Coherent and Incoherent Tunneling into Yu-Shiba-Rusinov States Revealed by Atomic Scale Shot-Noise Spectroscopy.

The pair breaking potential of individual magnetic impurities in s-wave superconductors generates localized states inside the superconducting gap commonly referred to as Yu-Shiba-Rusinov (YSR) states whose isolated nature makes them promising building blocks for artificial structures that may host Majorana fermions. One of the challenges in this endeavor is to understand their intrinsic lifetime, ℏ/Λ, which is expected to be limited by the inelastic coupling with the continuum thus leading to decoherence. Here we use shot-noise scanning tunneling microscopy to reveal that electron tunneling into superconducting 2H-NbSe_{2} mediated by YSR states is not Poissonian, but ordered as a function of time, as evidenced by a reduction of the noise.

Inflammatory bowel disease and risk of adenocarcinoma and neuroendocrine tumors in the small bowel.

Background: Uncertainty prevails about the magnitude of excess risk of small bowel cancer in patients with inflammatory bowel disease (IBD).

Patients And Methods: To quantify the risk of small bowel adenocarcinoma and neuroendocrine tumors in patients with ulcerative colitis (UC) and Crohn's disease (CD), we undertook a population-based cohort study of all patients with IBD diagnosed in Norway and Sweden from 1987 to 2016. Patients were followed through linkage to national registers.

Unveiling Odd-Frequency Pairing around a Magnetic Impurity in a Superconductor.

We study the unconventional superconducting correlations caused by a single isolated magnetic impurity in a conventional s-wave superconductor. Because of the local breaking of time-reversal symmetry, the impurity induces unconventional superconductivity, which is even in both space and spin variables but odd under time inversion. We derive an exact proportionality relation between the even-frequency component of the local electron density of states and the imaginary part of the odd-frequency local pairing function.

Probing Trions at Chemically Tailored Trapping Defects.

Trions, charged excitons that are reminiscent of hydrogen and positronium ions, have been intensively studied for energy harvesting, light-emitting diodes, lasing, and quantum computing applications because of their inherent connection with electron spin and dark excitons. However, these quasi-particles are typically present as a minority species at room temperature making it difficult for quantitative experimental measurements. Here, we show that by chemically engineering the well depth of sp quantum defects through a series of alkyl functional groups covalently attached to semiconducting carbon nanotube hosts, trions can be efficiently generated and localized at the trapping chemical defects.

Alternative PDGFD rearrangements in dermatofibrosarcomas protuberans without PDGFB fusions.

Dermatofibrosarcoma protuberans is underlined by recurrent collagen type I alpha 1 chain-platelet-derived growth factor B chain (COL1A1-PDGFB) fusions but ~ 4% of typical dermatofibrosarcoma protuberans remain negative for this translocation in routine molecular screening. We investigated a series of 21 cases not associated with the pathognomonic COL1A1-PDGFB fusion on routine fluorescence in situ hybridization (FISH) testing. All cases displayed morphological and clinical features consistent with the diagnosis of dermatofibrosarcoma protuberans.

Transcriptomic definition of molecular subgroups of small round cell sarcomas.

Sarcoma represents a highly heterogeneous group of tumours. We report here the first unbiased and systematic search for gene fusions combined with unsupervised expression analysis of a series of 184 small round cell sarcomas. Fusion genes were detected in 59% of samples, with half of them being observed recurrently.

Relative velocity distribution of inertial particles in turbulence: A numerical study.

The distribution of relative velocities between particles provides invaluable information on the rates and characteristics of particle collisions. We show that the theoretical model of Gustavsson and Mehlig [K. Gustavsson and B.

Preferred location of droplet collisions in turbulent flows.

This study investigates the local flow characteristics near droplet-droplet collisions by means of direct numerical simulation of isotropic cloudlike turbulence. The key finding is that, generally, droplets do not collide where they preferentially concentrate. Preferential concentration is found to happen as expected in regions of low enstrophy (vorticity magnitude), but collisions tend to take place in regions with significantly higher dissipation rates (up to a factor of 2.

Targeting the EWSR1-FLI1 oncogene-induced protein kinase PKC-β abolishes ewing sarcoma growth.

Ewing sarcoma is a rare but aggressive disease most common in young adults. This cancer is driven by a unique chimeric fusion oncogene but targeted strategies have been elusive. Here we report the identification of the protein kinase PKC-ß (PRKCB) as a disease-specific druggable target for treatment of Ewing sarcoma.

Determinants of patient satisfaction in ambulatory oncology: a cross sectional study based on the OUT-PATSAT35 questionnaire.

Background: The aim of this study was to identify factors associated with satisfaction with care in cancer patients undergoing ambulatory treatment. We investigated associations between patients' baseline clinical and socio-demographic characteristics, as well as self-reported quality of life, and satisfaction with care.

Methods: Patients undergoing ambulatory chemotherapy or radiotherapy in 2 centres in France were invited, at the beginning of their treatment, to complete the OUT-PATSAT35, a 35 item and 13 scale questionnaire evaluating perception of doctors, nurses and aspects of care organisation.

Synchrotron infrared microspectroscopy detecting the evolution of Huntington's disease neuropathology and suggesting unique correlates of dysfunction in white versus gray brain matter.

