[Synthesis and spectral characteristic of Ga-Fe3O4 at room temperature].

Gallium bearing ferrites with different gallium content were synthesized by oxidation of ferrous and gallium ions under alkaline condition and room temperature. The samples were subjected to IR, XRD, Mossbauer spectral analysis and magnetization characterization. The results indicated that the green-rust intermediate phase would be produced during the procedure of Ga-Fe3O4 formation, and the green-rust intermediate phase was converted to ferrites with spinel structure during the drying under hot-N2 atmosphere.

[Preparation and evaluation of sustained-release microsphere of Sanguis Draconis in vitro].

Objective: To prepare sustained-release microsphere containing extract of Sanguis Draconis and to measure its dissolution in vitro.

Method: Sustained-release microsphere was prepared with polylactic acid (PLA) as carriers using the oil-in-water (O/W) emulsion solvent evaporation method. The powder particle's characteristics of sustainded-release microsphere were evaluated comprehensively, and its dissolution characteristics in vitro were studied.

[Establishment of stable expression cell lines for HBsAg variants and analysis of antigenicity].

Objective: To study the mechanism of hepatitis B virus infected patients who is negative for HbsAg.

Methods: DNA sequences of 46 patients were analyzed. In these patients, HBsAg was negative but HBV DNA was positive and six new HBsAg variants were identified.

Detection of interleukin-6 and -12 in of hepatitis B patients and its clinical significance.

OBJECTIVE: To investigate the clinical significance of detecting interleukin-6 (IL-6) and interleukin-12 (IL-12) in the immunological mechanism of hepatitis B virus infection (HBV). METHODS: Serum IL-6 and IL-12 levels were determined using enzyme-linked immunosorbent assay in patients with chronic, acute or advanced hepatitis B as well as in healthy subjects. RESULTS: In chronic, acute, severe hepatitis B patients, serum IL-6 levels were significantly elevated as hepatitis worsened (199.

Hot-spot mutations in HBV pre-C region in HBeAg-negative patients with severe hepatitis B.

OBJECTIVE: To investigate the association of hot-spot mutations in hepatitis B virus (HBV) pre-C region with the occurrence and outcome of severe hepatitis B. METHODS: A total of 68 patients with severe hepatitis B negative for hepatits B e antigen (HBeAg) were enrolled in this study, including 6 cases of acute, 38 cases of subacute and 24 chronic severe hepatitis B, with another 44 HBeAg-positive patients with chronic hepatitis B serving as control. Mismatch PCR and restriction fragment length polymorphism analysis were employed to examine the mutations of T1862 and A1896 in this 2 groups of patients.

Determination and analysis of complete nucleotide sequence of Chinese genotype D hepatitis B virus: the first report.

OBJECTIVE: To determine the complete nucleotide sequence of a Chinese hepatitis B virus (HBV) strain of genotype D. METHOD: The complete nucleotide sequence of HBV derived from a Chinese chronic asymptomatic carrier was amplified by PCR and cloned to conduct sequence analysis. Homology of the resulted nucleotide sequence with those of published HBV strains was assessed by using DNASIS, and complete sequence analysis of the phylogenetic tree of 30 genotype D HBV strains conducted by the assistance of Clustalw.

Construction of recombinant eukaryotic expression plasmid containing hepatitis B virus genome with partial deletion of the core promoter.

OBJECTIVE: To construct an eukaryotic expression vector containing the full-length genome with partially deleted core promoter of hepatitis B virus (HBV). METHODS: A linearized genome containing the entire HBV 3.5 kb mRNA transcriptional units (P3.

[Construction and biological activity assessment of core mutants of hepatitis B virus adr subtype].

Objective: To construct the core mutant (L97 and V60) plasmids of hepatitis B virus (HBV) and assess their biological activity.

Methods: Site-directed mutagenesis was performed to induce specific core point mutations in HBV adr suhtype 1.2 copy genome plasmid p3.