Bichromatic Rabi Control of Semiconductor Qubits.

Electrically driven spin resonance is a powerful technique for controlling semiconductor spin qubits. However, it faces challenges in qubit addressability and off-resonance driving in larger systems. We demonstrate coherent bichromatic Rabi control of quantum dot hole spin qubits, offering a spatially selective approach for large qubit arrays. By applying simultaneous microwave bursts to different gate electrodes, we observe multichromatic resonance lines and resonance anticrossings that are caused by the ac Stark shift. Our theoretical framework aligns with experimental data, highlighting interdot motion as the dominant mechanism for bichromatic driving.

Electrical Control of Uniformity in Quantum Dot Devices.

Highly uniform quantum systems are essential for the practical implementation of scalable quantum processors. While quantum dot spin qubits based on semiconductor technology are a promising platform for large-scale quantum computing, their small size makes them particularly sensitive to their local environment. Here, we present a method to electrically obtain a high degree of uniformity in the intrinsic potential landscape using hysteretic shifts of the gate voltage characteristics. We demonstrate the tuning of pinch-off voltages in quantum dot devices over hundreds of millivolts that then remain stable at least for hours. Applying our method, we homogenize the pinch-off voltages of the plunger gates in a linear array for four quantum dots, reducing the spread in pinch-off voltages by one order of magnitude. This work provides a new tool for the tuning of quantum dot devices and offers new perspectives for the implementation of scalable spin qubit arrays.

High Mobility Stemless InSb Nanowires.

High aspect-ratio InSb nanowires (NWs) of high chemical purity are sought for implementing advanced quantum devices. The growth of InSb NWs is challenging, generally requiring a stem of a foreign material for nucleation. Such a stem tends to limit the length of InSb NWs and its material becomes incorporated in the InSb segment. Here, we report on the growth of chemically pure InSb NWs tens of microns long. Using a selective-area mask in combination with gold as a catalyst allows complete omission of the stem, thus demonstrating that InSb NWs can grow directly from the substrate. The introduction of the selective-area mask gives rise to novel growth kinetics, demonstrating high growth rates and complete suppression of layer deposition on the mask for Sb-rich conditions. The crystal quality and chemical purity of these NWs is reflected in the significant enhancement of low-temperature electron mobility, yielding an average of 4.4 × 104 cm2/(V s), compared to previously studied InSb NWs grown on stems.

Effect of neonatal isolation on outcome following neonatal seizures in rats--the role of corticosterone.

Emerging evidence indicates that early maternal care permanently modifies the activity of hypothalamic-pituitary-adrenal (HPA) axis and is a critical factor in determining the capacity of the brain to compensate for later encountered insults. The purpose of this study was to determine the role of corticosterone (CORT) in the detrimental effects of neonatal isolation (NI) on seizures. Rats were assigned randomly to the following five groups: (1) control (CONT) rats; (2) NI rats that underwent daily separation from their dams from postnatal day 2 (P2) to P9; (3) status epilepticus (SE) rats, induced by lithium-pilocarpine (Li-Pilo) model at P10; (4) NI plus SE (NIS) rats and (5) NISM rats, a subset of NIS rats receiving metyrapone (100 mg/kg), a CORT synthesis inhibitor, immediately after SE induction. At P10, plasma CORT levels were compared at baseline in CONT and NI rats and in response to Li-Pilo-induced SE among SE, NIS and NISM rats. We evaluated the spatial memory in the Morris water maze at P50 approximately 55, the expression of hippocampal cyclic adenosine monophosphate (cAMP)-responsive element-binding protein phosphorylation at serine-133 (pCREBSer-133) at P55, hippocampal neuronal damage at P80 and seizure threshold at P100. The isolated rats exhibited higher CORT release in response to SE than non-isolated rats, and the NIS rats had greater cognitive deficits and decreased seizure threshold compared to the CONT, NI and SE groups. By contrast, the NISM group, compared to the NIS group, showed a normal CORT response to SE and better spatial memory but no difference in seizure threshold. Compared to the CONT group, the hippocampal pCREBSer-133 level was significantly reduced in all experimental groups (NI, SE, NIS, NISM) with no differences between groups. All rats were free of spontaneous seizures later in life and had no discernible neuronal loss in the hippocampus. Results in this model demonstrate repetitive NI enhances response of plasma CORT to SE, and exacerbates the neurological consequences of neonatal SE. Amelioration of neurological sequelae following reduction of the SE-induced excessive rise in plasma CORT implicates CORT in the pathogenesis of NI increasing the vulnerability to seizures.

Long-term effects of early-life malnutrition and status epilepticus: assessment by spatial navigation and CREB(Serine-133) phosphorylation.

