De Novo Design of Activatable Photoacoustic/Fluorescent Probes for Imaging Acute Lung Injury In Vivo.

Effective monitoring of the physiological progression of acute lung injury (ALI) in real time is crucial for early theranostics to reduce its high mortality. In particular, activatable fluorescence and photoacoustic molecule probes have attracted attention to assess ALI by detecting related indicators. However, the existing fluorophores often encounter issues of low retention in the lungs and slow clearance from the body, which compromise the probe's actual capability for in situ imaging by intravenous injection in vivo. Herein, a novel near-infrared hemicyanines fluorophore (FJH) bearing a quaternary ammonium group was first developed by combining with the rational design and screening strategy. The properties of good hydrophilicity and blood circulation effectively enable FJH accumulation for lung imaging. Inspired by the high retention efficiency, the probe FJH-C that turns on fluorescence and photoacoustic signals in response to the ALI indicator (esterase) was subsequently synthesized. Notably, the probe FJH-C successfully achieved the selectivity and sensitivity toward esterase in vitro and in living cells. More importantly, FJH-C can be further used to assess lipopolysaccharides and silica-induced ALI through the desired fluo-photoacoustic signal. Therefore, this study not only shows the first activatable probe for real-time imaging of lung function but also highlights the fluorophore structure with high lung retention. It is believed that FJH and FJH-C can serve as an efficient platform to reveal the pathological progression of other lung diseases for early diagnosis and medical intervention.

Engineering a Ratiometric Photoacoustic Probe with a Hepatocyte-Specific Targeting Ability for Liver Injury Imaging.

In situ imaging of biological indicators is imperative for pathological research by utilizing an activatable photoacoustic (PA) probe. However, precise imaging in actual applications is hampered by the inevitable poor accumulation and low sensitivity. Herein, an amphiphilic molecular probe (AP) was rationally constructed as proof of concept for in situ imaging of drug-induced liver injury, which consists of a hydrophilic target unit and a superoxide anion radical (O2•-)-sensitive small-molecule PA moiety. The probe AP successfully realizes the selectivity and sensitivity toward O2•- in vitro and in living cells. Notably, the amphiphilic probe AP can be selectively retained in the liver and activated toward endogenous O2•- through receptor-mediated endocytosis inside hepatocytes. By virtue of the highly efficient accumulation at the liver, AP was further applied to assess isoniazid-induced liver injury through desired ratiometric PA signals. In addition, based on the fluctuation of O2•-, the therapeutic efficacy of hepatoprotective medicines for hepatotoxicity was analyzed in vivo. Therefore, the O2•--specific probe could serve as a promising molecular tool for early diagnosis study of other liver diseases and analysis of new potential therapeutic agents.

Diagnostic value of NKG2D promoter methylation in hepatitis B virus-associated hepatocellular carcinoma.

Aim: Natural killer cell receptor group 2D (NKG2D) plays an important role in the immune regulation of tumors. We speculate that DNA methylation are involved in the regulation of NKG2D gene. Methods: We investigated the methylation status of the NKG2D promoter in peripheral blood mononuclear cells of hepatocellular carcinoma (HCC) patients, chronic hepatitis B patients and healthy controls by methylation-specific PCR and the mRNA expression level was examined by real-time quantitative PCR. Results: The methylation frequency of NKG2D promoter in HCC patients was higher than that of chronic hepatitis B patients and healthy controls. NKG2D promoter methylation has a good predictive value for HCC diagnosis. Conclusion: NKG2D promoter methylation can be used as a noninvasive marker for detecting HCC.

BATF Interference Blocks Th17 Cell Differentiation and Inflammatory Response in Hepatitis B Virus Transgenic Mice.

