Emission and its back-reaction accompanying electron motion in relativistically strong and QED-strong pulsed laser fields

The emission from an electron in the field of a relativistically strong laser pulse is analyzed. At pulse intensities of J > 2 10^22 W/cm2 the emission from counter-propagating electrons is modified by the effects of Quantum ElectroDynamics (QED), as long as the electron energy is sufficiently high: E > 1 GeV. The radiation force experienced by an electron is for the first time derived from the QED principles and its applicability range is extended towards the QED-strong fields.Comment: 14 pages, 5 figures. Submitted to Phys.Rev.

Radiation back-reaction in relativistically strong and QED-strong laser fields

The emission from an electron in the field of a relativistically strong laser pulse is analyzed. At the pulse intensities of \ge 10^{22} W/cm^2 the emission from counter-propagating electrons is modified by the effects of Quantum ElectroDynamics (QED), as long as the electron energy is sufficiently high: E \ge 1 GeV. The radiation force experienced by an electron is for the first time derived from the QED principles and its applicability range is extended towards the QED-strong fields.Comment: 4 pages, 4 figure

Generation of GeV protons from 1 PW laser interaction with near critical density targets

The propagation of ultra intense laser pulses through matter is connected with the generation of strong moving magnetic fields in the propagation channel as well as the formation of a thin ion filament along the axis of the channel. Upon exiting the plasma the magnetic field displaces the electrons at the back of the target, generating a quasistatic electric field that accelerates and collimates ions from the filament. Two-dimensional Particle-in-Cell simulations show that a 1 PW laser pulse tightly focused on a near-critical density target is able to accelerate protons up to an energy of 1.3 GeV. Scaling laws and optimal conditions for proton acceleration are established considering the energy depletion of the laser pulse.Comment: 26 pages, 8 figure

X-ray phase contrast imaging of biological specimens with tabletop synchrotron radiation

Since their discovery in 1896, x-rays have had a profound impact on science, medicine and technology. Here we show that the x-rays from a novel tabletop source of bright coherent synchrotron radiation can be applied to phase contrast imaging of biological specimens, yielding superior image quality and avoiding the need for scarce or expensive conventional sources

Accelerating Protons to Therapeutic Energies with Ultra-Intense Ultra-Clean and Ultra-Short Laser Pulses

Proton acceleration by high-intensity laser pulses from ultra-thin foils for hadron therapy is discussed. With the improvement of the laser intensity contrast ratio to 10-11 achieved on Hercules laser at the University of Michigan, it became possible to attain laser-solid interactions at intensities up to 1022 W/cm2 that allows an efficient regime of laser-driven ion acceleration from submicron foils. Particle-In-Cell (PIC) computer simulations of proton acceleration in the Directed Coulomb explosion regime from ultra-thin double-layer (heavy ions / light ions) foils of different thicknesses were performed under the anticipated experimental conditions for Hercules laser with pulse energies from 3 to 15 J, pulse duration of 30 fs at full width half maximum (FWHM), focused to a spot size of 0.8 microns (FWHM). In this regime heavy ions expand predominantly in the direction of laser pulse propagation enhancing the longitudinal charge separation electric field that accelerates light ions. The dependence of the maximum proton energy on the foil thickness has been found and the laser pulse characteristics have been matched with the thickness of the target to ensure the most efficient acceleration. Moreover the proton spectrum demonstrates a peaked structure at high energies, which is required for radiation therapy. 2D PIC simulations show that a 150-500 TW laser pulse is able to accelerate protons up to 100-220 MeV energies.Comment: 26 pages, 6 figure

Dynamics of Emitting Electrons in Strong Electromagnetic Fields

We derive a modified non-perturbative Lorentz-Abraham-Dirac equation. It satisfies the proper conservation laws, particularly, it conserves the generalized momentum, the latter property eliminates the symmetry-breaking runaway solution. The equation allows a consistent calculation of the electron current, the radiation effect on the electron momentum, and the radiation itself, for a single electron or plasma electrons in strong electromagnetic fields. The equation is applied to a simulation of a strong laser pulse interaction with a plasma target. Some analytical solutions are also provided.Comment: The original form of this paper was submitted to Phys. Rev. Lett. on August 3, 2008. The current version of the paper is substantially extended and includes modifications resulting from points raised during the review proces

