Simulation Studies on Robust Contacts in V₂CT₂/MoSi₂N₄ (TO, F, OH) van der Waals Heterojunction Nanostructures: Implications for Optoelectronic Devices

Research on metal electrode–semiconductor contacts has primarily focused on adjusting the Schottky barrier height (SBH), with little attention paid to the stability of electronic properties upon contact. Herein, we comprehensively investigate the sensitivity of contact properties to the external electric field (ΔE), out-plane strain (Δd), and in-plane biaxial strain (Δδ) taking the V2C(T2)/MoSi2N4 (TO, OH, F) van der Waals heterojunction (vdWH) as an example. Our findings suggest that surface functionalization (-T termination) is a powerful tool for controlling contact characteristics. Importantly, when ΔE0.3 V/nm, Δd = −0.1 Å, and Δδ < 0%, the intrinsic contact properties of V2C/MoSi2N4 may be changed. However, V2CT2/MoSi2N4 can maintain the intrinsic contact properties over a wider range of ΔE, Δd, and Δδ. Furthermore, we design a p–i–n optoelectronic transistor (V2CO2/MoSi2N4/V2CO2H2), which has excellent tunneling probability (100%), photocurrent density (11.336 A/m2), responsivity (0.322 AW–1), and external quantum efficiency (71.061%). Our work not only serves as a reference for eliminating the error of information transmission and the degradation of device performance caused by contact property sensitivity to electric field and strain but also provides theoretical guidance for the experimental design of high-performance MoSi2N4-based optoelectronic devices

Comparative expression levels miRNAs in young cells (or tissues) (x axis) and senescent cells (or tissues) (y axis).

<p>(A) replicative senescence in HUVECs (the expression data was log2 transformed). (B) Oncogene-induced senescence in IMR90 cells. (C) Aging tissues in rhesus macaque brain.</p

List of the miRNA expression datasets used in this study.

<p>List of the miRNA expression datasets used in this study.</p

Result of enrichment analysis of deregulated miRNAs during cellular senescence in two cancer miRNA sets.

<p>(A) Tumor suppressing miRNAs. (B) oncogenic miRNAs. Red color represents senescent cells. Green color represents young cell. 1 Replicative senescence in HUVECs. 2 Oncogene-induced senescence in IMR90 cells. 3 Aging tissues in rhesus macaque brain.</p

Model of relationship between miRNA abundance and protein accumulation during cellular senescence.

<p>Globally low expression of miRNAs in senescent cells decreased the suppression of RNA translating into proteins, which results in the accumulation of proteins accompanied with the increased proteins synthesis mediated by autophagy.</p

Synthesis of Polysubstituted Pyrazoles by a Platinum-Catalyzed Sigmatropic Rearrangement/Cyclization Cascade

A highly efficient Pt-catalyzed [3,3] sigmatropic rearrangement/cyclization cascade of <i>N</i>-propargyl­hydra­zones is reported. The process provides expedient access to a variety of highly functionalized pyrazoles. The substrate has good substituted group compatibility, and the bioactive 3-CF₃ pyrazoles could be synthesized easily with this method

Synthesis of 5,6-Dihydro­pyrazolo­[1,5‑<i>c</i>]quina­zolines through Gold-Catalyzed Chemoselective Bicyclization of <i>N</i>‑Propargylic Sulfonylhydrazones

An efficient method for the preparation of 5,6-dihydro­pyrazolo­[1,5-<i>c</i>]­quinazolines via gold­(I)-catalyzed chemoselective bicyclization of <i>N</i>-propargylic sulfonyl­hydrazones has been developed. This process relies on the chemoselective cyclization of the hydrazone nitrogen instead of the usually favored aniline nitrogen onto the alkyne. The synthetic utility of the current strategy is demonstrated through the synthesis of a potential Eg5/Kinesin spindle protein inhibitor

Senescence as a novel mechanism involved in β-adrenergic receptor mediated cardiac hypertrophy

<div><p>Pathological cardiac hypertrophy used to be elucidated by biomechanical, stretch-sensitive or neurohumoral mechanisms. However, a series of hints have indicated that hypertrophy process simulates senescence program. However, further evidence need to be pursued. To verify this hypothesis and examine whether cardiac senescence is a novel mechanism of hypertrophy induced by isoproterenol, 2-month-old male Sprague Dawley rats were subjected to isoproterenol infusion (0.25mg/kg/day) for 7 days by subcutaneous injection). Key characteristics of senescence (senescence-associated β-galactosidase activity, lipofuscin, expression of cyclin-dependent kinase inhibitors) were examined in cardiac hypertrophy model. Senescence-like phenotype, such as increased senescence-associated β-galactosidase activity, accumulation of lipofuscin and high levels of cyclin-dependent kinase inhibitors (e.g. p16, p19, p21 and p53) was found along the process of cardiac hypertrophy. Cardiac-specific transcription factor GATA4 increased in isoproterenol-treated cardiomyocytes as well. We further found that myocardial hypertrophy could be inhibited by resveratrol, an anti-aging compound, in a dose-dependent manner. Our results showed for the first time that cardiac senescence is involved in the process of pathological cardiac hypertrophy induced by isoproterenol.</p></div

Expression of CDKIs and GATA4 increased in ISO-treated cells.

<p>(A) The protein level of cell cycle inhibitors and Eif5 (loading control) was examined by western blotting. (B) The protein level was quantified by densitometry. (C) The protein level of GATA4 and Eif5 was examined by western blotting and (D) quantified by densitometry. The gene expression of SASP factors (E) and (F) was examined with the use of quantitative RT-PCR. Data are means ± SEM (n = 6; *P < 0.05, ***P < 0.001 <i>vs</i>. vehicle; # P < 0.05, ## P < 0.01,###P < 0.001 <i>vs</i>. 2 months. The mean value for 2-month-old rats was expressed as 1 unit).</p

Increased number of senescence associated β-galactosidase (SA-β-gal)-positive cardiomyocytes and amount of lipofuscin in aging and treated cells.

<p>(A) Cardiomyocytes were incubated with 10⁻⁵ mol/L ISO for 48h. Cells were then stained for the presence of SA-β-gal as described in the Methods. Data are means ± SEM (n = 3; *P < 0.05 <i>vs</i>. vehicle). (B) The percentage of SA-β-gal-positive cells was calculated. (C) Frozen heart tissue sections were analyzed for SA-β-gal staining, and (D) the number of SA-gal-positive cells was counted. (E), Frozen heart tissue sections were analyzed for lipofuscin and (F) the percentage of lipofuscin-positive cells was calculated. Data are means ± SEM (n = 6; ***P < 0.001 vs.vehicle group; ###P < 0.001 <i>vs</i>. 2 months.).</p