BACKGROUND: B cell-activating transcription factor (BATF) contributes to Th17 cell differentiation and pathological inflammatory responses. AIMS: This study explored BATF as a regulator of Th17 differentiation in normal and hepatitis B virus (HBV) transgenic mice. METHODS: Normal mice were divided into control, short hairpin RNA (shRNA) scramble, and shRNA BATF groups. HBV transgenic mice were divided into control, entecavir, shRNA scramble, entecavir + vector control, entecavir + shRNA scramble, shRNA BATF, and entecavir + shRNA BATF groups. Serum concentrations of AST, ALT, HBV-DNA, BATF, IL-17, and IL-22 and Th17 cell frequencies in the liver were compared among the groups. Correlations of serum HBV surface antigen (HBsAg), e-antigen (HBeAg), and core antigen (HBcAg) concentrations with BATF mRNA expression and the proportion of Th17 cells in the livers of HBV transgenic mice were also analyzed. RESULTS: Serum AST, ALT, BATF, IL-17, and IL-22 concentrations and Th17 cell proportions were higher in HBV transgenic mice relative to normal controls. Positive correlations of the HBcAg concentration with BATF mRNA and the proportion of Th17 cells were observed in HBV transgenic mice. BATF interference reduced the proportion of Th17 cells and serum IL-17 and IL-22 concentrations and led to obvious downregulation of AST, ALT, BATF, IL-17, and IL-22 expression and a reduced proportion of Th17 cells when combined with entecavir. CONCLUSION: HBV markedly upregulated BATF expression and promoted Th17 cell activation. By contrast, BATF interference significantly impeded the proliferation of Th17 cells and secretion of IL-17 and IL-22 while alleviating hepatic lesions.

Combined detection of insulin-like growth factor-binding protein 7 promoter methylation improves the diagnostic efficacy of AFP in hepatitis B virus-associated hepatocellular carcinoma.

This study quantitatively assessed serum insulin-like growth factor-binding protein 7 (IGFBP7) promoter methylation in hepatocellular carcinoma (HCC), and explored its clinical value. A total of 80 patients with hepatitis B virus-associated HCC, 35 patients with chronic hepatitis B (CHB), and 20 healthy controls (HC) were enrolled. MethyLight was used to quantitatively assess the methylation levels of serum IGFBP7 promoter. A logistic regression model was established for the combined evaluation of AFP and serum IGFBP7 promoter methylation. The results showed that mean methylation levels of serum IGFBP7 promoter were significantly higher in HCC (5.33%, interquartile range [IQR] 1.14-15.70%) patients than in individuals with CHB (1.54%, IQR 0.64-2.45%; P<0.01) and HC (0.63%, IQR 0.22-0.98%; P<0.01). In HCC subgroups, patients with vascular invasion, tumor size >3cm and advanced tumor node metastasis (TNM) showed higher methylation levels compared with the remaining groups (P<0.05). Compared with AFP alone, combined determination based on logistic regression analysis significantly improved the area under the receiver operating characteristic (ROC) curve (AUC) (0.759 vs 0.623, P<0.05). In addition, the Youden index was increased from 5.71%, 11.25% and 15.18%, when considering AFP alone at cut-off values of 20, 200, and 400ng/ml, respectively, to 45.71% with IGFBP7 promoter methylation taken into consideration (all P<0.05). These results suggested that combined quantitative measurement of serum IGFBP7 promoter methylation could enhance the diagnostic ability of AFP in distinguishing hepatitis B virus-associated HCC from CHB.

Methylation status of the estrogen receptor 1 promoter predicts poor prognosis of acute-on-chronic hepatitis B liver failure

