Critical-point scaling function for the specific heat of a Ginzburg-Landau superconductor

If the zero-field transition in high temperature superconductors such as YBa_2Cu_3O_7-\delta is a critical point in the universality class of the 3-dimensional XY model, then the general theory of critical phenomena predicts the existence of a critical region in which thermodynamic functions have a characteristic scaling form. We report the first attempt to calculate the universal scaling function associated with the specific heat, for which experimental data have become available in recent years. Scaling behaviour is extracted from a renormalization-group analysis, and the 1/N expansion is adopted as a means of approximation. The estimated scaling function is qualitatively similar to that observed experimentally, and also to the lowest-Landau-level scaling function used by some authors to provide an alternative interpretation of the same data. Unfortunately, the 1/N expansion is not sufficiently reliable at small values of N for a quantitative fit to be feasible.Comment: 20 pages; 4 figure

Renormalization group and 1/N expansion for 3-dimensional Ginzburg-Landau-Wilson models

A renormalization-group scheme is developed for the 3-dimensional O($2N$)-symmetric Ginzburg-Landau-Wilson model, which is consistent with the use of a 1/N expansion as a systematic method of approximation. It is motivated by an application to the critical properties of superconductors, reported in a separate paper. Within this scheme, the infrared stable fixed point controlling critical behaviour appears at $z=0$, where $z=\lambda^{-1}$ is the inverse of the quartic coupling constant, and an efficient renormalization procedure consists in the minimal subtraction of ultraviolet divergences at $z=0$. This scheme is implemented at next-to-leading order, and the standard results for critical exponents calculated by other means are recovered. An apparently novel result of this non-perturbative method of approximation is that corrections to scaling (or confluent singularities) do not, as in perturbative analyses, appear as simple power series in the variable $y=zt^{\omega\nu}$. At least in three dimensions, the power series are modified by powers of $\ln y$.Comment: 20 pages; 5 figure

Theory of finite temperature crossovers near quantum critical points close to, or above, their upper-critical dimension

A systematic method for the computation of finite temperature ($T$) crossover functions near quantum critical points close to, or above, their upper-critical dimension is devised. We describe the physics of the various regions in the $T$ and critical tuning parameter ($t$) plane. The quantum critical point is at $T=0$, $t=0$, and in many cases there is a line of finite temperature transitions at $T = T_c (t)$, $t < 0$ with $T_c (0) = 0$. For the relativistic, $n$-component $\phi^4$ continuum quantum field theory (which describes lattice quantum rotor ($n \geq 2$) and transverse field Ising ($n=1$) models) the upper critical dimension is $d=3$, and for $d<3$, $\epsilon=3-d$ is the control parameter over the entire phase diagram. In the region $|T - T_c (t)| \ll T_c (t)$, we obtain an $\epsilon$ expansion for coupling constants which then are input as arguments of known {\em classical, tricritical,} crossover functions. In the high $T$ region of the continuum theory, an expansion in integer powers of $\sqrt{\epsilon}$, modulo powers of $\ln \epsilon$, holds for all thermodynamic observables, static correlators, and dynamic properties at all Matsubara frequencies; for the imaginary part of correlators at real frequencies ($\omega$), the perturbative $\sqrt{\epsilon}$ expansion describes quantum relaxation at $\hbar \omega \sim k_B T$ or larger, but fails for $\hbar \omega \sim \sqrt{\epsilon} k_B T$ or smaller. An important principle, underlying the whole calculation, is the analyticity of all observables as functions of $t$ at $t=0$, for $T>0$; indeed, analytic continuation in $t$ is used to obtain results in a portion of the phase diagram. Our method also applies to a large class of other quantum critical points and their associated continuum quantum field theories.Comment: 36 pages, 4 eps figure

Anthropogenic Space Weather

Anthropogenic effects on the space environment started in the late 19th century and reached their peak in the 1960s when high-altitude nuclear explosions were carried out by the USA and the Soviet Union. These explosions created artificial radiation belts near Earth that resulted in major damages to several satellites. Another, unexpected impact of the high-altitude nuclear tests was the electromagnetic pulse (EMP) that can have devastating effects over a large geographic area (as large as the continental United States). Other anthropogenic impacts on the space environment include chemical release ex- periments, high-frequency wave heating of the ionosphere and the interaction of VLF waves with the radiation belts. This paper reviews the fundamental physical process behind these phenomena and discusses the observations of their impacts.Comment: 71 pages, 35 figure

EXPRESS: Differential IL-1 signalling induced by BMPR2 deficiency drives pulmonary vascular remodelling

