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Biomedical subjects

Yong Sung Kim

Publications and source records attributed to Yong Sung Kim.

At least 19 recordsLinked to original sources

The epigenetic silencing of LIMS2 in gastric cancer and its inhibitory effect on cell migration.

Recent finding has shown that LIMS2 (also known as PINCH2) functions as a natural regulator of the LIMS1-ILK-parvin complex formation and is associated with cell spreading and migration via integrins at focal adhesions. Here, we report for the first time the epigenetic silencing of LIMS2 in gastric tumors. Downregulation of LIMS2 was detected in 91% (10 of 11) of gastric cancer cell lines by real-time quantitative RT-PCR and 80% (8 of 10) of the LIMS2-downregulated cell lines were associated with CpG island hypermethylation at a 5'-upstream region of LIMS2. Furthermore, LIMS2 was restored in its non-expressing cell lines after treatment with 5-Aza-dC and/or trichostatin A. Loss of expression of LIMS2 was also detected in 53% (51 of 96) of primary gastric tumors. This decrease in expression level significantly correlated with an increase of the CpG island hypermethylation. In addition, the methylation status in any normal-appearing gastric tissues was gradually increased in an age-dependent manner, suggesting that the positive methylation in normal-appearing gastric mucosa can be due to 'field cancerization effect' as an early event in gastric carcinogenesis. Moreover, the transient transfection of LIMS2-siRNA significantly stimulated cell migration in gastric cancer cells but had no effects on cell growth. These results suggest that the frequent inactivation of LIMS2 by epigenetic alteration in gastric cancer may be important in tumor progression events, such as invasion and metastasis. Thus, LIMS2 may be useful as a molecular biomarker and a therapeutic target by increasing its expression and activity in gastric cancer.

Adaptor Proteins, Signal Transducing↗

Membrane topology of helix 0 of the Epsin N-terminal homology domain.

Specific interaction of the epsin N-terminal homology (ENTH) domain with the plasma membrane appears to bridge other related proteins to the specific regions of the membrane that are invaginated to form endocytic vesicles. An additional a-helix, referred to as helix 0 (H0), is formed in the presence of the soluble ligand inositol-1,4,5-trisphosphate [Ins(1,4,5)P3] at the N terminus of the ENTH domain (amino acid residues 3-15). The ENTH domain alone and full-length epsin cause tubulation of liposomes made of brain lipids. Thus, it is believed that H0 is membrane-inserted when it is coordinated with the phospholipid phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P2], resulting in membrane deformation as well as recruitment of accessory factors to the membrane. However, formation of H0 in a real biological membrane has not been demonstrated. In the present study, the membrane structure of H0 was determined by measurement of electron paramagnetic resonance (EPR) nitroxide accessibility. H0 was located at the phosphate head-group region of the membrane. Moreover, EPR line-shape analysis indicated that no pre-formed H0-like structure were present on normal acidic membranes. PtdIns(4,5)P2 was necessary and sufficient for interaction of the H0 region with the membrane. H0 was stable only in the membrane. In conclusion, the H0 region of the ENTH domain has an intrinsic ability to form H0 in a PtdIns(4,5)P2-containing membrane, perhaps functioning as a sensor of membrane patches enriched with PtdIns(4,5)P2 that will initiate curvature to form endocytic vesicles.

Adaptor Proteins, Vesicular Transport↗

Identification of intrahepatic cholangiocarcinoma related genes by comparison with normal liver tissues using expressed sequence tags.

Intrahepatic cholangiocarcinoma (ICC), a malignant tumor derived from the bile duct epithelium, is one of the leading causes of death from cancer, worldwide. However, the mechanisms related to it remain largely unknown. In this study, an analysis of the gene expression profiles for ICC was done using the frequency of the ESTs obtained from nine cDNA libraries that constructed from 4 ICC cell lines and 4 normal liver tissues. One hundred and thirty-seven genes were identified as being either up- or down-regulated in human ICC cells. Thirty genes were randomly selected to confirm their differential expression in 4 human ICC cell lines and 5 ICC tissues compared to normal liver tissues by semi-quantitative RT-PCR. Among these genes, ANXA1, ANXA2, AMBP, and SERPINC1 were further verified by immunohistochemical analyses. In conclusion, these identified genes represent potential biomarkers for ICC and represent potential targets for elucidating the molecular mechanisms that are associated with ICC.

