Implications of Electronics Constraints for Solid-State Quantum Error Correction and Quantum Circuit Failure Probability

In this paper we present the impact of classical electronics constraints on a solid-state quantum dot logical qubit architecture. Constraints due to routing density, bandwidth allocation, signal timing, and thermally aware placement of classical supporting electronics significantly affect the quantum error correction circuit's error rate. We analyze one level of a quantum error correction circuit using nine data qubits in a Bacon-Shor code configured as a quantum memory. A hypothetical silicon double quantum dot quantum bit (qubit) is used as the fundamental element. A pessimistic estimate of the error probability of the quantum circuit is calculated using the total number of gates and idle time using a provably optimal schedule for the circuit operations obtained with an integer program methodology. The micro-architecture analysis provides insight about the different ways the electronics impact the circuit performance (e.g., extra idle time in the schedule), which can significantly limit the ultimate performance of any quantum circuit and therefore is a critical foundation for any future larger scale architecture analysis.Comment: 10 pages, 7 figures, 3 table

Vascular endothelial growth factor (VEGF) fails to improve blood flow and to promote collateralization in a diabetic mouse ischemic hindlimb model

BACKGROUND: Angiogenic therapy with vascular endothelial growth factor (VEGF) has been proposed as a treatment paradigm for patients suffering from an insufficiency of collateral vessels. Diabetes is associated with increase in the production of VEGF and therefore additional VEGF may not be beneficial. Accordingly, we sought to determine the efficacy of VEGF therapy to augment collateral formation and tissue perfusion in a diabetic mouse ischemic hindlimb model. METHODS: Diabetic and non-diabetic mice were studied in parallel for the efficacy of VEGF administration. Diabetes was induced with streptozotocin. Hindlimb ischemia was produced by severing the left iliac artery. An outlet tube from an osmotic infusion pump with placebo/ 500 micrograms of plasmid-DNA encoding VEGF was fenestrated and tunneled into the left quadriceps muscle. RESULTS: VEGF induced more rapid and complete restoration of blood flow in normal mice. However, in the setting of diabetes there was no difference between VEGF Vs. placebo in the rate or adequacy of flow restoration. There was a significant increase in smooth muscle actin and Factor-VIII antigen densities in diabetic animals and in animals which received VEGF. CONCLUSIONS: Angiogenic therapy with VEGF in the setting of diabetes does not appear to have the beneficial effects seen in the absence of diabetes

Haptoglobin genotype is a determinant of survival and cardiac remodeling after myocardial infarction in diabetic mice

<p>Abstract</p> <p>Background</p> <p>We have recently demonstrated in man that a functional allelic polymorphism in the Haptoglobin (Hp) gene plays a major role in determining survival and congestive heart failure after myocardial infarction (MI). We sought to recapitulate the effect of Hp type on outcomes and cardiac remodeling after MI in transgenic mice.</p> <p>Methods</p> <p>The Hp 2 allele exists only in man. Wild type C57Bl/6 mice carry the Hp 1 allele with high homology to the human Hp 1 allele. We genetically engineered a murine Hp 2 allele and targeted its insertion by homologous recombination to the murine Hp locus to create Hp 2 mice. Diabetes Mellitus (DM) was induced with streptozotocin. MI was produced by occlusion of the left anterior descending artery in DM C57Bl/6 mice carrying the Hp 1 or Hp 2 allele. MI size was determined with TTC staining. Left ventricular (LV) function and dimensions were assessed by 2-dimensional echocardiography.</p> <p>Results</p> <p>In the absence of DM, Hp 1-1 and Hp 2-2 mice had similar LV dimensions and LV function. MI size was similar in DM Hp 1-1 and 2-2 mice 24 hours after MI (50.2 ± 2.1%and 46.9 ± 5.5%, respectively, p = 0.6). However, DM Hp 1-1 mice had a significantly lower mortality rate than DM Hp 2-2 mice 30 days after MI (HR 0.41, 95% CI (0.19–0.95), p = 0.037 by log rank). LV chamber dimensions were significantly increased in DM Hp 2-2 mice compared to DM Hp 1-1 mice 30 days after MI (0.196 ± 0.01 cm²vs. 0.163 ± 0.01 cm², respectively; p = 0.029).</p> <p>Conclusion</p> <p>In DM mice the Hp 2-2 genotype is associated with increased mortality and more severe cardiac remodeling 30 days after MI.</p

