Detection of magnetic moment in thin films with a home-made vibrating sample magnetometer

This paper explores the optimization of an array of pick-up coils in a home-made vibrating sample magnetometer for the detection of magnetic moment in thin films. Sensitivity function of a 4-coils Mallinson configuration was numerically studied for the determination of the physical dimensions that enhance the sensitivity of the magnetometer. By performing numerical simulations using the Biot-Savart law combined with the principle of reciprocity we were able to determine the maximum values of sensitivity and the influence of the separation of the coils on the sensitivity function. After the optimization of the pick-up coils, the vibrating sample magnetometer was able to detect the magnetic moment of a 100 nm-thickness Fe19Ni81 magnetic thin film along and perpendicular to the in-plane anisotropy easy axis. The implemented vibrating sample magnetometer is able to detect changes in the magnetic moment of ∼2 × 10-4 emu.Fil: Jordán, D.. Universidad Nacional de Ingeniería. Facultad de Ciencias; PerúFil: González Chávez, D.. Centro Brasileiro de Pesquisas Físicas; BrasilFil: Laura, D.. Universidad Nacional de Ingeniería. Facultad de Ciencias; PerúFil: Leon Hilario, Ludwin Misael. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Ingeniería. Facultad de Ciencias; PerúFil: Monteblanco, E.. Universite de Lorraine; FranciaFil: Gutarra Espinoza, Abel. Universidad Nacional de Ingeniería. Facultad de Ciencias; PerúFil: Aviles Felix, Luis Steven. Comision Nacional de Energía Atómica. Gerencia de Área Investigaciones y Aplicaciones no Nucleares. Gerencia de Física (Centro Atómico Bariloche). División Resonancias Magnéticas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Auto-immune haematological complications occurring during the treatment of malignant lymphoproliferative diseases

Auto-immune haematological complications occurring during treatment for malignant Iymphoproliferative diseases are described in 5 patients. There appeared to be a temporal relationship between the development of these complications and the administration of chemotherapeutic drugs or extensive radiotherapy.S. Afr. Med. J., 48, 2143 (1974)

Gravitational Repulsion within a Black-Hole using the Stueckelberg Quantum Formalism

We wish to study an application of Stueckelberg's relativistic quantum theory in the framework of general relativity. We study the form of the wave equation of a massive body in the presence of a Schwarzschild gravitational field. We treat the mathematical behavior of the wavefunction also around and beyond the horizon (r=2M). Classically, within the horizon, the time component of the metric becomes spacelike and distance from the origin singularity becomes timelike, suggesting an inevitable propagation of all matter within the horizon to a total collapse at r=0. However, the quantum description of the wave function provides a different understanding of the behavior of matter within the horizon. We find that a test particle can almost never be found at the origin and is more probable to be found at the horizon. Matter outside the horizon has a very small wave length and therefore interference effects can be found only on a very small atomic scale. However, within the horizon, matter becomes totally "tachionic" and is potentially "spread" over all space. Small location uncertainties on the atomic scale become large around the horizon, and different mass components of the wave function can therefore interfere on a stellar scale. This interference phenomenon, where the probability of finding matter decreases as a function of the distance from the horizon, appears as an effective gravitational repulsion.Comment: 20 pages, 6 figure

Automatic System for the D.C. High Voltage Qualification of the Superconducting Electrical Circuits of the LHC Machine

A d.c. high voltage test system has been developed to verify automatically the insulation resistance of the powering circuits of the LHC. In the most complex case, up to 72 circuits share the same volume inside cryogenic lines. Each circuit can have an insulation fault versus any other circuit or versus ground. The system is able to connect up to 80 circuits and apply a voltage up to 2 kV D.C. The leakage current flowing through each circuit is measured within a range of 1 nA to 1.6 mA. The matrix of measurements allows characterizing the paths taken by the currents and locating weak points of the insulation between circuits. The system is composed of a D.C. voltage source and a data acquisition card. The card is able to measure with precision currents and voltages and to drive up to 5 high voltage switching modules offering 16 channels each. A LabVIEW application controls the system for an automatic and safe operation. This paper describes the hardware and software design, the testing methodology and the results obtained during the qualification of the LHC superconducting circuits

