Solving for Micro- and Macro- Scale Electrostatic Configurations Using the Robin Hood Algorithm

We present a novel technique by which highly-segmented electrostatic configurations can be solved. The Robin Hood method is a matrix-inversion algorithm optimized for solving high density boundary element method (BEM) problems. We illustrate the capabilities of this solver by studying two distinct geometry scales: (a) the electrostatic potential of a large volume beta-detector and (b) the field enhancement present at surface of electrode nano-structures. Geometries with elements numbering in the O(10^5) are easily modeled and solved without loss of accuracy. The technique has recently been expanded so as to include dielectrics and magnetic materials.Comment: 40 pages, 20 figure

The KATRIN Pre-Spectrometer at reduced Filter Energy

The KArlsruhe TRItium Neutrino experiment, KATRIN, will determine the mass of the electron neutrino with a sensitivity of 0.2 eV (90% C.L.) via a measurement of the beta-spectrum of gaseous tritium near its endpoint of E_0 =18.57 keV. An ultra-low background of about b = 10 mHz is among the requirements to reach this sensitivity. In the KATRIN main beam-line two spectrometers of MAC-E filter type are used in a tandem configuration. This setup, however, produces a Penning trap which could lead to increased background. We have performed test measurements showing that the filter energy of the pre-spectrometer can be reduced by several keV in order to diminish this trap. These measurements were analyzed with the help of a complex computer simulation, modeling multiple electron reflections both from the detector and the photoelectric electron source used in our test setup.Comment: 22 pages, 12 figure

Severe muscle trauma triggers heightened and prolonged local musculoskeletal inflammation and impairs adjacent tibia fracture healing

Objectives: Complicated fracture healing is often associated with the severity of surrounding muscle tissue trauma. Since inflammation is a primary determinant of musculoskeletal health and regeneration, it is plausible that delayed healing and non-unions are partly caused by compounding local inflammation in response to concomitant muscle trauma. Methods and results: To investigate this possibility, a Lewis rat open fracture model [tibia osteotomy with adjacent tibialis anterior (TA) muscle volumetric muscle loss (VML) injury] was interrogated. We observed that VML injury impaired tibia healing, as indicated by diminished mechanical strength and decreased mineralized bone within the fracture callus, as well as continued presence of cartilage instead of woven bone 28 days post-injury. The VML injured muscle presented innate and adaptive immune responses that were atypical of canonical muscle injury healing. Additionally, the VML injury resulted in a perturbation of the inflammatory phase of fracture healing, as indicated by elevations of CD3+ lymphocytes and CD68+ macrophages in the fracture callus at 3 and 14d post-injury, respectively. Conclusions: These data indicate that heightened and sustained innate and adaptive immune responses to traumatized muscle are associated with impaired fracture healing and may be targeted for the prevention of delayed and non-union following musculoskeletal trauma

A forest typology for monitoring sustainable forest management: The case of European Forest Types

Sustainable forest management (SFM) is presently widely accepted as the overriding objective for forest policy and practice. Regional processes are in progress all over the world to develop and implement criteria and indicators of SFM. In continental Europe, a set of 35 Pan-European indicators has been endorsed under the Ministerial Conference on the Protection of Forests in Europe (MCPFE) to measure progress towards SFM in the 44 countries of the region. The formulation of seven indicators (forest area, growing stock, age structure/diameter distribution, deadwood, tree species composition, damaging agents, naturalness) requires national data to be reported by forest types. Within the vast European forest area the values taken by these indicators show a considerable range of variation, due to variable natural conditions and anthropogenic influences. Given this variability, it is very difficult to grasp the meaning of these indicators when taken out of their ecological background. The paper discusses the concepts behind, and the requirements of, a classification more soundly ecologically framed and suitable for MCPFE reporting than the three (un-informative) classes adopted so far: broadleaved forest, coniferous forest, mixed broadleaved and coniferous forest. We propose a European Forest Types scheme structured into a reasonably higher number of classes, that would improve the specificity of the indicators reported under the MCPFE process and its understanding.L'articolo è disponibile sul sito dell'editore www.tandf.co.uk/journals

Achieving Acetylcholine Receptor Clustering in Tissue-Engineered Skeletal Muscle Constructs In vitro through a Materials-Directed Agrin Delivery Approach

