Valley-spin blockade and spin resonance in carbon nanotubes

Manipulation and readout of spin qubits in quantum dots made in III-V materials successfully rely on Pauli blockade that forbids transitions between spin-triplet and spin-singlet states. Quantum dots in group IV materials have the advantage of avoiding decoherence from the hyperfine interaction by purifying them with only zero-spin nuclei. Complications of group IV materials arise from the valley degeneracies in the electronic bandstructure. These lead to complicated multiplet states even for two-electron quantum dots thereby significantly weakening the selection rules for Pauli blockade. Only recently have spin qubits been realized in silicon devices where the valley degeneracy is lifted by strain and spatial confinement. In carbon nanotubes Pauli blockade can be observed by lifting valley degeneracy through disorder. In clean nanotubes, quantum dots have to be made ultra-small to obtain a large energy difference between the relevant multiplet states. Here we report on low-disorder nanotubes and demonstrate Pauli blockade based on both valley and spin selection rules. We exploit the bandgap of the nanotube to obtain a large level spacing and thereby a robust blockade. Single-electron spin resonance is detected using the blockade.Comment: 31 pages including supplementary informatio

Electrically driven single electron spin resonance in a slanting Zeeman field

The rapidly rising fields of spintronics and quantum information science have led to a strong interest in developing the ability to coherently manipulate electron spins. Electron spin resonance (ESR) is a powerful technique to manipulate spins that is commonly achieved by applying an oscillating magnetic field. However, the technique has proven very challenging when addressing individual spins. In contrast, by mixing the spin and charge degrees of freedom in a controlled way through engineered non-uniform magnetic fields, electron spin can be manipulated electrically without the need of high-frequency magnetic fields. Here we realize electrically-driven addressable spin rotations on two individual electrons by integrating a micron-size ferromagnet to a double quantum dot device. We find that the electrical control and spin selectivity is enabled by the micro-magnet's stray magnetic field which can be tailored to multi-dots architecture. Our results demonstrate the feasibility of manipulating electron spins electrically in a scalable way.Comment: 25 pages, 6 figure

Electrical control over single hole spins in nanowire quantum dots

Single electron spins in semiconductor quantum dots (QDs) are a versatile platform for quantum information processing, however controlling decoherence remains a considerable challenge. Recently, hole spins have emerged as a promising alternative. Holes in III-V semiconductors have unique properties, such as strong spin-orbit interaction and weak coupling to nuclear spins, and therefore have potential for enhanced spin control and longer coherence times. Weaker hyperfine interaction has already been reported in self-assembled quantum dots using quantum optics techniques. However, challenging fabrication has so far kept the promise of hole-spin-based electronic devices out of reach in conventional III-V heterostructures. Here, we report gate-tuneable hole quantum dots formed in InSb nanowires. Using these devices we demonstrate Pauli spin blockade and electrical control of single hole spins. The devices are fully tuneable between hole and electron QDs, enabling direct comparison between the hyperfine interaction strengths, g-factors and spin blockade anisotropies in the two regimes

Genomic aberrations associated with outcome in anaplastic oligodendroglial tumors treated within the EORTC phase III trial 26951

Despite similar morphological aspects, anaplastic oligodendroglial tumors (AOTs) form a heterogeneous clinical subgroup of gliomas. The chromosome arms 1p/19q codeletion has been shown to be a relevant biomarker in AOTs and to be perfectly exclusive from EGFR amplification in gliomas. To identify new genomic regions associated with prognosis, 60 AOTs from the EORTC trial 26951 were analyzed retrospectively using BAC-array-based comparative genomic hybridization. The data were processed using a binary tree method. Thirty-three BACs with prognostic value were identified distinguishing four genomic subgroups of AOTs with different prognosis (p < 0.0001). Type I tumors (25%) were characterized by: (1) an EGFR amplification, (2) a poor prognosis, (3) a higher rate of necrosis, and (4) an older age of patients. Type II tumors (21.7%) had: (1) loss of prognostic BACs located on 1p tightly associated with 19q deletion, (2) a longer survival, (3) an oligodendroglioma phenotype, and (4) a frontal location in brain. Type III AOTs (11.7%) exhibited: (1) a deletion of prognostic BACs located on 21q, and (2) a short survival. Finally, type IV tumors (41.7%) had different genomic patterns and prognosis than type I, II and III AOTs. Multivariate analysis showed that genomic type provides additional prognostic data to clinical, imaging and pathological features. Similar results were obtained in the cohort of 45 centrally reviewed–validated cases of AOTs. Whole genome analysis appears useful to screen the numerous genomic abnormalities observed in AOTs and to propose new biomarkers particularly in the non-1p/19q codeleted AOTs

