Unital quantum operators on the Bloch ball and Bloch region

For one qubit systems, we present a short, elementary argument characterizing unital quantum operators in terms of their action on Bloch vectors. We then show how our approach generalizes to multi-qubit systems, obtaining inequalities that govern when a ``diagonal'' superoperator on the Bloch region is a quantum operator. These inequalities are the n-qubit analogue of the Algoet-Fujiwara conditions. Our work is facilitated by an analysis of operator-sum decompositions in which negative summands are allowed.Comment: Revised and corrected, to appear in Physical Review

Entangling oscillators through environment noise

We consider two independent bosonic oscillators immersed in a common bath, evolving in time with a completely positive, markovian, quasi-free (Gaussian) reduced dynamics. We show that an initially separated Gaussian state can become entangled as a result of a purely noisy mechanism. In certain cases, the dissipative dynamics allows the persistence of these bath induced quantum correlations even in the asymptotic equilibrium state.Comment: 14 pages, plain-Te

Decoherence and entanglement degradation of a qubit-qutrit system in non-inertial frames

We study the effect of decoherence on a qubit-qutrit system under the influence of global, local and multilocal decoherence in non-inertial frames. We show that the entanglement sudden death can be avoided in non-inertial frames in the presence of amplitude damping, depolarizing and phase damping channels. However, degradation of entanglement is seen due to Unruh effect. It is shown that for lower level of decoherence, the depolarizing channel degrades the entanglement more heavily as compared to the amplitude damping and phase damping channels. However, for higher values of decoherence parameters, amplitude damping channel heavily degrades the entanglement of the hybrid system. Further more, no ESD is seen for any value of Rob's acceleration.Comment: 16 pages, 5 .eps figures, 1 table; Quantum Information Processing, published online, 5 July, 201

Biallelic <em>NDUFA13 </em>variants lead to a neurodevelopmental phenotype with gradual neurological impairment

\ua9 The Author(s) 2024.Biallelic variants in NADH (nicotinamide adenine dinucleotide (NAD) + hydrogen (H))-ubiquinone oxidoreductase 1 alpha subcomplex 13 have been linked to mitochondrial complex I deficiency, nuclear type 28, based on three affected individuals from two families. With only two families reported, the clinical and molecular spectrum of NADH-ubiquinone oxidoreductase 1 alpha subcomplex 13–related diseases remains unclear. We report 10 additional affected individuals from nine independent families, identifying four missense variants (including recurrent c.170G &gt; A) and three ultra-rare or novel predicted loss-of-function biallelic variants. Updated clinical–radiological data from previously reported families and a literature review compiling clinical features of all reported patients with isolated complex I deficiency caused by 43 genes encoding complex I subunits and assembly factors are also provided. Our cohort (mean age 7.8 \ub1 5.4 years; range 2.5–18) predominantly presented a moderate-to-severe neurodevelopmental syndrome with oculomotor abnormalities (84%), spasticity/hypertonia (83%), hypotonia (69%), cerebellar ataxia (66%), movement disorders (58%) and epilepsy (46%). Neuroimaging revealed bilateral symmetric T2 hyperintense substantia nigra lesions (91.6%) and optic nerve atrophy (66.6%). Protein modeling suggests missense variants destabilize a critical junction between the hydrophilic and membrane arms of complex I. Fibroblasts from two patients showed reduced complex I activity and compensatory complex IV activity increase. This study characterizes NADH-ubiquinone oxidoreductase 1 alpha subcomplex 13–related disease in 13 individuals, highlighting genotype–phenotype correlations

Mechanisms of extramedullary relapse in acute lymphoblastic leukemia Reconciling biological concepts and clinical issues

International audienceLong-term survival rates in childhood acute lymphoblastic leukemia (ALL) are currently above 85% due to huge improvements in treatment. However, 15-20% of children still experience relapses. Relapses can either occur in the bone marrow or at extramedullary sites, such as gonads or the central nervous system (CNS), formerly referred to as ALL-blast sanctuaries. The reason why ALL cells migrate to and stay in these sites is still unclear. In this review, we have attempted to assemble the evidence concerning the microenvironmental factors that could explain why ALL cells reside in such sites. We present criteria that make extramedullary leukemia niches and solid tumor metastatic niches comparable. Indeed, considering extramedullary leukemias as metastases could be a useful approach for proposing more effective treatments. In this context, we conclude with several examples of potential niche-based therapies which could be successfully added to current treatments of ALL

Hypoxia Regulates CD9 Expression and Migration of Lymphoblasts in Childhood B Acute Lymphoblastic Leukemia

International audienc