Trap-Assisted Complexes in Cold Atom-Ion Collisions.

We theoretically investigate the trap-assisted formation of complexes in atom-ion collisions and their impact on the stability of the trapped ion. The time-dependent potential of the Paul trap facilitates the formation of temporary complexes by reducing the energy of the atom, which gets temporarily stuck in the atom-ion potential. As a result, those complexes significantly impact termolecular reactions leading to molecular ion formation via three-body recombination. We find that complex formation is more pronounced in systems with heavy atoms, but the mass has no influence on the lifetime of the transient state. Instead, the complex formation rate strongly depends on the amplitude of the ion's micromotion. We also show that complex formation persists even in the case of a time-independent harmonic trap. In this case, we find higher formation rates and longer lifetimes than in Paul traps, indicating that the atom-ion complex plays an essential role in atom-ion mixtures in optical traps.

Observation of Chemical Reactions between a Trapped Ion and Ultracold Feshbach Dimers.

We measure chemical reactions between a single trapped ^{174}Yb^{+} ion and ultracold Li_{2} dimers. This produces LiYb^{+} molecular ions that we detect via mass spectrometry. We explain the reaction rates by modeling the dimer density as a function of the magnetic field and obtain excellent agreement when we assume the reaction to follow the Langevin rate. Our results present a novel approach towards the creation of cold molecular ions and point to the exploration of ultracold chemistry in ion molecule collisions. What is more, with a detection sensitivity below molecule densities of 10^{14} m^{-3}, we provide a new method to detect low-density molecular gases.

Trapped Ion Quantum Computing Using Optical Tweezers and Electric Fields.

We propose a new scalable architecture for trapped ion quantum computing that combines optical tweezers delivering qubit state-dependent local potentials with oscillating electric fields. Since the electric field allows for long-range qubit-qubit interactions mediated by the center-of-mass motion of the ion crystal alone, it is inherently scalable to large ion crystals. Furthermore, our proposed scheme does not rely on either ground-state cooling or the Lamb-Dicke approximation. We study the effects of imperfect cooling of the ion crystal, as well as the role of unwanted qubit-motion entanglement, and discuss the prospects of implementing the state-dependent tweezers in the laboratory.

Author Correction: Unifying scrambling, thermalization and entanglement through measurement of fidelity out-of-time-order correlators in the Dicke model.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Unifying scrambling, thermalization and entanglement through measurement of fidelity out-of-time-order correlators in the Dicke model.

Scrambling is the process by which information stored in local degrees of freedom spreads over the many-body degrees of freedom of a quantum system, becoming inaccessible to local probes and apparently lost. Scrambling and entanglement can reconcile seemingly unrelated behaviors including thermalization of isolated quantum systems and information loss in black holes. Here, we demonstrate that fidelity out-of-time-order correlators (FOTOCs) can elucidate connections between scrambling, entanglement, ergodicity and quantum chaos (butterfly effect). We compute FOTOCs for the paradigmatic Dicke model, and show they can measure subsystem Rényi entropies and inform about quantum thermalization. Moreover, we illustrate why FOTOCs give access to a simple relation between quantum and classical Lyapunov exponents in a chaotic system without finite-size effects. Our results open a path to experimental use FOTOCs to explore scrambling, bounds on quantum information processing and investigation of black hole analogs in controllable quantum systems.

Verification of a Many-Ion Simulator of the Dicke Model Through Slow Quenches across a Phase Transition.

We use a self-assembled two-dimensional Coulomb crystal of ∼70 ions in the presence of an external transverse field to engineer a simulator of the Dicke Hamiltonian, an iconic model in quantum optics which features a quantum phase transition between a superradiant (ferromagnetic) and a normal (paramagnetic) phase. We experimentally implement slow quenches across the quantum critical point and benchmark the dynamics and the performance of the simulator through extensive theory-experiment comparisons which show excellent agreement. The implementation of the Dicke model in fully controllable trapped ion arrays can open a path for the generation of highly entangled states useful for enhanced metrology and the observation of scrambling and quantum chaos in a many-body system.