Bile Duct Neoplasms↗

Effects of ranitidine for exercise induced gastric mucosal changes and bleeding.

AIM: To evaluate the effect of ranitidine on gastric mucosal changes and on GI bleeding in long distance runners. METHODS: Twenty-four long distance runners (M: 16, F: 8, age: 18.2 +/- 1.5 years) participated in this study. A symptom questionnaire, stool hemoccult test, and upper gastrointestinal (GI) endoscopy were performed on the subjects prior to the study. The subjects took oral ranitidine (150 mg, b.i.d.) for two weeks. The upper GI endoscopy and stool Hemoccult tests were repeated after the treatment. RESULTS: Twenty-two of the 24 runners had at least one upper GI mucosal lesion before the medication. The Endoscopic improvements were seen in eleven of the 14 cases of erosive gastritis and four of the 5 cases of esophagitis. Six subjects were Heme occult positive prior to the study, but only one was positive after the medication. CONCLUSION: Gastric mucosal lesions and GI bleeding in long distance runners seem to be associated to acid-related factors mediated by the high level of regular running. Ranitidine seems to be and effective prophylaxis to prevent gastric mucosal lesions and GI bleeding.

Adolescent↗

Functional polymorphism 57Val>Ile of aurora kinase A associated with increased risk of gastric cancer progression.

Overexpression or amplification of the aurora kinase A (AURKA) gene induces chromosomal instability and transformation. AURKA SNPs are associated with several human cancers but their association with gastric cancer has yet to be investigated. In this study, 501 gastric cancer patients and 427 controls were genotyped for two coding SNPs in AURKA, 91A>T (31Ile>Phe) and 169G>A (57Val>Ile). Allele or genotype association with gastric cancer susceptibility was not observed in comparisons between the patient and control samples. However, 169G/G genotype was significantly more frequent in advanced gastric cancers than in early gastric cancers (age/sex-adjusted OR=2.2, 95% CI=1.3-3.8, P=0.0042). Moreover, the elevated risk of gastric cancer progression was associated with 91T-169G (age/sex-adjusted OR=1.9, 95% CI=1.1-3.4, P=0.025) and 91A-169G (age/sex-adjusted OR=1.6, 95% CI=1.0-2.6, P=0.048) haplotypes, having approximately 2.5-fold higher kinase activity than 91T-169A haplotype. The results suggest that 169G>A in AURKA is associated with progression of gastric cancer by affecting relative kinase activities of AURKA variants.

Alleles↗

Comparative analysis of chimpanzee and human Y chromosomes unveils complex evolutionary pathway.

The mammalian Y chromosome has unique characteristics compared with the autosomes or X chromosomes. Here we report the finished sequence of the chimpanzee Y chromosome (PTRY), including 271 kb of the Y-specific pseudoautosomal region 1 and 12.7 Mb of the male-specific region of the Y chromosome. Greater sequence divergence between the human Y chromosome (HSAY) and PTRY (1.78%) than between their respective whole genomes (1.23%) confirmed the accelerated evolutionary rate of the Y chromosome. Each of the 19 PTRY protein-coding genes analyzed had at least one nonsynonymous substitution, and 11 genes had higher nonsynonymous substitution rates than synonymous ones, suggesting relaxation of selective constraint, positive selection or both. We also identified lineage-specific changes, including deletion of a 200-kb fragment from the pericentromeric region of HSAY, expansion of young Alu families in HSAY and accumulation of young L1 elements and long terminal repeat retrotransposons in PTRY. Reconstruction of the common ancestral Y chromosome reflects the dynamic changes in our genomes in the 5-6 million years since speciation.

Animals↗

Gene expression profiling of human HBV- and/or HCV-associated hepatocellular carcinoma cells using expressed sequence tags.

