Biomedical subjects

Hui Hui Liu

Publications and source records attributed to Hui Hui Liu.

3 recordsLinked to original sources

PubMed2006

Array-based nano-amplification technique was applied in detection of hepatitis E virus.

A rapid method for the detection of Hepatitis E Virus (HEV) was developed by utilizing nano-gold labeled oligonucleotide probes, silver stain enhancement and the microarray technique. The 5'-end -NH(2) modified oligonucleotide probes were immobilized on the surface of the chip base as the capture probe. The detection probe was made of the 3'-end -SH modified oligonucleotide probe and nano-gold colloid. The optimal concentrations of these two probes were determined. To test the detection sensitivity and specificity of this technique, a conservative fragment of the virus RNA was amplified by the RT-PCR/PCR one step amplification. The cDNA was hybridized with the capture probes and the detection probes on microarray. The detection signal was amplified by silver stain enhancement and could be identified by naked eyes.100 fM of amplicon could be detected out on the microarray. As the results, preparation of nano-gold was improved and faster. Development time also was shortened to 2 min. Thus, considering high efficiency, low cost, good specificity and high sensitivity, this technique is alternative for the detection of HEV.

Gold↗

PubMed2005

Elevated levels of serum soluble Fas are associated with organ and tissue damage in systemic lupus erythematosus among Chinese.

The aims of the present study are to evaluate the difference of the levels of soluble Fas (sFas) antigen between patients with systemic lupus erythematosus (SLE) and healthy controls and to explore whether sFas has a role in either the disease activity or the organ damage in SLE. Serum levels of sFas were measured in 40 Chinese patients with SLE and 15 age-, gender-, and race-matched healthy controls using double antibody ELISA. SLEDAI scores for disease activity were determined. Data of organ and tissue damage was obtained from clinical records. Serum sFas levels were significantly increased in both more active (mean=8043.8 pg/ml, P<0.001) and less active SLE patients (mean=4820.2 pg/ml, P<0.001) comparing to the healthy controls (mean=3253.4 pg/ml). There was also a significant difference in serum sFas levels between the more active SLE patients and less active SLE patients (P=0.04). But, the levels of sFas didn't correlate with SLEDAI. There was a significant difference in the serum sFas levels between patients with and without CNS disease (mean=9582.6, 6634.5 pg/ml; P=0.007). The same was true when patients with and without renal disease (mean=10972.7, 6520.1 pg/ml; P=0.019), as well as serositis (mean=10385.3, 6709.1 pg/ml; P=0.005) were analyzed. sFas is elevated in sera of SLE patients, especially in patients with active SLE. The elevated levels of sFas in the sera of patients with SLE may be closely associated with damage to the kidneys, central nervous system and serosa. Serum sFas may serve as a predictor of some organ and tissue damage in SLE.

Adolescent↗

PubMed2005

Polymorphisms in the promoter region of RANTES in Han Chinese and their relationship with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex multisystem autoimmune disease afflicting more than 600,000 individuals in China. RANTES (regulated on activation, normal T cell expressed and secreted, 17q11.2-q12) is a member of the proinflammatory cytokine family known as "chemokines". It plays an important role in the attraction and recruitment of lymphocytes, monocytes and eosinophils to sites of inflammation. A total of 146 SLE patients and 159 random healthy volunteer individuals in Han Chinese patients were enrolled in this study. Genotypes of RANTES -403 locus and -28 locus were observed to be different in all racial groups. The frequency of individuals who possessed G allele at -28 locus among SLE patients was not significantly different from that among normal controls. A total of seven compound genotypes at -403 locus and -28 locus were observed in this study. The frequency of this compound genotype (-403 G/G, -28 C/C) was different between the two groups. The distribution of genotypes and alleles at RANTES-403 locus was observed to be significantly different between renal damaged group and no renal damaged group (P<0.05), while there was no significant difference in distribution of genotypes and alleles at RANTES-28 locus between the two groups. These results suggest that (a) two genetic polymorphisms in the RANTES promoter do not correlate with SLE as individual polymorphisms. (b) interaction of the polymorphisms at two loci probably exerts a risk effect against SLE and (c) polymorphism at RANTES-403 locus is probably related with renal damage.

Alleles↗