Variational QMC study of a Hydrogen atom in jellium with comparison to LSDA and LSDA-SIC solutions

A Hydrogen atom immersed in a finite jellium sphere is solved using variational quantum Monte Carlo (VQMC). The same system is also solved using density functional theory (DFT), in both the local spin density (LSDA) and self-interaction correction (SIC) approximations. The immersion energies calculated using these methods, as functions of the background density of the jellium, are found to lie within 1eV of each other with minima in approximately the same positions. The DFT results show overbinding relative to the VQMC result. The immersion energies also suggest an improved performance of the SIC over the LSDA relative to the VQMC results. The atom-induced density is also calculated and shows a difference between the methods, with a more extended Friedel oscillation in the case of the VQMC result.Comment: 16 pages, 9 Postscript figure

A Joint Search for Gravitational Wave Bursts with AURIGA and LIGO

The first simultaneous operation of the AURIGA detector and the LIGO observatory was an opportunity to explore real data, joint analysis methods between two very different types of gravitational wave detectors: resonant bars and interferometers. This paper describes a coincident gravitational wave burst search, where data from the LIGO interferometers are cross-correlated at the time of AURIGA candidate events to identify coherent transients. The analysis pipeline is tuned with two thresholds, on the signal-to-noise ratio of AURIGA candidate events and on the significance of the cross-correlation test in LIGO. The false alarm rate is estimated by introducing time shifts between data sets and the network detection efficiency is measured with simulated signals with power in the narrower AURIGA band. In the absence of a detection, we discuss how to set an upper limit on the rate of gravitational waves and to interpret it according to different source models. Due to the short amount of analyzed data and to the high rate of non-Gaussian transients in the detectors noise at the time, the relevance of this study is methodological: this was the first joint search for gravitational wave bursts among detectors with such different spectral sensitivity and the first opportunity for the resonant and interferometric communities to unify languages and techniques in the pursuit of their common goal.Comment: 18 pages, IOP, 12 EPS figure

Searching for a Stochastic Background of Gravitational Waves with LIGO

The Laser Interferometer Gravitational-wave Observatory (LIGO) has performed the fourth science run, S4, with significantly improved interferometer sensitivities with respect to previous runs. Using data acquired during this science run, we place a limit on the amplitude of a stochastic background of gravitational waves. For a frequency independent spectrum, the new limit is $\Omega_{\rm GW} < 6.5 \times 10^{-5}$. This is currently the most sensitive result in the frequency range 51-150 Hz, with a factor of 13 improvement over the previous LIGO result. We discuss complementarity of the new result with other constraints on a stochastic background of gravitational waves, and we investigate implications of the new result for different models of this background.Comment: 37 pages, 16 figure

Glucose transporter-1 deficiency syndrome: the expanding clinical and genetic spectrum of a treatable disorder

Glucose transporter-1 deficiency syndrome is caused by mutations in the SLC2A1 gene in the majority of patients and results in impaired glucose transport into the brain. From 2004-2008, 132 requests for mutational analysis of the SLC2A1 gene were studied by automated Sanger sequencing and multiplex ligation-dependent probe amplification. Mutations in the SLC2A1 gene were detected in 54 patients (41%) and subsequently in three clinically affected family members. In these 57 patients we identified 49 different mutations, including six multiple exon deletions, six known mutations and 37 novel mutations (13 missense, five nonsense, 13 frame shift, four splice site and two translation initiation mutations). Clinical data were retrospectively collected from referring physicians by means of a questionnaire. Three different phenotypes were recognized: (i) the classical phenotype (84%), subdivided into early-onset (<2 years) (65%) and late-onset (18%); (ii) a non-classical phenotype, with mental retardation and movement disorder, without epilepsy (15%); and (iii) one adult case of glucose transporter-1 deficiency syndrome with minimal symptoms. Recognizing glucose transporter-1 deficiency syndrome is important, since a ketogenic diet was effective in most of the patients with epilepsy (86%) and also reduced movement disorders in 48% of the patients with a classical phenotype and 71% of the patients with a non-classical phenotype. The average delay in diagnosing classical glucose transporter-1 deficiency syndrome was 6.6 years (range 1 month-16 years). Cerebrospinal fluid glucose was below 2.5 mmol/l (range 0.9-2.4 mmol/l) in all patients and cerebrospinal fluid : blood glucose ratio was below 0.50 in all but one patient (range 0.19-0.52). Cerebrospinal fluid lactate was low to normal in all patients. Our relatively large series of 57 patients with glucose transporter-1 deficiency syndrome allowed us to identify correlations between genotype, phenotype and biochemical data. Type of mutation was related to the severity of mental retardation and the presence of complex movement disorders. Cerebrospinal fluid : blood glucose ratio was related to type of mutation and phenotype. In conclusion, a substantial number of the patients with glucose transporter-1 deficiency syndrome do not have epilepsy. Our study demonstrates that a lumbar puncture provides the diagnostic clue to glucose transporter-1 deficiency syndrome and can thereby dramatically reduce diagnostic delay to allow early start of the ketogenic die