Liver cancer is one of the leading causes of cancer death worldwide. To identify novel target genes that are related to liver carcinogenesis, we examined new genes that are differentially expressed in human hepatocellular carcinoma (HCC) cell lines and tissues based on the expressed sequence tag (EST) frequency. Eleven libraries were constructed from seven HCC cell lines and three normal liver tissue samples obtained from Korean patients. An analysis of gene expression profiles for HCC was performed using the frequency of ESTs obtained from these cDNA libraries. Genes were identified (n=120) as being either up- or down-regulated in human liver cancer cells. Among these, 14 genes (FTL, K-ALPHA1, LDHA, RPL4, ENO1, ANXA2, RPL9, RPL10, RPL13A, GNB2L1, AMBP, GC, A1BG, and SERPINC1), in addition to previously well-known liver cancer related genes, were confirmed to be differentially expressed in seven liver cancer cell lines and 17 HCC tissues by semi-quantitative RT-PCR. In addition, 73 genes, in which there was a significant difference (P>0.99) between HBV- and HCV-associated HCC cells, were selected. Of these, expression patterns of 14 (RPLP0, AKR1C, KRT8, GPX4, RPS15, ID1, RPS21, VIM, EEF1G, EIF4A1, HLA-C, FN1, CD44, and RPS10) were confirmed by semi-quantitative RT-PCR in four of HBV- and three of HCV-associated HCC cell lines. Among those genes, an immunohistochemical analysis for ANXA2 showed that it is expressed at high levels in HCC. Using an analysis of EST frequency, the newly identified genes, especially ANXA2, represent potential biomarkers for HCC and useful targets for elucidating the molecular mechanisms associated with HCC involving virological etiology.

Biomarkers, Tumor↗

Oncogenic effect of Polo-like kinase 1 expression in human gastric carcinomas.

Polo-like kinase 1 (Plk1) is one of the serine/threonine kinases involved in various mitotic processes, such as centrosome maturation and chromosome segregation. Although Plk1 is increased in several tumor types, the effect of Plk1 in gastric cancer is not clear because of the limited patient numbers in previous studies. This study was performed to investigate the prognostic significance and the expression profiles of Plk1 in gastric carcinoma tissues from 280 Korean patients. The expression of Plk1 was analyzed by reverse transcriptional PCR and a tissue array using immunohistochemical staining method in gastric adenocarcinoma tissues. The oncogenic potential of Plk1 was analyzed by using Plk1-specific small interference RNA in gastric cancer cells. The message of Plk1 was increased in various gastric cancer cell types and in primary cancer specimens in comparison with normal tissue. The expression rate of Plk1 was 95% (268/280) in gastric carcinoma patients. Although Plk1 expression had no specific correlation in male or female patients, among the differentiation types of cancer, its expression was generally increased in gastric cancers. Plk1 expression was significantly associated with accumulation of proliferation-related genes and oncogenes, and reversely correlated with tumor suppressor genes. When Plk1 expression was blocked, cancer cell growth was inhibited and apoptotic phenotypes were detected. Overexpression of Plk1 was important in abnormal proliferation and showed oncogenic potential in gastric cancer. Plk1 might have potential as a tumor prognostic marker for gastric cancer.

Adenocarcinoma↗

Transcriptome analysis of human gastric cancer.

To elucidate the genetic events associated with gastric cancer, 124,704 cDNA clones were collected from 37 human gastric cDNA libraries, including 20 full-length enriched cDNA libraries of gastric cancer cell lines and tissues from Korean patients. An analysis of the collected ESTs revealed that 97,930 high-quality ESTs coalesced into 13,001 clusters, of which 11,135 clusters (85.6%) were annotated to known ESTs. The analysis of the full-length cDNAs also revealed that 4862 clusters (51.7%) contained at least one putative full-length cDNA clone with an initiation codon, with the average length of the 5' UTR of 140 bp. A large number appear to have a diverse transcription start site (TSS). An examination of the TSS of some genes, such as TEGT and GAPD, using 5' RACE revealed that the predicted TSSs are actually found in human gastric cancer cells and that several TSSs differ depending on the specific gastric cell line. Furthermore, of the human gastric ESTs, 766 genes (9.5%) were present as putative alternatively spliced variants. Confirmation of the predicted spliced isoforms using RT-PCR showed that the predicted isoforms exist in gastric cancer cells and some isoforms coexist in gastric cell lines. These results provide potentially useful information for elucidating the molecular mechanisms associated with gastric oncogenesis.

