Relationship Between Neutrophil to Lymphocyte Ratio and Contrast-induced Nephropathy in Patients With Percutaneous Coronary Intervention / 中国循环杂志

Objective:To investigate the relationship between neutrophil to lymphocyte ratio (NLR) and contrast-induced nephropathy (CIN) in patients with percutaneous coronary intervention (PCI).Methods:A total of 176 patients received PCI in our hospital from 2015-05 to 2016-12 were enrolled.Blood levels of white blood cells (WBC),neutrophils (N),lymphocytes (L);serum creatinine (SCr),blood urea nitrogen (BUN),uric acid (UA),cystatin C (CysC) were examined within 24 h of admission and NLR was calculated.According to NLR,the patients were divided into 3 groups:Low NLR group,NLR＜1.60,n=58,Moderate NLR group,1.60≤NLR≤2.36,n=62 and High NLR group,NLR＞2.36,n=56.SCr and CysC were re-examined at 48 h and 72 h after PCI.Pearson analysis was conducted for correlation study and Logistic regression analysis was used to identify whether NLR was the risk factor for CIN occurrence.Results:Compared with baseline condition,SCr and CysC were increased in all 3 groups,all P＜0.05.Pearson analysis indicated that NLR was positively related to SCr and CysC elevation (r=0.785 and r=0.764),both P＜0.05;Logistic regression analysis presented that NLR was an independent risk factor for CIN occurrence.Conclusion:NLR was positively related to contrast induced kidney injury,it was the risk factor for CIN occurrence in PCI patients.

Relationship Between Neutrophil to Lymphocyte Ratio and Contrast-induced Nephropathy in Patients With Percutaneous Coronary Intervention / 中国循环杂志

Objective:To investigate the relationship between neutrophil to lymphocyte ratio (NLR) and contrast-induced nephropathy (CIN) in patients with percutaneous coronary intervention (PCI).Methods:A total of 176 patients received PCI in our hospital from 2015-05 to 2016-12 were enrolled.Blood levels of white blood cells (WBC),neutrophils (N),lymphocytes (L);serum creatinine (SCr),blood urea nitrogen (BUN),uric acid (UA),cystatin C (CysC) were examined within 24 h of admission and NLR was calculated.According to NLR,the patients were divided into 3 groups:Low NLR group,NLR＜1.60,n=58,Moderate NLR group,1.60≤NLR≤2.36,n=62 and High NLR group,NLR＞2.36,n=56.SCr and CysC were re-examined at 48 h and 72 h after PCI.Pearson analysis was conducted for correlation study and Logistic regression analysis was used to identify whether NLR was the risk factor for CIN occurrence.Results:Compared with baseline condition,SCr and CysC were increased in all 3 groups,all P＜0.05.Pearson analysis indicated that NLR was positively related to SCr and CysC elevation (r=0.785 and r=0.764),both P＜0.05;Logistic regression analysis presented that NLR was an independent risk factor for CIN occurrence.Conclusion:NLR was positively related to contrast induced kidney injury,it was the risk factor for CIN occurrence in PCI patients.

PNPLA3 rs738409 Polymorphism Associated with Hepatic Steatosis and Advanced Fibrosis in Patients with Chronic Hepatitis C Virus: A Meta-Analysis

BACKGROUND/AIMS: The recognition of a correlation between patatin-like phospholipase domain containing-protein 3 (PNPLA3) rs738409 (C>G) and the severity of liver steatosis or fibrosis in chronic hepatitis C (CHC) has not reached a consensus. This meta-analysis sought to investigate with accuracy the association between the PNPLA3 rs738409 (C>G) polymorphism and liver steatosis and advanced fibrosis in CHC patients. METHODS: We performed a comprehensive literature search from the PubMed, Embase, Web of Science, and Google Scholar databases up to December 31, 2014. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Statistical analyses were performed using Stata 12.0 software. RESULTS: The meta-analysis revealed the severity of liver fibrosis was significantly higher in CHC patients with PNPLA3 rs738409 GG in Caucasians (versus CC+CG: OR, 2.29; 95% CI, 1.57 to 3.35; pG) was associated with the risk of both advanced liver fibrosis and steatosis in patients with CHC, especially among Caucasian populations.

