Tohoku University

About: Tohoku University is a education organization based out in Sendai, Japan. It is known for research contribution in the topics: Magnetization & Population. The organization has 72116 authors who have published 170791 publications receiving 3941714 citations. The organization is also known as: Tōhoku daigaku.

The Molecular Mechanisms Regulating the KEAP1-NRF2 Pathway.

Abstract: The KEAP1-NRF2 pathway is the principal protective response to oxidative and electrophilic stresses. Under homeostatic conditions, KEAP1 forms part of an E3 ubiquitin ligase, which tightly regulates the activity of the transcription factor NRF2 by targeting it for ubiquitination and proteasome-dependent degradation. In response to stress, an intricate molecular mechanism facilitated by sensor cysteines within KEAP1 allows NRF2 to escape ubiquitination, accumulate within the cell, and translocate to the nucleus, where it can promote its antioxidant transcription program. Recent advances have revealed that KEAP1 contains multiple stress sensors and inactivation modalities, which together allow diverse cellular inputs, from oxidative stress and cellular metabolites to dysregulated autophagy, to regulate NRF2 activity. This integration of the KEAP1-NRF2 system into multiple cellular signaling and metabolic pathways places NRF2 activation as a critical regulatory node in many disease phenotypes and suggests that the pharmaceutical modulation of NRF2's cytoprotective activity will be beneficial for human health in a broad range of noncommunicable diseases.

A survey of routing attacks in mobile ad hoc networks

Abstract: Recently, mobile ad hoc networks became a hot research topic among researchers due to their flexibility and independence of network infrastructures, such as base stations. Due to unique characteristics, such as dynamic network topology, limited bandwidth, and limited battery power, routing in a MANET is a particularly challenging task compared to a conventional network. Early work in MANET research has mainly focused on developing an efficient routing mechanism in such a highly dynamic and resource-constrained network. At present, several efficient routing protocols have been proposed for MANET. Most of these protocols assume a trusted and cooperative environment. However, in the presence of malicious nodes, the networks are vulnerable to various kinds of attacks. In MANET, routing attacks are particularly serious. In this article, we investigate the state-of-the-art of security issues in MANET. In particular, we examine routing attacks, such as link spoofing and colluding misrelay attacks, as well as countermeasures against such attacks in existing MANET protocols.

Isolation and indentification on meiosis inducing substance in starfish Asterias amurensis.

Abstract: INVESTIGATIONS of the mechanism of starfish spawning induced by injection of a water extract of radial nerves have shown that an active polypeptide acts on the ovary and induces the production of a second substance which is, in the true sense, a meiosis inducing factor as well as a spawning inducing factor1–7. The neural substance has therefore been renamed gonad stimulating substance (GSS), and the second substance, produced in the ovary, is meiosis inducing substance (MIS)5,7. Isolated ovarian fragments immersed in seawater containing MIS discharge their eggs4,5,7, while isolated oocytes with germinal vesicles treated with MIS mature4–7. The production of MIS by GSS has been demonstrated in isolated ovarian fragments of seven species of starfish, and it seems to be non-species specific among starfishes7. MIS is heat stable (100° C, 30 min) and is not a peptide5,6.

Cyclic ADP-ribose in insulin secretion from pancreatic beta cells

Abstract: Inositol 1,4,5-trisphosphate (IP3) is thought to be a second messenger for intracellular calcium mobilization. However, in a cell-free system of islet microsomes, cyclic adenosine diphosphate-ribose (cADP-ribose), a nicotinamide adenine dinucleotide (NAD+) metabolite, but not IP3, induced calcium release. In digitonin-permeabilized islets, cADP-ribose and calcium, but not IP3, induced insulin secretion. Islet microsomes released calcium when combined with the extract from intact islets that had been incubated with high concentrations of glucose. Sequential additions of cADP-ribose inhibited the calcium release response to extracts from islets treated with high concentrations of glucose. Conversely, repeated additions of the islet extract inhibited the calcium release response to a subsequent addition of cADP-ribose. These results suggest that cADP-ribose is a mediator of calcium release from islet microsomes and may be generated in islets by glucose stimulation, serving as a second messenger for calcium mobilization in the endoplasmic reticulum.