Spatial profile measurement of femtosecond laser - Compton xrays

Abstract A femtosecond X-ray source was developed by Thomson scattering through interaction between a lowemittance picosecond electron beam and a terawatt femtosecond laser light at 90 o configuration. The observed X-ray intensity with peak energy of 2.3 keV and pulse duration of 270 fs rms was typically 1.4x10 4 photons/pulse. The pulse-to-pulse fluctuation of the X-ray intensity was measured to be 25%. The spatial profile of the X-rays was measured with a technique of X-ray imaging on a phosphor screen using an image-intensified CCD camera. The dependence of the X-ray beam profile on the scattering laser polarization was obtained and compared with theoretical analysis. INTRODUCATION A short pulse X-ray source is an important tool for studying the dynamics of the materials in the fundamental time scale. The development of femtosecond laser has made it possible to generate such ultrashort X-ray pulses in femtosecond region by means of 90-degree (90 o ) Thomson scattering with a relativistic ultrashort-pulse electron beam The intensity of the X-rays generated in Thomson scattering is proportional to the densities of both the electron and laser beam. It is important to tightly focus both the beams in the transverse direction to generate high-brightness X-rays. In addition, the small focused beam size should be required to reduce the interaction time in 90 o Thomson scattering for the generation of femtosecond X-ray pulse EXPERIMENTAL ARRANGEMENT The Thomson femtosecond X-ray source was consisted of a picosecond electron source and a tabletop terawatt femtosecond pulse laser An Electron Source The electron beam was produced by a S-band (2856 MHz) photocathode rf gun. The rf gun, which was constructed under the BNL/KEK/SHI collaboration [6], was consisted of two cells: a half cell and a full cell. A copper cathode was located on the side of the half cell. The length of the half cell was designed to be 0.6 times of the full cell length to reduce the beam divergence. At the exit of the rf gun, a single solenoid magnet was mounted for space-charge emittance compensation. The rf gun was driven by an all solid-state LD-pumped Nd:YAG picosecond laser. The laser was consisted of a passive mode-locked oscillator, a regenerative amplifier, a post amplifier and a frequency converter. The oscillator was phase-locked with a frequency of 119 MHz, the 24 th sub-harmonic of the accelerating 2856 MHz rf, by dynamically adjusting the cavity length of the oscillator with a semiconductor saturable absorber mirror controlled by a timing stabilizer. The output of the oscillator was amplified the pulse energy up to 2mJ in the regenerative amplifier and the post amplifier. The amplified laser pulse was frequency quadrupled to 262 nm ultraviolet (UV) light by a pair of frequency conversion crystals. The UV light was injected on the cathode surface at an incident angle of 68 o along the electron beam direction. The electron beam produced from the rf gun was accelerated with a 70 cm long standing-wave linear accelerator (linac) produced with an alternating-periodic structure. The linac is located at a position of 1.2 m from the cathode. The input rf peak power of both the rf gun and the linac was 7.5 MW that was produced with a 15 MW Klystron. The peak electric fields on axis in the rf gun and the linac were approximately 100 and 25 MV/m, respectively. The repetition rate of the operation was 10 Hz in the experiments. The accelerated electron beam was focused at the interaction point for scattering with the laser light by a triplet quadrupole magnet downstream of the linac. The scattered electrons were bended by a 90 o dipole magnet A Terawatt Femtosecond Laser The terawatt femtosecond laser was consisted of a mode-locked Ti:Sapphire laser oscillator, a pulse stretcher, a regenerative amplifier, a multi-pass post amplifier, and a pulse compressor. The oscillator generated 50 fs pulses at the repetition rate of 119 MHz. The frequency of the laser oscillator was phase-locked with the 119 MHz rf by the same method as the driving laser of the rf gun. ___________________________________________

DEVELOPMENT OF HIGH-BRIGHTNESS FEMTOSECOND X-RAY SOURCE

Abstract A high-brightness femtosecond X-ray source, based on Thomson scattering of a low-emittance electron beam with a femtosecond pulse laser at a 90-degree interaction configuration, has been developed and will be expected for the study of ultra-fast structural dynamics of materials. The electron beam was generated by a laser-driven photocathode RF gun and accelerated up to 14MeV with a linac. A 270fs pulse X-rays with a peak energy of 2.3keV were achieved experimentally in the interaction of a 3ps electron bunch with a 100fs Ti:Sapphire laser light. The intensity of the X-rays was obtained to be 1.4x10 4 /pulse under the experimental conditions of a 0.5nC electron bunch and a 100mJ laser pulse energy. The stability of the X-ray intensity was obtained to be 25%(rms)