Background: Bone morphogenetic protein receptor type 2 (BMPR2) mutations are present in patients with heritable and idiopathic pulmonary arterial hypertension (PAH). Circulating levels of Interleukin-1 (IL-1) are raised in patients and animal models. Whether interplay between BMP and IL- 1 signalling can explain the local manifestation of PAH in the lung remains unclear. Methods: Cell culture, siRNA and mRNA microarray analysis of RNA isolated from human Pulmonary artery (PASMC) and Aortic (AoSMC) smooth muscle cells were used. R899X+/- BMPR2 transgenic mice fed western diet for six weeks were given daily injections of IL-1ß prior to assessment for PAH and tissue collection. Results: PASMC have reduced inflammatory activation in response to IL-1ß compared with AoSMCs, however PASMC with reduced BMPR2 demonstrated an exaggerated response. Mice treated with IL-1ß had higher white blood cell counts, and significantly raised serum protein levels of IL-6 and OPG plasma levels recapitulating in vitro data. Phenotypically, IL-1ß treated mice demonstrated increased pulmonary vascular remodelling. Conclusions: IL-1ß induces an exaggerated pulmonary artery specific transcriptomic inflammatory response when BMPR2 signalling is reduced

Identification of cardiac MRI thresholds for risk stratification in pulmonary arterial hypertension

Rationale: Pulmonary arterial hypertension (PAH) is a life-shortening condition. The European Society of Cardiology and European Respiratory Society and the REVEAL (North American Registry to Evaluate Early and Long-Term PAH Disease Management) risk score calculator (REVEAL 2.0) identify thresholds to predict 1-year mortality. Objectives: This study evaluates whether cardiac magnetic resonance imaging (MRI) thresholds can be identified and used to aid risk stratification and facilitate decision-making. Methods: Consecutive patients with PAH (n = 438) undergoing cardiac MRI were identified from the ASPIRE (Assessing the Spectrum of Pulmonary Hypertension Identified at a Referral Center) MRI database. Thresholds were identified from a discovery cohort and evaluated in a test cohort. Measurements and Main Results: A percentage-predicted right ventricular end-systolic volume index threshold of 227% or a left ventricular end-diastolic volume index of 58 ml/m2 identified patients at low (10%) risk of 1-year mortality. These metrics respectively identified 63% and 34% of patients as low risk. Right ventricular ejection fraction >54%, 37–54%, and <37% identified 21%, 43%, and 36% of patients at low, intermediate, and high risk, respectively, of 1-year mortality. At follow-up cardiac MRI, patients who improved to or were maintained in a low-risk group had a 1-year mortality <5%. Percentage-predicted right ventricular end-systolic volume index independently predicted outcome and, when used in conjunction with the REVEAL 2.0 risk score calculator or a modified French Pulmonary Hypertension Registry approach, improved risk stratification for 1-year mortality. Conclusions: Cardiac MRI can be used to risk stratify patients with PAH using a threshold approach. Percentage-predicted right ventricular end-systolic volume index can identify a high percentage of patients at low-risk of 1-year mortality and, when used in conjunction with current risk stratification approaches, can improve risk stratification. This study supports further evaluation of cardiac MRI in risk stratification in PAH

Altered macrophage polarization induces experimental pulmonary hypertension and is observed in patients with pulmonary arterial hypertension.

Objective: To determine whether global reduction of CD68 (cluster of differentiation) macrophages impacts the development of experimental pulmonary arterial hypertension (PAH) and whether this reduction affects the balance of pro- and anti-inflammatory macrophages within the lung. Additionally, to determine whether there is evidence of an altered macrophage polarization in patients with PAH. Approach and Results: Macrophage reduction was induced in mice via doxycycline-induced CD68-driven cytotoxic diphtheria toxin A chain expression (macrophage low [MacLow] mice). Chimeric mice were generated using bone marrow transplant. Mice were phenotyped for PAH by echocardiography and closed chest cardiac catheterization. Murine macrophage phenotyping was performed on lungs, bone marrow–derived macrophages, and alveolar macrophages using immunohistochemical and flow cytometry. Monocyte-derived macrophages were isolated from PAH patients and healthy volunteers and polarization capacity assessed morphologically and by flow cytometry. After 6 weeks of macrophage depletion, male but not female MacLow mice developed PAH. Chimeric mice demonstrated a requirement for both MacLow bone marrow and MacLow recipient mice to cause PAH. Immunohistochemical analysis of lung sections demonstrated imbalance in M1/M2 ratio in male MacLow mice only, suggesting that this imbalance may drive the PAH phenotype. M1/M2 imbalance was also seen in male MacLow bone marrow–derived macrophages and PAH patient monocyte-derived macrophages following stimulation with doxycycline and IL (interleukin)-4, respectively. Furthermore, MacLow-derived alveolar macrophages showed characteristic differences in terms of their polarization and expression of diphtheria toxin A chain following stimulation with doxycycline. Conclusions: These data further highlight a sex imbalance in PAH and further implicate immune cells into this paradigm. Targeting imbalance of macrophage population may offer a future therapeutic option

Express: The incremental shuttle walk test predicts mortality in non-group 1 pulmonary hypertension: results from the ASPIRE Registry.

