Epitaxial top-gated atomic-scale silicon wire in a three-dimensional architecture.

Three-dimensional (3D) control of dopant profiles in silicon is a critical requirement for fabricating atomically precise transistors. We demonstrate conductance modulation through an atomic scale 3 nm wide δ-doped silicon-phosphorus wire using a vertically separated epitaxial doped Si:P top-gate. We show that intrinsic crystalline silicon grown at low temperatures (∼250 °C) serves as an effective gate dielectric permitting us to achieve large gate ranges (∼2.6 V) with leakage currents below 1 pA. Combining scanning tunneling lithography for precise lateral confinement, with monolayer doping and low temperature epitaxial overgrowth for precise vertical confinement, we can realize multiple layers of nano-patterned dopants in a single crystal material. These results demonstrate the viability of highly doped, vertically separated epitaxial gates in an all-crystalline architecture with long-term implications for monolithic 3D silicon circuits and for the realization of atomically precise donor architectures for quantum computing.

Interleukin-31 induces cytokine and chemokine production from human bronchial epithelial cells through activation of mitogen-activated protein kinase signalling pathways: implications for the allergic response.

Interleukin-31 (IL-31) is a novel T-helper-lymphocyte-derived cytokine that plays an important role in allergic skin inflammation and atopic dermatitis. It has recently been implicated in bronchial inflammation. We investigated the functions and mechanisms of IL-31-induced activation of human bronchial epithelial cells. The gene and protein expressions of candidate cytokines/chemokines from IL-31-stimulated human bronchial epithelial BEAS-2B cells were first quantified by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The activity of different mitogen-activated protein kinases (MAPKs) in IL-31-stimulated BEAS-2B cells was assessed by Western blot. The IL-31 could significantly elevate the gene and protein expressions of epidermal growth factor (EGF), vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1/CCL2) of BEAS-2B cells in both time-dependently and dose-dependently. Combination of IL-31 with either IL-4 or IL-13 further enhanced VEGF and CCL2 production while IL-31 could synergistically augment the release of EGF, VEGF, CCL2, IL-6 and IL-8 in cocultures of BEAS-2B cells and eosinophils. In addition, IL-31 could activate p38 MAPK, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) of BEAS-2B cells. Selective inhibitors of p38 MAPK (SB203580), ERK (PD98059), and JNK (SP600125) could differentially inhibit the production of EGF, VEGF and CCL2, thereby suggesting a role for MAPKs in IL-31 functions. In conclusion, the activation of MAPKs can be crucial for IL-31-mediated activation of bronchial epithelial cells, thereby providing an immunological role for IL-31 in bronchial inflammation, at least partly, via epithelial EGF, VEGF and CCL2 production.