Objective To develop specific targeted magnetic biomarkers which can selectively mark the senile plaques in Alzheimer' s disease (AD) and verify its feasibility and validity.Methods Aβ1-40 peptide and Tat-PTD ( Tat-protein transduction domain) was binded with dextran-coated ultrasmall superparamagnetic iron oxide ( USPIO) particles.Visualization of plaques in vivo in Alzheimer transgenic mice was investigated at 7.0 Tesla using T2 sequences after intravenous administration of the targeted nanoiron contrast agent and verified by histological staining.Results The targeted nano-iron contrast agent could enter the cultured neural stem cells,and was able to accelerate T2 relaxation rates of water protons in the cells and negatively reinforce the T2 signal intensity in the labeled cells.Plaques were specifically detected in vivo by magnetic resonance imaging ( MRI) and correlated well with histological staining after injection of nano-iron contrast agent into the APP/PS1 mice.Conclusion The targeted nano-iron contrast agent has the ability of selectively labeling the senile plaques in AD brain tissues in vivo,which might enable the early detection of plaques by MRI and can be further applied in the studies of early diagnosis of AD.

The purpose of this study is trying to analysis the homology between four lentogenic Class I genotype 3 Newcastle disease virus isolates from different hosts with NDV strain NDV 08-004, which was the first obtained complete genome sequence virus of class I genotype 3. The full-length genome of NDV isolates, JS/3/09/Ch, ZJ/3/10/Ch, AH/2/10/Du and JS/9/08/Go,were determined by RT-PCR and then an alyzed. All the genomes are 15 198 nucleotides (nt) in length. Compared with the full genome sequences of Class II NDV stains (genotype IV-IX),four isolates has a 6-nt deletion in the non-coding region of nuclear phosphoprotein gene between nucleotides 1 640-1 641 and 12-nt insertion in the coding region of phospho protein gene between nucleotides 2 381-2 382. All the isolates have the motifs 112EQ/RQE/GRL117 at the cleavage site of the fusion protein, which is typical of lenogenic NDV strains, and it is in agreement with the result of pathogenic tests. The full-length genome of 4 genotype 3 NDV isolates shared 93% nucleotide identity with NDV08-004. The results of alignment of 6 viral genes showed that NP gene shared the highest identity (98.3%-96.4%) and P gene shared the lowest identity (96.1%-91.9%). The results show the following two points. First, it is concluded that the isolates from different hosts share the same genotype has the insignificant divergence in the genetic information. Second, it is proposed that the mutation rates of NP/F/L genes are lower than P/M/HN genes.
Animals ; Genome, Viral ; genetics ; Genomics ; Genotype ; Host Specificity ; genetics ; Newcastle disease virus ; classification ; genetics ; isolation & purification ; Phylogeny

Objective: To determine the changes in peripheral plasma concentrations of interleukin-10 (IL-10), interleukin -12 (IL-12) and interfoeron-γ(IFN-γ) in the patients with chronic hepatitis B virus (HBV) infection and their correlations with HBV infection stage or HBV DNA load of HBV carriers. Methods: Data of 135 patients with chronic HBV infection from March 2016 to March 2017 were collected, the patients included 32 chronic HBV carriers, 61 with chronic hepatitis and 42 with cirrhosis. Forty healthy subjects served as controls. The concentrations of IL-10, IL-12 and IFN-γ were determined using enzyme-linked immunosorbent assay (ELISA). Correlation analysis was performed using the Pearson correlation test, which was performed to analyze the correlation between IL-10, IL-12, IFN-γ and HBV infection stage, HBV DNA load of HBV carriers. Results: Compared with those in healthy controls, plasma IL-10 and IL-12 levels in patients with chronic hepatitis and cirrhosis increased significantly (F=22.06, 15.67, P=0.013, 0.021), plasma IL-10 and IL-12 levels in cirrhosis cases were higher than those in chronic hepatitis (all P<0.001), plasma IL-10 and IL-12 levels in chronic hepatitis were higher than those in chronic HBV carriers (all P<0.001). Plasma IFN-γ level in chronic HBV carriers, chronic hepatitis and cirrhosis were significantly higher than those in healthy controls (F=18.36, P=0.017). There were statistically significant differences in IFN-γ levels among the three groups in the chronic HBV carriers, chronic hepatitis and cirrhosis. IL-10, IL-12 and IFN-γ levels of the low, medium and high HBV DNA load groups were statistically significant (all P<0.05). There was no correlation between IL-10 and HBV DNA. IFN-γ, IL-12 and HBV DNA load were negatively correlated. There was no correlation between IL-10 and IFN-γ (r=0.103, P>0.05), IL-12 and IFN-γ were significantly positively correlated (r=0.687, P<0.05). Conclusions IL-10, IL-12 and IFN-γ may play an important role in the chronic HBV infection.