Background: Acute-on-chronic hepatitis B liver failure (ACHBLF) is an acute deteriorating liver disease and rapidly progresses to multiple organ failure. There is currently no adequate accurate predictive models of ACHBLF prognosis. Aims: To identify the methylation frequency of the estrogen receptor 1 (ESR1) promoter in ACHBLF and analyze the associated prognostic significance. Methods: Methylation-specific PCR (MSP) was used to determine the methylation frequency of the ESR1 promoter in peripheral blood mononuclear cells from a training and validation cohort of patients. The training cohort included 113 patients with ACHBLF, 73 with chronic hepatitis B (CHB) and 40 healthy controls (HCs). The validation cohort consisted of 37 patients with ACHBLF. Another 18 patients with pre-ACHBLF who progressed to ACHBLF were used to dynamically evaluate ESR1 promoter methylation changes associated with a severe clinical condition. Results: Death from ACHBLF was associated with hyperbilirubinemia, a higher score in the model for end-stage liver disease (MELD), a higher incidence of hepatic encephalopathy (HE) and an increased frequency of ESR1 promoter methylation during the 28 day follow-up. HE, MELD score and ESR1 promoter methylation were the independent risk factors associated with 28-day mortality from ACHBLF. The frequency of ESR1 promoter methylation was significantly higher than in patients with CHB and HCs. Albumin and the MELD score were significantly associated with ESR1 promoter methylation. Moreover, ESR1 promoter methylation frequency increased with ACHBLF progression. More importantly, ESR1 promoter methylation was an independent risk factor and had a high value to predict 28-day mortality from ACHBLF. Conclusions: Abnormal ESR1 methylation could be a prognostic biomarker for ACHBLF (AU)

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Methylation status of the estrogen receptor 1 promoter predicts poor prognosis of acute-on-chronic hepatitis B liver failure.

BACKGROUND: Acute-on-chronic hepatitis B liver failure (ACHBLF) is an acute deteriorating liver disease and rapidly progresses to multiple organ failure. There is currently no adequate accurate predictive models of ACHBLF prognosis. AIMS: To identify the methylation frequency of the estrogen receptor 1 (ESR1) promoter in ACHBLF and analyze the associated prognostic significance. METHODS: Methylation-specific PCR (MSP) was used to determine the methylation frequency of the ESR1 promoter in peripheral blood mononuclear cells from a training and validation cohort of patients. The training cohort included 113 patients with ACHBLF, 73 with chronic hepatitis B (CHB) and 40 healthy controls (HCs). The validation cohort consisted of 37 patients with ACHBLF. Another 18 patients with pre-ACHBLF who progressed to ACHBLF were used to dynamically evaluate ESR1 promoter methylation changes associated with a severe clinical condition. RESULTS: Death from ACHBLF was associated with hyperbilirubinemia, a higher score in the model for end-stage liver disease (MELD), a higher incidence of hepatic encephalopathy (HE) and an increased frequency of ESR1 promoter methylation during the 28 day follow-up. HE, MELD score and ESR1 promoter methylation were the independent risk factors associated with 28-day mortality from ACHBLF. The frequency of ESR1 promoter methylation was significantly higher than in patients with CHB and HCs. Albumin and the MELD score were significantly associated with ESR1 promoter methylation. Moreover, ESR1 promoter methylation frequency increased with ACHBLF progression. More importantly, ESR1 promoter methylation was an independent risk factor and had a high value to predict 28-day mortality from ACHBLF. CONCLUSIONS: Abnormal ESR1 methylation could be a prognostic biomarker for ACHBLF.

Change in the Treg/Th17 cell imbalance in hepatocellular carcinoma patients and its clinical value.

Recent studies have indicated that the T cell mediated immune response plays an important role in the pathogenesis of hepatitis B virus-associated hepatocellular carcinoma (HCC), but the underlying mechanism remains unclear. In this study, we found an imbalance in Treg/Th17 cells in peripheral blood mononuclear cells from HCC patients. The percentages of CD4CD25FOXP3 Treg cells and CD4IL-17 Th17 cells were significantly higher in HCC patients than in the controls. The numbers of Treg and Th17 cells were increased and correlated in a positive linear manner. Moreover, the increased percentages of Treg and Th17 cells were closely related to the tumor stage and tumor size of HCC. Therefore, we concluded that Treg and Th17 cells might participate in the promotion of the invasion and progression of HCC and that a Treg/Th17 cell imbalance might be able to serve as an important indicator for determining the progression and prognosis of HCC. Further studies might provide novel therapeutic targets for HCC.