Comparison of experimental and bioelectrical impedance analysis methods in calculation of dry weight in peritoneal dialysis patients.

BACKGROUND: To optimize dialysis prescription and fluid balance of the peritoneal dialysis (PD) patients, it is important to assess their dry weight accurately. The experimental evaluation is the method which is widely used in PD centers which needs continuous and controlled reduction of the postdialysis weight down to the point where patient does not show any signs of hypotension and volume overload. This study intends to indicate that the bioelectrical impedance analysis (BIA) method can be used as an alternative method to evaluate the dry weight. MATERIALS AND METHODS: The demographic data of 101 continuous ambulatory peritoneal dialysis (CAPD) patients of Alzahra and Noor hospitals of Isfahan University (50 males and 51 females) who had been referred for periodical examinations from April 2009 to April 2010 were extracted from their files. The normal body volume was selected as the inclusion criteria and identified by an examiner group (a nephrologist, a general practitioner and a PD nurse). The patients' dry weights were calculated based on both methods. The bioelectrical impedance analysis method was done by the Maltron Bioscan ver916 and data were analyzed by SPSS program ver18. RESULTS: There were 49.5% males and 50.5% females with the mean age of 54.6±17 years. The mean dry weight in the experimental method was 63.4±13.3 kg in comparison to the other (61.5± 13.7 kg). There was a significant difference between the results (P value <0.001) depended on the gender t-test, but there was a 98% correlation between the results by two methods. No correlation observed between the patient's age, body mass index, blood pressure, previous hemodialysis history, PD duration time, and underlying disease. CONCLUSION: The study showed that there is significant difference between the two methods. However, there was 98% direct correlation between them. It is concluded that bioelectrical impedance analysis could be a better alternative for accurate evaluation of dry weight in PD patients because it is a fast and cheap method and does not depend on examiner's capability. Further studies based on the results of this method are recommended to consider this method as the gold standard.

First-order phase transitions in optical lattices with tunable three-body onsite interaction.

We study the two-dimensional Bose-Hubbard model in the presence of a three-body interaction term, both at a mean-field level and via quantum Monte Carlo simulations. The three-body term is tuned by coupling the triply occupied states to a trapped universal trimer. We find that, for a sufficiently attractive three-body interaction, the n=2 Mott lobe disappears and the system displays first-order phase transitions separating the n=1 from the n=3 lobes and the n=1 and n=3 Mott insulator from the superfluid. We also analyze the effect of finite temperature and find that transitions are still of first order at temperatures T~J, where J is the hopping matrix element.

Human CoQ10 deficiencies.

Coenzyme Q10 (CoQ10 or ubiquinone) is a lipid-soluble component of virtually all cell membranes and has multiple metabolic functions. A major function of CoQ10 is to transport electrons from complexes I and II to complex III in the respiratory chain which resides in the mitochondrial inner membrane. Deficiencies of CoQ10 (MIM 607426) have been associated with four major clinical phenotypes: 1) encephalomyopathy characterized by a triad of recurrent myoglobinuria, brain involvement, and ragged-red fibers; 2) infantile multisystemic disease typically with prominent nephropathy and encephalopathy; 3) cerebellar ataxia with marked cerebellar atrophy; and 4) pure myopathy. Primary CoQ10 deficiencies due to mutations in ubiquinone biosynthetic genes (COQ2, PDSS1, PDSS2, and ADCK3 [CABC1]) have been identified in patients with the infantile multisystemic and cerebellar ataxic phenotypes. In contrast, secondary CoQ10 deficiencies, due to mutations in genes not directly related to ubiquinone biosynthesis (APTX, ETFDH, and BRAF), have been identified in patients with cerebellar ataxia, pure myopathy, and cardiofaciocutaneous syndrome. In many patients with CoQ10 deficiencies, the causative molecular genetic defects remain unknown; therefore, it is likely that mutations in additional genes will be identified as causes of CoQ10 deficiencies.

