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This case–control study was aimed to assess the effect of genetic variants of tumor necrosis factor (TNF) α−308 and lymphotoxin (LT) α+252 on development of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Their gene–gene interaction was also investigated. We enrolled 200 pairs of age- and sex-matched patients with cirrhotic HBV-HCC and unrelated patients with HBV-cirrhosis alone. Polymorphisms of TNFα −308 and LTα +252 were genotyped. Synergy index was used to calculate interaction between the variant genotypes. The results indicated that the frequency distribution of the variant genotypes ( TNFα −308 G/A and LTα +252 G/G) in patients with HCC were significantly higher than those in patients with cirrhosis alone. Multivariate analysis indicated that TNFα −308 G/A (odds ratio [OR], 2.34) and LTα +252 G/G (OR, 2.04) were independent risk factors for HCC. By the clinical characteristics of study population, multivariate analysis demonstrated that independent factors associated with harboring the variant genotypes included cirrhosis with Child-Pugh C (OR = 6.47 in cases and OR = 11.56 in controls) and thrombocytopenia (OR = 8.86 in cases and OR = 7.74 in controls). Calculation of synergy index (SI) indicated that there are additive interaction between TNFα −308 G/A and LTα +252 G/G on risk of HCC (SI = 1.29). In conclusion: There are independent and additive interactions between TNFα −308 G/A and LTα +252 G/G on risk for HBV-HCC. They correlated with advanced hepatic fibrosis and severe liver damage, which might contribute to a higher risk for HCC.

Copper (Cu2+) ion was determined at micro level by diethyldithiocarbamate (DDTC) spectrophotometry after temperature-dependent solid–liquid separation using N-butyl pyridinium hexafluorophosphate ([BPy]PF6) as a solid solvent and DDTC as an extractant. The results showed that ions can be extracted 100% by DDTC–[BPy]PF6 at pH = 10·20. The extracted species was neutral Cu(DDTC)mCl2 (m = 1) based on slope analysis in the Cu2+–[BPy]PF6–DDTC temperature-dependent solid–liquid separation system. The recovery of Cu2+ extracted into DDTC–[BPy]PF6 can be achieved using 2 mol L−1 HNO3 as stripping agents. Back extraction method was adopted for the detection and quantification of Cu2+ ions using the DDTC spectrometry. The calibration curve was Y = 0·00328 + 0·10279X (correlation coefficient = 0·99922), the linear calibration range was 7·68 × 10−2 0·768 μg mL−1 and the limit of detection was 1·28 × 10−2 μg mL−1 for Cu2+. In this method, the contents of Cu2+ in Tieguanyin tea were determined with relative stan...

This case–control study aimed to assess the interactive effect between polymorphisms of lymphotoxin (LT) α +252 and habitual substance use on risk of hepatocellular carcinoma (HCC). We enrolled 150 pairs of sex- and age-matched HCC patients and unrelated healthy controls. LTα genotypes were detected with polymerase-chain reaction and restrictive fragment length polymorphisms. Information about habits of substance use was obtained through personal interview. Multivariate analysis indicated that LTα +252 G/G genotypes [odds ratio (OR) = 3.36], Hepatitis B surface antigen (OR = 16.68), antibodies to hepatitis C virus (OR = 34.88) and having at least two habits of substance use (OR = 2.50) were independent risk factors for HCC. There were additive interactions among LTα +252 G/G genotype, chronic viral hepatitis, and habit of each substance use. In conclusion: There are independent and additive interactions between LTα +252 G/G genotype, chronic viral hepatitis, and habits of substance use on risk of HCC.

Summary Background Peginterferon-α–based therapy frequently leads to neutropenia. It remains unclear whether neutropenia is associated with bacterial infection in chronic hepatitis C (CHC). Aim To evaluate the risk of bacterial infection and neutropenia in patients with CHC treated with peginterferon-α/ribavirin. Methods In all, 207 patients with CHC with (group A, n = 30) and without (group B, n = 177) baseline neutropenia were treated with peginterferon-α/ribavirin. Results Group A had significantly higher rates of moderate (

To evaluate the diagnostic application of serum insulin-like growth factor-II (IGF-II) and alpha-fetoprotein (AFP) levels in hepatocellular carcinoma (HCC), IGF-II and AFP were determined in 100 cirrhotic patients with HCC, 100 sex- and age-matched patients with cirrhosis alone and 50 healthy controls. The results indicated that IGF-II and AFP levels in patients with HCC were higher than in those with cirrhosis alone (p = 0.0001). There is an inverse correlation between IGF-II and (log)AFP (r = -0.410, p = 0.0001) in patients with HCC. Multivariate analysis indicated that IGF-II and AFP were closely associated, in a dose-related fashion, with the presence of HCC. Receiver operating characteristic curves were used to determine the optimal cutoff values of IGF-II (4.5 mg/g prealbumin) and AFP (100 ng/ml), respectively. Both IGF-II and AFP show a high specificity and positive likelihood ratio. The sensitivity was 42.0% for IGF-II and 73.0% for AFP. Determination of both markers in parallel significantly increased the diagnostic accuracy (96.5%) and sensitivity (97.9%), with a high specificity (95.1%) and positive likelihood ratio (19.9). In conclusion, IGF-II and AFP may be used as complementary tumor markers to discriminate HCC from cirrhosis.

