GRB10 is a novel factor associated with gastric cancer proliferation and prognosis.

GRB10 and its family members GRB7 and GRB14 were important adaptor proteins. They regulated many cellular functions by interacting with various tyrosine kinase receptors and other phosphorus-containing amino acid proteins. More and more studies have shown that the abnormal expression of GRB10 is closely related to the occurrence and development of cancer. In our current research, expression data for 33 cancers from the TCGA database was downloaded for analysis. It was found that GRB10 was up-regulated in cholangiocarcinoma, colon adenocarcinoma, head and neck squamous carcinoma, renal chromophobe, clear renal carcinoma, hepatocellular carcinoma, lung adenocarcinoma, lung squamous carcinoma, gastric adenocarcinoma and thyroid carcinoma. Especially in gastric cancer, the high GRB10 expression was closely associated with poorer overall survival. Further research showed that the knockdown of GRB10 inhibited proliferation and migration ability in gastric cancer. Also, there was a potential binding site for miR-379-5p on the 3'UTR of GRB10. Overexpression of miR-379-5p in gastric cancer cells reduced GRB10-regulated gastric cancer proliferation and migration capacity. In addition, we found that tumor growth was slower in a mice xenograft model with knock down of GRB10 expression. These findings suggested that miR-379-5p suppresses gastric cancer development by downregulating GRB10 expression. Therefore, miR-379-5p and GRB10 were expected to be potential targets for the treatment of gastric cancer.

[Temporal and Spatial Variations in Black Carbon Aerosol in Different Atmospheric Background Stations in China from 2006 to 2020].

Black carbon (BC) aerosol emissions are complex and have important environmental and meteorological effects. In China, the temporal and spatial variations in BC in different atmospheric environmental conditions need to be fully understood. Based on the long-term observational BC data in seven atmospheric background stations in China from 2006 to 2020, combined with meteorological data, emission source data, enhanced vegetation index (EVI) data, and aerosol optical depth (AOD) data, we comprehensively analyzed the characteristics of temporal and spatial variations, long-term evolution, and influencing factors of BC in China. The results showed that the BC and AOD values of different atmospheric environments in China were quite different, and BC positively contributed to AOD. The spatial distribution was high in the east and low in the west owing to the differences in emission sources and meteorological conditions. The ρ(BC) and AOD values were higher to the east of the "Hu Huanyong" line, such as at the Mt. Longfeng, Shangdianzi, Lin'an, and Jinsha stations, where the average values were (1699±2213)-(3392±2131) ng·m-3 and 0.36±0.32-0.72±0.37, respectively. These values were lower to the west of the "Hu Huanyong" line, such as at the Akedala, Mt. Waliguan, and Shangri-La stations, where the average values were (287±226)-(398±308) ng·m-3 and 0.20±0.13-0.22±0.19, respectively. The interannual variability in BC included differences between different atmospheric background stations, which could be divided into four categories:low interannual variability, such as at the Akedala station; an initial increase followed by a decrease and subsequent stabilization, such as at the Mt. Waliguan station; an initial decrease followed by stabilization, such as at the Shangri-La station; and an initial stabilization followed by a decrease, such as at the Mt. Longfeng, Shangdianzi, Jinsha, and Lin'an stations. Seasonal variations in BC included differences in different atmospheric background stations. The BC mass concentrations were lowest in autumn and higher in winter and spring west of the "Hu Huanyong" line and were highest in winter and lowest in summer east of the "Hu Huanyong" line. BC contributed to the AOD being larger in all stations in the spring and summer and contributed less at the stations west of the "Hu Huanyong" line in autumn and the stations east of the "Hu Huanyong" line in winter. The diurnal variations in BC were mainly bimodally distributed in the different atmospheric background stations, but the peak times varied in different stations and seasons.

Iron-Based Metal-Organic Frameworks as Platform for H2S Selective Conversion: Structure-Dependent Desulfurization Activity.

Three classical Fe-MOFs, viz., MIL-100(Fe), MIL-101(Fe), and MIL-53(Fe), were synthesized to serve as platforms for the investigation of structure-activity relationship and catalytic mechanism in the selective conversion of H2S to sulfur. The physicochemical properties of the Fe-MOFs were characterized by various techniques. It was disclosed that the desulfurization performances of Fe-MOFs with well-defined microstructures are obviously different. Among these, MIL-100(Fe) exhibits the highest catalytic performance (ca. 100% H2S conversion and 100% S selectivity at 100-180 °C) that is superior to that of commercial Fe2O3. Furthermore, the results of systematic characterization and DFT calculation reveal that the difference in catalytic performance is mainly because of discrepancy in the amount of Lewis acid sites. A plausible catalytic mechanism has been proposed for H2S selective conversion over Fe-MOFs. This work provides critical insights that are helpful for rational design of desulfurization catalysts.