Volumetric muscle loss (VML) can result from trauma, infection, congenital anomalies, or surgery, and produce permanent functional and cosmetic deficits. There are no effective treatment options for VML injuries, and recent advances toward development of muscle constructs lack the ability to achieve innervation necessary for long-term function. We sought to develop a proof-of-concept biomaterial construct that could achieve acetylcholine receptor (AChR) clustering on muscle-derived cells (MDCs) in vitro. The approach consisted of the presentation of neural (Z+) agrin from the surface of microspheres embedded with a fibrin hydrogel to muscle cells (C2C12 cell line or primary rat MDCs). AChR clustering was spatially restricted to areas of cell (C2C12)-microsphere contact when the microspheres were delivered in suspension or when they were incorporated into a thin (2D) fibrin hydrogel. AChR clusters were observed from 16 to 72 h after treatment when Z+ agrin was adsorbed to the microspheres, and for greater than 120 h when agrin was covalently coupled to the microspheres. Little to no AChR clustering was observed when agrin-coated microspheres were delivered from specially designed 3D fibrin constructs. However, cyclic stretch in combination with agrin-presenting microspheres led to dramatic enhancement of AChR clustering in cells cultured on these 3D fibrin constructs, suggesting a synergistic effect between mechanical strain and agrin stimulation of AChR clustering in vitro. These studies highlight a strategy for maintaining a physiological phenotype characterized by motor endplates of muscle cells used in tissue engineering strategies for muscle regeneration. As such, these observations may provide an important first step toward improving function of tissue-engineered constructs for treatment of VML injuries

Genetic Identification of a Network of Factors that Functionally Interact with the Nucleosome Remodeling ATPase ISWI

Nucleosome remodeling and covalent modifications of histones play fundamental roles in chromatin structure and function. However, much remains to be learned about how the action of ATP-dependent chromatin remodeling factors and histone-modifying enzymes is coordinated to modulate chromatin organization and transcription. The evolutionarily conserved ATP-dependent chromatin-remodeling factor ISWI plays essential roles in chromosome organization, DNA replication, and transcription regulation. To gain insight into regulation and mechanism of action of ISWI, we conducted an unbiased genetic screen to identify factors with which it interacts in vivo. We found that ISWI interacts with a network of factors that escaped detection in previous biochemical analyses, including the Sin3A gene. The Sin3A protein and the histone deacetylase Rpd3 are part of a conserved histone deacetylase complex involved in transcriptional repression. ISWI and the Sin3A/Rpd3 complex co-localize at specific chromosome domains. Loss of ISWI activity causes a reduction in the binding of the Sin3A/Rpd3 complex to chromatin. Biochemical analysis showed that the ISWI physically interacts with the histone deacetylase activity of the Sin3A/Rpd3 complex. Consistent with these findings, the acetylation of histone H4 is altered when ISWI activity is perturbed in vivo. These findings suggest that ISWI associates with the Sin3A/Rpd3 complex to support its function in vivo

Communications Biophysics

Contains reports on six research projects.National Institutes of Health (Grant 2 P01 GM-14940-01)Joint Services Electronics Programs (U. S. Army, U.S. Navy, and U.S. Air Force) under Contract DA 28-043-AMC-02536(E)National Aeronautics and Space Administration (Grant NsG-496)National Institutes of Health (Grant 2 ROl NB-05462-03

In vivo effects of antibodies from patients with anti-NMDA receptor encephalitis: further evidence of synaptic glutamatergic dysfunction

Background: A severe encephalitis that associates with auto-antibodies to the NR1 subunit of the NMDA receptor (NMDA-R) was recently reported. Patients' antibodies cause a decrease of the density of NMDA-R and synaptic mediated currents, but the in vivo effects on the extracellular glutamate and glutamatergic transmission are unknown. Methods. We investigated the acute metabolic effects of patients' CSF and purified IgG injected in vivo. Injections were performed in CA1 area of Ammon's horn and in premotor cortex in rats. Results: Patient's CSF increased the concentrations of glutamate in the extracellular space. The increase was dose-dependent and was dramatic with purified IgG. Patients' CSF impaired both the NMDA- and the AMPA-mediated synaptic regulation of glutamate, and did not affect the glial transport of glutamate. Blockade of GABA-A receptors was associated with a marked elevation of extra-cellular levels of glutamate following a pretreatment with patients' CSF. Conclusion: These results support a direct role of NMDA-R antibodies upon altering glutamatergic transmission. Furthermore, we provide additional evidence in vivo that NMDA-R antibodies deregulate the glutamatergic pathways and that the encephalitis associated with these antibodies is an auto-immune synaptic disorder. © 2010 Manto et al; licensee BioMed Central Ltd.SCOPUS: ar.jinfo:eu-repo/semantics/publishe