On the Zero-Bias Anomaly in Quantum Wires

Undoped GaAs/AlGaAs heterostructures have been used to fabricate quantum wires in which the average impurity separation is greater than the device size. We compare the behavior of the Zero-Bias Anomaly against predictions from Kondo and spin polarization models. Both theories display shortcomings, the most dramatic of which are the linear electron-density dependence of the Zero-Bias Anomaly spin-splitting at fixed magnetic field B and the suppression of the Zeeman effect at pinch-off

Low Temperature Transport in Undoped Mesoscopic Structures

Using high quality undoped GaAs/AlGaAs heterostructures with optically patterned insulation between two layers of gates, it is possible to investigate very low density mesoscopic regions where the number of impurities is well quantified. Signature appearances of the scattering length scale arise in confined two dimensional regions, where the zero-bias anomaly (ZBA) is also observed. These results explicitly outline the molecular beam epitaxy growth parameters necessary to obtain ultra low density large two dimensional regions as well as clean reproducible mesoscopic devices.Comment: 4 pages, 4 EPS fig

Personalised therapy in follicular lymphoma - is the dial turning?

Follicular lymphoma is the most common indolent lymphoma accounting for approximately 20%–25% of all new non-Hodgkin lymphoma diagnoses in western countries. Whilst outcomes are mostly favorable, the spectrum of clinical phenotypes includes high-risk groups with significantly inferior outcomes. This review discusses recent updates in risk stratification and treatment approaches from upfront treatment for limited and advanced stage follicular lymphoma to the growing options for relapsed, refractory disease with perspectives on how to approach this from a personalized lens. Notable gaps remain on how one can precisely and prospectively select optimal treatment for patients based on varying risks, with an anticipation that an increased understanding of the biology of these different phenotypes and increasing refinement of imaging- and biomarker-based tools will, in time, allow these gaps to be closed

Ultra-shallow quantum dots in an undoped GaAs/AlGaAs 2D electron gas

We report quantum dots fabricated on very shallow 2-dimensional electron gases, only 30 nm below the surface, in undoped GaAs/AlGaAs heterostructures grown by molecular beam epitaxy. Due to the absence of dopants, an improvement of more than one order of magnitude in mobility (at 2E11 /cm^2) with respect to doped heterostructures with similar depths is observed. These undoped wafers can easily be gated with surface metallic gates patterned by e-beam lithography, as demonstrated here from single-level transport through a quantum dot showing large charging energies (up to 1.75 meV) and excited state energies (up to 0.5 meV).Comment: 4 pages, 4 figures; added figures, references, equations, and text; results/conclusions otherwise unchange

Extreme sensitivity of the spin-splitting and 0.7 anomaly to confining potential in one-dimensional nanoelectronic devices

Quantum point contacts (QPCs) have shown promise as nanoscale spin-selective components for spintronic applications and are of fundamental interest in the study of electron many-body effects such as the 0.7 x 2e^2/h anomaly. We report on the dependence of the 1D Lande g-factor g* and 0.7 anomaly on electron density and confinement in QPCs with two different top-gate architectures. We obtain g* values up to 2.8 for the lowest 1D subband, significantly exceeding previous in-plane g-factor values in AlGaAs/GaAs QPCs, and approaching that in InGaAs/InP QPCs. We show that g* is highly sensitive to confinement potential, particularly for the lowest 1D subband. This suggests careful management of the QPC's confinement potential may enable the high g* desirable for spintronic applications without resorting to narrow-gap materials such as InAs or InSb. The 0.7 anomaly and zero-bias peak are also highly sensitive to confining potential, explaining the conflicting density dependencies of the 0.7 anomaly in the literature.Comment: 23 pages, 7 figure

Catheter Ablation of Atrial Fibrillation in Patients with Previous Lobectomy or Partial Lung Resection: Long-Term Results of an International Multicenter Study

Introduction: Data regarding the efficacy of catheter ablation in patients with atrial fibrillation (AF) and patients' previous history of pulmonary lobectomy/pneumonectomy are scanty. We sought to evaluate the efficacy and long-term follow-up of catheter ablation in this highly selected group of patients. Material and Methods: Twenty consecutive patients (8 females, 40%; median age 65.2 years old) with a history of pneumonectomy/lobectomy and paroxysmal or persistent AF, treated by means of pulmonary vein isolation (PVI) at ten participating centers were included. Procedural success, intra-procedural complications, and AF recurrences were considered. Results: Fifteen patients had a previous lobectomy and five patients had a complete pneumonectomy. A large proportion (65%) of PV stumps were electrically active and represented a source of firing in 20% of cases. PVI was performed by radiofrequency ablation in 13 patients (65%) and by cryoablation in the remaining 7 cases. Over a median follow up of 29.7 months, a total of 7 (33%) AF recurrences were recorded with neither a difference between patients treated with cryoablation or radiofrequency ablation or between the two genders. Conclusions: Catheter ablation by radiofrequency ablation or cryoablation in patients with pulmonary stumps is feasible and safe. Long-term outcomes are favorable, and a similar efficacy of catheter ablation has been noticed in both males and females