Spin-orbit qubit in a semiconductor nanowire

Motion of electrons can influence their spins through a fundamental effect called spin-orbit interaction. This interaction provides a way to electrically control spins and as such lies at the foundation of spintronics. Even at the level of single electrons, spin-orbit interaction has proven promising for coherent spin rotations. Here we report a spin-orbit quantum bit implemented in an InAs nanowire, where spin-orbit interaction is so strong that spin and motion can no longer be separated. In this regime we realize fast qubit rotations and universal single qubit control using only electric fields. We enhance coherence by dynamically decoupling the qubit from the environment. Our qubits are individually addressable: they are hosted in single-electron quantum dots, each of which has a different Land\'e g-factor. The demonstration of a nanowire qubit opens ways to harness the advantages of nanowires for use in quantum computing. Nanowires can serve as one-dimensional templates for scalable qubit registers. Unique to nanowires is the possibility to easily vary the material even during wire growth. Such flexibility can be used to design wires with suppressed decoherence and push semiconductor qubit fidelities towards error-correction levels. Furthermore, electrical dots can be integrated with optical dots in p-n junction nanowires. The coherence times achieved here are sufficient for the conversion of an electronic qubit into a photon, the flying qubit, for long-distance quantum communication

Relatively lower body mass index is associated with an excess of severe truncal asymmetry in healthy adolescents: Do white adipose tissue, leptin, hypothalamus and sympathetic nervous system influence truncal growth asymmetry?

<p>Abstract</p> <p>Background</p> <p>In healthy adolescents normal back shape asymmetry, here termed truncal asymmetry (TA), is evaluated by higher and lower subsets of BMI. The study was initiated after research on girls with adolescent idiopathic scoliosis (AIS) showed that higher and lower BMI subsets discriminated patterns of skeletal maturation and asymmetry unexplained by existing theories of pathogenesis leading to a new interpretation which has therapeutic implications <it>(double neuro-osseous theory)</it>.</p> <p>Methods</p> <p>5953 adolescents age 11–17 years (boys 2939, girls 3014) were examined in a school screening program in two standard positions, standing forward bending (FB) and sitting FB. The sitting FB position is thought to reveal intrinsic TA free from back humps induced by any leg-length inequality. TA was measured in both positions using a Pruijs scoliometer as angle of trunk inclinations (ATIs) across the back at each of three spinal regions, thoracic, thoracolumbar and lumbar. Abnormality of ATIs was defined as being outside 2 standard deviations for each age group, gender, position and spinal region, and termed <it>severe </it>TA.</p> <p>Results</p> <p>In the sitting FB position after correcting for age,<it>relatively lower BMIs </it>are statistically associated with a greater number of severe TAs than with relatively higher BMIs in both girls (thoracolumbar region) and boys (thoracolumbar and lumbar regions).</p> <p>The relative frequency of severe TAs is significantly higher in girls than boys for each of the right thoracic (56.76%) and thoracolumbar (58.82%) regions (p = 0.006, 0.006, respectively). After correcting for age, smaller BMIs are associated with more <it>severe TAs </it>in boys and girls.</p> <p>Discussion</p> <p>BMI is a surrogate measure for body fat and circulating leptin levels. The finding that girls with relatively lower BMI have significantly later menarche, and a significant excess of TAs, suggests a relation to energy homeostasis through the hypothalamus. The hypothesis we suggest for the pathogenesis of severe TA in girls and boys has the same mechanism as that proposed recently for AIS girls, namely: severe TAs are initiated by a <it>genetically-determined selectively </it>increased hypothalamic sensitivity (up-regulation, i.e. increased sensitivity) to leptin with asymmetry as an adverse response to stress (hormesis), mediated bilaterally mainly to the growing trunk via the sympathetic nervous system <it>(leptin-hypothalamic-sympathetic nervous system (LHS) concept)</it>. The putative autonomic dysfunction is thought to be increased by any lower circulating leptin levels associated with relatively lower BMIs. Sympathetic nervous system activation with asymmetry leads to asymmetries in ribs and/or vertebrae producing severe TA when beyond the capacity of postural mechanisms of the somatic nervous system to control the shape distortion of the trunk. A test of this hypothesis testing skin sympathetic responses, as in the Rett syndrome, is suggested.</p

