18 research outputs found

    Lowering the Schottky Barrier Height by Quasi-van der Waals Contacts for High-Performance p‑Type MoTe<sub>2</sub> Field-Effect Transistors

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    Two-dimensional (2D) transition-metal dichalcogenides (TMDs) offer advantages over traditional silicon in future electronics but are hampered by the prominent high contact resistance of metal–TMD interfaces, especially for p-type TMDs. Here, we present high-performance p-type MoTe2 field-effect transistors via a nondestructive van der Waals (vdW) transfer process, establishing low contact resistance between the 2D MoTe2 semiconductor and the PtTe2 semimetal. The integration of PtTe2 as contacts in MoTe2 field-effect transistors leads to significantly improved electrical characteristics compared to conventional metal contacts, evidenced by a mobility increase to 80 cm2 V–1 s–1, an on-state current rise to 5.0 μA/μm, and a reduction in Schottky barrier height (SBH) to 48 meV. Such a low SBH in quasi-van der Waals contacts can be assigned to the low electrical resistivity of PtTe2 and the high efficiency of carrier injection at the 2D semimetal/2D semiconductor interfaces. Imaging via transmission electron microscopy reveals that the 2D semimetal/two-dimensional semiconductor interfaces are atomically flat and exceptionally clean. This interface engineering strategy could enable low-resistance contacts based on vdW architectures in a facile manner, providing opportunities for 2D materials for next-generation optoelectronics and electronics

    The frequencies of both Th1 and Th17 cells in the spleen of Apo E<sup>−/−</sup> mice increase in parallel to the rise in the serum level of total cholesterol and IL-6.

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    <p>(a), the serum level of Total cholesterol levels in Apo E<sup>−/−</sup> mice were measured compared with age-matched C57BL/6 mice. Data are the mean ± SEM (n = 4) of one representative experiment. **p<0.01, ***p<0.001. (b), the serum level of IL-6 in Apo E<sup>−/−</sup> mice and age-matched C57BL/6 mice was measured by ELISA. Shown is one representative experiment of three performed. *p<0.05, **p<0.01. Apo E<sup>−/−</sup> mice were fed with standard chow diet and sacrificed at age 6, 12, 24, and 48 weeks. Splenocytes were stained with FITC-CD4, PE-IL-17A and APC-IFN-γ antibody, (c), Representative plots are shown. The frequencies of Th1and Th17 cells are shown in (d) and (e), respectively. Data are the mean ± SEM (n = 4) of one representative experiment out of three performed. **p<0.01, ***p<0.001.</p

    Accumulated Gr-1<sup>+</sup>CD11b<sup>+</sup> cells cause unresponsiveness of pro-inflammatory T cells to suppression by Treg cells in Apo E<sup>−/−</sup> mice.

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    <p>(a), CD4<sup>+</sup>CD25<sup>−</sup> T cells from C57BL/6 mice were cultured with or without Gr-1<sup>+</sup>CD11b<sup>+</sup> cells and Treg cells, T cell proliferation was determined by [3H] thymidine incorporation. Similar results were obtained in three independent experiments. (b), 6×10<sup>4</sup> CD4<sup>+</sup>CD25<sup>−</sup> T cells from C57BL/6 mice were cultured in the presence of indicated numbers of Gr-1<sup>+</sup>CD11b<sup>+</sup> cells from 20-week old Apo E<sup>−/−</sup> mice for 3 days. 1 µCi of [3H] thymidine was added in each well 18 hrs before harvest, T cell proliferation was determined by [3H] thymidine incorporation. Data are the mean ± SEM (n = 4) of one representative experiment out of three performed. (c), atherosclerotic Apo E<sup>−/−</sup> mice were pre-treated i.p. with 100 µg RB6-8C5 mAb or PBS twice a week before adoptive transfer of 1×107 CFSE-labeled C57BL/6 CD4<sup>+</sup>CD25<sup>−</sup> T cells. Three days after transfer, mice were sacrificed and CFSE dilution was analysis by flow cytometry. Data are the mean ± SEM (n = 5) of one representative experiment. Similar results were obtained in at least three independent experiments. n.s = not significant; *p<0.05, **p<0.01.</p

    The accumulation of Treg and IMC in the spleen of Apo E<sup>−/−</sup> mice.

