Objective To study the correlation between the drug-resistance variation and the genotypes of hepatitis B virus (HBV)detected by the PCR-reverse dot blot and the relation between the HBV variation loci with the liver function indexes and HBV DNA viral loading.Methods The serum samples from 462 patients with chronic hepatitis B treated by oral nucleoside drugs were screened.The PCR-reverse dot blot was adopted to detect the drug-resistance gene mutation loci and genotypes.The correla-tion between the HBV drug-resistance mutant with the genotypes,liver function indexes and HBV DNA viral loads was performed. Results Among 462 patients taking nucleoside drugs for treating chronic hepatitis B,45 drug-resistance mutants were detected with the mutation rate of 9.74%;in which,16 cases (35.5%)were 180M and 204I/V mutant,6 cases(13.3%)were 204V,13 ca-ses(28.9%)were 204I mutant,3 cases (6.7%)were 180V mutant and 3 cases(6.7%)were 236T mutant.The HBV genotyping showed 105 cases of genotype B,337 cases of genotype C,0 case of genotype D and 2 cases of other genotypes.Conclusion (1)The HBVgenotypes in Maoming area may be different from the genotypes in other southern regions and is dominated by HBV-C geno-type.(2)The PCR-reverse dot blot method is a detection method for fastly and accurately finding the drug-resistance loci after nu-cleosides therapy.(3)The clinical analysis demonstrates that the drug-resistance mutation loci has no correlation with the liver func-tion index ALT(P >0.05),but there was certain correlation between the drug-resistance mutation loci in hepatitis B and HBV DNA viral load(P <0.05).

Objective To investigate the effects of dexmedetomidine (DEX) on the mRNA expression of triggering receptor expressed on myeloid cells 1 (TREM-1) in peripheral blood mononuclear cells of rats with acute obstructive suppurative cholangitis (AOSC).Methods Sixty healthy male Wistar rat models of AOSC induced by complete common bile duct ligation and injection of E.coli into the bile duct through an intubation tube were replicated successfully.After modeling,the peripheral blood was collected and mononuclear cells were isolated and cultured.According to random number table method,the mononeuclear cells were divided into model group (no drug added in culture of mononuclear cells) and low,medium and high dose DEX groups (final concentrations 0.4,0.8,1.2 μg/L DEX were in low,medium and high DEX mononuclear cell cultures,respectively).After the mononuclear cells were cultured for 24 hours,the levels of tumor necrosis factor-α (TNF-α),interleukins (IL-1 and IL-6) in the supernatant of the cultured mononuclear cells were detected by enzyme linked immunosorbent assay (ELISA).The level of C-reactive protein (CRP) was detected by immunity transmission turbidimetry.The expression of TREM-1 mRNA in the mononuclear cells was detected by reverse trantscription-polymerase chain reaction (RT-PCR).Results Compared with the model group,the levels of TNF-α,IL-1,IL-6,CRP were decreased,the TREM-1 mRNA expressions were down-regulated in the different DEX dose groups,and the degrees of descent in medium and high dose groups were more significant than those in low dose group [TNF-oα (ng/L):95.5±8.6,88.9±5.3 vs.131.1 ± 14.2;IL-1 (ng/L):53.5±8.3,48.3 ± 6.7 vs.73.7 ± 12.8;IL-6 (ng/L):266.9±26.2,252.1 ± 17.7 vs.349.9±40.4;CRP (ng/L):4.3 ± 1.1,3.9 ±0.7 vs.5.6 ± 1.7;TREM-1 mRNA (A value):0.43 ± 0.18,0.39 ± 0.16 vs.0.65 ±0.25,all P ＜ 0.05].Conclusion DEX can down-regulate the expression of TREM-1 mRNA and inhibit the formation and secretion of inflammatory factors TNF-α,IL-1,IL-6 and CRP in peripheral blood mononuclear cells of rats with ASOC.

Objective Plasma circulating DNA can be em-ployed in place of bone marrow examination for the auxiliary diagnosis of leukemia.This study aimed to explore the clinical application of the plasma DNA level in evaluating the effect of chemotherapy on chronic leukemia. Methods We collected blood samples from 52 patients with chronic myelogenous leukemia (CML) (33 in the chronic phase, 7 in the acceleration phase, and 12 in the blast phase) , 85 with chron-ic lymphocytic leukemia (CLL) (28 with complete remission, 27 with partial remission, and 30 with no remission), 4 patients with hairy cell leukemia (HCL), and 80 healthy subjects.We simultaneously obtained plasma DNA and recombinant plasmid DNA using the BI-LATEST DNA Kit and examined the human β-actin gene and the level of plasmid DNA by real-time quantitative PCR. Results Before chemotherapy, the median value of plasma DNA was 149.46(30.63-496.91)ng/ml in the CML and 101.54(69.10-258.14) ng/ml in the CLL patients, both significantly higher than in the healthy controls (19.05[12.67-25.92]ng/ml) (P<0.01).After chemotherapy, the plasma DNA level of the CML patients was remarkably decreased, but still higher than that of the controls ( P<0.01).The CML patients in the chronic phase showed a markedly higher level of plasma DNA (302.89[93.33-541.52]ng/ml) than those in the blast phase (43.19[23.54-70.03]ng/ml) and acceleration phase (28.11[16.21-92.07]ng/ml) (P<0.05).The CLL patients with CR exhibited a significantly lower level of plasma DNA (24.29[14.64-30.74]ng/ml) than those with PR (106.88 [96.23-143.25]ng/ml) and NR (460.73[284.57-653.38〗ng/ml) (P<0.01), but all dramatically higher than that of the healthy controls (P<0.01) Conclusion The quantification of plasma DNA has a clinical application value in evaluating the effect of chemo-therapy on chronic leukemia.