Electrical Quality Assurance of the Superconducting Circuits during LHC Machine Assembly

Based on the LHC powering reference database, all-together 1750 superconducting circuits were connected in the various cryogenic transfer lines of the LHC machine. Testing the continuity, magnet polarity, and the quality of the electrical insulation were the main tasks of the Electrical Quality Assurance (ELQA) activities during the LHC machine assembly. With the assembly of the LHC now complete, the paper reviews the work flow, resources, and the qualification results including the different types of electrical non-conformities

Molecular correlates of axonal and synaptic pathology in mouse models of Batten disease

Neuronal ceroid lipofuscinoses (NCLs; Batten disease) are collectively the most frequent autosomal-recessive neurodegenerative disease of childhood, but the underlying cellular and molecular mechanisms remain unclear. Several lines of evidence have highlighted the important role that non-somatic compartments of neurons (axons and synapses) play in the instigation and progression of NCL pathogenesis. Here, we report a progressive breakdown of axons and synapses in the brains of two different mouse models of NCL: Ppt1−/− model of infantile NCL and Cln6nclf model of variant late-infantile NCL. Synaptic pathology was evident in the thalamus and cortex of these mice, but occurred much earlier within the thalamus. Quantitative comparisons of expression levels for a subset of proteins previously implicated in regulation of axonal and synaptic vulnerability revealed changes in proteins involved with synaptic function/stability and cell-cycle regulation in both strains of NCL mice. Protein expression changes were present at pre/early-symptomatic stages, occurring in advance of morphologically detectable synaptic or axonal pathology and again displayed regional selectivity, occurring first within the thalamus and only later in the cortex. Although significant differences in individual protein expression profiles existed between the two NCL models studied, 2 of the 15 proteins examined (VDAC1 and Pttg1) displayed robust and significant changes at pre/early-symptomatic time-points in both models. Our study demonstrates that synapses and axons are important early pathological targets in the NCLs and has identified two proteins, VDAC1 and Pttg1, with the potential for use as in vivo biomarkers of pre/early-symptomatic axonal and synaptic vulnerability in the NCLs

Neurodegeneration progresses despite complete elimination of clinical relapses in a mouse model of multiple sclerosis.

BACKGROUND: [corrected] Multiple Sclerosis has two clinical phases reflecting distinct but inter-related pathological processes: focal inflammation drives the relapse-remitting stage and neurodegeneration represents the principal substrate of secondary progression. In contrast to the increasing number of effective anti-inflammatory disease modifying treatments for relapse-remitting disease, the absence of therapies for progressive disease represents a major unmet clinical need. This raises the unanswered question of whether elimination of clinical relapses will prevent subsequent progression and if so how early in the disease course should treatment be initiated. Experimental autoimmune encephalomyelitis in the Biozzi ABH mouse recapitulates the clinical and pathological features of multiple sclerosis including relapse-remitting episodes with inflammatory mediated demyelination and progressive disability with neurodegeneration. To address the relationship between inflammation and neurodegeneration we used an auto-immune tolerance strategy to eliminate clinical relapses in EAE in a manner analogous to the clinical effect of disease modifying treatments. RESULTS: By arresting clinical relapses in EAE at two distinct stages, early and late disease, we demonstrate that halting immune driven demyelination even after the first major clinical event is insufficient to prevent long-term neurodegeneration and associated gliosis. Nonetheless, early intervention is partially neuroprotective, whereas later interventions are not. Furthermore early tolerisation is also associated with increased remyelination. CONCLUSIONS: These findings are consistent with both a partial uncoupling of inflammation and neurodegeneration and that the regenerative response of remyelination is negatively correlated with inflammation. These findings strongly support the need for early combinatorial treatment of immunomodulatory therapies and neuroprotective treatments to prevent long-term neurodegeneration in multiple sclerosis

