Resistive reduced MHD modeling of multi-edge-localized-mode cycles in Tokamak X-point plasmas.

The full dynamics of a multi-edge-localized-mode (ELM) cycle is modeled for the first time in realistic tokamak X-point geometry with the nonlinear reduced MHD code jorek. The diamagnetic rotation is found to be instrumental to stabilize the plasma after an ELM crash and to model the cyclic reconstruction and collapse of the plasma pressure profile. ELM relaxations are cyclically initiated each time the pedestal gradient crosses a triggering threshold. Diamagnetic drifts are also found to yield a near-symmetric ELM power deposition on the inner and outer divertor target plates, consistent with experimental measurements.

Mechanism of edge localized mode mitigation by resonant magnetic perturbations.

A possible mechanism of edge localized modes (ELMs) mitigation by resonant magnetic perturbations (RMPs) is proposed based on the results of nonlinear resistive magnetohydrodynamic modeling using the jorek code, realistic JET-like plasma parameters and an RMP spectrum of JET error-field correction coils (EFCC) with a main toroidal number n=2 were used in the simulations. Without RMPs, a large ELM relaxation is obtained mainly due to the most unstable medium-n ballooning mode. The externally imposed RMP drives nonlinearly the modes coupled to n=2 RMP which produce small multimode relaxations, mitigated ELMs. The modes driven by RMPs exhibit a tearinglike structure and produce additional islands. Mitigated ELMs deposit energy into the divertor mainly in the structures ("footprints") created by n=2 RMPs, however, slightly modulated by other nonlinearly driven even harmonics. The divertor power flux during a ELM phase mitigated by RMPs is reduced almost by a factor of 10. The mechanism of ELM mitigation by RMPs proposed here reproduces generic features of high collisionality RMP experiments, where large ELMs are replaced by small, much more frequent ELMs or magnetic turbulence. Total ELM suppression was also demonstrated in modeling at higher RMP amplitude.

Unraveling quasiperiodic relaxations of transport barriers with gyrokinetic simulations of tokamak plasmas.

The generation and dynamics of transport barriers governed by sheared poloidal flows are analyzed in flux-driven 5D gyrokinetic simulations of ion temperature gradient driven turbulence in tokamak plasmas. The transport barrier is triggered by a vorticity source that polarizes the system. The chosen source captures characteristic features of some experimental scenarios, namely, the generation of a sheared electric field coupled to anisotropic heating. For sufficiently large shearing rates, turbulent transport is suppressed and a transport barrier builds up, in agreement with the common understanding of transport barriers. The vorticity source also governs a secondary instability--driven by the temperature anisotropy (T(∥)≠T(⊥)). Turbulence and its associated zonal flows are generated in the vicinity of the barrier, destroying the latter due to the screening of the polarization source by the zonal flows. These barrier relaxations occur quasiperiodically, and generically result from the decoupling between the dynamics of the barrier generation, triggered by the source driven sheared flow, and that of the crash, triggered by the secondary instability. This result underlines that barriers triggered by sheared flows are prone to relaxations whenever secondary instabilities come into play.

Impact of energetic-particle-driven geodesic acoustic modes on turbulence.

The impact on turbulent transport of geodesic acoustic modes excited by energetic particles is evidenced for the first time in flux-driven 5D gyrokinetic simulations using the Gysela code. Energetic geodesic acoustic modes (EGAMs) are excited in a regime with a transport barrier in the outer radial region. The interaction between EGAMs and turbulence is such that turbulent transport can be enhanced in the presence of EGAMs, with the subsequent destruction of the transport barrier. This scenario could be particularly critical in those plasmas, such as burning plasmas, exhibiting a rich population of suprathermal particles capable of exciting energetic modes.

Prolonged low-dose dopamine infusion induces a transient improvement in renal function in hemodynamically stable, critically ill patients: a single-blind, prospective, controlled study.

OBJECTIVE: To evaluate the length of the effects of long-term (48 hrs), low-dose dopamine infusion on both renal function and systemic hemodynamic variables in stable nonoliguric critically ill patients. DESIGN: Prospective, single-blind, controlled clinical study. SETTING: University hospital, 19-bed multidisciplinary intensive care unit. PATIENTS: Eight hemodynamically stable, critically ill patients with a mild nonoliguric renal impairment (creatinine clearance between 30 and 80 mL/min). INTERVENTIONS: Each patient consecutively received 4 hrs of placebo, followed by a 3 microg/kg/min dopamine infusion during 48 hrs, then a new 4-hr placebo period. We measured cardiac output and other hemodynamic variables by using a pulmonary artery catheter. The bladder was emptied to determine urine volume and to collect urine samples. Measurements were performed at six times: after the initial control of 4 hrs of placebo (C1); after 4 hrs (H4), 8 hrs (H8), 24 hrs (H24), and 48 hrs (H48) of dopamine infusion; and after the second control of 4 hrs of placebo (C2). MEASUREMENTS AND MAIN RESULTS: We saw no significant change in systemic hemodynamic variables with dopamine at all times of infusion. Diuresis, creatinine clearance, and the fractional excretion of sodium (FENa) at C1 and C2 were not different. Urine flow, creatinine clearance, and FENa increased significantly 4 hrs after starting dopamine (for all these changes, p < .01 vs. C1 and C2). The maximum changes were obtained at H8, with an increase of 50% for diuresis, 37% for creatinine clearance, and 85% for FENa (for all these changes, p < .01 vs. C1 and C2). But these effects waned progressively from H24, and both creatinine clearance and FENa at H48 did not differ from control values. CONCLUSIONS: In stable critically ill patients, preventive low-dose dopamine increased creatinine clearance, diuresis, and the fractional excretion of sodium without concomitant hemodynamic change. These effects reached a maximum during 8 hrs of dopamine infusion. But despite a slight persistent increase in diuresis, improvement in creatinine clearance and FENa disappeared after 48 hrs. According to these data, it is likely that tolerance develops to dopamine-receptor agonists in critically ill patients at risk of developing acute renal failure.

Long-term radiographic follow-up in a patient with osteosclerotic sarcoidosis of the spine and pelvis.

Eight-year clinical and radiographic data in a patient with sarcoidosis manifesting as pelvic and spinal osteosclerosis and as mediastinal lymphadenopathy are described, extending the initial report of this case written after three years of follow-up. The osteosclerotic lesions involved the right iliac and sacral wings, as well as two lumbar vertebras, which had an ivory appearance. There was also evidence of right sacroiliitis, pubic symphysitis and T7-T8 discitis. The diagnosis was established by bone and mediastinal lymph node biopsies. Follow-up was eight years at the time of this writing. The osteosclerotic lesions improved, disappearing almost completely at the lumbar spine, and fusion occurred at the right sacroiliac joint, pubic symphysis, and T7-T8 intervertebral disk. A review of the literature found 13 similar cases, with noticeably shorter follow-ups. The characteristics of axial osteosclerotic sarcoidosis are reviewed, and the indications of corticosteroid therapy are discussed.

Tumoral calcinosis in hemodialysis patients. A review of three cases.

Soft tissue calcification are common in chronic hemodialysis patients and often affect the periarticular tissues, where they occasionally form tumoral masses. In a retrospective study of 254 hemodialysis patients we identified three such cases. Affected sites were the wrist, shoulder, and chest wall. None of the patients had secondary hyperparathyroidism. A discussion is provided of the roentgenographic and clinical features of tumoral calcinosis, of current pathogenic hypotheses, and of available treatments.