The Plasma Wave Experiment (PWE) on board the Arase (ERG) satellite

The Exploration of energization and Radiation in Geospace (ERG) project aims to study acceleration and loss mechanisms of relativistic electrons around the Earth. The Arase (ERG) satellite was launched on December 20, 2016, to explore in the heart of the Earth’s radiation belt. In the present paper, we introduce the specifications of the Plasma Wave Experiment (PWE) on board the Arase satellite. In the inner magnetosphere, plasma waves, such as the whistler-mode chorus, electromagnetic ion cyclotron wave, and magnetosonic wave, are expected to interact with particles over a wide energy range and contribute to high-energy particle loss and/or acceleration processes. Thermal plasma density is another key parameter because it controls the dispersion relation of plasma waves, which affects wave–particle interaction conditions and wave propagation characteristics. The DC electric field also plays an important role in controlling the global dynamics of the inner magnetosphere. The PWE, which consists of an orthogonal electric field sensor (WPT; wire probe antenna), a triaxial magnetic sensor (MSC; magnetic search coil), and receivers named electric field detector (EFD), waveform capture and onboard frequency analyzer (WFC/OFA), and high-frequency analyzer (HFA), was developed to measure the DC electric field and plasma waves in the inner magnetosphere. Using these sensors and receivers, the PWE covers a wide frequency range from DC to 10 MHz for electric fields and from a few Hz to 100 kHz for magnetic fields. We produce continuous ELF/VLF/HF range wave spectra and ELF range waveforms for 24 h each day. We also produce spectral matrices as continuous data for wave direction finding. In addition, we intermittently produce two types of waveform burst data, “chorus burst” and “EMIC burst.” We also input raw waveform data into the software-type wave–particle interaction analyzer (S-WPIA), which derives direct correlation between waves and particles. Finally, we introduce our PWE observation strategy and provide some initial results

Common Variants in a Novel Gene, FONG on Chromosome 2q33.1 Confer Risk of Osteoporosis in Japanese

Osteoporosis is a common disease characterized by low bone mass, decreased bone quality and increased predisposition to fracture. Genetic factors have been implicated in its etiology; however, the specific genes related to susceptibility to osteoporosis are not entirely known. To detect susceptibility genes for osteoporosis, we conducted a genome-wide association study in Japanese using ∼270,000 SNPs in 1,747 subjects (190 cases and 1,557 controls) followed by multiple levels of replication of the association using a total of ∼5,000 subjects (2,092 cases and 3,114 controls). Through these staged association studies followed by resequencing and linkage disequilibrium mapping, we identified a single nucleotide polymorphism (SNP), rs7605378 associated with osteoporosis. (combined P = 1.51×10−8, odds ratio = 1.25). This SNP is in a previously unknown gene on chromosome 2q33.1, FONG. FONG is predicted to encode a 147 amino-acid protein with a formiminotransferase domain in its N-terminal (FTCD_N domain) and is ubiquitously expressed in various tissues including bone. Our findings would give a new insight into osteoporosis etiology and pathogenesis

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Sweet's syndrome is an acute inflammatory disease of unknown etiology that is clinically characterized by the following four signs: 1) fever; 2) neutrophil polymorphonuclear leukocytosis of the blood; 3) raised painful plaques on the limbs, face, and neck; and 4) histologically, dense dermal infiltration with Abstract Neurological disorders are one of the rare complication

Detailed Anatomy of Bridging Veins Around the Foramen Magnum: a Multicenter Study Using Three-dimensional Angiography

Background and Purpose　There has been limited literature regarding the bridging veins (BVs) of the medulla oblongata around the foramen magnum (FM). The present study aims to analyze the normal angioarchitecture of the BVs around the FM using slab MIP images of three-dimensional (3D) angiography. Methods　We collected 3D angiography data of posterior fossa veins and analyzed the BVs around the FM using slab MIP images. We analyzed the course, outlet, and number of BVs around the FM. We also examined the detection rate and mean diameter of each BV. Results　Of 57 patients, 55 patients (96%) had any BV. The median number of BVs was two (range: 0–5). The BVs originate from the perimedullary veins and run anterolaterally to join the anterior condylar vein (ACV), inferior petrosal sinus, sigmoid sinus, or jugular bulb, inferolaterally to join the suboccipital cavernous sinus (SCS), laterally or posterolaterally to join the marginal sinus (MS), and posteriorly to join the MS or occipital sinus. We classified BVs into five subtypes according to the draining location: ACV, jugular foramen (JF), MS, SCS, and cerebellomedullary cistern (CMC). ACV, JF, MS, SCS, and CMC BVs were detected in 11 (19%), 18 (32%), 32 (56%), 20 (35%), and 16 (28%) patients, respectively. The mean diameter of the BVs other than CMC was 0.6 mm, and that of CMC BV was 0.8 mm. Conclusion　Using venous data from 3D angiography, we detected FM BVs in most cases, and the BVs were connected in various directions

Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis

The mechanisms by which mixed-lineage leukemia (MLL) fusion products resulting from in utero translocations in 11q23 contribute to leukemogenesis and infant acute leukemia remain elusive. It is still controversial whether the MLL fusion protein is sufficient to induce acute leukemia without additional genetic alterations, although carcinogenesis in general is known to result from more than 1 genetic disorder accumulating during a lifetime. Here we demonstrate that the fusion partner–mediated homo-oligomerization of MLL-SEPT6 is essential to immortalize hematopoietic progenitors in vitro. MLL-SEPT6 induced myeloproliferative disease with long latency in mice, but not acute leukemia, implying that secondary genotoxic events are required to develop leukemia. We developed in vitro and in vivo model systems of leukemogenesis by MLL fusion proteins, where activated FMS-like receptor tyrosine kinase 3 (FLT3) together with MLL-SEPT6 not only transformed hematopoietic progenitors in vitro but also induced acute biphenotypic or myeloid leukemia with short latency in vivo. In these systems, MLL-ENL, another type of the fusion product that seems to act as a monomer, also induced the transformation in vitro and leukemogenesis in vivo in concert with activated FLT3. These findings show direct evidence for a multistep leukemogenesis mediated by MLL fusion proteins and may be applicable to development of direct MLL fusion–targeted therapy

Disruption of Sept6, a Fusion Partner Gene of MLL, Does Not Affect Ontogeny, Leukemogenesis Induced by MLL-SEPT6, or Phenotype Induced by the Loss of Sept4

Septins are evolutionarily conserved GTP-binding proteins that can heteropolymerize into filaments. Recent studies have revealed that septins are involved in not only diverse normal cellular processes but also the pathogenesis of various diseases, including cancer. SEPT6 is ubiquitously expressed in tissues and one of the fusion partner genes of MLL in the 11q23 translocations implicated in acute leukemia. However, the roles of this septin in vivo remain elusive. We have developed Sept6-deficient mice that exhibited neither gross abnormalities, changes in cytokinesis, nor spontaneous malignancy. Sept6 deficiency did not cause any quantitative changes in any of the septins evaluated in this study, nor did it cause any additional changes in the Sept4-deficient mice. Even the depletion of Sept11, a close homolog of Sept6, did not affect the Sept6-null cells in vitro, thus implying a high degree of redundancy in the septin system. Furthermore, a loss of Sept6 did not alter the phenotype of myeloproliferative disease induced by MLL-SEPT6, thus suggesting that Sept6 does not function as a tumor suppressor. To our knowledge, this is the first report demonstrating that a disruption of the translocation partner gene of MLL in 11q23 translocation does not contribute to leukemogenesis by the MLL fusion gene