Immunosenescence and lymphomagenesis

One of the most important determinants of aging-related changes is a complex biological process emerged recently and called \u201cimmunosenescence\u201d. Immunosenescence refers to the inability of an aging immune system to produce an appropriate and effective response to challenge. This immune dysregulation may manifest as increased susceptibility to infection, cancer, autoimmune disease, and vaccine failure. At present, the relationship between immunosenescence and lymphoma in elderly patients is not defined in a satisfactory way. This review presents a brief overview of the interplay between aging, cancer and lymphoma, and the key topic of immunosenescence is addressed in the context of two main lymphoma groups, namely Non Hodgkin Lymphoma (NHL) and Hodgkin Lymphoma (HL). Epstein Barr Virus (EBV) plays a central role in the onset of neoplastic lymphoproliferation associated with immunological changes in aging, although the pathophysiology varies vastly among different disease entities. The interaction between immune dysfunction, immunosenescence and Epstein Barr Virus (EBV) infection appears to differ between NHL and HL, as well as between NHL subtypes

Oral treatment with a zinc complex of acetylsalicylic acid prevents diabetic cardiomyopathy in a rat model of type-2 diabetes: activation of the Akt pathway.

BACKGROUND: Type-2 diabetics have an increased risk of cardiomyopathy, and heart failure is a major cause of death among these patients. Growing evidence indicates that proinflammatory cytokines may induce the development of insulin resistance, and that anti-inflammatory medications may reverse this process. We investigated the effects of the oral administration of zinc and acetylsalicylic acid, in the form of bis(aspirinato)zinc(II)-complex Zn(ASA)2, on different aspects of cardiac damage in Zucker diabetic fatty (ZDF) rats, an experimental model of type-2 diabetic cardiomyopathy. METHODS: Nondiabetic control (ZL) and ZDF rats were treated orally with vehicle or Zn(ASA)2 for 24 days. At the age of 29-30 weeks, the electrical activities, left-ventricular functional parameters and left-ventricular wall thicknesses were assessed. Nitrotyrosine immunohistochemistry, TUNEL-assay, and hematoxylin-eosin staining were performed. The protein expression of the insulin-receptor and PI3K/AKT pathway were quantified by Western blot. RESULTS: Zn(ASA)2-treatment significantly decreased plasma glucose concentration in ZDF rats (39.0 +/- 3.6 vs 49.4 +/- 2.8 mM, P < 0.05) while serum insulin-levels were similar among the groups. Data from cardiac catheterization showed that Zn(ASA)2 normalized the increased left-ventricular diastolic stiffness (end-diastolic pressure-volume relationship: 0.064 +/- 0.008 vs 0.084 +/- 0.014 mmHg/microl; end-diastolic pressure: 6.5 +/- 0.6 vs 7.9 +/- 0.7 mmHg, P < 0.05). Furthermore, ECG-recordings revealed a restoration of prolonged QT-intervals (63 +/- 3 vs 83 +/- 4 ms, P < 0.05) with Zn(ASA)2. Left-ventricular wall thickness, assessed by echocardiography, did not differ among the groups. However histological examination revealed an increase in the cardiomyocytes' transverse cross-section area in ZDF compared to the ZL rats, which was significantly decreased after Zn(ASA)2-treatment. Additionally, a significant fibrotic remodeling was observed in the diabetic rats compared to ZL rats, and Zn(ASA)2-administered ZDF rats showed a similar collagen content as ZL animals. In diabetic hearts Zn(ASA)2 significantly decreased DNA-fragmentation, and nitro-oxidative stress, and up-regulated myocardial phosphorylated-AKT/AKT protein expression. Zn(ASA)2 reduced cardiomyocyte death in a cellular model of oxidative stress. Zn(ASA)2 had no effects on altered myocardial CD36, GLUT-4, and PI3K protein expression. CONCLUSIONS: We demonstrated that treatment of type-2 diabetic rats with Zn(ASA)2 reduced plasma glucose-levels and prevented diabetic cardiomyopathy. The increased myocardial AKT activation could, in part, help to explain the cardioprotective effects of Zn(ASA)2. The oral administration of Zn(ASA)2 may have therapeutic potential, aiming to prevent/treat cardiac complications in type-2 diabetic patients

Exome reanalysis and proteomic profiling identified TRIP4 as a novel cause of cerebellar hypoplasia and spinal muscular atrophy (PCH1)

TRIP4 is one of the subunits of the transcriptional coregulator ASC-1, a ribonucleoprotein complex that participates in transcriptional coactivation and RNA processing events. Recessive variants in the TRIP4 gene have been associated with spinal muscular atrophy with bone fractures as well as a severe form of congenital muscular dystrophy. Here we present the diagnostic journey of a patient with cerebellar hypoplasia and spinal muscular atrophy (PCH1) and congenital bone fractures. Initial exome sequencing analysis revealed no candidate variants. Reanalysis of the exome data by inclusion in the Solve-RD project resulted in the identification of a homozygous stop-gain variant in the TRIP4 gene, previously reported as disease-causing. This highlights the importance of analysis reiteration and improved and updated bioinformatic pipelines. Proteomic profile of the patient’s fibroblasts showed altered RNA-processing and impaired exosome activity supporting the pathogenicity of the detected variant. In addition, we identified a novel genetic form of PCH1, further strengthening the link of this characteristic phenotype with altered RNA metabolism