Huntington's disease (HD), caused by a mutation of the corresponding gene encoding the protein huntingtin (htt), is characterized by progressive deterioration of cognitive and motor functions, paralleled by extensive loss of striatal neurons. At the cellular level, pathogenesis involves an early and prolonged period of neuronal dysfunction followed by neuronal death. Understanding the molecular events driving these deleterious processes is critical to the successful development of therapies to slow down or halt the progression of the disease.

Automated genome-wide visual profiling of cellular proteins involved in HIV infection.

Recent genome-wide RNAi screens have identified >842 human genes that affect the human immunodeficiency virus (HIV) cycle. The list of genes implicated in infection differs between screens, and there is minimal overlap. A reason for this variance is the interdependence of HIV infection and host cell function, producing a multitude of indirect or pleiotropic cellular effects affecting the viral infection during RNAi screening.

Partial inhibition of human immunodeficiency virus replication by type I interferons: impact of cell-to-cell viral transfer.

Type I interferons (IFN) inhibit several steps of the human immunodeficiency virus type 1 (HIV) replication cycle. Some HIV proteins, like Vif and Vpu, directly counteract IFN-induced restriction factors. Other mechanisms are expected to modulate the extent of IFN inhibition.

Sustained effects of nonallele-specific Huntingtin silencing.

Objective: Huntington's disease (HD) is a fatal autosomal dominant neurodegenerative disorder caused by a polyglutamine expansion in the huntingtin (htt) protein. No cure is available to date to alleviate neurodegeneration. Recent studies have demonstrated that RNA interference represents a promising approach for the treatment of autosomal dominant disorders.

Implication of the JNK pathway in a rat model of Huntington's disease.

Huntington's disease (HD) is a neurodegenerative disorder resulting from the expansion of a glutamine repeat (polyQ) in the N-terminus of the huntingtin (htt) protein. Expression of polyQ-containing proteins has been previously shown to induce various cellular stress responses. Among these, activation of the c-Jun N-terminal kinase (JNK) cascade has been observed in cellular models of HD.

Dysregulation of gene expression in primary neuron models of Huntington's disease shows that polyglutamine-related effects on the striatal transcriptome may not be dependent on brain circuitry.

Gene expression changes are a hallmark of the neuropathology of Huntington's disease (HD), but the exact molecular mechanisms of this effect remain uncertain. Here, we report that in vitro models of disease comprised of primary striatal neurons expressing N-terminal fragments of mutant huntingtin (via lentiviral gene delivery) faithfully reproduce the gene expression changes seen in human HD. Neither viral infection nor unrelated (enhanced green fluorescent protein) transgene expression had a major effect on resultant RNA profiles.

Characterization of the mechanical nonlinear behavior of piezoelectric ceramics.

A characterization of the nonlinear behavior with high signal excitation in piezoceramic resonators was carried out. The behavior of power devices working at resonance, in which high strains are involved, is explained. A theoretical model previously described is used to explain the motional impedance variation proportional to the square of the motional current.

Haloperidol protects striatal neurons from dysfunction induced by mutated huntingtin in vivo.

Huntington's disease (HD) results from an abnormal polyglutamine extension in the N-terminal region of the huntingtin protein. This mutation causes preferential degeneration of striatal projection neurons. We previously demonstrated, in vitro, that dopaminergic D2 receptor stimulation acted synergistically with mutated huntingtin (expHtt) to increase aggregate formation and striatal death.

Genetic and phenotypic features of blood and genital viral populations of clinically asymptomatic and antiretroviral-treatment-naive clade a human immunodeficiency virus type 1-infected women.

In the present study, we assessed whether human immunodeficiency virus type 1 (HIV-1) genetic compartmentalization was associated with phenotypic CCR5 (R5) or CXCR4 (X4) coreceptor usage differences between the systemic and the genital viral populations. Four clinically asymptomatic and treatment-naïve clade A HIV-1-infected patients were selected from a cohort of 274 African women, because they were free of all the biological cofactors known to modify the kinetics of viral production in the genital tract. HIV RNA envelope sequences (V1 to V3) derived from plasma and cervicovaginal secretions (CVS) were amplified, subcloned, and sequenced.

Neuroprotection by Hsp104 and Hsp27 in lentiviral-based rat models of Huntington's disease.

Huntington's disease (HD) is an inherited neurodegenerative disorder caused by an expansion of glutamine repeats in the huntingtin (htt) protein. Abnormal protein folding and the accumulation of mutated htt are hallmarks of HD neuropathology. Heat-shock proteins (hsps), which refold denatured proteins, might therefore mitigate HD.

Progressive and selective striatal degeneration in primary neuronal cultures using lentiviral vector coding for a mutant huntingtin fragment.

A lentiviral vector expressing a mutant huntingtin protein (htt171-82Q) was used to generate a chronic model of Huntington's disease (HD) in rat primary striatal cultures. In this model, the majority of neurons expressed the transgene so that Western blot analysis and flow cytometry measurement could complement immunohistological evaluation. Mutant huntingtin produced a slowly progressing pathology characterized after 1 month by the appearance of neuritic aggregates followed by intranuclear inclusions, morphological anomalies of neurites, loss of neurofilament 160, increased expression in stress response protein Hsp70, and later loss of neuronal markers such as NeuN and MAP-2.

Akt is altered in an animal model of Huntington's disease and in patients.

The insulin-like growth factor I (IGF-1)/Akt pathway plays a crucial role in Huntington's disease by phosphorylating the causative protein, polyQ-huntingtin, and abolishing its toxic properties [Humbert et al. (2002)Dev. Cell, 2, 831-837; Rangone et al.