Hypomethylated Ubiquitin-Conjugating Enzyme2 Q1 (UBE2Q1) Gene Promoter in the Serum Is a Promising Biomarker for Hepatitis B Virus-Associated Hepatocellular Carcinoma.

Aberrant DNA methylation, which can be detected in circulating cell-free DNA (cfDNA), is one of the major epigenetic alterations in hepatocellular carcinoma (HCC). UBE2Q1, a putative member of the ubiquitin-conjugating enzyme family, might play substantial roles in tumorigenesis. However, the methylation status of the UBE2Q1 gene in HCC remains unknown. We aimed to determine the methylation status of the UBE2Q1 gene promoter and to evaluate its potential clinical significance for HCC detection. The methylation-specific polymerase chain reaction (MSP) assay was used to detect the UBE2Q1 gene methylation status in serum samples from 80 patients with hepatitis B virus (HBV)-related HCC, 40 patients with liver cirrhosis (LC), 40 patients with chronic hepatitis B (CHB), and 20 healthy controls (HCs). Significantly lower methylation frequencies were detected in HCC patients (33.75%) compared with LC patients (55.00%, p = 0.026) and CHB patients (60.00%, p = 0.006) and HCs (65.00%, p = 0.011). Hypomethylation of the UBE2Q1 gene was negatively associated with the tumor node metastasis stage (rs = -0.30, p = 0.008). The UBE2Q1 gene methylation status combined with alpha fetoprotein using cut-off points of 20, 200 and 400 ng/ml showed sensitivity and specificity values of 58.8% and 75.0%, 53.8% and 87.5%, and 37.5% and 88.7%, respectively, and yielded a significantly increased area under the ROC curve (0.720, 0.760 and 0.694, respectively) for discriminating HCC from LC and CHB. Our study results suggest that hypomethylation of the UBE2Q1 gene promoter is a potential biomarker for detecting HBV-associated HCC.

A model to predict the onset of non-alcoholic fatty liver disease within 2 years in elderly adults.

BACKGROUND AND AIM: Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic hepatitis, which leads to cirrhosis and hepatocellular carcinoma. However, it is difficult to identify subjects at high risk for NAFLD onset. This study aims to construct a model to predict the onset of NAFLD within 2 years in elderly adults. METHODS: This study included and followed 3378 initial NAFLD-free subjects aged 60 years or over for 2 years, which were randomly divided into a training set and a validation set. NAFLD was diagnosed on ultrasound. Clinical and laboratory data were recorded at baseline. A model was constructed in the training set to predict the onset of NAFLD and validated in the validation set. RESULTS: Body mass index, hemoglobin, fasting blood glucose, and triglycerides were identified as predictors for the onset of NAFLD. A risk score (R) was calculated by them. It classified the subjects into low-risk group (R ≤ -2.88), moderate-risk group (-2.88 < R ≤ -1.26), and high-risk group (R > -1.26). In the training set, 4.68% of the participants in the low-risk group, 11.59% of the participants in the moderate-risk group, and 31.02% of the participants in the high-risk group developed NAFLD. In the validation set, 5.84% of the participants in the low-risk group, 10.57% of the participants in the moderate-risk group, and 29.44% of the participants in the high-risk group developed NAFLD. CONCLUSIONS: This study developed a model to predict the onset of NAFLD in elderly adults, which might provide indications for intervention to these subjects.

Methylation of the Glutathione-S-Transferase P1 Gene Promoter Is Associated with Oxidative Stress in Patients with Chronic Hepatitis B.