Sp6 and Sp8 transcription factors control AER formation and dorsal-ventral patterning in limb development

The formation and maintenance of the apical ectodermal ridge (AER) is critical for the outgrowth and patterning of the vertebrate limb. The induction of the AER is a complex process that relies on integrated interactions among the Fgf, Wnt, and Bmp signaling pathways that operate within the ectoderm and between the ectoderm and the mesoderm of the early limb bud. The transcription factors Sp6 and Sp8 are expressed in the limb ectoderm and AER during limb development. Sp6 mutant mice display a mild syndactyly phenotype while Sp8 mutants exhibit severe limb truncations. Both mutants show defects in AER maturation and in dorsal-ventral patterning. To gain further insights into the role Sp6 and Sp8 play in limb development, we have produced mice lacking both Sp6 and Sp8 activity in the limb ectoderm. Remarkably, the elimination or significant reduction in Sp6;Sp8 gene dosage leads to tetra-amelia; initial budding occurs, but neither Fgf8 nor En1 are activated. Mutants bearing a single functional allele of Sp8 (Sp6-/-;Sp8+/-) exhibit a split-hand/foot malformation phenotype with double dorsal digit tips probably due to an irregular and immature AER that is not maintained in the center of the bud and on the abnormal expansion of Wnt7a expression to the ventral ectoderm. Our data are compatible with Sp6 and Sp8 working together and in a dose-dependent manner as indispensable mediators of Wnt/βcatenin and Bmp signaling in the limb ectoderm. We suggest that the function of these factors links proximal-distal and dorsal-ventral patterning

Pathogenesis of adolescent idiopathic scoliosis in girls - a double neuro-osseous theory involving disharmony between two nervous systems, somatic and autonomic expressed in the spine and trunk: possible dependency on sympathetic nervous system and hormones with implications for medical therapy

Anthropometric data from three groups of adolescent girls - preoperative adolescent idiopathic scoliosis (AIS), screened for scoliosis and normals were analysed by comparing skeletal data between higher and lower body mass index subsets. Unexpected findings for each of skeletal maturation, asymmetries and overgrowth are not explained by prevailing theories of AIS pathogenesis. A speculative pathogenetic theory for girls is formulated after surveying evidence including: (1) the thoracospinal concept for right thoracic AIS in girls; (2) the new neuroskeletal biology relating the sympathetic nervous system to bone formation/resorption and bone growth; (3) white adipose tissue storing triglycerides and the adiposity hormone leptin which functions as satiety hormone and sentinel of energy balance to the hypothalamus for long-term adiposity; and (4) central leptin resistance in obesity and possibly in healthy females. The new theory states that AIS in girls results from developmental disharmony expressed in spine and trunk between autonomic and somatic nervous systems. The autonomic component of this double neuro-osseous theory for AIS pathogenesis in girls involves selectively increased sensitivity of the hypothalamus to circulating leptin (genetically-determined up-regulation possibly involving inhibitory or sensitizing intracellular molecules, such as SOC3, PTP-1B and SH2B1 respectively), with asymmetry as an adverse response (hormesis); this asymmetry is routed bilaterally via the sympathetic nervous system to the growing axial skeleton where it may initiate the scoliosis deformity (leptin-hypothalamic-sympathetic nervous system concept = LHS concept). In some younger preoperative AIS girls, the hypothalamic up-regulation to circulating leptin also involves the somatotropic (growth hormone/IGF) axis which exaggerates the sympathetically-induced asymmetric skeletal effects and contributes to curve progression, a concept with therapeutic implications. In the somatic nervous system, dysfunction of a postural mechanism involving the CNS body schema fails to control, or may induce, the spinal deformity of AIS in girls (escalator concept). Biomechanical factors affecting ribs and/or vertebrae and spinal cord during growth may localize AIS to the thoracic spine and contribute to sagittal spinal shape alterations. The developmental disharmony in spine and trunk is compounded by any osteopenia, biomechanical spinal growth modulation, disc degeneration and platelet calmodulin dysfunction. Methods for testing the theory are outlined. Implications are discussed for neuroendocrine dysfunctions, osteopontin, sympathoactivation, medical therapy, Rett and Prader-Willi syndromes, infantile idiopathic scoliosis, and human evolution. AIS pathogenesis in girls is predicated on two putative normal mechanisms involved in trunk growth, each acquired in evolution and unique to humans