Hyperfine-mediated transitions between a Zeeman split doublet in GaAs quantum dots: The role of the internal field

We consider the hyperfine-mediated transition rate between Zeeman split spin states of the lowest orbital level in a GaAs quantum dot. We separate the hyperfine Hamiltonian into a part which is diagonal in the orbital states and another one which mixes different orbitals. The diagonal part gives rise to an effective (internal) magnetic field which, in addition to an external magnetic field, determines the Zeeman splitting. Spin-flip transitions in the dots are induced by the orbital mixing part accompanied by an emission of a phonon. We evaluate the rate for different regimes of applied magnetic field and temperature. The rates we find are bigger that the spin-orbit related rates provided the external magnetic field is sufficiently low.Comment: 8 pages, 3 figure

Nucleus-mediated spin-flip transitions in GaAs quantum dots

Spin-flip rates in GaAs quantum dots can be quite slow, thus opening up the possibilities to manipulate spin states in the dots. We present here estimations of inelastic spin-flip rates mediated by hyperfine interaction with nuclei. Under general assumptions the nucleus mediated rate is proportional to the phonon relaxation rate for the corresponding non-spin-flip transitions. The rate can be accelerated in the vicinity of a singlet-triplet excited states crossing. The small proportionality coefficient depends inversely on the number of nuclei in the quantum dot. We compare our results with known mechanisms of spin-flip in $GaAs$ quantum dot.Comment: RevTex 4 pages, 1 figure, submitted to Phys. Rev.

3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

Lesions of ERBB2, PTEN, and PIK3CA activate the phosphati- dylinositol 3-kinase (PI3K) pathway during cancer development by increasing levels of phosphatidylinositol-3,4,5-triphosphate (PIP3). 3-Phosphoinositide-dependent kinase 1 (PDK1) is the first node of the PI3K signal output and is required for activation of AKT. PIP3 recruits PDK1 and AKT to the cell membrane through interactions with their pleckstrin homology domains, allowing PDK1 to activate AKT by phosphorylating it at residue threonine-308. We show that total PDK1 protein and mRNA were overexpressed in a majority of human breast cancers and that 21% of tumors had five or more copies of the gene encoding PDK1, PDPK1. We found that increased PDPK1 copy number was associated with upstream pathway lesions (ERBB2 amplification, PTEN loss, or PIK3CA mutation), as well as patient survival. Examination of an independent set of breast cancers and tumor cell lines derived from multiple forms of human cancers also found increased PDK1 protein levels associated with such upstream pathway lesions. In human mammary cells, PDK1 enhanced the ability of upstream lesions to signal to AKT, stimulate cell growth and migration, and rendered cells more resistant to PDK1 and PI3K inhibition. After orthotopic transplantation, PDK1 overexpression was not oncogenic but dramatically enhanced the ability of ERBB2 to form tumors. Our studies argue that PDK1 overexpression and increased PDPK1 copy number are common occurrences in cancer that potentiate the oncogenic effect of upstream lesions on the PI3K pathway. Therefore, we conclude that alteration of PDK1 is a critical component of oncogenic PI3K signaling in breast cancer

A high-throughput platform for stem cell niche co-cultures and downstream gene expression analysis

Stem cells reside in 'niches', where support cells provide critical signalling for tissue renewal. Culture methods mimic niche conditions and support the growth of stem cells in vitro. However, current functional assays preclude statistically meaningful studies of clonal stem cells, stem cell-niche interactions, and genetic analysis of single cells and their organoid progeny. Here, we describe a 'microraft array' (MRA) that facilitates high-throughput clonogenic culture and computational identification of single intestinal stem cells (ISCs) and niche cells. We use MRAs to demonstrate that Paneth cells, a known ISC niche component, enhance organoid formation in a contact-dependent manner. MRAs facilitate retrieval of early enteroids for quantitative PCR to correlate functional properties, such as enteroid morphology, with differences in gene expression. MRAs have broad applicability to assaying stem cell-niche interactions and organoid development, and serve as a high-throughput culture platform to interrogate gene expression at early stages of stem cell fate choices