Serum iron levels are an independent predictor of in-hospital mortality of critically ill patients: a retrospective, single-institution study.

OBJECTIVE: This study aimed to examine the relationship between serum iron levels and in-hospital mortality in critically ill patients. METHODS: We retrospectively studied 250 critically ill patients who received treatment at the intensive care unit between June 2015 and May 2017. Blood chemistry and hepatic and renal function were measured. Kaplan-Meier survival curves were plotted according to serum iron levels. Correlations between serum iron levels and other variables were analyzed. RESULTS: A total of 165 (66.0%) patients had abnormally low serum iron levels (<10.6 µmol/L). Patients who died during hospitalization had markedly higher Acute Physiology and Chronic Health Evaluation II scores and significantly lower serum iron levels compared with those who survived. Cumulative survival was significantly lower in patients with low serum iron levels than in those with normal serum iron levels in subgroup analysis of older patients (n = 192). Multivariate regression analysis showed that, after adjusting for relevant factors, low serum iron levels remained an independent risk for in-hospital mortality (odds ratio 2.014; 95% confidence interval 1.089, 3.725). CONCLUSIONS: Low serum iron levels are present in a significant proportion of critically ill patients and are associated with higher in-hospital mortality, particularly in older patients.

Intrafibrillar silicified collagen scaffold modulates monocyte to promote cell homing, angiogenesis and bone regeneration.

The immunomodulatory functions of monocytes are increasingly being recognized. Silicified collagen scaffolds (SCSs), produced by infiltrating collagen matrices with intrafibrillar amorphous silica, exhibit osteogenic and angiogenic potential and are promising candidates in tissue engineering. Here, we demonstrate that SCS promotes in situ bone regeneration and angiogenesis via monocyte immunomodulation. Increased numbers of TRAP-positive monocytes, nestin-positive bone marrow stromal cells (BMSCs) and CD31-positive and endomucin-positive new vessels can be identified from new bone formation regions in a murine calvarial defect model. In addition, sustained release of silicic acid by SCS stimulates differentiation of blood-derived monocytes into TRAP-positive cells, with increased expressions of SDF-1α, TGF-ß1, VEGFa and PDGF-BB. These cytokines further promote homing of BMSCs and endothelial progenitor cells as well as neovascularization. Taken together, these novel findings indicate that SCSs possess the ability to enhance recruitment of progenitor cells and promote osteogenesis and angiogenesis by immunomodulation of monocytes.

[Weekend Effect in Distributions of Particulate Matters, Main Gas Pollutants and Aerosol Size in Spring of Jiaxing].

To investigate the discrepancy of distributions of major gas pollutants and aerosol size between weekdays and weekends, trace gases (SO2, NO2, CO and O3), PM (PM10 and PM2.5) and aerosol spectral distributions at 10 nm-10 µm were monitored in May 2015 at Nanhu district in Jiaxing. The results showed that the gas pollutants of SO2, NO2, CO and O3 had significant weekend effects in Jiaxing. The O3 concentration on daytime of weekends was lower than that of weekdays. The peak of O3 occurred at 14:00 on weekends, which was 1 hour later than that on weekdays. The weekend effect of PM2.5 was observed to be much more obvious compared to that of PMPM2.5. The ratios of PMPM2.5/PM10 were 0.7 and 0.6 on weekends and weekdays, respectively. The aerosol number concentration was mostly concentrated at particle size below 500 nm, with values of 16,602 cm⁻³ and 23,309 cm⁻³ on weekends and weekdays. The most remarkable weekend effect was found for aerosol number concentration in nuclei mode, for surface area concentration in nuclei and coarse mode, and for mass concentration in accumulation and coarse mode. The spectra of aerosol number concentration, surface area concentration and mass concentration showed unimodal, trimodal and four-peak distributions, respectively.

Intrafibrillar-silicified collagen scaffolds enhance the osteogenic capacity of human dental pulp stem cells.