Glutathione-S-transferase P1 (GSTP1) and glutathione-S-transferase M3 (GSTM3) catalyze the glutathione-related clearance of xenobiotics. The methylation of these gene promoters was associated with oxidative stress that induced liver damage. This study aims to explore the relationship among GSTP1 and GSTM3 methylation, DNA methyltransferases (DNMTs) expression, and oxidative stress in patients with chronic hepatitis B (CHB). We retrospectively enrolled 153 patients with CHB and 40 healthy controls (HCs). The GSTP1 and GSTM3 methylation status, DNMTs mRNA levels in peripheral mononuclear cells (PBMCs) and TNF-α and malondialdehyde (MDA) levels in plasma were detected. GSTP1 methylation was significantly higher in patients with CHB than HCs (P = 0.047). Patients with HBeAg-positive CHB showed significantly higher GSTP1 methylation than those with HBeAg-negative CHB (P = 0.017) and HCs (P = 0.007). No significant difference was observed between GSTP1 methylation in HBeAg-negative CHB and HCs (P = 0.191). DNMT1 and DNMT3a mRNA levels were significantly higher in participants with GSTP1 methylation than those without. In patients with CHB, the degree of GSTP1 promoter methylation was significantly correlated with DNMT1 mRNA, DNMT3a mRNA, TNF-α, MDA, HBeAg, ALT, AST and TBIL. In contrast, no significant difference was found between GSTM3 methylation in patients with CHB and HCs (P = 0.079). Meanwhile, no significant difference could be observed between GSTM3 promoter methylation in patients with HBeAg-positive CHB and HBeAg-negative CHB (P = 0.146). Therefore, this study demonstrated that GSTP1 hypermethylation was associated with DNMT1, DNMT3a overexpression and oxidative stress in patients with HBeAg-positive CHB.

[Distributions and influencing factors of total dissolved inorganic antimony in the coastal area of Zhejiang and Fujian].

Antimony has been ubiquitously present in the aquatic environment as a toxic and rare metalloid element. The contamination of antimony and its compounds in the environment is increasingly severe, so it has been received extensive attention by the international scientific community. The cruise was carried out in the coastal area of Zhejiang and Fujian provinces in the East China Sea (ECS) in May 2008. The concentrations of total dissolved inorganic antimony (TDISb) were measured by Hydride Generation-Atomic Fluorescence (HG-AFS). The concentration ranges of TDISb in the surface and bottom layer were 0.68-5.64 nmol x L(-1) and 0.71-5.25 nmol x L(-1) with averages of 2.25 and 1.79 nmol x L(-1), respectively. The concentration of TDISb in the study area was lower than the environmental quality standards for surface water of China and drinking water standards of World Health Organization (about 41.08 nmol x L(-1)), indicating that it remained at the pristine level. The concentration of TDISb decreased gradually from the coastal area to the central ECS shelf with higher concentration in the surface layer than the bottom. Water mass mixing, adsorption/desorption behavior on the surface of the suspended particulate matters (SPM) and biological activities were the main influence factors of TDISb biogeochemistry in the study area.

Enhanced demethylation of interferon-γ gene promoter in peripheral blood mononuclear cells is associated with acute-on-chronic hepatitis B liver failure.

Acute-on-chronic hepatitis B liver failure (ACHBLF) refers to liver failure occurring in patients with chronic hepatitis B (CHB) related liver diseases. Interferon-γ (IFN-γ) plays an important role in the exacerbation of liver function. However, the exact mechanism, by which IFN-γ mediates ACHBLF, is not fully understood. Forty patients with ACHBLF, fifteen patients with CHB and ten healthy controls were included in this present study. ELISA was performed to measure the level of serum IFN-γ. The methylation status of IFN-γ promoter in peripheral blood mononuclear cells (PBMCs) was determined using methylation-specific PCR. Model for End-stage Liver Disease (MELD) scoring was performed for evaluating the severity of liver failure. The serum level of IFN-γ in patients with ACHBLF or CHB was significantly lower than that in healthy controls, while the serum IFN-γ level in ACHBLF patients was significantly higher than that in CHB patients. In ACHBLF patients, the level of IFN-γ was positively correlated with total bilirubin and MELD score, but negatively correlated with prothrombin time activity. These results suggest the involvement of IFN-γ in the pathogenesis of ACHBLF. Importantly, the degree of methylation of the IFN-γ gene promoter in ACHBLF patients (60%, 24/40) was significantly lower than that in CHB patients (93%, 14/15), but was higher than that in the control group (20%, 2/10). Furthermore, in ACHBLF patients, the serum IFN-γ level was significantly higher in unmethylation group than that in methylation group. In conclusion, enhanced demethylation of IFN-γ gene promoter in PBMCs may be associated with the onset of ACHBLF.