Pulmonary hypertension (PH) is classified into 5 groups based on disease etiology but there is only limited information on the prognostic value of exercise testing in non-Group 1 PH. In Group 1 PH the incremental shuttle walking test (ISWT) distance has been shown to correlate with pulmonary hemodynamics and predict survival without a ceiling-effect. This study assessed the ISWT in non-group 1 PH. Data were retrieved from the ASPIRE registry (Assessing the Spectrum of Pulmonary hypertension Identified at a REferral centre) for consecutive patients diagnosed with PH. Patients were required to have been systematically assessed as Group 2-5 PH and to have a baseline ISWT within 3 months of cardiac catheterization. Patients were stratified according to incremental shuttle walk test distance (ISWD) and ISWT distance percent predicted (ISWD%pred). 479 patients with non-Group 1 PH were identified. ISWD and ISWD%pred correlated significantly with symptoms and hemodynamic severity. ISWD and ISWD%pred predicted survival with no ceiling-effect. The test was prognostic in Groups 2, 3 and 4. ISWD and ISWD%pred and change in ISWD and ISWD%pred at 1 year were all significant predictors of outcome. In patients with non-Group 1 PH the Incremental Shuttle Walk Test is a simple non-invasive test that is easy to perform, is predictive of survival at baseline and follow-up, reflects change and can be used in the assessment of PH of any etiology

Incremental Shuttle Walking Test Distance and Autonomic Dysfunction Predict Survival in Pulmonary Arterial Hypertension

Background To ensure effective monitoring of pulmonary arterial hypertension (PAH), a simple, reliable assessment of exercise capacity applicable over a range of disease severity is needed. The aim of this study was to assess the ability of the incremental shuttle walk test (ISWT) to correlate with disease severity, measure sensitivity to change, and predict survival in PAH. Methods We enrolled 418 treatment-naïve patients with PAH with baseline ISWT within 3 months of cardiac catheterization. Clinical validity and prognostic value of ISWT distance were assessed at baseline and 1 year. Results ISWT distance was found to correlate at baseline with World Health Organization functional class, Borg score, and hemodynamics without a ceiling effect (all p 18 beats/min, highest SBP, change in SBP, and 3-minute SBP ratio) were significant predictors of survival (all p < 0.05). Conclusions In patients with PAH, the ISWT is simple to perform, allows assessment of maximal exercise capacity, is sensitive to treatment effect, predicts outcome, and has no ceiling effect. Also, measures of autonomic function made post-exercise predict survival in PAH

Maximal exercise testing using the incremental shuttle walking test can be used to risk stratify patients with pulmonary arterial hypertension

Rationale: Exercise capacity predicts mortality in pulmonary arterial hypertension but limited data exist on the routine use of maximal exercise testing. Objectives: This study evaluates a simple to perform maximal test, the incremental shuttle walking test, and its utility in risk stratification in pulmonary arterial hypertension (PAH). Methods: Consecutive patients with pulmonary hypertension were identified from the ASPIRE registry (2001-2018). Thresholds for levels of risk were identified at baseline, tested at follow-up and incorporation into current risk stratification approaches assessed. Results: Of 4524 treatment-naïve patients with pulmonary hypertension who underwent maximal exercise testing 1,847 patients had PAH. A step-wise reduction in one-year-mortality was seen between levels 1 (≤30m; 32% mortality) and 7 (340-420m; 1% mortality) with no mortality for levels 8-12 (≥430m) in idiopathic and connective tissue disease related PAH. Thresholds derived at baseline of ≤180m (>10%; high-risk), 190-330m (5-10%; intermediate-risk) and ≥340m (<5%; low-risk of one-year mortality) were applied at follow-up and also accurately identified levels of risk. Thresholds were incorporated into the REVEAL 2.0 risk score calculator and French low-risk approach to risk stratification and distinct categories of risk remained. Conclusion: We have demonstrated that maximal exercise testing in PAH stratifies mortality-risk at baseline and follow-up. This study highlights the potential value of the incremental shuttle walking test as an alternative to the 6-minute-walk-test, combining some of the advantages of maximal exercise testing whilst maintaining the simplicity of a simple to perform field test