Nanocrystalline magnetite Fe3O4 samples with a grain size of about 40 nm have been synthesized by an optimized sol-gel method. The single phase of spinel magnetite was confirmed by both X-ray diffraction and transmission electron microscopy. It has been found that the magnetoresistance of the samples at low field (LFMR) is relatively large, and with the decrease of temperature its value at a field of 0.5 T changes dramatically from -2.5% at 300 K to -17.0% at 55 K. With the further decrease of temperature a sharp drop occurs for the magnitude of the magnetoresistance (MR), regarded as a spin (cluster) glass transition in the surface region of the grains that can be confirmed by the zero-field-cooled and field-cooled magnetization and ac susceptibility measurement. The mechanism of the magnetic and transport properties was discussed.

Genetic variants in matrix metalloproteinase (MMP) gene may influence the biological function of these enzymes and change their role in carcinogenesis and progression. The effect of MMP2 C-1306T and MMP9 C-1562T polymorphisms on genetic susceptibility has been investigated in various kinds of cancer. However, the relationship between these polymorphisms and risk of recurrence of hepatocellular carcinoma (HCC) after liver transplantation (LT) has not been reported. The present study was designed to investigate the association of these two loci with the risk of HCC recurrence in 93 HCC patients treated with LT. Genotyping was performed using direct DNA sequencing. For MMP2 C-1306T variant, patients with CT heterozygous conferred a 58% reduction in recurrence risk (risk ratio: 0.419; 95% confidence interval: 0.177-0.994). The mean recurrence-free survival for CT genotype was significantly longer than that for homozygous CC patients (30.4 vs 19.3 months, p = 0.019). However, no association was found between MMP9 C-1562T polymorphisms and recurrence of HCC (p = 0.259). These findings suggest that MMP2 promoter polymorphisms may provide some predictive value for HCC recurrence after LT.

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ABSTRACT. Nuclear factor (NF)-κB is a transcription factor that controls cell proliferation, differentiation, and immunity. Activated NF-κB1 is associated with the pathogenesis of coronary artery disease (CAD) and genetic polymorphisms in NF-κB1 have a plausible role in modulating the risk of CAD. To identify markers that contribute to the genetic susceptibility to CAD, we examined the potential association between CAD and single nucleotide polymorphisms (SNPs; rs28362491, rs230531, rs230528, rs1005819, rs4648055, rs3774964, and rs3774968) in the NF-κB1 gene using SNaPshot SNP genotyping assay. Participants included 361 patients with CAD and 385 healthy controls. The genotype and allele frequencies of the rs28362491 (promoter region) polymorphism in the CAD patients were significantly different from those in the healthy controls. The frequency of the D allele was significantly higher in CAD patients than 2 X.L. Guo et al. Genetics and Molecular Research 15 (3): gmr.15038072 in the healthy controls (P = 0.005 after Bonferroni correction). Strong linkage disequilibrium was observed in one block (D' > 0.9). Haplotype analysis revealed that haplotypes in block 1 of the NF-κB1 gene did not display a risk or protective effect (P > 0.05). These data suggest that NF-κB1 gene polymorphisms confer susceptibility to CAD and also support the notion that dysfunction of NF-κB1 is involved in the pathophysiological process of CAD.

In order to solve the problem that the location prediction rate of the base station is low due to the insufficient MR data within the coverage range of the base station, based on the inspiration of the grip rule, the longitude and latitude correction model of the base station in the main cell based on big data is established by using the coarse positioning data and fine positioning data of adjacent cells. Taking Guangdong Telecom as an example, the experimental results show that the prediction rate of base station location is significantly improved from 69% to 92%.

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