An evaluation of geomagnetic harmonic series for 1100 kilometers altitude

Geomagnetic harmonic series evaluation for 1100 kilometers altitude using satellite observation

The scaler magnetic intensity at 1100 kilometers in middle and low latitudes

Satellite borne magnetometer for measuring scalar magnetic intensities in middle and low latitudes at 1100 km altitud

The Molecular Interstellar Medium in Ultraluminous Infrared Galaxies

We present CO observations of a large sample of ultraluminous IR galaxies out to z = 0.3. Most of the galaxies are interacting, but not completed mergers. All but one have high CO(1-0) luminosities, log(Lco [K-km/s-pc^2]) = 9.92 +/- 0.12. The dispersion in Lco is only 30%, less than that in the FIR luminosity. The integrated CO intensity correlates Strongly with the 100 micron flux density, as expected for a black body model in which the mid and far IR radiation are optically thick. We use this model to derive sizes of the FIR and CO emitting regions and the enclosed dynamical masses. Both the IR and CO emission originate in regions a few hundred parsecs in radius. The median value of Lfir/Lco = 160 Lsun/(K-km/s-pc^2), within a factor of two of the black body limit for the observed FIR temperatures. The entire ISM is a scaled up version of a normal galactic disk with densities a factor of 100 higher, making even the intercloud medium a molecular region. Using three different techniques of H2 mass estimation, we conclude that the ratio of gas mass to Lco is about a factor of four lower than for Galactic molecular clouds, but that the gas mass is a large fraction of the dynamical mass. Our analysis of CO emission reduces the H2 mass from previous estimates of 2-5e10 Msun to 0.4-1.5e10 Msun, which is in the range found for molecular gas rich spiral galaxies. A collision involving a molecular gas rich spiral could lead to an ultraluminous galaxy powered by central starbursts triggered by the compression of infalling preexisting GMC's.Comment: 34 pages LaTeX with aasms.sty, 14 Postscript figures, submitted to ApJ Higher quality versions of Figs 2a-f and 7a-c available by anonymous FTP from ftp://sbast1.ess.sunysb.edu/solomon/

Synergistic Effects of Processing and Nanofiber Reinforcement on the mechanical and Ferroelectric Performance of Geopolymer Matrix Composites

tThis study involved the evaluation of mechanical and ferroelectric properties of a new classof nanofiller infused inorganic polymer (geopolymer, GP). To evaluate the mechanical per-formance, compressive strength and fracture resistance of neat and nanofillers infused GPwere studied at various treatment temperatures. It was found that, addition of 5 vol% alu-mina nanofiber (ANF), increased compressive strength and modulus by over 30% and 60%,respectively, while it increased fracture toughness (KIC) by over 60% compared to the baselinespecimens. Simultaneously, ferroelectric properties were investigated at various treatmenttemperatures (250◦C, 650◦C and 870◦C). Remarkably, higher ferroelectric hysteresis wasobserved with the GP treated at 870◦C and remnant polarization increased with the addi-tion of alumina nanofiber. Scanning Electron Microscopy confirmed that neat materials arecomposed of particles embedded into the poly-condensed matrix, where particle natureexisted until the treatment temperature reached above 870◦C. X-ray diffraction analysissuggests that, baseline geopolymer started becoming crystalline while the particle naturegradually disappeared with heating at or beyond 870◦C. The bonding between the polymerand alumina nanofiber tends to be stronger with increasing treatment temperature. Theincrease in KICwith the addition of 2 vol% and 5 vol% alumina nanofibers (ANF) is due tohomogeneous dispersion of high interfacial strength nanofillers, which essentially createstrong crack bridging and crack deflection effect. The increase in ferroelectric hysteresisis potentially due to the formation of hierarchical order and domain reorientation of thematerials

Competition between Intramolecular and Intermolecular Interactions in an Amyloid-Forming Protein

