Characterization of SiGe/Si Heterostructures Formed by Ge+ and C+ Implantation

Formation of SiGe/Si heterostructures by germanium ion implantation was investigated. A germanium‐implanted layer was grown epitaxially in the solid phase by thermal annealing. Two kinds of crystalline defects were observed. One is a misfit dislocation, and the other is a residual dislocation caused by ion bombardment. The p‐n junction formed in the SiGe layer has a leakage current three orders of magnitude larger than that of a pure Si p‐n junction fabricated with an identical process except for the Ge+ implantation. Carbon doping in the SiGe layer improves its crystalline quality and the junction characteristics

Improved Crystalline Quality of Si\u3csub\u3e1-x\u3c/sub\u3eGe\u3csub\u3ex\u3c/sub\u3e Formed by Low-temperature Germanium Ion Implantation

Improvement of crystalline quality in Si1-xGex formed by germanium ion implantation has been found. End‐of‐range defects were drastically reduced in number by lowering the substrate temperature during implantation with doses on the order of 1016 cm−2. This improvement was confirmed by electrical characterization of p‐n junctions formed in the SiGe layer as well as by transmission electron microscopy

Double-Free-Layer Stochastic Magnetic Tunnel Junctions with Synthetic Antiferromagnets

Stochastic magnetic tunnel junctions (sMTJ) using low-barrier nanomagnets have shown promise as fast, energy-efficient, and scalable building blocks for probabilistic computing. Despite recent experimental and theoretical progress, sMTJs exhibiting the ideal characteristics necessary for probabilistic bits (p-bit) are still lacking. Ideally, the sMTJs should have (a) voltage bias independence preventing read disturbance (b) uniform randomness in the magnetization angle between the free layers, and (c) fast fluctuations without requiring external magnetic fields while being robust to magnetic field perturbations. Here, we propose a new design satisfying all of these requirements, using double-free-layer sMTJs with synthetic antiferromagnets (SAF). We evaluate the proposed sMTJ design with experimentally benchmarked spin-circuit models accounting for transport physics, coupled with the stochastic Landau-Lifshitz-Gilbert equation for magnetization dynamics. We find that the use of low-barrier SAF layers reduces dipolar coupling, achieving uncorrelated fluctuations at zero-magnetic field surviving up to diameters exceeding ($D\approx 100$ nm) if the nanomagnets can be made thin enough ($\approx 1$-$2$ nm). The double-free-layer structure retains bias-independence and the circular nature of the nanomagnets provides near-uniform randomness with fast fluctuations. Combining our full sMTJ model with advanced transistor models, we estimate the energy to generate a random bit as $\approx$ 3.6 fJ, with fluctuation rates of $\approx$ 3.3 GHz per p-bit. Our results will guide the experimental development of superior stochastic magnetic tunnel junctions for large-scale and energy-efficient probabilistic computation for problems relevant to machine learning and artificial intelligence

Verwey transition in Fe3_{3}O4_{4} at high pressure: quantum critical behavior at the onset of metallization

We provide evidence for the existence of a {\em quantum critical point} at the metallization of magnetite Fe$_{3}$O$_{4}$ at an applied pressure of $p_{c} \approx 8$ GPa. We show that the present ac magnetic susceptibility data support earlier resistivity data. The Verwey temperature scales with pressure $T_{V}\sim (1-p/p_{c})^{\nu}$, with $\nu\sim 1/3$. The resistivity data shows a temperature dependence $\rho(T)=\rho_{0}+AT^{n}$, with $n\simeq 3$ above and 2.5 at the critical pressure, respectively. This difference in $n$ with pressure is a sign of critical behavior at $p_{c}$. The magnetic susceptibility is smooth near the critical pressure, both at the Verwey transition and near the ferroelectric anomaly. A comparison with the critical behavior observed in the Mott-Hubbard and related systems is made.Comment: 5 pages, 5 figure

Mamld1 Knockdown Reduces Testosterone Production and Cyp17a1 Expression in Mouse Leydig Tumor Cells

MAMLD1 is known to be a causative gene for hypospadias. Although previous studies have indicated that MAMLD1 mutations result in hypospadias primarily because of compromised testosterone production around the critical period for fetal sex development, the underlying mechanism(s) remains to be clarified. Furthermore, although functional studies have indicated a transactivation function of MAMLD1 for the non-canonical Notch target Hes3, its relevance to testosterone production remains unknown. To examine these matters, we performed Mamld1 knockdown experiments.Mamld1 knockdown was performed with two siRNAs, using mouse Leydig tumor cells (MLTCs). Mamld1 knockdown did not influence the concentrations of pregnenolone and progesterone but significantly reduced those of 17-OH pregnenolone, 17-OH progesterone, dehydroepiandrosterone, androstenedione, and testosterone in the culture media. Furthermore, Mamld1 knockdown significantly decreased Cyp17a1 expression, but did not affect expressions of other genes involved in testosterone biosynthesis as well as in insulin-like 3 production. Hes3 expression was not significantly altered. In addition, while 47 genes were significantly up-regulated (fold change >2.0×) and 38 genes were significantly down-regulated (fold change <0.5×), none of them was known to be involved in testosterone production. Cell proliferation analysis revealed no evidence for compromised proliferation of siRNA-transfected MLTCs.The results, in conjunction with the previous data, imply that Mamld1 enhances Cyp17a1 expression primarily in Leydig cells and permit to produce a sufficient amount of testosterone for male sex development, independently of the Hes3-related non-canonical Notch signaling

Mouse Suppressor of fused is a negative regulator of Sonic hedgehog signaling and alters the subcellular distribution of Gli1

AbstractThe Hedgehog (Hh) signaling pathway has critical functions during embryogenesis of both invertebrate and vertebrate species [1]; defects in this pathway in humans can cause developmental disorders as well as neoplasia [2]. Although the Gli1, Gli2, and Gli3 zinc finger proteins are known to be effectors of Hh signaling in vertebrates, the mechanisms regulating activity of these transcription factors remain poorly understood [3,4]. In Drosophila, activity of the Gli homolog Cubitus interruptus (Ci) is likely to be modulated by its interaction with a cytoplasmic complex containing several other proteins [5,6], including Costal2, Fused (Fu), and Suppressor of fused (Su(fu)), the last of which has been shown to interact directly with Ci [7]. We have cloned mouse Suppressor of fused (mSu(fu)) and detected its 4.5 kb transcript throughout embryogenesis and in several adult tissues. In cultured cells, mSu(fu) overexpression inhibited transcriptional activation mediated by Sonic hedgehog (Shh), Gli1 and Gli2. Co-immunoprecipitation of epitope-tagged proteins indicated that mSu(fu) interacts with Gli1, Gli2, and Gli3, and that the inhibitory effects of mSu(fu) on Gli1's transcriptional activity were mediated through interactions with both amino- and carboxy-terminal regions of Gli1. Gli1 was localized primarily to the nucleus of both HeLa cells and the Shh-responsive cell line MNS-70; co-expression with mSu(fu) resulted in a striking increase in cytoplasmic Gli1 immunostaining. Our findings indicate that mSu(fu) can function as a negative regulator of Shh signaling and suggest that this effect is mediated by interaction with Gli transcription factors