Efficient laser-overdense plasma coupling via surface plasma waves and steady magnetic field generation

International audienceThe efficiency of laser overdense plasma coupling via surface plasma wave excitation is investigated. Two-dimensional particle-in-cell simulations are performed over a wide range of laser pulse intensity from 10 15 to 10 20 W cm À2 lm 2 with electron density ranging from 25 to 100n c to describe the laser interaction with a grating target where a surface plasma wave excitation condition is fulfilled. The numerical studies confirm an efficient coupling with an enhancement of the laser absorption up to 75%. The simulations also show the presence of a localized, quasi-static magnetic field at the plasma surface. Two interaction regimes are identified for low (Ik 2 10 17 W cm À2 lm 2) laser pulse intensities. At " relativistic " laser intensity, steady magnetic fields as high as $580 MG lm/k 0 at 7 Â 10 19 W cm À2 lm 2 are obtained in the simulations

Self-generation of megagauss magnetic fields during the expansion of a plasma

International audienceThe expansion of a plasma slab into a vacuum is studied using one-dimensional and two-dimensional particle-in-cell simulations. As electrons transfer their longitudinal kinetic energy to ions during the expansion, the electron temperature becomes anisotropic. Once this anisotropy exceeds a threshold value, it drives the Weibel instability, leading to magnetic fields in the megagauss range. These fields induce energy transfer between the longitudinal and transverses directions, which influences the expansion. The impact of a cold electron population on this phenomenon is also investigated. Plasma expansion is a fundamental process which occurs in very different fields, such as astrophysics ͓1,2͔, laser-plasma ion acceleration ͓3–5͔ and thin-film deposition ͓6͔. This phenomenon is usually described by simple one-dimensional models ͓7–9͔. Yet, even when the system is translation-invariant along the plasma surface, several effects ͑e.g., Coulomb collisions ͓10͔͒ can induce momentum transfer between the longitudinal and transverse directions. The purely one-dimensional ͑1D͒ description is thus, in general, inaccurate. In this paper, we show that self-generated magnetic fields can lead to such momentum transfer during the expansion of a collisionless plasma slab. This study is of particular interest in the context of laser-plasma ion acceleration , where an intense laser pulse is focused on a thin foil to create a hot electron population that transfers progressively its energy to ions via the ambipolar electric field at the plasma surface ͓11͔. We assume here that the electron distribution is initially Maxwellian with an isotropic temperature. As the plasma expands, the longitudinal temperature T ʈ decreases and the anisotropy parameter A = T Ќ / T ʈ − 1 increases, which eventually leads to the growth of the Weibel instability ͓12–18͔. The most unstable modes are obtained for k = k x e x , where e x is a unit vector normal to the plasma surface. In this case, the maximum unstable wave vector is k

Influence of the Weibel instability on the expansion of a plasma slab into a vacuum

International audienceThe development of the Weibel instability during the expansion of a thin plasma foil heated by an intense laser pulse is investigated, using both analytical models and relativistic particle-in-cell simulations. When the plasma has initially an anisotropic electron distribution, this electromagnetic instability develops from the beginning of the expansion. Then it contributes to suppress the anisotropy and eventually saturates. After the saturation, the strength of the magnetic field decreases because of the plasma expansion until it becomes too weak to maintain the distribution isotropic. For this time, the anisotropy rises as electrons give progressively their longitudinal energy to ions, so that a new instability can develop

Visibility of dichalcogenide nanolayers

Dichalcogenides with the common formula MX2 are layered materials with electrical properties that range from semiconducting to superconducting. Here, we describe optimal imaging conditions for optical detection of ultrathin, two-dimensional dichalcogenide nanocrystals containing single, double and triple layers of MoS2, WSe2 and NbSe2. A simple optical model is used to calculate the contrast for nanolayers deposited on wafers with varying thickness of SiO2. The model is extended for imaging using the green channel of a video camera. Using AFM and optical imaging we confirm that single layers of MoS2, WSe2 and NbSe2 can be detected on 90nm and 270 nm SiO2 using optical means. By measuring contrast under broad-band green illumination we are also able to distinguish between nanostructures containing single, mono and triple layers of MoS2, WSe2 and NbSe2

Search for the best indicators for the presence of a VPS13B gene mutation and confirmation of diagnostic criteria in a series of 34 patients genotyped for suspected Cohen syndrome

