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.

IJER editorial: The future of the internal combustion engine:

Abstract: Internal combustion (IC) engines operating on fossil fuel oil provide about 25% of the world’s power (about 3000 out of 13,000 million tons oil equivalent per year—see Figure 1), and in doing so, they produce about 10% of the world’s greenhouse gas (GHG) emissions (Figure 2). Reducing fuel consumption and emissions has been the goal of engine researchers and manufacturers for years, as can be seen in the two decades of ground-breaking peer-reviewed articles published in this International Journal of Engine Research (IJER). Indeed, major advances have been made, making today’s IC engine a technological marvel. However, recently, the reputation of IC engines has been dealt a severe blow by emission scandals that threaten the ability of this technology to make significant and further contributions to the reduction of transportation sector emissions. In response, there have been proposals to replace vehicle IC engines with electric-drives with the intended goals of further reducing fuel consumption and emissions, and to decrease vehicle GHG emissions. Indeed, some potential students and researchers are being dissuaded from seeking careers in IC engine research due to disparaging statements made in the popular press and elsewhere that disproportionately blame IC engines for increasing atmospheric GHGs. Without a continuous influx of enthusiastic, welltrained engineers into the profession, the potential further benefits that improved IC engines can still provide will not be realized. As responsible automotive engineers and as stewards of the environment for future generations, it is up to our community to make an honest assessment of the progress made in the development of IC engines over the past century, with their almost universal adoption to meet the world’s mobility and power generation needs. Considering that the maturity of IC engine technology is something that many other technologies/possibilities do not have, we also need to assess the potential for future progress, as well as to assess the benefits offered by competitor technologies, in order to make responsible recommendations for future directions. Factors impacting that future are discussed in this editorial and include the following:

Analysis of a human DNA excision repair gene involved in group A xeroderma pigmentosum and containing a zinc-finger domain

Abstract: Xeroderma pigmentosum (XP) is an autosomal recessive disease, characterized by a high incidence of sunlight-induced skin cancer. Cells from people with this condition are hypersensitive to ultraviolet because of a defect in DNA repair. There are nine genetic complementation groups of XP, groups A-H and a variant. We have cloned the mouse DNA repair gene that complements the defect of group A, the XPAC gene. Here we report molecular cloning of human and mouse XPAC complementary DNAs. Expression of XPAC cDNA confers ultraviolet-resistance on several group A cell lines, but not on lines of other XP groups. Almost all group A lines tested showed abnormality or absence of XPAC messenger RNAs. These results indicate that a defective XPAC gene causes group A XP. The human and mouse XPAC genes are located on chromosome 9q34.1 and chromosome 4C2, respectively. Human XPAC cDNA encodes a protein of 273 amino acids with a zinc-finger motif.

The structure of Atg4B-LC3 complex reveals the mechanism of LC3 processing and delipidation during autophagy.

Abstract: Atg8 is conjugated to phosphatidylethanolamine (PE) by ubiquitin-like conjugation reactions. Atg8 has at least two functions in autophagy: membrane biogenesis and target recognition. Regulation of PE conjugation and deconjugation of Atg8 is crucial for these functions in which Atg4 has a critical function by both processing Atg8 precursors and deconjugating Atg8–PE. Here, we report the crystal structures of catalytically inert human Atg4B (HsAtg4B) in complex with processed and unprocessed forms of LC3, a mammalian orthologue of yeast Atg8. On LC3 binding, the regulatory loop and the N-terminal tail of HsAtg4B undergo large conformational changes. The regulatory loop masking the entrance of the active site of free HsAtg4B is lifted by LC3 Phe119, so that a groove is formed along which the LC3 tail enters the active site. At the same time, the N-terminal tail masking the exit of the active site of HsAtg4B in the free form is detached from the enzyme core and a large flat surface is exposed, which might enable the enzyme to access the membrane-bound LC3–PE.

Synergistic effect of Nod1 and Nod2 agonists with Toll-like receptor agonists on human dendritic cells to generate interleukin-12 and T helper type 1 cells

Abstract: A synthetic Nod2 agonist, muramyldipeptide (MDP), and two Nod1 agonists, FK565 and FK156, mimic the bacterial peptidoglycan moiety and are powerful adjuvants that induce cell-mediated immunity, especially delayed-type hypersensitivity. In this study, we used human dendritic cell (DC) cultures to examine possible T helper type 1 (Th1) responses induced by MDP and FK565/156 in combination with various synthetic Toll-like receptor (TLR) agonists, including synthetic lipid A (TLR4 agonist), the synthetic triacyl lipopeptide Pam3CSSNA (TLR2 agonist), poly(I:C) (TLR3 agonist), and CpG DNA (TLR9 agonist). Immature DCs derived from human monocytes expressed mRNAs for Nod1, Nod2, TLR2, TLR3, TLR4, and TLR9. The stimulation of DCs with MDP and FK565 in combination with lipid A, poly(I:C), and CpG DNA, but not with Pam3CSSNA, synergistically induced interleukin-12 (IL-12) p70 and gamma interferon (IFN-γ), but not IL-18, in culture supernatants and induced IL-15 on the cell surface. In correlation with the cytokine induction, an upregulation of the mRNA expression of these cytokine genes was observed. Notably, IL-12 p35 mRNA expression increased >1,000-fold upon stimulation with lipid A plus either MDP or FK565 compared with stimulation with each stimulant alone. In contrast, for the expression of CD83 and costimulatory molecules such as CD40, CD80, and CD86, no synergistic effects were observed upon stimulation with Nod plus TLR agonists. The culture supernatants of DCs stimulated with lipid A plus either MDP or FK565 activated human T cells to produce high levels of IFN-γ, and the activity was attributable to DC-derived IL-12. These findings suggest that Nod1 and Nod2 agonists in combination with TLR3, TLR4, and TLR9 agonists synergistically induce IL-12 and IFN-γ production in DCs to induce Th1-lineage immune responses.