Effects of cake collapse caused by deposition of fractal aggregates on pressure drop during ceramic filtration.

A cake collapse model was developed by taking the combined effects of fractal dimension, relaxation ratio, coordination number, and aggregate diameter into consideration. The cake porosity including intraaggregate and interaggregate porosities was modeled successively by three typical coordination numbers (n = 6, 8, and 12). Accordingly, an inversion method made it possible to deduce the coordination number using the measured cake porosities, and the reverse-calculated value with minimum error and the corresponding relaxation ratios were applied as the parameters for the model. As a result, the profiles of intraaggregate and interaggregate porosities and cake porosity were respectively predicted in contrast to the integrated variation of the relaxation ratio and the fractal dimension. Furthermore, a comparison between the model predictions of the cake pressure drop gradients with and without aggregate compression was conducted to validate the presence of cake collapse. The results show that the predictions based on the proposed collapse model are in agreement with the experiments, and the coordination number is one of the key factors that must be incorporated into the cake collapse models.

Plasma alpha-tocopherol is negatively correlated with hepatocyte apoptosis in chronic hepatitis B patients.

AIM: Hepatocyte apoptosis is involved in the pathogenesis of liver diseases, while at the same time oxidative stress plays an important role in liver cell damage. This prompted us to evaluate the possible relationship between hepatocyte apoptosis and oxidative stress in patients with chronic hepatitis B. METHODS: CHB patients were placed in groups A (ALT >40 IU/L) and B (ALT

[Study on the relationship of serum vitamin E and liver pathological features in the patients with chronic hepatitis B].

OBJECTIVE: To study on the relationship of serum vitamin E and liver pathological features in the patients with chronic hepatitis B. METHODS: Sixty-six patients with chronic hepatitis B and ten healthy controls were enrolled in this present study. The serum vitamin E level was measured spectrophotometrically. Comparisons of liver function test, HBeAg and HBV DNA level were conducted among different liver pathological features including inflammatory grading and fibrosis staging. RESULTS: Compared with healthy controls, the serum level of vitamin E was significantly decreased in the patients with chronic hepatitis B, especially in those with elevated ALT activity. In comparison between HBeAg positive group and HBeAg negative group, the serum level of vitamin E of the former group did not significantly changed (P > 0.05). Furthermore, the serum level of vitamin E has been demonstrated to be negatively associated with the inflammation grading in the patients with chronic hepatitis B. However, there was no significant association between the serum vitamin E and liver fibrosis staging. CONCLUSION: Vitamin E, as one of the important anti-oxidants, was demonstrated to be implicated in the progression of liver inflammation in the patients with chronic hepatitis B. Furthermore, the supplement of vitamin E would be a potential therapy for attenuate the inflammatory response.

[Study of serum level of cortisol and peripheral T lymphocyte subsets state in the hepatitis B virus carriers].

OBJECTIVE: To study of serum level of cortisol and peripheral T lymphocyte subsets state in the hepatitis B virus (HBV) carriers. METHODS: Sixty chronic HBV carriers and ten healthy controls were all enrolled in this present study. Serum expression of cortisol was determined by radioimmunoassay, and also flow cytometry was performed to evaluate peripheral blood T lymphocyte subset. RESULTS: Compared with those in normal controls, the serous levels of cortisol in chronic HBV carriers were significantly elevated, while there was no distinct difference in the proportion of CD4+ T lymphocytes ( P > 0.05) with the decreased odds of CD4+/CD8+ lymphocytes( P < 0.05) and obvious higher proportion of CD8+ T lymphocytes( P < 0.05). In comparison between HBeAg positive group and HBeAg negative group, the serous levels of cortisol of the former group were significantly higher ( P < 0.05), and so proportion of CD8+ T was too ( P < 0.05). However, there is no significant differences in the proportion of CD4+ T lymphocyte ( P > 0.05). CONCLUSION: The elevated serum cortisol and increased CD8+ T lymphocytes subsets in the chronic HBV carriers, suggested that there was disturbance of endocrine-immune response in the chronicity of HBV infection.

