Magnetized Ekman Layer and Stewartson Layer in a Magnetized Taylor-Couette Flow

In this paper we present axisymmetric nonlinear simulations of magnetized Ekman and Stewartson layers in a magnetized Taylor-Couette flow with a centrifugally stable angular-momemtum profile and with a magnetic Reynolds number below the threshold of magnetorotational instability. The magnetic field is found to inhibit the Ekman suction. The width of the Ekman layer is reduced with increased magnetic field normal to the end plate. A uniformly-rotating region forms near the outer cylinder. A strong magnetic field leads to a steady Stewartson layer emanating from the junction between differentially rotating rings at the endcaps. The Stewartson layer becomes thinner with larger Reynolds number and penetrates deeper into the bulk flow with stronger magnetic field and larger Reynolds number. However, at Reynolds number larger than a critical value $\sim 600$, axisymmetric, and perhaps also nonaxisymmetric, instabilities occur and result in a less prominent Stewartson layer that extends less far from the boundary.Comment: 24 pages, 12 figures, accepted by PRE, revision according to referee

Second primary malignancies in thyroid cancer patients

The late health effects associated with radioiodine ((131)I) given as treatment for thyroid cancer are difficult to assess since the number of thyroid cancer patients treated at each centre is limited. The risk of second primary malignancies (SPMs) was evaluated in a European cohort of thyroid cancer patients. A common database was obtained by pooling the 2-year survivors of the three major Swedish, Italian, and French cohorts of papillary and follicular thyroid cancer patients. A time-dependent analysis using external comparison was performed. The study concerned 6841 thyroid cancer patients, diagnosed during the period 1934-1995, at a mean age of 44 years. In all, 17% were treated with external radiotherapy and 62% received (131)I. In total, 576 patients were diagnosed with a SPM. Compared to the general population of each of the three countries, an overall significantly increased risk of SPM of 27% (95% CI: 15-40) was seen in the European cohort. An increased risk of both solid tumours and leukaemias was found with increasing cumulative activity of (131)I administered, with an excess absolute risk of 14.4 solid cancers and of 0.8 leukaemias per GBq of (131)I and 10(5) person-years of follow-up. A relationship was found between (131)I administration and occurrence of bone and soft tissue, colorectal, and salivary gland cancers. These results strongly highlight the necessity to delineate the indications of (131)I treatment in thyroid cancer patients in order to restrict its use to patients in whom clinical benefits are expected

Stability and turbulent transport in Taylor–Couette flow from analysis of experimental data

International audienceThis paper provides a prescription for the turbulent viscosity in rotating shear flows for use e.g. in geophysical and astrophysical contexts. This prescription is the result of the detailed analysis of the experimental data obtained in several studies of the transition to turbulence and turbulent transport in Taylor-Couette flow. We first introduce a new set of control parameters, based on dynamical rather than geometrical considerations, so that the analysis applies more naturally to rotating shear flows in general and not only to Taylor-Couette flow. We then investigate the transition thresholds in the supercritical and the subcritical regime in order to extract their general dependencies on the control parameters. The inspection of the mean profiles provides us with some general hints on the mean to laminar shear ratio. Then the examination of the torque data allows us to propose a decomposition of the torque dependence on the control parameters in two terms, one completely given by measurements in the case where the outer cylinder is at rest, the other one being a universal function provided here from experimental fits. As a result, we obtain a general expression for the turbulent viscosity and compare it to existing prescription in the literature. Finally, throughout all the paper we discuss the influence of additional effects such as stratification or magnetic fields

Stability of quasi-Keplerian shear flow in a laboratory experiment

Context: Subcritical transition to turbulence has been proposed as a source of turbulent viscosity required for the associated angular momentum transport for fast accretion in Keplerian disks. Previously cited laboratory experiments in supporting this hypothesis were performed either in a different type of flow than Keplerian or without quantitative measurements of angular momentum transport and mean flow profile, and all of them appear to suffer from Ekman effects, secondary flows induced by nonoptimal axial boundary conditions. Such Ekman effects are expected to be absent from astronomical disks, which probably have stress-free vertical boundaries unless strongly magnetized. Aims: To quantify angular momentum transport due to subcritical hydrodynamic turbulence, if exists, in a quasi-Keplerian flow with minimized Ekman effects. Methods: We perform a local measurement of the azimuthal--radial component of the Reynolds stress tensor in a novel laboratory apparatus where Ekman effects are minimized by flexible control of axial boundary conditions. Results: We find significant Ekman effects on angular momentum transport due to nonoptimal axial boundary conditions in quasi-Keplerian flows. With the optimal control of Ekman effects, no statistically meaningful angular momentum transport is detected in such flows at Reynolds number up to two millions. Conclusions: Either a subcritical transition does not occur, or, if a subcritical transition does occur, the associated radial transport of angular momentum in optimized quasi-Keplerian laboratory flows is too small to directly support the hypothesis that subcritical hydrodynamic turbulence is responsible for accretion in astrophysical disks. Possible limitations in applying laboratory results to astrophysical disks due to experimental geometry are discussed.Comment: 24 pages, 13 figures, published in Astron. Astrophy