Despite much progress in understanding the folding and the aggregation processes of proteins, the rules defining their interplay have yet to be fully defined. This problem is of particular importance since many diseases are initiated by protein unfolding and hence the propensity to aggregate competes with intramolecular collapse and other folding events. Here, we describe the roles of intramolecular and intermolecular interactions in defining the length of the lag time and the apparent rate of elongation of the 100-residue protein human β2-microglobulin at pH 2.5, commencing from an acid-denatured state that lacks persistent structure but contains significant non-random hydrophobic interactions. Using a combination of site-directed mutagenesis, quantitative kinetic analysis and computational methods, we show that only a single region of about 10 residues in length, determines the rate of fibril formation, despite the fact that other regions exhibit a significant intrinsic propensity for aggregation. We rationalise these results by analysing the effect of incorporating the conformational properties of acid-unfolded β2-microglobulin and its variants at pH 2.5 as measured by NMR spectroscopy into the Zyggregator aggregation prediction algorithm. These results demonstrate that residual structure in the precursor state modulates the intrinsic propensity of the polypeptide chain to aggregate and that the algorithm developed here allows the key regions for aggregation to be more clearly identified and the rates of their self-association to be predicted. Given the common propensity of unfolded chains to form non-random intramolecular interactions as monomers and to self-assemble subsequently into amyloid fibrils, the approach developed should find widespread utility for the prediction of regions important in amyloid formation and their rates of self-assembly. © 2009 Elsevier Ltd. All rights reserved

Neuropathologic basis of frontotemporal dementia in progressive supranuclear palsy.

BackgroundProgressive supranuclear palsy (PSP) is a neurodegenerative disorder characterized by neuronal loss in the extrapyramidal system with pathologic accumulation of tau in neurons and glia. The most common clinical presentation of PSP, referred to as Richardson syndrome, is that of atypical parkinsonism with vertical gaze palsy, axial rigidity, and frequent falls. Although cognitive deficits in PSP are often ascribed to subcortical dysfunction, a subset of patients has dementia with behavioral features similar to the behavioral variant of frontotemporal dementia. In this study we aimed to identify the clinical and pathological characteristics of PSP presenting with frontotemporal dementia.MethodsIn this study, we compared clinical and pathologic characteristics of 31 patients with PSP with Richardson syndrome with 15 patients with PSP with frontotemporal dementia. For pathological analysis, we used semiquantitative methods to assess neuronal and glial lesions with tau immunohistochemistry, as well image analysis of tau burden using digital microscopic methods.ResultsWe found greater frontal and temporal neocortical neuronal tau pathology in PSP with frontotemporal dementia compared with PSP with Richardson syndrome. White matter tau pathology was also greater in PSP with frontotemporal dementia than PSP with Richardson syndrome. Genetic and demographic factors were not associated with atypical distribution of tau pathology in PSP with frontotemporal dementia.ConclusionsThe results confirm the subset of cognitive-predominant PSP mimicking frontotemporal dementia in PSP. PSP with frontotemporal dementia has distinct clinical features that differ from PSP with Richardson syndrome, as well as differences in distribution and density of tau pathology. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society

Characterization of the Response of Primary Cells Relevant to Dialysis-Related Amyloidosis to β2-Microglobulin Monomer and Fibrils

The formation of insoluble amyloid fibrils is associated with an array of devastating human diseases. Dialysis-related amyloidosis (DRA) is a severe complication of hemodialysis that results in the progressive destruction of the bones and joints. Elevated concentrations of β2-microglobulin (β2m) in the serum of subjects on hemodialysis promote the formation of amyloid fibrils in the osteoarticular tissues, but the cellular basis for the destruction of these tissues in DRA is poorly understood. In this study we performed a systematic analysis of the interaction of monomeric and fibrillar β2m with primary human cells of the types present in the synovial joints of subjects with DRA. Building upon observations that macrophages infiltrate β2m amyloid deposits in vivo we demonstrate that monocytes, the precursors of macrophages, cannot degrade β2m fibrils, and that both monomeric β2m and fibrillar β2m are cytotoxic to these cells. β2m fibrils also impair the formation of bone resorbing osteoclasts from monocytes and reduce the viability of osteoblasts, the cell type that produces bone. As a consequence, we predict that β2m amyloid will disrupt the remodelling of the bone, which is critical for the maintenance of this tissue. Moreover, we show that β2m fibrils reduce the viability of chondrocytes, rationalizing the loss of cartilage in DRA. Together, our observations demonstrate that β2m cytotoxicity has multiple cellular targets in the osteoarticular tissues and is likely to be a key factor in the bone and joint destruction characteristic of DRA