The global carbon budget 1959-2011

Accurate assessments of anthropogenic carbon dioxide (CO2) emissions and their redistribution among the atmosphere, ocean, and terrestrial biosphere is important to better understand the global carbon cycle, support the climate policy process, and project future climate change. Present-day analysis requires the combination of a range of data, algorithms, statistics and model estimates and their interpretation by a broad scientific community. Here we describe datasets and a methodology developed by the global carbon cycle science community to quantify all major components of the global carbon budget, including their uncertainties. We discuss changes compared to previous estimates, consistency within and among components, and methodology and data limitations. CO2 emissions from fossil fuel combustion and cement production (EFF) are based on energy statistics, while emissions from Land-Use Change (ELUC), including deforestation, are based on combined evidence from land cover change data, fire activity in regions undergoing deforestation, and models. The global atmospheric CO2 concentration is measured directly and its rate of growth (GATM) is computed from the concentration. The mean ocean CO2 sink (SOCEAN) is based on observations from the 1990s, while the annual anomalies and trends are estimated with ocean models. Finally, the global residual terrestrial CO2 sink (SLAND) is estimated by the difference of the other terms. For the last decade available (2002–2011), EFF was 8.3 &pm; 0.4 PgC yr−1, ELUC 1.0 &pm; 0.5 PgC yr−1, GATM 4.3 &pm; 0.1PgC yr−1, SOCEAN 2.5 &pm; 0.5 PgC yr−1, and SLAND 2.6 &pm; 0.8 PgC yr−1. For year 2011 alone, EFF was 9.5 &pm; 0.5 PgC yr−1, 3.0 percent above 2010, reflecting a continued trend in these emissions; ELUC was 0.9 &pm; 0.5 PgC yr−1, approximately constant throughout the decade; GATM was 3.6 &pm; 0.2 PgC yr−1, SOCEAN was 2.7 &pm; 0.5 PgC yr−1, and SLAND was 4.1 &pm; 0.9 PgC yr−1. GATM was low in 2011 compared to the 2002–2011 average because of a high uptake by the land probably in response to natural climate variability associated to La Niña conditions in the Pacific Ocean. The global atmospheric CO2 concentration reached 391.31 &pm; 0.13 ppm at the end of year 2011. We estimate that EFF will have increased by 2.6% (1.9–3.5%) in 2012 based on projections of gross world product and recent changes in the carbon intensity of the economy. All uncertainties are reported as &pm;1 sigma (68% confidence assuming Gaussian error distributions that the real value lies within the given interval), reflecting the current capacity to characterise the annual estimates of each component of the global carbon budget. This paper is intended to provide a baseline to keep track of annual carbon budgets in the future

The effect of the systemic inflammatory response on plasma vitamin 25 (OH) D concentrations adjusted for albumin

&lt;b&gt;Aim&lt;/b&gt;&lt;p&gt;&lt;/p&gt; To examine the relationship between plasma 25(OH)D, CRP and albumin concentrations in two patient cohorts.&lt;p&gt;&lt;/p&gt; &lt;b&gt;Methods&lt;/b&gt;&lt;p&gt;&lt;/p&gt; 5327 patients referred for nutritional assessment and 117 patients with critical illness were examined. Plasma 25 (OH) D concentrations were measured using standard methods. Intra and between assay imprecision was &#60;10%.&lt;p&gt;&lt;/p&gt; &lt;b&gt;Result&lt;/b&gt;&lt;p&gt;&lt;/p&gt; In the large cohort, plasma 25 (OH) D was significantly associated with CRP (rs = −0.113, p&#60;0.001) and albumin (rs = 0.192, p&#60;0.001). 3711 patients had CRP concentrations ≤10 mg/L; with decreasing albumin concentrations ≥35, 25–34 and &#60;25 g/l, median concentrations of 25 (OH) D were significantly lower from 35 to 28 to 14 nmol/l (p&#60;0.001). This decrease was significant when albumin concentrations were reduced between 25–34 g/L (p&#60;0.001) and when albumin &#60;25 g/L (p&#60;0.001). 1271 patients had CRP concentrations between 11–80 mg/L; with decreasing albumin concentrations ≥35, 25–34 and &#60;25 g/l, median concentrations of 25 (OH) D were significantly lower from 31 to 24 to 19 nmol/l (p&#60;0.001). This decrease was significant when albumin concentration were 25–34 g/L (p&#60;0.001) and when albumin &#60;25 g/L (p&#60;0.001). 345 patients had CRP concentrations &#62;80 mg/L; with decreasing albumin concentrations ≥35, 25–34 and &#60;25 g/l, median concentrations of 25 (OH) D were not significantly altered varying from 19 to 23 to 23 nmol/l. Similar relationships were also obtained in the cohort of patients with critical illness.&lt;p&gt;&lt;/p&gt; &lt;b&gt;Conclusion&lt;/b&gt;&lt;p&gt;&lt;/p&gt; Plasma concentrations of 25(OH) D were independently associated with both CRP and albumin and consistent with the systemic inflammatory response as a major confounding factor in determining vitamin D status.&lt;p&gt;&lt;/p&gt