BACKGROUND: Cohen syndrome is a rare autosomal recessive inherited disorder that results from mutations of the VPS13B gene. Clinical features consist of a combination of mental retardation, facial dysmorphism, postnatal microcephaly, truncal obesity, slender extremities, joint hyperextensibility, myopia, progressive chorioretinal dystrophy, and intermittent neutropenia.PATIENTS AND METHODS: The aim of the study was to determine which of the above clinical features were the best indicators for the presence of VPS13B gene mutations in a series of 34 patients with suspected Cohen syndrome referred for molecular analysis of VPS13B. RESULTS: 14 VPS13B gene mutations were identified in 12 patients, and no mutation was found in 22 patients. The presence of chorioretinal dystrophy (92% vs 32%, p=0.0023), intermittent neutropenia (92% vs 5%, p<0.001), and postnatal microcephaly (100% vs 48%, p=0.0045) was significantly higher in the group of patients with a VPS13B gene mutation compared to the group of patients without a mutation. All patients with VPS13B mutations had chorioretinal dystrophy and/or intermittent neutropenia. The Kolehmainen diagnostic criteria provided 100% sensibility and 77% specificity when applied to this series. CONCLUSION: From this study and a review of more than 160 genotyped cases from the literature, it is concluded that, given the large size of the gene, VPS13B screening is not indicated in the absence of chorioretinal dystrophy or neutropenia in patients aged over 5 years. The follow-up of young patients could be a satisfactory alternative unless there are some reproductive issues

Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions

Creatine and guanidinoacetate reference values in a French population

Creatine and guanidinoacetate are biomarkers of creatine metabolism. Their assays in body fluids may be used for detecting patients with primary creatine deficiency disorders (PCDD), a class of inherited diseases. Their laboratory values in blood and urine may vary with age, requiring that reference normal values are given within the age range. Despite the long known role of creatine for muscle physiology, muscle signs are not necessarily the major complaint expressed by PCDD patients. These disorders drastically affect brain function inducing, in patients, intellectual disability, autistic behavior and other neurological signs (delays in speech and language, epilepsy, ataxia, dystonia and choreoathetosis), being a common feature the drop in brain creatine content. For this reason, screening of PCDD patients has been repeatedly carried out in populations with neurological signs. This report is aimed at providing reference laboratory values and related age ranges found for a large scale population of patients with neurological signs (more than 6 thousand patients) previously serving as a background population for screening French patients with PCDD. These reference laboratory values and age ranges compare rather favorably with literature values for healthy populations. Some differences are also observed, and female participants are discriminated from male participants as regards to urine but not blood values including creatine on creatinine ratio and guanidinoacetate on creatinine ratio values. Such gender differences were previously observed in healthy populations; they might be explained by literature differential effects of testosterone and estrogen in adolescents and adults, and by estrogen effects in prepubertal age on SLC6A8 function. Finally, though they were acquired on a population with neurological signs, the present data might reasonably serve as reference laboratory values in any future medical study exploring abnormalities of creatine metabolism and transport

Clinical reappraisal of SHORT syndrome with PIK3R1 mutations: towards recommendation for molecular testing and management

International audienceSHORT syndrome has historically been defined by its acronym: short stature (S), hyperextensibility of joints and/or inguinal hernia (H), ocular depression (O), Rieger abnormality (R) and teething delay (T). More recently several research groups have identified PIK3R1 mutations as responsible for SHORT syndrome. Knowledge of the molecular etiology of SHORT syndrome has permitted a reassessment of the clinical phenotype. The detailed phenotypes of 32 individuals with SHORT syndrome and PIK3R1 mutation, including eight newly ascertained individuals, were studied to fully define the syndrome and the indications for PIK3R1 testing. The major features described in the SHORT acronym were not universally seen and only half (52%) had 4 or more of the classic features. The commonly observed clinical features of SHORT syndrome seen in the cohort included IUGR \textless 10(th) percentile, postnatal growth restriction, lipoatrophy and the characteristic facial gestalt. Anterior chamber defects and insulin resistance or diabetes were also observed but were not as prevalent. The less specific, or minor features of SHORT syndrome include teething delay, thin wrinkled skin, speech delay, sensorineural deafness, hyperextensibility of joints and inguinal hernia. Given the high risk of diabetes mellitus, regular monitoring of glucose metabolism is warranted. An echocardiogram, ophthalmological and hearing assessments are also recommended