Unfolding dynamics of proteins under applied force

Understanding the mechanisms of protein folding is a major challenge that is being addressed effectively by collaboration between researchers in the physical and life sciences. Recently, it has become possible to mechanically unfold proteins by pulling on their two termini using local force probes such as the atomic force microscope. Here, we present data from experiments in which synthetic protein polymers designed to mimic naturally occurring polyproteins have been mechanically unfolded. For many years protein folding dynamics have been studied using chemical denaturation, and we therefore firstly discuss our mechanical unfolding data in the context of such experiments and show that the two unfolding mechanisms are not the same, at least for the proteins studied here. We also report unexpected observations that indicate a history effect in the observed unfolding forces of polymeric proteins and explain this in terms of the changing number of domains remaining to unfold and the increasing compliance of the lengthening unstructured polypeptide chain produced each time a domain unfolds

Charmonium states in QCD-inspired quark potential model using Gaussian expansion method

We investigate the mass spectrum and electromagnetic processes of charmonium system with the nonperturbative treatment for the spin-dependent potentials, comparing the pure scalar and scalar-vector mixing linear confining potentials. It is revealed that the scalar-vector mixing confinement would be important for reproducing the mass spectrum and decay widths, and therein the vector component is predicted to be around 22%. With the state wave functions obtained via the full-potential Hamiltonian, the long-standing discrepancy in M1 radiative transitions of $J/\psi$ and $\psi^{\prime}$ are alleviated spontaneously. This work also intends to provide an inspection and suggestion for the possible $c\bar{c}$ among the copious higher charmonium-like states. Particularly, the newly observed X(4160) and X(4350) are found in the charmonium family mass spectrum as $M(2^1D_2)= 4164.9$ MeV and $M(3^3P_2)= 4352.4$ MeV, which strongly favor the $J^{PC}=2^{-+}, 2^{++}$ assignments respectively. The corresponding radiative transitions, leptonic and two-photon decay widths have been also predicted theoretically for the further experimental search.Comment: 16 pages,3 figure

Granulocyte-macrophage colony stimulating factor (GM-CSF) after high-dose melphalan in patients with advanced colon cancer.

Nine patients with progressive, metastatic disease from primary carcinoma of the colon were entered into a phase I/II study using continuous intravenous infusions of granulocyte-macrophage colony-stimulating factor (GM-CSF) and high dose melphalan (120 mg m-2). GM-CSF was given alone to six patients during the first part of the study to determine a dose that would produce a peripheral leucocyte count (WCC) greater than or equal to 50 X 10(9) 1(-1) and was initially given at 3 micrograms kg-1 day-1 and escalated to 10 micrograms kg-1 day-1 after 10 days. The infusion was discontinued when the WCC exceeded 50 X 10(9) 1(-1) and after a gap of one week, melphalan was given over 30 min. GM-CSF was recommenced 8 h later and was continued until the neutrophil count had exceeded 0.5 X 10(9) 1(-1) for greater than 1 week. One patient achieved a WCC greater than 50 X 10(9) 1(-1) with GM-CSF 3 micrograms kg-1 day-1, but the other five who entered this phase of the study required dose escalation to 10 micrograms kg-1. No toxicity attributed to GM-CSF was seen. After melphalan, the median times to severe neutropenia (less than 0.5 X 10(9) 1(-1] and thrombocytopenia (greater than 20 X 10(9) 1(-1] were 6 and 9 days respectively. The median durations of neutropenia and thrombocytopenia were 14 and 10 days respectively. All patients required intensive support with a median duration of inpatient stay of 24 days. There was one treatment related death due to renal failure. One complete and two partial remissions (33% response rate) were seen but these were of short duration (median of 10 weeks). This study demonstrates that GM-CSF given by continuous intravenous infusion produces significant increments of peripheral granulocyte counts at 3 and 10 micrograms kg-1 day-1 and is not associated with any toxicity. The duration of neutropenia and thrombocytopenia induced by high-dose melphalan appears to be reduced by the subsequent administration of GM-CSF to times which are at least as short as have been reported in historical series which have used autologous bone marrow rescue