5' Untranslated Regions↗

Effect of itopride, a new prokinetic, in patients with mild GERD: a pilot study.

AIM: Itopride is a newly developed prokinetic agent, which enhances gastric motility through both antidopaminergic and anti-acetylcholinesterasic actions. The importance of esophageal motor dysfunction in the pathogenesis of gastro-esophageal reflux disease (GERD) makes it interesting to examine the effect of itopride on esophageal acid exposure. METHODS: The effect of itopride on esophageal acid reflux variables for 24 h was studied in 26 patients with GERD symptoms, pre-entry total acid exposure time (pH<4) of more than 5% and mild esophagitis (Savary-Miller grades I, II) proven by endoscopy. Ambulatory 24-h pH-metry and symptom assessment were performed after treatments with 150 or 300 mg itopride thrice a day (t.i.d.) for 30 d in random order, using an open label method. For evaluating the safety of itopride, blood biochemical laboratory test was performed and the serum prolactin level was also examined before and after treatment. RESULTS: Total symptom score was significantly decreased after treatment in 150- or 300-mg group. Itopride 300 mg was significantly effective than 150 mg on decreasing the total per cent time with pH<4, total time with pH<4 and DeMeester score. No serious adverse effects were observed with administration of itopride in both groups. CONCLUSION: Itopride 100 mg t.i.d. is effective on decreasing pathologic reflux in patient with GERD and therefore it has the potential to be effective in the treatment of this disease.

Adult↗

Role of FLASH in caspase-8-mediated activation of NF-kappaB: dominant-negative function of FLASH mutant in NF-kappaB signaling pathway.

Caspase-8 is the most receptor-proximal, upstream caspase in the caspase cascade and plays a key role in cell death triggered by various death receptors. Here, we addressed the role of endogenous caspase-8 in tumor necrosis factor (TNF)-alpha-induced activation of NF-kappaB. Direct targeting of caspase-8 with siRNA and antisense (AS) approaches abolished TNF-alpha-induced activation of NF-kappaB in NIH3T3, HeLa, and HEK293 cells as determined with luciferase reporter gene and cell fractionation assays. Reconstitution of caspase-8-deficient C33A cells with processing-defective (P/D) mutant of caspase-8 sensitized the cells to TNF-alpha for NF-kappaB activation. In contrast to wild-type caspase-8, death effector domain mutant replacing Asp73 with Ala (caspase-8 (D73A)) failed to activate NF-kappaB and to bind FLICE-associated huge protein (FLASH) in vitro and in vivo. Instead, caspase-8 (D73A) mutant bound to caspase-8 and blocked NF-kappaB activation triggered by TNF-alpha and caspase-8. In addition, expression of an NF-kappaB-activating domain-deletion mutant of FLASH or transfection of FLASH AS oligonucleotides abolished TNF-alpha and caspase-8, but not phorbol 12-myristate 13-acetate, -induced activation of NF-kappaB. Further, immunoprecipitation assays showed that caspase-8 formed triple complex with TRAF2 and FLASH. Taken together, these results suggest that endogenous caspase-8 mediates TNF-alpha-induced activation of NF-kappaB via FLASH.

Animals↗

Identification of gastric cancer-related genes using a cDNA microarray containing novel expressed sequence tags expressed in gastric cancer cells.

