ABSTRACT
A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
ABSTRACT
BACKGROUND: Polyacrylic acid (PAA)-coated gold nanorods (GNRs) were prepared in this research, and then the structure, stability, temperature increment efficiency, and biocompatibility of GNRs@PAA were detected. METHODS: It was demonstrated that GNRs@PAA coupled with an 808 nm laser had superior efficiency of hyperthermia therapy for MG63 human osteosarcoma cell. RESULTS: The mechanism of photothermal therapy of GNRs@PAA was explored, and it was proved that damaged cell membrane and DNA integration caused cell apoptosis and death, and the cell apoptosis rate had been obviously promoted by in vitro photothermal therapy which exhibited time-dose dependence. CONCLUSION: The results demonstrated that the GNRs@PAA could be a promising candidate for phototherapeutic applications in human osteosarcoma.
ABSTRACT
Hepatitis B virus (HBV) has been suspected to contribute to several autoimmune diseases, including Sjögren's syndrome (SS), although the exact mechanism is unknown. The 2'-5' oligoadenylate synthetase (OAS1) is one of the most important components of the immune system and has significant antiviral functions. We studied a polymorphism rs10774671 of OAS1 gene in Han Chinese descent. The minor allele G was significantly associated with a decreased risk for SS, anti-SSA-positive SS, and anti-SSA-positive SS complicated with HBV infection, which have not been seen in anti-SSA-negative SS and HBcAb-negative SS patients. Gene expression analysis showed that the risk-conferring A allele was correlated with lower expression of p46 and increased expression of p42, p48, and p44. A functional study of enzymatic activities revealed that the p42, p44, and p48 isoforms display a reduced capacity to inhibit HBV replication in HepG2 cells compared to the normal p46 isoform. Our data demonstrated that the functional variant, rs10774671, is associated with HBV infection and anti-SSA antibody-positive SS. The SAS variant switches the primary p46 isoform to three alternatives with decreased capacities to inhibit HBV replication. These data indicated that individuals harboring the risk allele might be susceptible to hepatitis B infection and SS development.