Magnetostructural correlations in antiperovskite manganese nitrides were investigated systematically for stoichiometric and solid solution Mn3Cu1−xAxN (A = Co, Ni, Zn, Ga, Ge, Rh, Pd, Ag, In, Sn or Sb). This class of nitrides is attracting great attention because of their giant negative thermal expansion, which is achieved by doping Ge or Sn into the A site as a relaxant of the sharp volume contraction on heating (spontaneous volume magnetostriction ωs) because of the magnetovolume effects. The physical background of large ωs and mechanism of how the volume contraction becomes gradual with temperature are central concerns for the physics and applications of these nitrides. An entire dataset of thermal expansion, crystal structure and magnetization demonstrates that the cubic triangular antiferromagnetic state is crucial for large ωs. The intimate relationship between ωs and the magnetic structure is discussed in terms of geometrical frustration related to the Mn6N octahedron and magnetic stress concept. The results presented herein also show that ωs depends on the number of d electrons in the A atom, suggesting the important role of the d orbitals of the A atom. Not all the dopants in the A site, but the elements that disturb the cubic triangular antiferromagnetic state, are effective in broadening the volume change. This fact suggests that instability neighboring the phase boundary is related to the broadening. The relation between the gradual volume change and the local structure anomaly is suggested by recent microprobe studies.

We found that: 1) a significant number of patients with APA had somatic mutations of the KCNJ5 gene; 2) KCNJ5 mRNA levels were higher in the APA with KCNJ5 mutations; and 3) the expression of KCNJ5 mRNA was significantly higher in APA than cortisol-producing adenomas and pheochromocytomas.

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The role of superoxide anion (O 2 ؊) and nitric oxide (NO) in the host defense mechanism against Salmonella typhimurium (LT-2) was examined by focusing on xanthine oxidase (XO) as an O 2 ؊-generating system and on inducible NO synthase (iNOS). When ICR mice were infected with a 0.1 50% lethal dose (2 ؋ 10 5 CFU) of S. typhimurium, bacterial growth in the liver reached a peak value 3 days after infection (10 4.32 CFU/g of liver) and decreased thereafter. XO activity in the liver became maximum at 7 days after infection; the value was 34.6 ؎ 1.4 mU/g of liver at 7 days (compared with 11.0 ؎ 1.3 mU/g of liver before infection). The time profile of NO production in the liver as determined by electron spin resonance spectroscopy was consistent with that of XO activity. Histological examination of infected liver showed the formation of multiple microabscesses with granulomatous lesions consisting of polymorphonuclear cells and mononuclear cells, and iNOS-expressing cells were localized in the confined areas of the microabscesses. When XO inhibitors such as allopurinol and 4-amino-6-hydroxypyrazolo[3,4-d]pyrimidine (AHPP) were administered to the infected mice, the mortality of the mice was significantly increased (10 of 21 and 11 of 20 for the allopurinol-and AHPP-treated groups, respectively, versus 2 of 20 for control mice), and bacterial growth was significantly enhanced. A similar exacerbation of the infection was obtained with N-monomethyl-L-arginine (L-NMMA) treatment of the mice. Of considerable importance is that granuloma formation in the liver was poorly developed by treatment with either XO inhibitors or L-NMMA. These results suggest that XO and NO play an important role in the antimicrobial mechanism against S. typhimurium in mice.

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder associated mainly with tumors of multiple endocrine organs. Mutations in the MEN1 gene that encodes for the menin protein are the predominant cause for hereditary MEN1 syndrome. Though menin is a tumor suppressor, its molecular mechanism of action has not been defined. Here, we report that menin interacts with AKT1 in vitro and in vivo. Menin downregulates the level of active AKT and its kinase activity. Through interaction with AKT1, menin suppresses both AKT1-induced proliferation and antiapoptosis in nonendocrine and endocrine cells. Confocal microscopy analysis revealed that menin regulates AKT1 in part by reducing the translocation of AKT1 from the cytoplasm to the plasma membrane during growth factor stimulation. Our findings may be generalizable to other cancers, insofar as we found that loss of menin expression was also associated with AKT activation in a mouse model of pancreatic islet adenoma. Together, our results suggest menin as an important novel negative regulator of AKT kinase activity. Cancer Res; 71(2); 371-82. Ó2010 AACR.