PURPOSE: Gastric cancer is one of the most frequently diagnosed malignancies in the world, especially in Korea and Japan. To understand the molecular mechanism associated with gastric carcinogenesis, we attempted to identify novel gastric cancer-related genes using a novel 2K cDNA microarray. EXPERIMENTAL DESIGN: A 2K cDNA microarray was fabricated from 1,995 novel expressed sequence tags (ESTs) showing no hits or a low homology with ESTs in public databases from our 143,452 ESTs collected from gastric cancer cell lines and tissues. An analysis of the gene expression for human gastric cancer cell lines to a normal cell line was done using this cDNA microarray. Data for the different expressed genes were verified using semiquantitative reverse transcription-PCR, Western blotting, and immunohistochemical staining in the gastric cell lines and tissues. RESULTS: Forty genes were identified as either up-regulated or down-regulated genes in human gastric cancer cells. Among these, genes such as SKB1, NT5C3, ZNF9, p30, CDC20, and FEN1, were confirmed to be up-regulated genes in nine gastric cell lines and in 25 pairs of tissue samples from patients by semiquantitative reverse transcription-PCR. On the other hand, genes such as MT2A and CXX1 were identified as down-regulated genes. In particular, the SKB1, CDC20, and FEN1 genes were overexpressed in > or =68% of tissues and the MT2A gene was down-expressed in 72% of the tissues. Western blotting and immunohistochemical analyses for CDC20 and SKB1 showed overexpression and localization changes of the corresponding protein in human gastric cancer tissues. CONCLUSIONS: Novel genes that are related to human gastric cancer were identified using cDNA microarray developed in our laboratory. In particular, CDC20 and MT2A represent a potential biomarker of human gastric cancer. These newly identified genes should provide a valuable resource for understanding the molecular mechanism associated with tumorigenesis of gastric carcinogenesis and for the discovery of potential diagnostic markers of gastric cancer.

Biomarkers, Tumor↗

Gene expression analysis of cultured amniotic fluid cell with Down syndrome by DNA microarray.

Complete or partial triplication of human chromosome 21 results in Down syndrome (DS). To analyze differential gene expressions in amniotic fluid (AF) cells of DS, we used a DNA microarray system to analyze 102 genes, which included 24 genes on chromosome 21, 28 genes related to the function of brain and muscle, 36 genes related to apoptosis, 4 genes related to extracellular matrix, 8 genes related to other molecular function and 2 house-keeping genes. AF cells were collected from 12 pregnancies at 16-18 weeks of gestation in DS (n=6) and normal (n=6) subjects. Our DNA microarray experiments showed that the expressions of 11 genes were altered by at least 2-folds in DS, as follows. Ten genes, COL6A1, CASP5, AKT2, JUN, PYGM, BNIP1, OSF-2, PRSS7, COL3A1, and MBLL were down-regulated and GSTT1 was only up-regulated. The differential expressions of GSTT1 and COL3A1 were further confirmed by semi-quantitative RT-PCR for each sample. The gene dosage hypothesis on chromosome 21 may explain the neurological and other symptoms of DS. However, our results showed that only two genes (COL6A1 and PRSS7), among 24 genes on chromosome 21, were down-regulated in the AF cells of DS. Our data may provide the basis for a more systematic identification of biological markers of fetal DS, thus leading to an improved understanding of pathogenesis for fetal DS.

Amniocentesis↗

[A case of spontaneous biloma complicated with choledocholithiasis and chronic cholecystitis].

A biloma is an encapsulated bile collection outside the biliary tree. Most cases of biloma are caused by iatrogenic injury or trauma. Intrahepatic rupture of the biliary tree due to nontraumatic cause is a rare event. A 68- year-old man was admitted because of abdominal pain and fever. He had no past history of abdominal surgery, instrumentation or trauma. Computed tomography (CT) scan and magnetic resonance cholangiopancreatography (MRCP) demonstrated a large subcapsular fluid collection in the right liver associated with choledocholithiasis and cholecystitis. Biloma was confirmed by sono-guided percutaneous needle aspiration and was drained through a pigtail catheter. After the successful treatment by percutaneous drainage and endoscopic sphincterotomy, the patient recovered. Here, we report an uncommon case of spontaneous biloma formation in association with choledocholithiasis with a review of literatures.