Pathogenic Lrrk2 substitutions and Amyotrophic lateral sclerosis.

Pathogenic Lrrk2 Y1699C substitution observed in a large German-Canadian kindred presents a neurodegenerative disorder that is reminiscent of amyotrophic lateral sclerosis and Parkinsonism-Dementia Complex. We screened 54 patients with ALS for seven known Lrrk2 pathogenic substitutions in the Roc, COR and kinase domains. No mutations were observed suggesting that this locus does not have a major influence on the ALS phenotype. However we can not rule out other genetic variation at the LRRK2 locus may play a role in parkinsonian disorders with amyotrophic lateral sclerosis and may be considered candidates for genetic screening.

Measurement of ATP production in mitochondrial disorders.

Mitochondrial diseases are a heterogeneous group of disorders caused by mutations in both nuclear DNA (nDNA) and mitochondrial DNA (mtDNA). Mitochondrial disease leads to impaired respiratory chain function and reduced ATP production. The aim of this study was to compare disturbances in mitochondrial function by measuring ATP synthesis in fibroblasts derived from patients with nDNA and mtDNA defects. Skin fibroblasts derived from 22 patients with either nDNA-related disorders (n = 8) or mtDNA-related disorders (n = 14) were analysed. ATP synthesis was markedly decreased in fibroblasts derived from patients with nDNA-related disorders but only variably so in patients with mtDNA mutations. In fibroblasts with the MELAS 3243A > G mutation, ATP synthesis correlated with mutant load. We believe that the observed differences in ATP production between cell lines derived from patients with nDNA-related disorders and mtDNA-related disorders may help in the assessment of patients with undiagnosed mitochondrial disease. The clinical comparisons observed in patients with nDNA- and mtDNA-related disorders may be explained by differences in the disturbance of ATP synthesis measured in the two conditions.

Coenzyme Q10 deficiency and isolated myopathy.

Three unrelated, sporadic patients with muscle coenzyme Q10 (CoQ10) deficiency presented at 32, 29, and 6 years of age with proximal muscle weakness and elevated serum creatine kinase (CK) and lactate levels, but without myoglobinuria, ataxia, or seizures. Muscle biopsy showed lipid storage myopathy, combined deficiency of respiratory chain complexes I and III, and CoQ10 levels below 50% of normal. Oral high-dose CoQ10 supplementation improved muscle strength dramatically and normalized serum CK.

Infantile encephalomyopathy and nephropathy with CoQ10 deficiency: a CoQ10-responsive condition.

Coenzyme Q10 (CoQ10) deficiency has been associated with various clinical phenotypes, including an infantile multisystem disorder. The authors report a 33-month-old boy who presented with corticosteroid-resistant nephrotic syndrome in whom progressive encephalomyopathy later developed. CoQ10 was decreased both in muscle and in fibroblasts. Oral CoQ10 improved the neurologic picture but not the renal dysfunction.

Coenzyme Q deficiency and cerebellar ataxia associated with an aprataxin mutation.

Primary muscle coenzyme Q10 (CoQ10) deficiency is an apparently autosomal recessive condition with heterogeneous clinical presentations. Patients with these disorders improve with CoQ10 supplementation. In a family with ataxia and CoQ10 deficiency, analysis of genome-wide microsatellite markers suggested linkage of the disease to chromosome 9p13 and led to identification of an aprataxin gene (APTX) mutation that causes ataxia oculomotor apraxia (AOA1 [MIM606350]). The authors' observations indicate that CoQ10 deficiency may contribute to the pathogenesis of AOA1.

Late-onset cerebellar ataxia with hypogonadism and muscle coenzyme Q10 deficiency.

Two brothers had late-onset progressive ataxia, cerebellar atrophy, and hypergonadotropic hypogonadism associated with coenzyme Q10 (CoQ10) deficiency in skeletal muscle. Both patients improved on high-dose CoQ10 supplementation, stressing the importance of CoQ10 deficiency in the differential diagnosis of cerebellar ataxia, even when onset is late.