OBJECTIVES: The present study investigated the effects of intrafibrillar-silicified collagen scaffolds (ISCS) on the osteogenic differentiation of human dental pulp stem cells (hDPSCs) in vitro and in vivo. METHODS: The hDPSCs were co-cultured with ISCS or nonsilicified collagen scaffolds (NCS) in control medium (CM) or osteogenic differentiation medium (ODM). Cell cycle and cell apoptosis were analyzed with flow cytometry to measure the viability of hDPSCs. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to evaluate the expression levels of osteogenic marker genes and proteins of hDPSCs. Alkaline phosphatase (ALP) staining and alizarin red S assay were used to evaluate the ALP activity of hDPSCs and their calcium deposition potential. In addition, hDPSCs and scaffolds were implanted subcutaneously in nude mice for 8 weeks. Harvested tissues were immunohistochemically stained for osteocalcin (OCN) expression from hDPSCs, and stained with alizarin red S for examination of their calcium deposition in vivo. RESULTS: The ISCS had no adverse effect on hDPSCs, promoted their proliferation, and significantly up-regulated the expression of osteogenesis-related genes and proteins. The hDPSCs co-cultured with ISCS in ODM exhibited the highest ALP activity and calcium deposition in vitro. The ISCS promoted the OCN expression and calcium deposition of hDPSCs after ectopic transplantation in vivo. CONCLUSIONS: Intrafibrillar-silicified collagen scaffolds significantly promoted the proliferation, osteogenic differentiation and mineralization of hDPSCs, when compared with NCS. This study demonstrates combining the use of hDPSCs and ISCS to promote bone-like tissue formation is a promising approach for clinical bone repair and regeneration.

Validity and reliability of Patient Health Questionnaire-9 and Patient Health Questionnaire-2 to screen for depression among college students in China.

INTRODUCTION: This study examined the validity and reliability of the Patient Health Questionnaire-9 (PHQ-9) and Patient Health Questionnaire-2 (PHQ-2). The optimal cutoff score when screening for depression among Chinese college students was also determined. METHODS: A total of 959 participants completed the PHQ-9 and the Beck Depression Inventory (BDI) questionnaire. The Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders was used to diagnose depression. Statistical tests were performed to determine the reliability, validity, and receiver operating characteristic curve of the data. The concurrent validity was tested by examining associations between PHQ-9 and BDI. The sensitivity and specificity, as well as the positive and negative predictive values, were calculated for different cutoff scores of PHQ-9 and PHQ-2. RESULTS: The internal consistency values of PHQ-9 and PHQ-2 were 0.854 and 0.727, respectively. The test-retest reliability values of PHQ-9 and PHQ-2 were 0.873 and 0.829, respectively. The scores of PHQ-9 (r = 0.790) and PHQ-2 (r = 0.651) were significantly associated with that of BDI. PHQ-9 had an optimal cutoff score of 11, which indicated a sensitivity of 0.89 and a specificity of 0.97, with an area under the curve of 0.977 (95% confidence interval: 0.966-0.988). The PHQ-2 demonstrated satisfactory sensitivity (0.81) and specificity (0.96) at the cutoff score of 3, and its area under the curve was 0.939. DISCUSSION: The PHQ-9 and the PHQ-2 are valid and reliable tools to screen depression in Chinese college students. For screening purposes, cutoff scores of 11 and 3 are recommended for PHQ-9 and PHQ-2, respectively.

[The effects of p38MAPK and HBxAg on cell proliferation and apoptosis in human hepatocarcinogenesis].

