Heat transport in the XXZXXZ spin chain: from ballistic to diffusive regimes and dephasing enhancement

In this work we study the heat transport in an XXZ spin-1/2 Heisenberg chain with homogeneous magnetic field, incoherently driven out of equilibrium by reservoirs at the boundaries. We focus on the effect of bulk dephasing (energy-dissipative) processes in different parameter regimes of the system. The non-equilibrium steady state of the chain is obtained by simulating its evolution under the corresponding Lindblad master equation, using the time evolving block decimation method. In the absence of dephasing, the heat transport is ballistic for weak interactions, while being diffusive in the strongly-interacting regime, as evidenced by the heat-current scaling with the system size. When bulk dephasing takes place in the system, diffusive transport is induced in the weakly-interacting regime, with the heat current monotonically decreasing with the dephasing rate. In contrast, in the strongly-interacting regime, the heat current can be significantly enhanced by dephasing for systems of small size

Abnormalities of the ventilatory equivalent for carbon dioxide in patients with chronic heart failure

Introduction. The relation between minute ventilation (VE) and carbon dioxide production (VCO2) can be characterised by the instantaneous ratio of ventilation to carbon dioxide production, the ventilatory equivalent for CO2 (VEqCO2). We hypothesised that the time taken to achieve the lowest VEqCO2 (time to VEqCO2 nadir) may be a prognostic marker in patients with chronic heart failure (CHF). Methods. Patients and healthy controls underwent a symptom-limited, cardiopulmonary exercise test (CPET) on a treadmill to volitional exhaustion. Results. 423 patients with CHF (mean age 63±12 years; 80% males) and 78 healthy controls (62% males; age 61±11 years) were recruited. Time to VEqCO2 nadir was shorter in patients than controls (327±204 s versus 514±187 s; P=0.0001). Univariable predictors of all-cause mortality included peak oxygen uptake (X 2 =53.0), VEqCO2 nadir (X 2 =47.9), and time to VEqCO2 nadir (X 2 =24.0). In an adjusted Cox multivariable proportional hazards model, peak oxygen uptake (X 2 =16.7) and VEqCO2 nadir (X 2 =17.9) were the most significant independent predictors of all-cause mortality. Conclusion. The time to VEqCO2 nadir was shorter in patients with CHF than in normal subjects and was a predictor of subsequent mortality. © 2012 Lee Ingle et al

Effects of human recombinant growth hormone on exercise capacity, cardiac structure, and cardiac function in patients with adult-onset growth hormone deficiency

Objective Epidemiological studies suggest that adult-onset growth hormone deficiency (AGHD) might increase the risk of death from cardiovascular causes. Methods This was a 6-month double-blind, placebo-controlled, randomised, cross-over trial followed by a 6-month open-label phase. Seventeen patients with AGHD received either recombinant human growth hormone (rGH) (0.4 mg injection daily) or placebo for 12 weeks, underwent washout for 2 weeks, and were then crossed over to the alternative treatment for a further 12 weeks. Cardiac magnetic resonance imaging, echocardiography, and cardiopulmonary exercise testing were performed at baseline, 12 weeks, 26 weeks, and the end of the open phase (12 months). The results were compared with those of 16 age- and sex-matched control subjects. Results At baseline, patients with AGHD had a significantly higher systolic blood pressure, ejection fraction, and left ventricular mass than the control group, even when corrected for body surface area. Treatment with rGH normalised the insulin-like growth factor 1 concentration without an effect on exercise capacity, cardiac structure, or cardiac function. Conclusion Administration of rGH therapy for 6 to 9 months failed to normalise the functional and structural cardiac differences observed in patients with AGHD when compared with a control group

Severe loss-of-function mutations in the adrenocorticotropin receptor (ACTHR, MC2R) can be found in patients diagnosed with salt-losing adrenal hypoplasia

Objective: Familial glucocorticoid deficiency type I (FGD1) is a rare form of primary adrenal insufficiency resulting from recessive mutations in the ACTH receptor (MC2R, MC2R). Individuals with this condition typically present in infancy or childhood with signs and symptoms of cortisol insufficiency, but disturbances in the renin-angiotensin system, aldosterone synthesis or sodium homeostasis are not a well-documented association of FGD1. As ACTH stimulation has been shown to stimulate aldosterone release in normal controls, and other causes of hyponatraemia can occur in children with cortisol deficiency, we investigated whether MC2R changes might be identified in children with primary adrenal failure who were being treated for mineralocorticoid insufficiency. Design: Mutational analysis of MC2R by direct sequencing. Patients: Children (n = 22) who had been diagnosed with salt-losing forms of adrenal hypoplasia (19 isolated cases, 3 familial), and who were negative for mutations in DAX1 (NR0B1) and SF1 (NR5A1). Results: MC2R mutations were found in three individuals or kindred (I: homozygous S74I; II: novel compound heterozygous R146H/560delT; III: novel homozygous 579-581delTGT). These changes represent severely disruptive loss-of-function mutations in this G-protein coupled receptor, including the first reported homozygous frameshift mutation. The apparent disturbances in sodium homeostasis were mild, manifest at times of stress (e.g. infection, salt-restriction, heat), and likely resolved with time. Conclusions: MC2R mutations should be considered in children who have primary adrenal failure with apparent mild disturbances in renin-sodium homeostasis. These children may have been misdiagnosed as having salt-losing adrenal hypoplasia. Making this diagnosis has important implications for treatment, counselling and long-term prognosi

Measuring failed disruption propagation in genetic programming

Information theory explains the robustness of deep GP trees, with on average up to 83.3% of crossover run time disruptions failing to propagate to the root node, and so having no impact on fitness, leading to phenotypic convergence. Monte Carlo simulations of perturbations covering the whole tree demonstrate a model based on random synchronisation of the evaluation of the parent and child which cause parent and offspring evaluations to be identical. This predicts the effectiveness of fitness measurement grows slowly as O(log(n)) with number n of test cases. This geometric distribution model is tested on genetic programming symbolic regression

Sle1 (\u3cem\u3eaaa\u3c/em\u3e) and Alpha Hemolysin (\u3cem\u3ehla\u3c/em\u3e) \u3cem\u3eStaphylococcus aureus\u3c/em\u3e Antigens as a Potential Vaccine for Cows

Knowledge of Staphylococcus aureus is essential to understanding how this pathogen causes different types of infections in humans. It can cause skin superficial infections and gastroenteritis. It can also cause infections in the joints and wounds, therefore causing humans to be severely ill by causing sepsis or infection in the blood. It is also very commonly antibiotic-resistant. In the lab, we are working with this priority pathogen because of antibiotic resistance. Cows can get S. aureus from humans, and it causes mastitis. This affects the dairy industry which is very important in the United States, but also specifically important in Idaho. We are making our vaccine through what\u27s called a chimera, we are fusing antigen proteins from S. aureus to cholera toxin (CT). The antigens we are using is Aaa/Sle1; a peptidoglycan hydrolase and adhesin, and Hla, a hemolytic pore protein. We have performed PCR and cloned this gene into a vector for chimera expression. The importance of this research is to improve productivity and quality of life by preventing S. aureus in cows. Everything that we learn about developing a vaccine for a cow can also translate to developing a vaccine for humans