Deficient sustained attention to response task and P300 characteristics in early Huntington’s disease

Evidence for the extent and nature of attentional impairment in premanifest and manifest Huntington’s disease (HD) is inconsistent. Understanding such impairments may help to better understand early functional changes in HD and could have consequences concerning care for HD patients. We investigated attentional control in both early and premanifest HD. We studied 17 early HD subjects (mean age: 51 years), 12 premanifest HD subjects (mean age: 43 years), and 15 healthy controls (mean age: 51 years), using the sustained attention to response task (SART), a simple Go/No-go test reflecting attentional and inhibitory processes through reaction time (RT) and error rates. Simultaneously recorded EEG yielded P300 amplitudes and latencies. The early HD group made more Go errors (p < 0.001) and reacted slower (p < 0.005) than the other groups. The RT pattern during the SART was remarkably different for early HD subjects compared to the other two groups (p < 0.005), apparent as significant post-error slowing. P300 data showed that for early HD the No-go amplitude was lower than for the other two groups (p < 0.05). Subjects with early HD showed a reduced capacity to effectively control attention. They proved unable to resume the task directly after having made an error, and need more time to return to pre-error performance levels. No attentional control deficits were found for the premanifest HD group

Systematic Review of Potential Health Risks Posed by Pharmaceutical, Occupational and Consumer Exposures to Metallic and Nanoscale Aluminum, Aluminum Oxides, Aluminum Hydroxide and Its Soluble Salts

Aluminum (Al) is a ubiquitous substance encountered both naturally (as the third most abundant element) and intentionally (used in water, foods, pharmaceuticals, and vaccines); it is also present in ambient and occupational airborne particulates. Existing data underscore the importance of Al physical and chemical forms in relation to its uptake, accumulation, and systemic bioavailability. The present review represents a systematic examination of the peer-reviewed literature on the adverse health effects of Al materials published since a previous critical evaluation compiled by Krewski et al. (2007). Challenges encountered in carrying out the present review reflected the experimental use of different physical and chemical Al forms, different routes of administration, and different target organs in relation to the magnitude, frequency, and duration of exposure. Wide variations in diet can result in Al intakes that are often higher than the World Health Organization provisional tolerable weekly intake (PTWI), which is based on studies with Al citrate. Comparing daily dietary Al exposures on the basis of “total Al”assumes that gastrointestinal bioavailability for all dietary Al forms is equivalent to that for Al citrate, an approach that requires validation. Current occupational exposure limits (OELs) for identical Al substances vary as much as 15-fold. The toxicity of different Al forms depends in large measure on their physical behavior and relative solubility in water. The toxicity of soluble Al forms depends upon the delivered dose of Al+ 3 to target tissues. Trivalent Al reacts with water to produce bidentate superoxide coordination spheres [Al(O2)(H2O4)+ 2 and Al(H2O)6 + 3] that after complexation with O2•−, generate Al superoxides [Al(O2•)](H2O5)]+ 2. Semireduced AlO2• radicals deplete mitochondrial Fe and promote generation of H2O2, O2 • − and OH•. Thus, it is the Al+ 3-induced formation of oxygen radicals that accounts for the oxidative damage that leads to intrinsic apoptosis. In contrast, the toxicity of the insoluble Al oxides depends primarily on their behavior as particulates. Aluminum has been held responsible for human morbidity and mortality, but there is no consistent and convincing evidence to associate the Al found in food and drinking water at the doses and chemical forms presently consumed by people living in North America and Western Europe with increased risk for Alzheimer\u27s disease (AD). Neither is there clear evidence to show use of Al-containing underarm antiperspirants or cosmetics increases the risk of AD or breast cancer. Metallic Al, its oxides, and common Al salts have not been shown to be either genotoxic or carcinogenic. Aluminum exposures during neonatal and pediatric parenteral nutrition (PN) can impair bone mineralization and delay neurological development. Adverse effects to vaccines with Al adjuvants have occurred; however, recent controlled trials found that the immunologic response to certain vaccines with Al adjuvants was no greater, and in some cases less than, that after identical vaccination without Al adjuvants. The scientific literature on the adverse health effects of Al is extensive. Health risk assessments for Al must take into account individual co-factors (e.g., age, renal function, diet, gastric pH). Conclusions from the current review point to the need for refinement of the PTWI, reduction of Al contamination in PN solutions, justification for routine addition of Al to vaccines, and harmonization of OELs for Al substances