Using Mixed Methods to Examine the Role of Veterans\u27 Illness Perceptions on Depression Treatment Utilization and HEDIS Concordance

BACKGROUND: Although depression screening occurs annually in the Department of Veterans Affairs (VA) primary care, many veterans may not be receiving guideline-concordant depression treatment. OBJECTIVES: To determine whether veterans\u27 illness perceptions of depression may be serving as barriers to guideline-concordant treatment. RESEARCH DESIGN: We used a prospective, observational design involving a mailed questionnaire and chart review data collection to assess depression treatment utilization and concordance with Healthcare Effectiveness Data and Information Set guidelines adopted by the VA. The Self-Regulation Model of Illness Behavior guided the study. SUBJECTS: Veterans who screened positive for a new episode of depression at 3 VA primary care clinics in the US northeast. MEASURES: The Illness Perceptions Questionnaire-Revised, measuring patients\u27 perceptions of their symptoms, cause, timeline, consequences, cure or controllability, and coherence of depression and its symptoms, was our primary measure to calculate veterans\u27 illness perceptions. Treatment utilization was assessed 3 months after the positive depression screen through chart review. Healthcare Effectiveness Data and Information Set (HEDIS) guideline-concordant treatment was determined according to a checklist created for the study. RESULTS: A total of 839 veterans screened positive for a new episode of depression from May 2009-June 2011; 275 (32.8%) completed the survey. Ninety-two (33.9%) received HEDIS guideline-concordant depression treatment. Veterans\u27 illness perceptions of their symptoms, cause, timeline, and controllability of depression predicted receiving guideline-concordant treatment. CONCLUSIONS: Many veterans are not receiving guideline-concordant treatment for depression. HEDIS guideline measures may not be assessing all aspects of quality depression care. Conversations about veterans\u27 illness perceptions and their specific needs are encouraged to ensure that appropriate treatment is achieved

Glucose transporter-1 deficiency syndrome: the expanding clinical and genetic spectrum of a treatable disorder

Glucose transporter-1 deficiency syndrome is caused by mutations in the SLC2A1 gene in the majority of patients and results in impaired glucose transport into the brain. From 2004–2008, 132 requests for mutational analysis of the SLC2A1 gene were studied by automated Sanger sequencing and multiplex ligation-dependent probe amplification. Mutations in the SLC2A1 gene were detected in 54 patients (41%) and subsequently in three clinically affected family members. In these 57 patients we identified 49 different mutations, including six multiple exon deletions, six known mutations and 37 novel mutations (13 missense, five nonsense, 13 frame shift, four splice site and two translation initiation mutations). Clinical data were retrospectively collected from referring physicians by means of a questionnaire. Three different phenotypes were recognized: (i) the classical phenotype (84%), subdivided into early-onset (&lt;2 years) (65%) and late-onset (18%); (ii) a non-classical phenotype, with mental retardation and movement disorder, without epilepsy (15%); and (iii) one adult case of glucose transporter-1 deficiency syndrome with minimal symptoms. Recognizing glucose transporter-1 deficiency syndrome is important, since a ketogenic diet was effective in most of the patients with epilepsy (86%) and also reduced movement disorders in 48% of the patients with a classical phenotype and 71% of the patients with a non-classical phenotype. The average delay in diagnosing classical glucose transporter-1 deficiency syndrome was 6.6 years (range 1 month–16 years). Cerebrospinal fluid glucose was below 2.5 mmol/l (range 0.9–2.4 mmol/l) in all patients and cerebrospinal fluid : blood glucose ratio was below 0.50 in all but one patient (range 0.19–0.52). Cerebrospinal fluid lactate was low to normal in all patients. Our relatively large series of 57 patients with glucose transporter-1 deficiency syndrome allowed us to identify correlations between genotype, phenotype and biochemical data. Type of mutation was related to the severity of mental retardation and the presence of complex movement disorders. Cerebrospinal fluid : blood glucose ratio was related to type of mutation and phenotype. In conclusion, a substantial number of the patients with glucose transporter-1 deficiency syndrome do not have epilepsy. Our study demonstrates that a lumbar puncture provides the diagnostic clue to glucose transporter-1 deficiency syndrome and can thereby dramatically reduce diagnostic delay to allow early start of the ketogenic die