Coherent Electron Transport by Adiabatic Passage in an Imperfect Donor Chain

Coherent Tunneling Adiabatic Passage (CTAP) has been proposed as a long-range physical qubit transport mechanism in solid-state quantum computing architectures. Although the mechanism can be implemented in either a chain of quantum dots or donors, a 1D chain of donors in Si is of particular interest due to the natural confining potential of donors that can in principle help reduce the gate densities in solid-state quantum computing architectures. Using detailed atomistic modeling, we investigate CTAP in a more realistic triple donor system in the presence of inevitable fabrication imperfections. In particular, we investigate how an adiabatic pathway for CTAP is affected by donor misplacements, and propose schemes to correct for such errors. We also investigate the sensitivity of the adiabatic path to gate voltage fluctuations. The tight-binding based atomistic treatment of straggle used here may benefit understanding of other donor nanostructures, such as donor-based charge and spin qubits. Finally, we derive an effective 3 × 3 model of CTAP that accurately resembles the voltage tuned lowest energy states of the multi-million atom tight-binding simulations, and provides a translation between intensive atomistic Hamiltonians and simplified effective Hamiltonians while retaining the relevant atomic-scale information. This method can help characterize multi-donor experimental structures quickly and accurately even in the presence of imperfections, overcoming some of the numeric intractabilities of finding optimal eigenstates for non-ideal donor placements

Haptoglobin phenotype is an independent risk factor for cardiovascular disease in individuals with diabetes the strong heart study

AbstractObjectivesThe goal of this study was to determine if the haptoglobin phenotype was predictive of cardiovascular disease (CVD) in diabetic mellitus (DM).BackgroundCardiovascular disease is the most frequent, severe, and costly complication of type 2 DM. There are clear geographic and ethnic differences in the risk of CVD among diabetic patients that cannot be fully explained by differences in conventional CVD risk factors. We have demonstrated that a functional allelic polymorphism in the haptoglobin gene acts as a major determinant of susceptibility for the development of diabetic microvascular complications.MethodsWe sought to determine if this paradigm concerning the haptoglobin gene could be extended to CVD in DM. We tested this hypothesis in a case-control sample from the Strong Heart study, a population-based longitudinal study of CVD in American Indians. Haptoglobin phenotype was determined by polyacrylamide gel electrophoresis in 206 CVD cases and 206 matched controls age 45 to 74 years. Median follow-up was six years.ResultsIn multivariate analyses controlling for conventional CVD risk factors, haptoglobin phenotype was a highly statistically significant, independent predictor of CVD in DM. The odds ratio of having CVD in DM with the haptoglobin 2-2 phenotype was 5.0 times greater than in DM with the haptoglobin 1-1 phenotype (p = 0.002). An intermediate risk of CVD was associated with the haptoglobin 2-1 phenotype.ConclusionsThis study suggests that determination of haptoglobin phenotype may contribute to the algorithm used in CVD risk stratification, and in evaluation of new therapies to prevent CVD in the diabetic patient

Haptoglobin Genotype and the Rate of Renal Function Decline in the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Study

Many patients with type 1 diabetes develop renal disease despite moderately good metabolic control, suggesting other risk factors may play a role. Recent evidence suggests that the haptoglobin (HP) 2-2 genotype, which codes for a protein with reduced antioxidant activity, may predict renal function decline in type 1 diabetes. We examined this hypothesis in 1,303 Caucasian participants in the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) study. HP genotype was determined by polyacrylamide gel electrophoresis. Glomerular filtration rate was estimated by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation and albumin excretion based on timed urine samples. Participants were followed up for a mean of 22 years. HP genotype was significantly associated with the development of sustained estimated glomerular filtration rate (GFR) \u3c60 mL/min/1.73 m2and with end-stage renal disease (ESRD), with HP 2-2 having greater risk than HP 2-1 and 1-1. No association was seen with albuminuria. Although there was no treatment group interaction, the associations were only significant in the conventional treatment group, where events rates were much higher. We conclude that the HP genotype is significantly associated with the development of reduced GFR and ESRD in the DCCT/EDIC study

Haptoglobin genotype predicts development of coronary artery calcification in a prospective cohort of patients with type 1 diabetes

<p>Abstract</p> <p>Background</p> <p>Coronary artery disease has been linked with genotypes for haptoglobin (Hp) which modulates extracorpuscular hemoglobin. We hypothesized that the Hp genotype would predict progression of coronary artery calcification (CAC), a marker of subclinical atherosclerosis.</p> <p>Methods</p> <p>CAC was measured three times in six years among 436 subjects with type 1 diabetes and 526 control subjects participating in the Coronary Artery Calcification in Type 1 Diabetes (CACTI) study. Hp typing was performed on plasma samples by polyacrylamide gel electrophoresis.</p> <p>Results</p> <p>The Hp 2-2 genotype predicted development of significant CAC only in subjects with diabetes who were free of CAC at baseline (OR: 1.95, 95% CI: 1.07-3.56, p = 0.03), compared to those without the Hp 2-2 genotype, controlling for age, sex, blood pressure and HDL-cholesterol. Hp 2 appeared to have an allele-dose effect on development of CAC. Hp genotype did not predict CAC progression in individuals without diabetes.</p> <p>Conclusions</p> <p>Hp genotype may aid prediction of accelerated coronary atherosclerosis in subjects with type 1 diabetes.</p