Ca2+-Dependent Phosphorylation of RyR2 Can Uncouple Channel Gating from Direct Cytosolic Ca2+ Regulation

Phosphorylation of the cardiac ryanodine receptor (RyR2) is thought to be important not only for normal cardiac excitation-contraction coupling but also in exacerbating abnormalities in Ca2+ homeostasis in heart failure. Linking phosphorylation to specific changes in the single-channel function of RyR2 has proved very difficult, yielding much controversy within the field. We therefore investigated the mechanistic changes that take place at the single-channel level after phosphorylating RyR2 and, in particular, the idea that PKA-dependent phosphorylation increases RyR2 sensitivity to cytosolic Ca2+. We show that hyperphosphorylation by exogenous PKA increases open probability (Po) but, crucially, RyR2 becomes uncoupled from the influence of cytosolic Ca2+; lowering [Ca2+] to subactivating levels no longer closes the channels. Phosphatase (PP1) treatment reverses these gating changes, returning the channels to a Ca2+-sensitive mode of gating. We additionally found that cytosolic incubation with Mg2+/ATP in the absence of exogenously added kinase could phosphorylate RyR2 in approximately 50% of channels, thereby indicating that an endogenous kinase incorporates into the bilayer together with RyR2. Channels activated by the endogenous kinase exhibited identical changes in gating behavior to those activated by exogenous PKA, including uncoupling from the influence of cytosolic Ca2+. We show that the endogenous kinase is both Ca2+-dependent and sensitive to inhibitors of PKC. Moreover, the Ca2+-dependent, endogenous kinase–induced changes in RyR2 gating do not appear to be related to phosphorylation of serine-2809. Further work is required to investigate the identity and physiological role of this Ca2+-dependent endogenous kinase that can uncouple RyR2 gating from direct cytosolic Ca2+ regulation

Validity of arthroscopic measurement of glenoid bone loss using the bare spot

Katsutoshi Miyatake, Yoshitsugu Takeda, Koji Fujii, Tomoya Takasago, Toshiyuki Iwame Department of Orthopaedic Surgery, Tokushima Red Cross Hospital, Komatsushima, Tokushima, Japan Purpose: Our aim was to test the validity of using the bare spot method to quantify glenoid bone loss arthroscopically in patients with shoulder instability. Methods: Twenty-seven patients with no evidence of instability (18 males, nine females; mean age 59.1 years) were evaluated arthroscopically to assess whether the bare spot is consistently located at the center of the inferior glenoid. Another 40 patients with glenohumeral anterior instability who underwent shoulder arthroscopy (30 males, ten females; mean age 25.9 years) were evaluated for glenoid bone loss with preoperative three-dimensional computed tomography (3D-CT) and arthroscopic examination. In patients without instability, the distances from the bare spot of the inferior glenoid to the anterior (Da) and posterior (Dp) glenoid rim were measured arthroscopically. In patients with instability, we compared the percentage glenoid bone loss calculated using CT versus arthroscopic measurements. Results: Among patients without instability, the bare spot could not be identified in three of 27 patients. Da (9.5±1.2 mm) was smaller than Dp (10.1±1.5 mm), but it was not significantly different. However, only 55% of glenoids showed less than 1 mm of difference between Da and Dp, and 18% showed more than 2 mm difference in length. The bare spot could not be identified in five of 40 patients with instability. Pearson's correlation coefficient showed significant (P<0.001) and strong (R2=0.63) correlation in percentage glenoid bone loss between the 3D-CT and arthroscopy method measurements. However, in ten shoulders (29%), the difference in percentage glenoid bone loss between 3D-CT and arthroscopic measurements was greater than 5%. Conclusion: The bare spot was not consistently located at the center of the inferior glenoid, and the arthroscopic measurement of glenoid bone loss using the bare spot as a landmark was inaccurate in some patients with anterior glenohumeral instability. Level of evidence: Level II, prospective comparative study. Keywords: shoulder instability, glenoid defect, arthroscopy, Bankart repair, 3D-CT, bone graft, shoulder dislocatio