Evolution of hepatitis B virus quasispecies during antiviral therapy in one chronic hepatitis B patient / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the evolution of hepatitis B virus (HBV) quasispecies in one patient during lamivudine (LAM) monotherapy and switching to entecavir (ETV) rescue treatment.</p><p><b>METHODS</b>Serum samples were taken at seven different time points during antiviral therapy (0, 24, 48, 60, 72, 96, 152 weeks, respectively), the HBV DNA polymerase gene was amplified, cloned and sequenced to analyze the amino acid substitutions within HBV DNA polymerase gene and distribution of virus quasispecies. Quantitative detection of the HBV wild strains and total virus was performed by amplification refractory mutation system real-time PCR (ARMS-PCR).</p><p><b>RESULTS</b>Three mutation patterns detected during antiviral therapy in the patient: rtM204V, rtM204V+rtL180M and rtM204I. The HBV quasispecies were found always in dynamic variation. The HBV populations were completely replaced with the LAM-resistant variants when the viral breakthrough was encountered during LAM monotherapy. Interestingly, the wild-type variants presented gradually dominant (79.3%) with the decline of HBV DNA load after switching to ETV rescue administration. ARMS-PCR results showed that the wild-type variants account ed for 68.55% of the HBV populations at baseline and this proportion declined to 0.21% when the viral breakthrough emerged under LAM therapy. The wild-type variants gradually increased from week 24 after switching to ETV rescue therapy and the proportion of HBV wild-type variants in the population fluctuated between 16.01% to 26.93%.</p><p><b>CONCLUSIONS</b>The distribution of virus quasispecies were always in dynamic variation during sequential therapy with nucleotide analogs in chronic hepatitis B patients. Different patterns of dynamic HBV quasispecies may have different contribution in ETV resistance in LMV refractory patients with ETV administration.</p>

Dissection of mechanism for the adefovir dipivoxil resistance in chronic hepatitis B patients / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To explore the mechanism for adefovir dipivoxil (ADV) resistance occurred in chronic hepatitis B patients of a series of phase III clinical trails.</p><p><b>METHODS</b>30 resistant HBV strains were selected out from 177 cases of ADV treated chronic hepatitis B patients. HBV polymerase RT region were amplified by nested PCR and analyzed with the standard nucleotide sequence of HBV strains deposited in GeneBank.</p><p><b>RESULTS</b>21 out of 30 HBV strains were primary resistant strains, among them 5 HBV strains (23.8%, 5/21) had the polymorphism site of rtN118H. While the other 9 HBV strains showed secondary resistance, variations in conservative region C (rtM207V) and other non-conservative regions were found. The classic mutation sites such as rtN236T and rtA181V/T were not found.</p><p><b>CONCLUSIONS</b>Polymorphism site of rtN118H might be responsible for HBV primary resistance to ADV therapy. rtM207V variation in HBV RT C domain and other variation sites might play a role in HBV secondary resistance to ADV treatment, and natural resistant quasispecies may be the basis for the ADV quick resistance. These conclusions await further confirmation by phenotype test.</p>

Comparison of antiviral responses to adefovir dipivoxil therapy of genotype B and genotype C HBV infected patients / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the role of HBV genotypes on their response to adefovir dipivoxil (ADV) antiviral therapy.</p><p><b>METHODS</b>HBV genotypes from 177 HBeAg-positive chronic hepatitis B (CHB) patients were identified and the patients were treated with ADV 10 mg per day for 48 weeks. The clinical data in terms of serum HBV DNA seroclearance, mean HBV DNA reduction (log value), HBeAg loss, anti-HBe seroconversion and serum ALT of those patients were analyzed against their HBV genotypes.</p><p><b>RESULTS</b>Genotype B and genotype C were found in 102 and 65 cases, respectively. The mean HBV DNA reduction in patients with genotype B and genotype C at their treatment times of 12, 24 and 48 weeks was 2.2 log10copies/ml, 2.1 log10copies/ml (P more than 0.05), 2.7 log10copies/ml, 2.4 log10copies/ml (P more than 0.05) and 3.6 log10copies/ml, 3.1 log10copies/ml (P less than 0.05), respectively. At the end of the therapy (48 weeks), 43 (42.2%) patients with genotype B HBV infection and 22 (33.8%) patients with genotype C HBV infection had achieved HBV DNA seroclearance (P less than 0.05).</p><p><b>CONCLUSIONS</b>Our results suggest that genotype B HBV has a better virological response to ADV therapy in HBeAg-positive chronic hepatitis B patients than that of genotype C. Longer terms of ADV treatment are needed to confirm this conclusion.</p>