Reversion of mtDNA depletion in a patient with TK2 deficiency.

Mutations in the thymidine kinase 2 (TK2) gene cause a myopathic form of the mitochondrial DNA depletion syndrome (MDS). Here, the authors report the unusual clinical, biochemical, and molecular findings in a 14-year-old patient in whom pathogenic mutations were identified in the TK2 gene. This report extends the phenotypic expression of primary TK2 deficiency and suggests that factors other than TK2 may modify expression of the clinical phenotype in patients with MDS syndrome.

Cerebellar ataxia and coenzyme Q10 deficiency.

The authors measured coenzyme Q10 (CoQ10) concentration in muscle biopsies from 135 patients with genetically undefined cerebellar ataxia. Thirteen patients with childhood-onset ataxia and cerebellar atrophy had markedly decreased levels of CoQ10. Associated symptoms included seizures, developmental delay, mental retardation, and pyramidal signs. These findings confirm the existence of an ataxic presentation of CoQ10 deficiency, which may be responsive to CoQ10 supplementation.

Mitochondrial DNA depletion: mutations in thymidine kinase gene with myopathy and SMA.

BACKGROUND: The mitochondrial DNA (mtDNA) depletion syndrome (MDS) is an autosomal recessive disorder of early childhood characterized by decreased mtDNA copy number in affected tissues. Recently, MDS has been linked to mutations in two genes involved in deoxyribonucleotide (dNTP) metabolism: thymidine kinase 2 (TK2) and deoxy-guanosine kinase (dGK). Mutations in TK2 have been associated with the myopathic form of MDS, and mutations in dGK with the hepatoencephalopathic form. OBJECTIVES: To further characterize the frequency and clinical spectrum of these mutations, the authors screened 20 patients with myopathic MDS. RESULTS: No patient had dGK gene mutations, but four patients from two families had TK2 mutations. Two siblings were compound heterozygous for a previously reported H90N mutation and a novel T77M mutation. The other siblings harbored a homozygous I22M mutation, and one of them had evidence of lower motor neuron disease. The pathogenicity of these mutations was confirmed by reduced TK2 activity in muscle (28% to 37% of controls). CONCLUSIONS: These results show that the clinical expression of TK2 mutations is not limited to myopathy and that the myopathic form of MDS is genetically heterogeneous.

Identification of a novel mutation in Cu/Zn superoxide dismutase gene associated with familial amyotrophic lateral sclerosis.

We report a new missense mutation (Ala140Gly) in exon 5 of the Cu/Zn superoxide dismutase (SOD-1) gene in a 73-year-old man with familial amyotrophic lateral sclerosis (FALS). The enzymatic activity of mutated SOD-1 measured in erythrocyte lysate was 70% of control. This heterozygote mutation, which is associated with the late onset of the disease, is located in the active site of the enzyme.

Biochemical studies of patients with Cuban epidemic neuropathy.

In 1992-1994, a disorder known as the epidemic neuropathy afflicted more than 50,000 Cubans. Three different forms of the illness were identified: epidemic optic neuropathy, peripheral neuropathy and mixed optic and peripheral neuropathy. The causes are still unknown. Skeletal muscle biopsy samples were analyzed by standard histological techniques and by biochemical assays. Elevated activities of citrate synthase, a non-respiratory-chain mitochondrial matrix enzyme, suggested possible mitochondrial proliferation in 7 of the 8 patients. Nicotinamide adenine dinucleotide phosphate (NADP(+)) levels were higher in the patients than in the controls (p = 0.04). Levels of nicotinamide adenine dinucleotide (NAD) and the reduced compounds NADH and NADPH were comparable in patients and controls. Elevations of succinate dehydrogenase and citrate synthase activities and high NADP(+) levels suggest that alterations of mitochondrial functions may be associated with this disorder.