livers (B, D and E, left panels) and lungs (B, D and E, right panels) were examined by quantitative PCR at 3 h post-PBS or LPS challenge. iNOS protein levels in the livers (C, left panel) and lungs (C, right panel) were examined by Western blot at 24 h post-LPS challenge. Data are shown as means ±SE (n = 4) of one representative experiment. *P<0.05; **P<0.01; ***P<0.001.</p
Increased IκBα, JNK and p38 phosphorylation in TIPE2-deficient macrophages.
<p>Peritoneal macrophages from WT and <i>TIPE2<sup>−/−</sup></i> mice (n = 4) were incubated with or without LPS (100 ng/mL) for the indicated times. Total cell lysates were examined with antibodies to total or phosphorylated IκBα, JNK1/2, p38 and ERK1/2 by Western blot. β-actin was served as a protein loading control.</p
TIPE2 deficiency increases NO production but decreases urea production in macropahges.
<p>Peritoneal macrophages from WT and <i>TIPE2<sup>−/−</sup></i> mice were treated with 100 ng/mL LPS for 0 h, 3 h, and 24 h. iNOS mRNA (<b>A</b>) and protein (<b>B</b>) levels were determined by quantitative PCR and Western blot, respectively. Expression levels of arginase I and arginase II mRNA were examined by quantitative RT-PCR (<b>D</b> and <b>C</b>). Cells were stimulated with 100 ng/mL LPS for 24 h, and culture supernatants were harvested for measurement of NO and urea (<b>E</b> and <b>F</b>). Data are shown as means ±SE (n = 4) of one representative experiment. *<i>P</i><0.05.</p
Multiheterojunction Phototransistors Based on Graphene–PbSe Quantum Dot Hybrids
Graphene-semiconductor
quantum dot (QD) hybrid field effect phototransistors (FEpTs) have
attracted much interest due to their ultrahigh gain and responsivity
in photo detection. However, most reported results are based on single-layer
heterojunction, and the multiheterojunction FEpTs are often ignored.
Here, we design two typical multiheterojunction FEpTs based on graphene–PbSe
quantum dot (QD) hybrids, including QD at the bottom layer (QD-bottom)
and graphene at the bottom layer (G-bottom) FEpTs. Through a comparative
study, G-bottom FEpTs showed a multisaturation behavior due to the
multigraphene layer effect, which was absent in the QD-bottom FEpTs.
The mobilities for electrons and holes were μ<sub>E</sub> =
147 cm<sup>2</sup> V<sup>–1</sup> s<sup>–1</sup> and
μ<sub>E</sub> = 137 cm<sup>2</sup> V<sup>–1</sup> s<sup>–1</sup> in the G-bottom FEpTs and μ<sub>E</sub> = 14
cm<sup>2</sup> V<sup>–1</sup> s<sup>–1</sup> and μ<sub>E</sub> = 59 cm<sup>2</sup> V<sup>–1</sup> s<sup>–1</sup> in the QD-bottom FEpTs. Higher responsivity (∼10<sup>6</sup> A W<sup>–1</sup>) and faster response rate were both achieved
by the G-bottom FEpTs. All of the advantages in G-bottom FEpTs were
attributed to the back-gate effect. Therefore, high performance is
expected in those FEpTs whose heterojunctions are designed to be close
to the back-gate
Additional file 1: of CD317 Promotes the survival of cancer cells through apoptosis-inducing factor
Supporting Online Material for âCD317 Promotes the survival of cancer cells through apoptosis-inducing factorâ. (DOCX 550Â kb