Genotyping 238 HBV strains using type-specific primer PCR combined with type-specific nucleotide analysis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To establish a set of suitable and reliable methods for HBV genotyping and to study the distribution of HBV genotypes.</p><p><b>METHODS</b>Type-specific nucleotides were searched through alignment of S genes (more than 1000 sequences) listed in GenBank. Then, type-specific primers were designed and type-specific primer PCR was used to genotype the 238 HBV strains. S genes of the untyped strains were further amplified and sequenced to find out their genotypes with type-specific nucleotide analysis.</p><p><b>RESULTS</b>All the 238 HBV strains were genotyped. 159 (66.8%) cases were genotype B, 69 (28.9%) were genotype C, 6 (2.5%) were mixtures of genotypes B and C and 4 (1.6%) were mixtures of genotypes B and D. No genotypes of A, E, F, G, and H were found.</p><p><b>CONCLUSION</b>Genotypes B and C are the most common types for HBV strains. Mixtures of genotypes B and C or genotypes B and D coinfection rarely existed. There is no relationship between the gender of the patients and HBV genotypes (X2 = 0.794, P more than 0.05).</p>

The relationship between histone acetylation modification and IFN-gamma responsive gene regulation / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To study the role of histone modification in the regulation of IFN-gamma-activated gene using chromatin immunoprecipitation technique.</p><p><b>METHODS</b>Real-time PCR was used to measure the mRNA level of interferon-gamma-inducible protein 10 (IP-10) in Hela cells. Chromatin immunoprecipitation combined with Real-time PCR was used to check the histone H4 acetylation level at IFN-stimulated response element (ISRE) locus of IP-10 gene.</p><p><b>RESULTS</b>IP-10 was strongly activated by IFN-gamma. The histone H4 deacetylation happened at the ISRE locus when IP-10 was induced by IFN-gamma. The activation of IP-10 and the deacetylation of histone H4 at the ISRE site induced by IFN-gamma were inhibited or blocked by histone deacetylase (HDAC) inhibitor trichostatin A (TSA).</p><p><b>CONCLUSION</b>The histone H4 deacetylation at the ISRE site is related with the activation of IP-10 by IFN-gamma.</p>

A method of HPRE synthesis via transcription by T7 RNA polymerase in vitro / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To synthesize highly pure HBV post-transcriptional regulatory element (HPRE) via transcription in vitro by T7 RNA polymerase.</p><p><b>METHODS</b>HPRE gene was amplified by PCR from a template containing HBV complete genomic DNA and cloned into plasmid pGEM-11zf. The cloned DNA sequence was transcribed by T7 RNA polymerase.</p><p><b>RESULTS</b>The construction of HPRE gene recombinant plasmid and production of HPRE via transcription in vitro was successful.</p><p><b>CONCLUSION</b>In vitro transcription by T7 RNA polymerase can be used to synthesize highly pure HPRE.</p>

A new method for amplification and sequence analysis of the full-length of HBV genome / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To develop a new method for amplifying and sequencing the full-length of HBV genome.</p><p><b>METHODS</b>A pair of primers located at the nick region of HBV molecule and a thermostable polymerase with high fidelity and sensitivity were used. After cloning the PCR products into a plasmid, the sequences of HBV genome were analyzed.</p><p><b>RESULTS</b>The full-length of HBV genome were acquired using this method. The sensitivity and fidelity of the new method were also analyzed. The least quantity of initial templates was 10(2) and the artificial mutation rate was 1.2 bp/kb.</p><p><b>CONCLUSION</b>This method can be used in amplification and sequence analysis of the full-length of HBV genome on a large scale.</p>