Hokkaido University

About: Hokkaido University is a education organization based out in Sapporo, Hokkaidô, Japan. It is known for research contribution in the topics: Catalysis & Population. The organization has 53925 authors who have published 115403 publications receiving 2651647 citations. The organization is also known as: Hokudai & Hokkaidō daigaku.

Genomic analysis of immunity in a Urochordate and the emergence of the vertebrate immune system: “waiting for Godot”

Abstract: Genome-wide sequence analysis in the invertebrate chordate, Ciona intestinalis, has provided a comprehensive picture of immune-related genes in an organism that occupies a key phylogenetic position in vertebrate evolution. The pivotal genes for adaptive immunity, such as the major histocompatibility complex (MHC) class I and II genes, T-cell receptors, or dimeric immunoglobulin molecules, have not been identified in the Ciona genome. Many genes involved in innate immunity have been identified, including complement components, Toll-like receptors, and the genes involved in intracellular signal transduction of immune responses, and show both expansion and unexpected diversity in comparison with the vertebrates. In addition, a number of genes were identified which predicted integral membrane proteins with extracellular C-type lectin or immunoglobulin domains and intracellular immunoreceptor tyrosine-based inhibitory motifs (ITIMs) and immunoreceptor tyrosine-based activation motifs (ITAMs) (plus their associated signal transduction molecules), suggesting that activating and inhibitory receptors have an MHC-independent function and an early evolutionary origin. A crucial component of vertebrate adaptive immunity is somatic diversification, and the recombination activating genes (RAG) and activation-induced cytidine deaminase (AID) genes responsible for the Generation of diversity are not present in Ciona. However, there are key V regions, the essential feature of an immunoglobulin superfamily VC1-like core, and possible proto-MHC regions scattered throughout the genome waiting for Godot.

FDG Uptake and Glucose Transporter Subtype Expressions in Experimental Tumor and Inflammation Models

Abstract: Although FDG uptake is closely related to the expression of the glucose transporter (GLUT) in malignant tumors, such a relationship has not been fully investigated in inflammatory lesions. The aim of our study was to determine the expression of GLUT subtypes in experimental inflammatory lesions and to compare the results with those in malignant tumors in relation to FDG accumulation. Methods: Rats were inoculated with a suspension of Staphylococcus aureus or allogenic hepatoma cells (KDH-8) into the left calf muscle. Five days after S. aureus inoculation (n 5 9) and 14 d after KDH-8 inoculation (n 5 11), [14C]FDG was injected intravenously and its accumulation in the infectious and tumor tissues was determined as the percentage activity of the injected dose per gram of tissue (%ID/g). The expression of glucose transporters (GLUT-1 to GLUT-5) was investigated by immunostaining the infectious tissues (n 5 6) and the tumor tissues (n 5 6). Immunohistochemical grading was assessed semiquantitatively by 5 observers. Results: The [ 14 C]FDG uptake was significantly higher in the tumor lesion than in the inflammatory lesion (2.04 6 0.38 %ID/g vs. 0.72 6 0.15 %ID/g; P , 0.0001). The tumor and inflammatory tissues highly expressed GLUT-1 and GLUT-3. The GLUT-1 expression level was significantly higher in the tumor tissue than in the inflammatory tissue (P , 0.05). Conclusion: The results based on our models showed a high FDG uptake and high GLUT-1 expression level not only in the tumor lesion but also in the inflammatory lesion. The higher GLUT-1 expression level in the tumor lesion may partially explain the higher FDG accumulation in the tumor than in the inflammatory lesion.