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    <p>(a), Splenocytes were stained with FITC-CD4 and PE-FoxP3 antibody, the frequencies of Treg cells at time points mentioned above were measured by flow cytometry. Representative plots are shown in (b). Data are the mean ± SEM (n = 4) of one representative experiment out of three performed. (c), Splenocytes were stained with FITC-Gr-1 and PE-CD11b antibody, the frequencies of IMC in the spleen at indicated time points were measured by flow cytometry. Representative plots are shown in (d). Data are the mean ± SEM (n = 4) of one representative experiment out of three performed. n.s = not significant, *p<0.05, **p<0.01.</p

    Gr-1<sup>+</sup>CD11b<sup>+</sup> cell-induced unresponsiveness of pro-inflammatory T cells to suppression is IL-6 dependent.

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    <p>(a), Gr-1<sup>+</sup>CD11b<sup>+</sup> cells were isolated from the spleen of 20-week old Apo E<sup>−/−</sup> and C57BL/6 mice and EL-4 tumor-bearing mice. The mRNA expression of Arg 1, iNOS 2, TGF-β1 and IL-6 was measured by qRT-PCR. (b), CD4<sup>+</sup>CD25<sup>−</sup> T cells from C57BL/6 mice were cultured with or without Gr-1<sup>+</sup>CD11b<sup>+</sup> cells and Treg cells as well as 20 µg/ml IL-6 antibody, T cell proliferation was determined by [3H] thymidine incorporation. Data are the mean ± SEM (n = 4) of one representative experiment. Atherosclerotic Apo E<sup>−/−</sup> mice were pre-treated i.p. with 100 µg RB6-8C5 mAb or Jak inhibitor tofacitinib (CP-690,550) 30 mg/kg twice a week, (c), Phosphorylation of stat1 and stat3 as well as Erk was detected by immunoblot. Shown is one representative experiment out of three. the serum levels of IL-6 (d), INF-γ (e), IL-17A (f) and TGF-β1 (g) were measured by ELISA. Data are the mean ± SEM (n = 4) of one representative experiment. Similar results were obtained in at least three independent experiments. n.s = not significant; *p<0.05, **p<0.01.</p

    Resistance of pro-inflammatory T cells to suppression, instead of impaired Treg cells, contributes to the ongoing inflammatory response in atherosclerotic Apo E<sup>−/−</sup> mice.

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    <p>(a), 6×10<sup>4</sup> CD4<sup>+</sup>CD25<sup>−</sup> T cells from C57BL/6 mice were stimulated with 3 µg/ml CD3 and 1 µg/ml CD28, in the presence or not of indicated numbers of Treg from 20-week old Apo E<sup>−/−</sup> mice or age-matched C57BL/6 mice for 3 days. 1 µCi of [3H] thymidine was added in each well 18 hrs before harvest, T cell proliferation was determined by [3H] thymidine incorporation. Data are the mean ± SEM (n = 4) of one representative experiment out of three performed. CD4<sup>+</sup>CD25<sup>−</sup> T cells isolated from 20-week old Apo E<sup>−/−</sup> mice or age-matched C57BL/6 mice were cultured alone or with Treg cells isolated from 20-week old Apo E<sup>−/−</sup> mice at 3∶1 ratio, T cell proliferation was examined as shown in (b). The amounts of IFN-γ (c) and IL-17A (d) in supernatant were measured by ELISA (n = 4). Data are representative of three independent experiments. n.s = not significant; *p<0.05, **p<0.01, ***p<0.001.</p

    Comparison of some parameters between the eddy and ordinary stations.

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    <p><sup>a</sup> The values in parentheses stand for the number of samples.</p><p><sup>b</sup> E and O refer to the eddy and ordinary stations. The <i>p</i> values were obtained from <i>t</i>-tests assuming <i>α</i> = 0.05.</p><p>E/O is the ratio of a specific parameter in the eddy to the surrounding water. The errors represent the standard deviation for data used to calculate the means.</p
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