[Safety and tolerance study of single oral dose of adefovir dipivoxil tablets in healthy volunteers].

BACKGROUND: To assess the safety and tolerance of adefovir dipivoxil tablet in Chinese healthy volunteers. METHODS: Totally 42 healthy volunteers were enrolled in the study, 21 were female and 21 were male and their age ranged from 19 to 26 years. The subjects were randomly divided into 5, 10, 20, 40 and 60 mg dose-groups (6-10 subjects in each group) based on sex and weight, beginning with the 5 mg dose-group. Clinical symptoms, vital signs, electrocardiogram, routine blood test, routine urine test, prothrombin time and blood biochemical tests were recorded and evaluated. RESULTS: No significant changes were found in clinical symptoms, vital signs and laboratory tests after dosing, except slight elevations of alanine aminotransferase in 2 subjects and bilirubin in 6 subjects observed and some gastrointestinal symptoms such as nausea and diarrhea found in 3 subjects, but the frequency and severity of all the adverse reactions were not found to be related to the dosages. CONCLUSION: The results showed that single oral dose of adefovir dipivoxil 60 mg or less was safe and tolerable.

[Oxidative stress in patients with chronic hepatitis B].

BACKGROUND: To study oxidative stress in patients with chronic hepatitis B. METHODS: Malondialdehyde (MDA), total anti-oxidative ability and ascorbic acid were measured as markers of oxidative stress in 30 patients with chronic hepatitis B, besides HBV DNA and ALT. RESULTS: MDA was significantly higher in patients with hepatitis B than the controls (P less than 0.05). Ascorbic acid was significantly higher in patients with normal ALT than the controls (P less than 0.01). MDA was significantly higher in patients with increased ALT than the controls and in patients with normal ALT. MDA was significantly positively correlated with ALT (r=0.61), and ascorbic acid was significantly negatively correlated with ALT (r=-0.64) in patients with hepatitis B. No significant relationship was found between HBV DNA and other indices of oxidative stress. No significant difference in total anti-oxidative ability was found among all groups. CONCLUSION: There was a disturbance between oxidative stress and anti-oxidative ability in patients with chronic hepatitis B. In patients with increased ALT, oxidative stress became high. In patients with normal ALT, oxidative stress level was low. The indices of oxidative stress should be detected in patients with hepatitis B, in addition to HBV markers.

[Hemorheologic changes in patients with liver diseases].

BACKGROUND: To study the variation of the hemorheology and microcirculation in different period of liver diseases. METHODS: Indices for hemorheology, liver function, HBV DNA and transfusion transmitted virus (TTV) DNA were measured in 82 patients with liver diseases and correlative analysis was made. RESULTS: The low-shear whole blood viscosity (BV) and RBC aggregation index were significantly higher in hepatitis B group than those in the control group (P less than 0.05). No correlation was found between HBV DNA and indices of hemorheology (P greater than 0.05). The high-shear and low-shear BV and hematocrit (HCT) were significantly lower in decompensated cirrhosis group than those in the control group (P less than 0.05). RBC aggregation index, plasma viscosity (PV) and the low-shear BV were significantly higher in compensated cirrhosis group than those in the control group (P less than 0.05). The high-shear and low-shear BV were significantly higher in TTV positive group than those in the control group. CONCLUSION: There is disturbance of microcirculation in the body of patients with hepatitis B or TTV infection. The blood of patients with compensated cirrhosis is in highly viscose status and in low viscose status in patients with decompensated cirrhosis. TTV seems to be harmful to some degree to the body. The hemorheology should be an index in detecting liver diseases in addition to HBV markers.