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In the work, high nitrogen γ-Fe based alloy was fabricated by N2pressure sintering in which the diffused N content could be up to 0.521wt%. Microstructure and mechanical properties were systematically studied. The increased activity of N atom with the added N2pressure accelerated the generation of MnSiN2, which had an orthorhombic structure of an orientation relation of (11¯1)γ-Fe//(121¯)MnSiN2with γ-Fe. HRTEM map displayed the incoherent interface of duplex phase on account of a large difference of the crystal plane distance between (11¯1)γ-Fe(d11¯1 = 0.2082 nm) and (121¯)MnSiN2(d121¯ = 0.2428 nm). Besides, due to the solute N atoms in γ-Fe, an ordered structure with a superlattice structure of selective electron diffraction spots was formed. The elevated nanohardness for austenite grains implied the solution strengthening mechanism of N. The EBSD diagrams showed that the grain sizes of austenite are 9.81, 7.27 and 6.22um respectively, indicating that the formation and precipitation of MnSiN2hindered the grain growth and led to the finer grain structure with the increased pressure of 0.05Mpa, 0.5Mpa and 1Mpa. The combination of solution strengthening and fine crystal reinforcing was the main reinforcement mechanism which enhanced the hardness austenite grains and wear resistance.

O6-Alkylguanine-DNA alkyltransferase (AGT, EC 2.1.1.63) is a principle DNA repair protein in repairing O6-alkylguanine in DNA, a major premutagenic lesion produced by environmental and therapeutic alkylating agents. AGT plays a critical role in protecting cells against mutation and cytotoxicity induced by these alkylating agents. The existence of a large interindividual variation in human AGT activity level has been observed and we hypothesize that genetic polymorphism of AGT could be an important determinant for this variation. The present study reports the identification of a novel missense polymorphism in the human AGT gene. The polymorphic alteration occurs at codon 143 in exon 5, converting isoleucine (ATC) to valine (GTC). Because Ile143is adjacent to the alkeyl acceptor Cys145of the AGT active site and is conserved among mammalian AGTs, amino acid substitution at this position may affect the function of AGT. The codon 143 polymorphism appears to be linked to another new polymorphic alteration at codon 178, which converts lysine (AAG) to arginine (AGG). Because it has been reported that human AGT can be truncated at position 176 without loss of activity, the codon 178 polymorphism may not affect AGT activity. The codon 143/178 polymorphism was found in two of 90 (2) esophageal cancer patients residing in a high incidence area of China, but was not detected in 60 normal individuals residing in the same area. Six of 28 (21) non-cancer Caucasian individuals, however, were found to carry this polymorphic allele, suggesting a significant ethnic difference in distribution of this codon 143/178 polymorphism between Chinese and Caucasian individuals. In addition, we confirmed the existence of a codon 84 genetic polymorphism previously identified in a Japanese population, which converts leucine (CTT) to phenylalanine (TTT). The distribution of codon 84 polymorphism was 16, 20 and 36, respectively, in the Chinese esophageal cancer patients, Chinese and Caucasian non-cancer individuals. Coexistence of codons 84 and 143/178 polymorphic alterations was found in one Caucasian individual. In all the Chinese (n= 150) and Caucasian (n= 28) samples examined, we were unable to detect a previously reported codon 160 polymorphism (Gly to Arg) which occurred in 10–25 of the Japanese individuals and was shown to affect the reaction of AGT with the drug O6-benzylguanine. The functional significance of the codon 143/178 genetic polymorphism of human AGT and its role in determining an Individual's susceptibility to environmental alkylating carcinogens and response to alkylating chemotherapeutic drugs both remain to be studied. Pharmacogenetics 9:81–87 © 1999 Lippincott Williams & Wilkins

The obgene mRNA expression in rat brown adipose tissue (BAT) and epididymal white adipose tissue (WAT) was measured on Northern blots hybridized with a rat obgene probe. The level of obgene mRNA in BAT was about 40% of that in WAT. Fasting (36 h) or semi‐starvation (10 days) decreased the obgene mRNA level in both tissues by 62–68%, and cold exposure at 6°C (24 h) decreased it in BAT (−84%)_but not in WAT. Acute administration of the β3‐adrenergic agonist Ro 16‐8714 decreased the obgene mRNA level in BAT (−51%) and WAT (−28%) of lean Zucker rats and only in BAT (−74%) of obese falfarats. This study demonstrates that, in the rat, the obgene is not only expressed in WAT but also in BAT, and suggests that in these two tissues, the modulation of the obgene expression might be more closely associated with known alterations in cell lipid content than with changes in sympathetic activity.