Neuron-glia cross talk in rat striatum after transient forebrain ischemia

Striatum is highly vulnerable to transient forebrain ischemia induced by the 4 vessel occlusion (4V0) method (Brierley 1976. Pulsinelli et al. 1982, Zini et al. 1990a). Massive degeneration and loss of Nissl-stained neurons occur within 24 hr from an ischemia of long duration (30 min) (Pulsinelli et al. 1982). Neuronal loss is mainly restricted to the lateral part of caudate-putamen (Pulsinelli et al. 1982, Zini et al. 1990a). Cellular alterations include loss of medium-size spiny projection neurons (Pulsinelli et al. 1982, Francis and Pulsinelli 1982), largely corresponding to dopaminoceptive neurons (Benfenati et al. 1989, Zoli et al. 1989), and increase in reactive astrocytes (Pulsinelli et al. 1982, Grimaldi et al. 1990) and microglia (Gehrmann et al. 1982). On the other hand, large cholinergie (Francis and Pulsinelli 1982) and medium-size aspiny somatostatin (SS)/neuropeptide Y (NPY)-containing interneurons are resistant to the ischemic insult (Pulsinelli et al. 1982, Grimaldi et al. 1990). In a few instances, such as in the case of SS and NPY immunoreactivity (IR), the initial loss is followed by full recovery within 7 (SS) or 40 (NPY) days post-ischemia (Grimaldi et al. 1990). However, it is not known whether some kind of recovery is present for the bulk of medium-size spiny projections neurons after the first days post-ischemia

The role of the complement system in traumatic brain injury: a review

Traumatic brain injury (TBI) is an important cause of disability and mortality in the western world. While the initial injury sustained results in damage, it is the subsequent secondary cascade that is thought to be the significant determinant of subsequent outcomes. The changes associated with the secondary injury do not become irreversible until some time after the start of the cascade. This may present a window of opportunity for therapeutic interventions aiming to improve outcomes subsequent to TBI. A prominent contributor to the secondary injury is a multifaceted inflammatory reaction. The complement system plays a notable role in this inflammatory reaction; however, it has often been overlooked in the context of TBI secondary injury. The complement system has homeostatic functions in the uninjured central nervous system (CNS), playing a part in neurodevelopment as well as having protective functions in the fully developed CNS, including protection from infection and inflammation. In the context of CNS injury, it can have a number of deleterious effects, evidence for which primarily comes not only from animal models but also, to a lesser extent, from human post-mortem studies. In stark contrast to this, complement may also promote neurogenesis and plasticity subsequent to CNS injury. This review aims to explore the role of the complement system in TBI secondary injury, by examining evidence from both clinical and animal studies. We examine whether specific complement activation pathways play more prominent roles in TBI than others. We also explore the potential role of complement in post-TBI neuroprotection and CNS repair/regeneration. Finally, we highlight the therapeutic potential of targeting the complement system in the context of TBI and point out certain areas on which future research is needed

Oligodendrocytes: biology and pathology

Oligodendrocytes are the myelinating cells of the central nervous system (CNS). They are the end product of a cell lineage which has to undergo a complex and precisely timed program of proliferation, migration, differentiation, and myelination to finally produce the insulating sheath of axons. Due to this complex differentiation program, and due to their unique metabolism/physiology, oligodendrocytes count among the most vulnerable cells of the CNS. In this review, we first describe the different steps eventually culminating in the formation of mature oligodendrocytes and myelin sheaths, as they were revealed by studies in rodents. We will then show differences and similarities of human oligodendrocyte development. Finally, we will lay out the different pathways leading to oligodendrocyte and myelin loss in human CNS diseases, and we will reveal the different principles leading to the restoration of myelin sheaths or to a failure to do so