Malnutrition and/or seizure in the developing brain cause hippocampal damages. However, underlying mechanisms remain unclear. The malnutrition group (MN) subjected with malnutrition alone was culled to 20-22 rats per dam on postnatal day 1 (P1). The rats subjected to lithium-pilocarpine (Li/PC)-induced status epilepticus at P21 were grouped as the SE group. The rats subjected to malnutrition and subsequent status epilepticus were grouped as the MS group. Visual-spatial memory test using the Morris water maze task was performed at P80. Following behavioral tests, the hippocampus was evaluated for histological lesions and phosphorylated cAMP-responsive, element-binding protein at serine-133 (pCREB(Ser-133)), an important transcription factor underlying learning and memory in the mammalian brain. Here, the MN group exhibited decreased body weight at P21. There was no significant difference in the seizure duration and mortality between the SE and MS groups. In adulthood (P80), both the SE and MS groups showed the spatial learning deficit, hippocampal cell loss and decreased pCREB(Ser133) level within hippocampal CA1 region. Although the MN group demonstrated a decreased level of pCREB(Ser133), no distinguishable changes in the cognitive deficit and hippocampal neuronal loss were detected. Collectively, the present results suggest that early-life malnutrition led to a reduced phosphorylation of CREB(Ser133) in hippocampal CA1 in the absence of the long-term spatial learning deficit. This decreased phosphorylation of CREB(Ser133) could suggest that cascades of signal transduction responsible for the phosphorylation of CREB(Ser133) might be disturbed by early-life malnutrition. In addition, malnutrition caused no discernible synergistic effects on Li/PC-induced status epilepticus.

An enriched environment improves cognitive performance after early-life status epilepticus accompanied by an increase in phosphorylation of extracellular signal-regulated kinase 2.

An enriched environment can enhance brain recovery in animals with early-life status epilepticus (SE). The purpose of this study was to determine the effects of early-life SE on spatial memory and hippocampal extracellular signal-regulated kinase (ERK) level, and the possible therapeutic effects of the enriched environment. Rats were assigned randomly to four groups: (1) control rats (nonenriched control); (2) control rats housed in an enriched environment from Postnatal Day (P) 25 to P40 (enriched control); (3) rats in which SE was induced with lithium-pilocarpine (Li-PC) at P21 (nonenriched SE); and (4) rats in which SE was induced with Li-PC at P21 and then housed in an enriched environment from P25 to P40 (enriched SE). As adults, the rats underwent spatial learning and memory tests in the Morris water maze between P50 and P55. At P55, subsets of animals were evaluated for expression of hippocampal ERK1/2 phosphorylation immediately following completion of the Morris water maze. At ~P100, another set of animals was tested for seizure threshold. When studied as adults, only the nonenriched SE group had a spatial memory deficit. The nonenriched SE group also exhibited lower levels of phosphorylated ERK2 as compared with the nonenriched control, enriched control, and enriched SE groups. Both the nonenriched SE and enriched SE groups had reduced seizure thresholds as compared with the nonenriched control and enriched control groups. Results from this study demonstrate that an enriched environment improves spatial memory in rats subjected to early-life SE, possibly through upregulation of phosphorylated ERK2 in the hippocampus. However, an enriched environment has no effect on seizure threshold.

Cord blood myeloperoxidase in preterm infants with periventricular hyperechogenicity.

BACKGROUND: Cytokines, adhesion molecules, and inflammatory mediators are believed to play central roles in the pathophysiologic mechanisms of brain white matter lesions. To examine the relationships of cytokines, adhesion molecules, and inflammatory mediators in the cord blood of preterm infants and neonatal cerebral ultrasound periventricular hyperechogenicity (PVH), cord blood cytokines, adhesion molecules, and inflammatory mediators were analyzed, and routine cerebral ultrasound scans were performed in all 96 premature infants. METHODS: The non-PVH group consisted of 20 infants with normal cerebral ultrasound findings during the first week of life. The PVH group consisted of 20 infants with PVH during the first week of life. Cytokines, adhesion molecules, and inflammatory mediators in cord blood including interleukin-8 (IL-8), prostaglandin E2 (PGE2), P-selectin, soluble vascular cell adhesion molecules (sVCAMs), and myeloperoxidase (MPO) were examined by enzyme-linked immunosorbent assay. RESULTS: There were no significant differences in IL-8, PGE2, P-selectin, and sVCAM levels between patients with and without PVH. Interestingly, MPO levels were marginally significantly higher in patients with PVH than those without PVH (7.46 +/- 3.6 vs. 4.81 +/- 3.5; p = 0.024). CONCLUSIONS: It is concluded that MPO from leukocytes may contribute to the occurrence of PVH in premature infants.