Consolidating the association of biallelic MAPKAPK5 pathogenic variants with a distinct syndromic neurodevelopmental disorder

BACKGROUND: MAPK-activated protein kinase 5 (MAPKAPK5) is an essential enzyme for diverse cellular processes. Dysregulation of the pathways regulated by MAPKAPK enzymes can lead to the development of variable diseases. Recently, homozygous loss-of-function variants in MAPKAPK5 were reported in four patients from three families presenting with a recognisable neurodevelopmental disorder, so-called 'neurocardiofaciodigital' syndrome. OBJECTIVE AND METHODS: In order to improve characterisation of the clinical features associated with biallelic MAPKAPK5 variants, we employed a genotype-first approach combined with reverse deep-phenotyping of three affected individuals. RESULTS: In the present study, we identified biallelic loss-of-function and missense MAPKAPK5 variants in three unrelated individuals from consanguineous families. All affected individuals exhibited a syndromic neurodevelopmental disorder characterised by severe global developmental delay, intellectual disability, characteristic facial morphology, brachycephaly, digital anomalies, hair and nail defects and neuroradiological findings, including cerebellar hypoplasia and hypomyelination, as well as variable vision and hearing impairment. Additional features include failure to thrive, hypotonia, microcephaly and genitourinary anomalies without any reported congenital heart disease. CONCLUSION: In this study, we consolidate the causality of loss of MAPKAPK5 function and further delineate the molecular and phenotypic spectrum associated with this new ultra-rare neurodevelopmental syndrome

Consolidating the association of biallelic MAPKAPK5 pathogenic variants with a distinct syndromic neurodevelopmental disorder

[Background]: MAPK-activated protein kinase 5 (MAPKAPK5) is an essential enzyme for diverse cellular processes. Dysregulation of the pathways regulated by MAPKAPK enzymes can lead to the development of variable diseases. Recently, homozygous loss-of-function variants in MAPKAPK5 were reported in four patients from three families presenting with a recognisable neurodevelopmental disorder, so-called ‘neurocardiofaciodigital’ syndrome. [Objective and methods]: In order to improve characterisation of the clinical features associated with biallelic MAPKAPK5 variants, we employed a genotype-first approach combined with reverse deep-phenotyping of three affected individuals. [Results]: In the present study, we identified biallelic loss-of-function and missense MAPKAPK5 variants in three unrelated individuals from consanguineous families. All affected individuals exhibited a syndromic neurodevelopmental disorder characterised by severe global developmental delay, intellectual disability, characteristic facial morphology, brachycephaly, digital anomalies, hair and nail defects and neuroradiological findings, including cerebellar hypoplasia and hypomyelination, as well as variable vision and hearing impairment. Additional features include failure to thrive, hypotonia, microcephaly and genitourinary anomalies without any reported congenital heart disease. [Conclusion]: In this study, we consolidate the causality of loss of MAPKAPK5 function and further delineate the molecular and phenotypic spectrum associated with this new ultra-rare neurodevelopmental syndrome.HH is funded by the MRC (MR/S01165X/1, MR/S005021/1, G0601943), the National Institute for Health Research University College London Hospitals Biomedical Research Centre, Rosetree Trust, Ataxia UK, MSA Trust, Brain Research UK, Sparks GOSH Charity, Muscular Dystrophy UK (MDUK), Muscular Dystrophy Association (MDA USA). SE is supported by an MRC strategic award to establish an International Centre for Genomic Medicine in Neuromuscular Diseases (ICGNMD) MR/S005021/1’

Femtosecond Diode-Pumped Cr : Lisgaf Lasers

The design and performance of diode-pumped Cr : LiSGAF lasers mode-locked by Kerr-Iens mode-locking and a solid-state saturable absorber are described. The different regimes of operation of the laser mode-locked by the saturable absorber are discussed. Both lasers generate 100-fs pulses with average powers of 40 mW and low fluctuations