Phantom: A smoothed particle hydrodynamics and magnetohydrodynamics code for astrophysics

Abstract: We present Phantom, a fast, parallel, modular, and low-memory smoothed particle hydrodynamics and magnetohydrodynamics code developed over the last decade for astrophysical applications in three dimensions. The code has been developed with a focus on stellar, galactic, planetary, and high energy astrophysics, and has already been used widely for studies of accretion discs and turbulence, from the birth of planets to how black holes accrete. Here we describe and test the core algorithms as well as modules for magnetohydrodynamics, self-gravity, sink particles, dust–gas mixtures, H2 chemistry, physical viscosity, external forces including numerous galactic potentials, Lense–Thirring precession, Poynting–Robertson drag, and stochastic turbulent driving. Phantom is hereby made publicly available.

Synoptic relationships between surface Chlorophyll- a and diagnostic pigments specific to phytoplankton functional types

Abstract: . Error-quantified, synoptic-scale relationships between chlorophyll-a (Chl-a) and phytoplankton pigment groups at the sea surface are presented. A total of ten pigment groups were considered to represent three Phytoplankton Size Classes (PSCs, micro-, nano- and picoplankton) and seven Phytoplankton Functional Types (PFTs, i.e. diatoms, dinoflagellates, green algae, prymnesiophytes (haptophytes), pico-eukaryotes, prokaryotes and Prochlorococcus sp.). The observed relationships between Chl-a and PSCs/PFTs were well-defined at the global scale to show that a community shift of phytoplankton at the basin and global scales is reflected by a change in Chl-a of the total community. Thus, Chl-a of the total community can be used as an index of not only phytoplankton biomass but also of their community structure. Within these relationships, we also found non-monotonic variations with Chl-a for certain pico-sized phytoplankton (pico-eukaryotes, Prokaryotes and Prochlorococcus sp.) and nano-sized phytoplankton (Green algae, prymnesiophytes). The relationships were quantified with a least-square fitting approach in order to enable an estimation of the PFTs from Chl-a where PFTs are expressed as a percentage of the total Chl-a. The estimated uncertainty of the relationships depends on both PFT and Chl-a concentration. Maximum uncertainty of 31.8% was found for diatoms at Chl-a = 0.49 mg m−3. However, the mean uncertainty of the relationships over all PFTs was 5.9% over the entire Chl-a range observed in situ (0.02

Mutations in COQ2 in familial and sporadic multiple-system atrophy the multiple-system atrophy research collaboration

Abstract: BACKGROUND Multiple-system atrophy is an intractable neurodegenerative disease characterized by autonomic failure in addition to various combinations of parkinsonism, cerebellar ataxia, and pyramidal dysfunction. Although multiple-system atrophy is widely considered to be a nongenetic disorder, we previously identified multiplex families with this disease, which indicates the involvement of genetic components. METHODS In combination with linkage analysis, we performed whole-genome sequencing of a sample obtained from a member of a multiplex family in whom multiple-system atrophy had been diagnosed on autopsy. We also performed mutational analysis of samples from members of five other multiplex families and from a Japanese series (363 patients and two sets of controls, one of 520 persons and one of 2383 persons), a European series (223 patients and 315 controls), and a North American series (172 patients and 294 controls). On the basis of these analyses, we used a yeast complementation assay and measured enzyme activity of parahydroxybenzoate-polyprenyl transferase. This enzyme is encoded by the gene COQ2 and is essential for the biosynthesis of coenzyme Q10. Levels of coenzyme Q10 in lymphoblastoid cells and brain tissue were measured on high-performance liquid chromatography. RESULTS We identified a homozygous mutation (M78V-V343A/M78V-V343A) and compound heterozygous mutations (R337X/V343A) in COQ2 in two multiplex families. Furthermore, we found that a common variant (V343A) and multiple rare variants in COQ2, all of which are functionally impaired, are associated with sporadic multiple-system atrophy. The V343A variant was exclusively observed in the Japanese population. CONCLUSIONS Functionally impaired variants of COQ2 were associated with an increased risk of multiple-system atrophy in multiplex families and patients with sporadic disease, providing evidence of a role of impaired COQ2 activities in the pathogenesis of this disease. (Funded by the Japan Society for the Promotion of Science and others.).