OBJECTIVE: To investigate the effects of host-derived p38 mitogen-activated protein kinase subunit 38 (p38MAPK) and the hepatitis B virus X antigen (HbxAg) on cell proliferation and apoptosis in human hepatocellular carcinoma (HCC), and to study the mechanism underlying hepatocarcinogenesis. METHODS: Liver tissues were biopsied from healthy individuals and patients with chronic hepatitis B (CHB), liver cirrhosis, paratumor cirrhosis, and HCC. Immunohistochemical staining was used to detect expressions of HBxAg, p38MAPK, cell cycle G2/M phase-related factors (cdc25B, p34cdc2, cyclin B1), and cell proliferation factor ki-67.The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method (known as TUNEL) was used to detect apoptosis. RESULTS: The highest rates of HBxAg were detected in CHB (65.0%) and HCC (44.4%) liver samples, and the antigen was mainly expressed in nuclei. Increasingly higher rates of p38MAPK, cdc25B, cyclin B1, and p34cdc2 expression were detected with increases in disease severity: normal liver (40.0%, 20.0%, 20.0%, and 30.0%, respectively), chronic hepatitis B (60.0%, 65.0%, 40.0%, and 50.0%, respectively), liver cirrhosis (65.0%, 75.0%, 70.0%, and 55.0%, respectively), paratumor cirrhosis (66.7%, 75.0%, 75.0%, and 63.9%, respectively), and HCC (77.8%, 80.6%, 80.6%, and 72.2%, respectively). In addition, the intracellular location of p38MAPK expression was different under different disease conditions, showing nuclear expression in CHB and liver cirrhosis samples and cytoplasmic expression in paratumor cirrhosis and HCC samples (x2 = 1.11, P more than 0.05). The proliferation index (PI) and the apoptosis index (AI) were both increased along with disease severity (normal more than CHB more than paratumor cirrhosis more than HCC) (PI: 0.0000+/-0.000, 0.0502+/-0.011, 0.0411+/-0.009, 0.0762+/-0.017; AI: 0.0351+/-0.024, 0.0607+/-0.022, 0.0562+/-0.013, 0.0716+/-0.011), with the notable exception for liver cirrhosis (PI: 0.1810+/-0.036 and AI: 0.1200+/-0.018). PI in poorly-differentiated HCC (0.2285+/-0.062) was significantly higher than in well-differentiated HCC (0.1216+/-0.032, t = 2.082, P = 0.044). AI in well-differentiated HCC (0.152+/-0.026) was significantly higher than in poorly-differentiated HCC (0.081+/-0.022, t = 2.129, P = 0.041). CONCLUSIONS: In the process of hepatocarcinogenesis, HBxAg may cause a series of abnormal changes in cell cycle, proliferation and apoptosis by affecting the expression of p38MAPK.

[Role of p38MAPK in apoptosis of human paratumor cirrhosis hepatocellular cell line QSG-7701 induced by cisplatin].

OBJECTIVE: To investigate the roles of p38 MAPK in apoptosis of the normal liver cell, the paratumor cirrhosis hepatocellular cell and the hepatocellular carcinoma cell. METHODS: Three cell lines were adopted (the normal liver cell line HL-7702, the paratumor cirrhosis hepatocellular cell line QSG-7701 and the hepatocellular carcinoma cell line QGY-7703) and treated with Diamminedichloroplatin (DDP, cisplatin) and p38MAPK inhibitor SB203580. The apoptosis and cell cycles were detected by flow cytometry and electromicroscopy. The expressions of p38MAPK, CDC25B, p34cdc2 and cyclinB1 were detected by immunocytochemical staining , confocal microscopy and western blot. RESULTS: The apoptotic rates in all three cell lines pretreated with DDP increased obviously and the rates in normal liver cells and HCC cells increased continuously even after SB203580 treatment, whereas in paratumor cirrhosis cells the rate decreased and the cell cycle stopped at S phase. CONCLUSION: Cisplatin induces apoptosis in the paratumor cirrhosis hepatocellular cell line QSG-7701 via activation of p38MAPK pathway and it differs in the normal liver cells from the hepatocellular carcinoma cells.

Angiogenic study in Graves' disease treated with thyroid arterial embolization.

PURPOSE: To investigate angiogenesis in the thyroid of Graves' disease (GD) treated with thyroid arterial embolization through analysis of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and microvessel density (MVD). MATERIALS AND METHODS: Forty-two GD patients were treated with thyroid arterial embolization and followed up for 1-68 months after embolization. Before embolization and at 7 days, 3, 6, 12, 36 and 48 months following embolization, TT3, TT4, FT3, FT4, TSH and thyroid stimulating antibody (TSAb) were tested respectively. Thyroid biopsy was performed under the guidance of computed tomography for immunohistochemical staining of VEGF and bFGF, and MVD within the thyroid gland was marked by CD34. RESULTS: VEGF and bFGF were mostly expressed in the cytoplasm and on the cell membrane. The expression of VEGF was increased (P < 0.05) at < or = 6 months compared with before embolization and decreased (P < 0.05) at > or = 1 year compared with either at < or = 6 months or before embolization. The expression of bFGF was not statistically different at < or = 6 months compared with before embolization but was decreased (P < 0.05) at > or = 1 year compared with either at ?6 months or before embolization. Thyroid MVD marked by CD34 had similar changes to those of the VEGF expression after embolization. There was a positive correlation between VEGF and bFGF (P < 0.05) and between VEGF or bFGF and MVD (P < 0.05). Thyroid hormones mostly returned to normal and TSAb was decreased in longer follow-up. CONCLUSION: Thyroid arterial embolization can decrease the expression of VEGF, bFGF and MVD. Consequently, angiogenesis within the GD thyroid will be decreased in the long term after embolization and may serve as the basis for reduced thyroid size and function.