In 1979, a mass poisoning of more than 2000 people occurred in central Taiwan due to consumption of rice-bran oil contaminated with PCBs and their heat-degraded byproducts. The incident was later referred to as Yucheng (oil disease). Serum samples from 56 women with the 1979 exposure were collected in February 1992 and analyzed for their contaminant content using sample enrichment and isotope dilution mass spectrometry. In most of the samples, levels of PCDFs and PCBs were detectable, and the median values of 2,3,4,7,8-PCDFs and 1,2,3,4,7,8-PCDFs were 1,030 and 2,220 ng/kg serum lipid, respectively. The median level of the total PCBs on a whole weight basis was 8,730 ng/kg. The PCB/PCDF concentrations in Yucheng women 14 years after the toxic exposure were still one to two orders of magnitude higher than controls. Concentrations of PCB levels in 1992 were positively correlated with the 1980-1981 measured PCB levels in these women and both PCBs and PCDFs were negatively correlated with the total duration when these women breast fed their children between 1979 and 1992. It is concluded that serum levels of congener-specific PCBs/PCDFs in exposed women are good indicators of previous exposure and may provide important information for more reliable estimation of dose-response relationship.

This case–control study aimed to evaluate the diagnostic application of urinary transforming growth factor (TGF) α and serum α-fetoprotein (AFP) in hepatocellular carcinoma (HCC). TGFα and AFP were determined in 90 pairs of age- and gender-matched patients with cirrhotic HCC and patients with cirrhosis alone and 60 healthy controls. The results indicated that TGFα and AFP levels in patients with HCC were higher than in those with cirrhosis alone or healthy controls (each P = 0.0001). Multivariate analysis indicated that TGFα (odds ratio (OR) 1.03, 95 % confidence interval (CI) 1.05–1.16) and AFP (OR 1.03, 95 % CI 1.01–1.06) were closely associated, in a dose-related fashion, with the development of HCC. The optimal cutoff values, determined with the receiver operating characteristic (ROC) curves, were 29 μg/g creatinine for TGFα and 100 ng/ml for AFP, respectively. The areas under ROC curve (AUC) were 0.74 for TGFα and 0.78 for AFP, respectively. Both biomarkers showed the same sensitivity (52.2 %), high specificity, high positive predictive value, and moderate positive likelihood ratio. Determination of both markers in parallel significantly increased the AUC (0.91) and diagnostic accuracy (92.2 %), with a high sensitivity (86.7 %), specificity (97.8 %), positive predictive value (PPV; 97.5 %), and moderate positive likelihood ratio (PLR; 39.4). Among 31 cirrhotic HCC with AFP ≤ 20 ng/ml, the calculated AUC for TGFα was 0.79, with a sensitivity of 64.5 %, specificity of 96.7 %, PPV of 87.0 %, and PLR of 19.5. In conclusion, urinary TGFα and serum AFP are complementary tumor markers for detection of HCC with low AFP production.

Background: Cerebrovascular disease is one of the leading causes of death worldwide. Hepatitis C virus (HCV) infection, a well-accepted causal agent for liver-related diseases, has been reported to increase the risk for atherothrombosis. However, the association between HCV infection and cerebrovascular diseases remains inconclusive and the dose-response relationship between serum HCVRNA levels and cerebrovascular death has never been elucidated. Methods: This study enrolled 23,665 residents aged between 30–65 years in community during 1991–1992. They were personally interviewed using structured questionnaires and provided blood samples for various serological and biochemical testing at study entry. Those who were seropositive for antibodies against HCV (anti-HCV) were examined for serum HCVRNA levels. HCV genotypes were determined in participants who had detectable serum HCVRNA. Cerebrovascular deaths of participants during follow-up were ascertained by computerized linkage with National Death Certification profiles from 1991 to 2007 (ICD-9: 430–438). Person-years at risk were calculated for each person as time from enrollment date to either the date of death, or to the end of 2007, whichever came first. Cox proportional hazards models were used to estimate relative risks and 95% confidence intervals for magnitude of HCV after adjustment of other risk factors. Results: There were 240 cerebrovascular deaths with 361,171 person-years of follow-up, giving a mortality of 66.5 per 100,000 person-years in this population. The cumulative risks for cerebrovascular death were 1.0% and 2.7% for anti-HCV seronegatives and anti-HCV seropositives (p < 0.001). Participants seropositive for anti-HCV had increased risk of cerebrovascular death, with a multivariate-adjusted relative risk (95% confidence interval) of 2.27 (1.56–3.30). Elevated serum HCVRNA levels increased the risk for cerebrovascular death with dose-response trend (p < 0.001). The adjusted relative risks were 1.52 (0.67– 3.44), 1.73 (0.43–6.98), 2.31 (1.25–4.25), and 3.45 (1.76– 6.75) in corresponding to participants with serum HCVRNA level