Physiological and pharmacological insights into the role of ionic channels in cardiac pacemaker activity

The generation of cardiac pacemaker activity is a complex phenomenon which requires the coordinated activity of different membrane ionic channels, as well as intracellular signalling factors including Ca(2+) and second messengers. The precise mechanism initiating automaticity in primary pacemaker cells is still matter of debate and certain aspects of how channels cooperate in the regulation of pacemaking by the autonomic nervous system have not been entirely elucidated. Research in the physiopathology of cardiac automaticity has also gained a considerable interest in the domain of cardiovascular pharmacology, since accumulating clinical and epidemiological evidence indicate a link between an increase in heart rate and the risk of cardiac mortality and morbidity. Lowering the heart rate by specific bradycardic agents in patients with heart disease constitutes a promising way to increase cardioprotection and improve survival. Thus, the elucidation of the mechanisms underlying the generation of pacemaker activity is necessary for the development of new therapeutic molecules for controlling the heart rate. Recent work on genetically modified mouse models provided new and intriguing evidence linking the activity of ionic channels genes to the generation and regulation of pacemaking. Importantly, results obtained on genetically engineered mouse strains have demonstrated that some channels are specifically involved in the generation of cardiac automaticity and conduction, but have no functional impact on the contractile activity of the heart. In this article, we will outline the current knowledge on the role of ionic channels in cardiac pacemaker activity and suggest new potential pharmacological targets for controlling the heart rate without concomitant negative inotropism

Voltage-dependent calcium channels and cardiac pacemaker activity: From ionic currents to genes

The spontaneous activity of pacemaker cells in the sino-atrial node controls the heart rhythm and rate under physiological conditions. Compared to working myocardial cells, pacemaker cells express a specific array of ionic channels. The functional importance of different ionic channels in the generation and regulation of cardiac automaticity is currently subject of an extensive research effort and has long been controversial. Among families of ionic channels, Ca(2+) channels have been proposed to substantially contribute to pacemaking. Indeed, Ca(2+) channels are robustly expressed in pacemaker cells, and influence the cell beating rate. Furthermore, they are regulated by the activity of the autonomic nervous system in both a positive and negative way. In this manuscript, we will first discuss how the concept of the involvement of Ca(2+) channels in cardiac pacemaking has been proposed and then subsequently developed by the recent advent in the domain of cardiac physiology of gene-targeting techniques. Secondly, we will indicate how the specific profile of Ca(2+) channels expression in pacemaker tissue can help design drugs which selectively regulate the heart rhythm in the absence of concomitant negative inotropism. Finally, we will indicate how the new possibility to assign a specific gene activity to a given ionic channel involved in cardiac pacemaking could implement the current postgenomic research effort in the construction of the cardiac Physiome

Functional role of L-type Ca(v)1.3 Ca(2+) channels in cardiac pacemaker activity

The spontaneous activity of pacemaker cells in the sino-atrial node (SAN) controls the heart rhythm and rate under physiological conditions. Pacemaker activity in SAN cells is due to the presence of the diastolic depolarization, a slow depolarization phase that drives the membrane voltage from the end of an action potential to the threshold of a new action potential. SAN cells express a wide array of ionic channels, but we have limited knowledge about their functional role in pacemaker activity and we still do not know which channels play a prominent role in the generation of the diastolic depolarization. It is thus important to provide genetic evidence linking the activity of genes coding for ionic channels to specific alterations of pacemaker activity of SAN cells. Here, we show that target inactivation of the gene coding for α(1D) (Ca(v)1.3) Ca(2+) channels in the mouse not only significantly slows pacemaker activity but also promotes spontaneous arrhythmia in SAN pacemaker cells. These alterations of pacemaker activity are linked to abolition of the major component of the L-type current (I(Ca,L)) activating at negative voltages. Pharmacological analysis of I(Ca,L) demonstrates that Ca(v)1.3 gene inactivation specifically abolishes I(Ca,L) in the voltage range corresponding to the diastolic depolarization. Taken together, our data demonstrate that Ca(v)1.3 channels play a major role in the generation of cardiac pacemaker activity by contributing to diastolic depolarization in SAN pacemaker cells