Graves' disease treated with thyroid arterial embolization.

PURPOSE: To study pathological changes in the thyroid gland of patients with Graves' disease (GD) treated with thyroid arterial embolization. METHODS: Thirty-seven patients with GD were treated through transcatheter thyroid arterial embolization. Of these patients, twenty-two had biopsy of the thyroid gland at different time points before and after the embolization for the study of pathology. Serum thyroid hormones, TSH and TRAb were also studied at these time points. Thyroid size was evaluated in all patients using color Doppler ultrasound or CT scan. RESULTS: Thyroid size decreased immediately or several days following embolization. Pathological study demonstrated mainly acute infarction and necrosis at 7 days post embolization. At 6 months, chronic inflammation and fibrous hyperplasia were the primary findings in the gland, and at 3 years following embolization, mesenchyma hyperplasia and follicle atrophy were primarily present in the embolized thyroid tissue. The thyroid hormones and TSH gradually resumed to normal range after embolization while TRAb decreased significantly. CONCLUSION: Thyroid arterial embolization can cause GD thyroid gland a series of pathological changes of acute ischemia and necrosis and later, chronic inflammation, fibroplasia and atrophy to decrease secretion of thyroid. The pathological changes within the thyroid gland after embolization form the basis of thyroid arterial embolization in treating GD hyperthyroidism.

Apoptotic study in Graves disease treated with thyroid arterial embolization.

OBJECTIVE: To investigate apoptosis in the thyroid of Graves disease (GD) induced by thyroid arterial embolization. MATERIALS AND METHODS: Forty one patients with clinically and laboratorily ascertained GD were treated with thyroid arterial embolization and followed up for 3-54 months following embolization. Prior to embolization and at 1, 3, 6, 12 and 36 months following embolization, thyroid autoimmunue antibodies were tested respectively, including thyroid stimulating antibody (TSAb), thyroglobulin antibody (TGAb) and thyroid microsomal antibody (TMAb). Thyroid biopsy was performed under the guidance of computed tomography for immunohistochemistry examination using semi-quantity analysis. RESULTS: The positive staining of Fas and FasL was mostly in the cytoplasma and cell membrane, the positive expression of Bax was mainly in the cytoplasma, and no positive expression of P53 was detected in the thyroid cells before embolization. After arterial embolziation, the positive cell number and staining degree of these genes were both greater than before embolization. CONCLUSION: The treatment method of thyroid arterial embolization can effectively enhance the positive expression of pro-apoptotic genes of Fas, FasL, Bax, Bcl-2 and P53 in GD thyroid, thus promoting apoptosis of GD thyroid and helping restore the thyroid size and function to normal conditions.

Expression and hypermethylation of p27 kip1 in hepatocarcinogenesis.

AIM: To study the expressions of p27 kip1 protein and p27mRNA, the hypermethylation of p27 kip1 and the relation between them in various stages of hepatocarcinogenesis. METHODS: p27 protein and p27mRNA were detected by immunohistochemical staining and in situ hybridization respectively in 68 cases of normal liver, liver cirrhosis, pericancerous cirrhosis and hepatocellular carcinoma (HCC). The hypermethylation of p27 kip1 was detected by methylation-specific PCR (MSP) in 44 cases of normal liver, liver cirrhosis, and HCC. RESULTS: The positive rate of p27 protein was 66.7% (4/6) in normal liver, 60.0% (6/10) in liver cirrhosis, 50.0% (12/24) in pericancerous cirrhosis and 21.4% (6/28) in HCC. There were no statistical differences in normal liver, liver cirrhosis and pericancerous cirrhosis, but the positive rate of p27 protein significantly decreased in HCC compared to that in the other groups (P = 0.006, chi2 = 7.664). The positive rate of p27 kip1 mRNA was 83.3% (5/6) in normal liver, 70.0% (7/10) in liver cirrhosis, 75.0% (18/24) in pericancerous cirrhosis and 25.0% (7/28) in HCC. There were no statistical differences in normal liver, liver cirrhosis and pericancerous cirrhosis, but the positive rate of p27 kip1 mRNA also significantly decreased in HCC compared to that in the other groups (P = 0.000, chi2 = 16.600). In addition, there was a significant correlation between the expression of p27 protein and p27mRNA in the integrated group of normal liver and liver cirrhosis. However, no significant correlation was found between pericancerous cirrhosis and HCC. Using MSP, we found that 1 HCC in 44 cases (including 6 cases of normal liver, 10 cases of liver cirrhosis and 28 cases of HCC) was methylated, whose p27 protein and p27mRNA were negative. CONCLUSION: The reduction or loss of p27 protein and p27mRNA are potentially involved in hepatocarcinogenesis. The hypermethylation of p27 might lead to the loss of p27mRNA transcription.

