Synthesis of titanium nitride for self-aligned gate AlGaN/GaN heterostructure field-effect transistors

In this study, titanium nitride (TiN) is synthesized using reactive sputtering for a self-aligned gate process. The Schottky barrier height of the TiN on n-GaN is around 0.5 to 0.6 eV and remains virtually constant with varying nitrogen ratios. As compared with the conventional Ni electrode, the TiN electrode presents a lower turn-on voltage, while its reverse leakage current is comparable with that of Ni. The results of annealing evaluation at different temperatures and duration times show that the TiN/W/Au gate stack can withstand the ohmic annealing process at 800°C for 1 or 3 min. Finally, the self-aligned TiN-gated AlGaN/GaN heterostructure field-effect transistors are obtained with good pinch-off characteristics

Thermal analysis of AlGaN/GaN hetero-structural Gunn diodes on different substrates through numerical simulation

GaN-based planar Gunn diodes are promising terahertz sources for monolithic microwave and terahertz integrated circuits (MMICs and MTICs, respectively) due to high output power and easiness of fabrication and circuit integration. However, high lateral current in the 2DEG channel may lead to failures such as early breakdown and suppression of oscillations. In this paper, we will, for the first time, systematically investigate the thermal effect on DC IV and output RF characteristics of AlGaN/GaN hetero-structural planar Gunn diodes on different substrates including diamond, SiC, Si and sapphire. Our simulation results show that the best RF output performance comes with the devices on diamond substrate and no oscillating current is observed for devices on sapphire substrate. The suppress of Gunn oscillation in the device on sapphire is mainly due to the excessive heat generated in the channel that leads to increase of the dead zone and attenuation of electronic domains. These results will lay theoretical and experimental foundation for realizing not only milliwatt GaN-based terahertz semiconductor oscillators but also other power devices

Baicalein inhibits acinar-to-ductal metaplasia of pancreatic acinal cell AR42J via improving the inflammatory microenvironment

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive cancers. Recent research has demonstrated that chronic pancreatitis (CP) is associated with an increased risk of PDAC, partly due to acinar-to-ductal metaplasia (ADM). Baicalein has been shown to exert anti-inflammatory and anti-tumor effects for CP or PDAC, respectively. The aim of our study was to investigate the effect of baicalein, and the putative underlying mechanism, on inflammatory cytokines-induced ADM of rat pancreatic acinar cell line AR42J. To investigate ADM and baicalein effects in vitro, AR42J were treated with recombinant rat Tumor Necrosis Factor alpha (rTNFα) with or without baicalein for 5 days. Results showed that rTNFα-induced AR42J cells switched their phenotype from dominantly amylase-positive acinar cells to dominantly cytokeratin 19-positive ductal cells. Moreover, expression of the transcripts for TNFα or Hes-1, a Notch target, was up-regulated in these cells. Interestingly, baicalein reduced the population of ADM as well as cytokines gene expression but not Hes-1. Baicalein inhibited NF-κB activation induced by rTNFα in AR42J, but no effect on Notch 1activation. Moreover, baicalein suppressed the secretion of TNFα and Nitric Oxide (NO) in macrophages stimulated with LPS and further inhibited ADM of conditional medium-treated AR42J cells. Baicalein also suppressed the inflammatory response of LPS-activated macrophages, thereby inhibited ADM of AR42J by altering their microenvironment. Taken together, our study indicates that baicalein reduces rTNFα-induced ADM of AR42J cells by inhibiting NF-κB activation. It also sheds new light on Chinese material medica therapy of pancreatitis and thereby prevention of PDAC

Potential landscape of high dimensional nonlinear stochastic dynamics with large noise

Quantifying stochastic processes is essential to understand many natural phenomena, particularly in biology, including the cell-fate decision in developmental processes as well as the genesis and progression of cancers. While various attempts have been made to construct potential landscape in high dimensional systems and to estimate transition rates, they are practically limited to the cases where either noise is small or detailed balance condition holds. A general and practical approach to investigate real-world nonequilibrium systems, which are typically high-dimensional and subject to large multiplicative noise and the breakdown of detailed balance, remains elusive. Here, we formulate a computational framework that can directly compute the relative probabilities between locally stable states of such systems based on a least action method, without the necessity of simulating the steady-state distribution. The method can be applied to systems with arbitrary noise intensities through A-type stochastic integration, which preserves the dynamical structure of the deterministic counterpart dynamics. We demonstrate our approach in a numerically accurate manner through solvable examples. We further apply the method to investigate the role of noise on tumor heterogeneity in a 38-dimensional network model for prostate cancer, and provide a new strategy on controlling cell populations by manipulating noise strength

AMPK- mediated formation of stress granules is required for dietary restriction- induced longevity in Caenorhabditis elegans

Stress granules (SGs) are nonmembranous organelles that are dynamically assembled and disassembled in response to various stressors. Under stressed conditions, polyadenylated mRNAs and translation factors are sequestrated in SGs to promote global repression of protein synthesis. It has been previously demonstrated that SG formation enhances cell survival and stress resistance. However, the physiological role of SGs in organismal aging and longevity regulation remains unclear. In this study, we used TIAR- 1::GFP and GTBP- 1::GFP as markers to monitor the formation of SGs in Caenorhabditis elegans. We found that, in addition to acute heat stress, SG formation could also be triggered by dietary changes, such as starvation and dietary restriction (DR). We found that HSF- 1 is required for the SG formation in response to acute heat shock and starvation but not DR, whereas the AMPK- eEF2K signaling is required for starvation and DR- induced SG formation but not heat shock. Moreover, our data suggest that this AMPK- eEF2K pathway- mediated SG formation is required for lifespan extension by DR, but dispensable for the longevity by reduced insulin/IGF- 1 signaling. Collectively, our findings unveil a novel role of SG formation in DR- induced longevity.In addition to heat stress, starvation and dietary restriction (DR) can activate stress granule (SG) formation in Caenorhabditis elegans. HSF- 1 and AMPK are two key regulators for the SG formations. HSF- 1 is required for the SG formation in response to acute heat shock and starvation but not DR, whereas the AMPK- eEF2K pathway is required for starvation and DR- induced SG formation but not heat shock. Furthermore, AMPK- mediated SG formation contributes to DR- induced longevity.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/1/acel13157-sup-0008-Figurelegends.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/2/acel13157-sup-0001-FigS1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/3/acel13157-sup-0006-TableS1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/4/acel13157-sup-0007-TableS2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/5/acel13157-sup-0005-FigS5.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/6/acel13157-sup-0003-FigS3.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/7/acel13157.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/8/acel13157-sup-0002-FigS2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/9/acel13157-sup-0004-FigS4.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/155936/10/acel13157_am.pd