Amyloid precursor protein accumulates in white matter at the margin of a focal ischaemic lesion

Amyloid precursor protein (APP) is transported by fast anterograde axonal transport. Since disruption of this transport results in APP accumulation, APP has been proposed as a sensitive marker of axonal injury. In the present study, axonal injury in subcortical white matter and myelinated fibre tracts permeating the striatum, 24 h after permanent middle cerebral artery occlusion in the rat, has been examined by assessing the location and extent of APP immunoreactivity. Increased APP immunoreactivity was present in both areas. This was localised to a circumscribed zone immediately adjacent to the boundary of the ischaemic lesion in grey matter. The amount of APP immunoreactivity was associated with the volume of the ischaemic lesion in individual animals. Increased APP immunoreactivity in subcortical white matter and myelinated fibre tracts at the margin of the ischaemic zone may prove to be a valuable marker for assessing strategies to protect axons after an ischaemic insult

Topographical and quantitative assessment of white matter injury following a focal ischaemic lesion in the rat brain

Axonal injury following cerebral ischaemia has attracted less attention than damage in grey matter. However, it is becoming increasingly recognised that axons are highly vulnerable to focal ischaemia [D. Dewar, D.A. Dawson, Changes of cytoskeletal protein immunostaining in myelinated fibre tracts after focal cerebral ischaemia in the rat, Acta. Neuropathol., 93 (1997) 71–77] [2]; [L. Pantoni, J.H. Garcia, J.A. Gutierrez, Cerebral white matter is highly vulnerable to ischemia, Stroke, 27 (1996) 1641–1647] [10]; [P.S. Yam, T. Takasago, D. Dewar, D.I. Graham, J. McCulloch, Amyloid precursor protein accumulates in white matter at the margin of a focal ischaemic lesion, Brain Res., 760 (1997) 150–157] [15]. Since white matter does not contain neuronal cell bodies or synapses it is likely that the mechanisms of injury and strategies for its protection are different from those in grey matter. In order that the effect of therapeutic intervention on the protection of axons can be assessed, a method by which axonal injury can be mapped and quantified is required. For this purpose, we investigated immunocytochemical methods using amyloid precursor protein (APP) following permanent middle cerebral artery occlusion in the rat. APP is transported by fast anterograde axonal transport [E.H. Koo, S.S. Sisodia, D.R. Archer, L.J. Martin, A. Weidemann, K. Beyreuther, P. Fischer, C.L. Masters, D.L. Price, Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport, Proc. Natl. Acad. Sci. U.S.A. 87 (1990) 1561–1565] [7]and has been shown to accumulate following a variety of insults to axons, indicative of dysfunction of axonal transport [R.N. Kalaria, S.U. Bhatti, E.A. Palatinsky, D.H. Pennington, E.R. Shelton, H.W. Chan, G. Perry, W.D. Lust, Accumulation of the beta amyloid precursor protein at sites of ischemic injury in rat brain, Neuroreport, 4 (1993) 211–214] [4]; [T. Kawarabayashi, M. Shoji, Y. Harigaya, H. Yamaguchi, S. Hirai, Expression of APP in the early stage of brain damage, Brain Res., 563 (1991) 334–338] [5]; [N. Otsuka, M. Tomonaga, K. Ikeda, Rapid appearance of beta-amyloid precursor protein immunoreactivity in damaged axons and reactive glial cells in rat brain following needle stab injury, Brain Res., 568 (1991) 335–338] [9]; [K. Shigematsu, P.L. McGeer, Accumulation of amyloid precursor protein in neurons after intraventricular injection of colchicine, Am. J. Pathol., 140 (1992) 787–794] [12]. We have been able to map the topographical relationship between APP accumulation and region of infarction using immunocytochemistry and image analysis techniques. Additionally, using a semi-quantitative scoring system, we have demonstrated that there is a relationship between the amount of APP accumulation and the volume of infarction following middle cerebral artery occlusion. These methods will be useful in the future for the assessment of therapeutic interventions on the protection of axons following ischaemic injury