Detection of HBV, PCNA and GST-pi in hepatocellular carcinoma and chronic liver diseases.

AIM: To investigate the change of HBV DNA, PCNA and GST-pi in chronic liver disease and hepatocellular carcinoma (HCC). METHODS: Hepatitis B surface antigen (HBsAg), proliferating cell nuclear antigen (PCNA) and glutathione S-transferases (GST-pi) were detected by immunohistochemical staining and HBV DNA was detected by in situ hybridization (ISH) in formalin-fixed and paraffin-embedded sections with a total of 111 specimens of chronic hepatitis, liver cirrhosis, paratumorous tissue, HCC and normal liver tissue. RESULTS: The positive rates of HBsAg and HBVDNA were 62.5 %(15/24) and 75.0 %(12/16) in chronic hepatitis, 64.0 %(16/25) and 83.3 %(15/18) in liver cirrhosis, 72.7 %(16/22) and 85.7 %(12/14) in the paratumorous tissu and 45.0 %(14/31) and 64.3 %(9/14) in HCC. The positive HBVDNA granules in chronic hepatitis, liver cirrhosis and the paratumorous tissue were more intense than that in HCC. The positive rates of PCNA and GST-pi were 34.8 %(8/23) and 25.0 %(4/16) in chronic hepatitis, 73.7 %(14/19) and 17.6 %(3/17) in liver cirrhosis, 86.7 %(13/15) and 53.3 %(8/15) in the paratumorous tissue, 100 %(15/15) and 60.0 %(9/15) in HCC, respectively, and the positive rate of GST-pi in the paratumorous tissue was significantly higher than that in the liver cirrhosis without tumor (P<0.05), but same as that in HCC (P>0.05). CONCLUSION: The HBV infection may increase expression of PCNA and GST-pi. The paratumor cirrhosis may be a sequential lesion of precancerous cirrhosis around HCC.

[Expression of GST-pi and HBV infection in hepatocellular carcinoma].

BACKGROUND & OBJECTIVE: The expression of glutathione S-transferases(GST-pi) might abnormally increase in many carcinogenesis, and the alteration of GST-pi preceded than that alteration of cell morphology. This study was designed to investigate the expression of glutathione S-transferases (GST-pi) and its relationship with hepatitis B virus (HBV) infection in hepatocellular carcinoma (HCC). METHODS: Hepatitis B surface antigen (HBsAg), Hepatitis B core antigen (HBcAg), and GST-pi were detected by immunohistochemical staining and HBV DNA was detected by in situ hybridization (ISH) in total 86 samples of chronic hepatitis, liver cirrhosis, paratumor cirrhosis, HCC, and normal liver tissue. RESULTS: The positive expression rates of HBsAg, HBcAg, and HBV DNA were 61.9% (13/21), 42.9% (9/21), and 75.0% (12/16) in chronic hepatitis; 64.0% (16/25), 36.0% (9/25), and 83.3% (15/18) in liver cirrhosis; 72.7% (16/22), 61.1% (11/18), and 85.7% (12/14) in the paratumor cirrhosis, as well as 45.0% (14/31), 50.0% (14/28) and 64.3% (9/14) in HCC. HBV DNA positive granules in chronic hepatitis, liver cirrhosis, and the paratumor cirrhosis were more and stronger than that in HCC, respectively. The positive expression rates of GST-pi were 25.0% (4/16), 17.6% (3/17), 53.3% (8/15), and 60.0% (9/15) in chronic hepatitis, liver cirrhosis, the Paratumor cirrhosis, and HCC, respectively. The positive rate of GST-pi in the paratumor cirrhosis was significantly higher than that in the liver cirrhosis without tumor (P < 0.05), but the same as in HCC (P > 0.05). CONCLUSIONS: Most of the HCC cases were closely associated with chronic hepatitis and liver cirrhosis of HBV infection. The HBV infection may increase expression of GST-pi. The paratumor cirrhosis may be a sequential lesion of precancerous cirrhosis around HCC.