Aged↗

Identification of novel genes associated with the response to 5-FU treatment in gastric cancer cell lines using a cDNA microarray.

The 5-Fluorouracil (5-FU) is an anticancer drug that is widely used in the treatment of cancer. To identify novel genes associated with 5-FU in gastric cancer, the time-dependent expression profiling of genes in response to 5-FU was examined in 5-FU sensitive and/or resistant gastric cancer cell lines using a 'KUGI 14 K cDNA chip' containing 14,081 unigenes obtained from human gastric cancer cell lines and tissues. By this analysis, we obtained 13 genes which are directly associated with sensitivity or resistance to 5-FU. Of these genes, 11 were found to be commonly up-regulated only in the 5-FU sensitive cell lines, and 2 were oppositely regulated in both of 5-FU sensitive and resistant cell lines. These genes were determined to be involved in cell surface, apoptosis, cell cycle and signal transduction. Of these genes, the expression levels of ZFP100, 4F2hc, FLJ11021, CSTF3, PPP1R14A, DDB2, C6orf139, CDKN1A, HOXC11 and FLJ38860 were confirmed by semi-quantitative RT-PCR. In addition, seven genes containing RRMI, UP1 and K-EST0037597 were found to be commonly up-regulated in both cell lines. In addition, the expression of genes such as TP, OPRT, TS and DPD, which have been previously known to be involved in 5-FU metabolism, were examined in both of 5-FU sensitive and resistant cell lines. These results provide not only predictive biomarkers for 5-FU sensitivity or resistance to human gastric cancer, but also a new molecular basis for understanding the mechanism of cellular cytoxicity to 5-FU.

Antimetabolites, Antineoplastic↗

Construction of multi-purpose vectors, pCNS and pCNS-D2, are suitable for collection and functional study of large-scale cDNAs.

To efficiently perform collection and functional studies of large-scale cDNAs, we constructed multi-functional cDNA vectors for efficient full-length cDNA cloning, direct sequencing, easy screening, and the expression of cDNA in vitro and in vivo without subcloning the cDNA into other vectors. The constructed vectors, pCNS and pCNS-D2, contain a multi-cloning site for uni-directional full-length cDNA cloning, T7 and Sp6 RNA polymerase promoters for in vitro transcription and translation, and hCMV immediate early promoter and BGH poly(A) to allow expression in mammalian cells. Using these vectors, we constructed full-length enriched cDNA libraries containing 60-75% of the full-length cDNAs using two different oligo-capping methods. The subtracted cDNA libraries could also be constructed by removing of EF1-alpha cDNA, a highly expressed cDNA. In addition, we confirmed the translation of EF1-alpha cDNA in vitro and the expression of luciferase cDNA in mammalian cells. The expression efficiency of luciferase cDNA in different cell lines, such as HeLa, Hep3B, SNU638, and SNU668, showed that pCNS vectors can highly express target genes in different cell types. These results indicated that our multi-purpose vectors, pCNS and pCNS-D2, are useful tools for the construction of full-length cDNA libraries and high-throughput based functional study of cDNAs.

Animals↗

Gene cataloging and expression profiling in human gastric cancer cells by expressed sequence tags.

To understand the molecular mechanism associated with gastric carcinogenesis, we identified genes expressed in gastric cancer cell lines and tissues. Of 97,609 high-quality ESTs sequenced from 36 cDNA libraries, 92,545 were coalesced into 10,418 human Unigene clusters (Build 151). The gene expression profile was produced by counting the cluster frequencies in each library. Although the profiles of highly expressed genes varied greatly from library to library, those genes related to cell structure formation, heat shock proteins, the glycolysis pathway, and the signaling pathway were highly represented in human gastric cancer cell lines and in primary tumors. Conversely, the genes encoding immunoglobulins, ribosomal proteins, and digestive proteins were down-regulated in gastric cancer cell lines and tissues compared to normal tissues. The transcription levels of some of these genes were confirmed by RT-PCR. We found that genes related to cell adhesion, apoptosis, and cytoskeleton formation were particularly up-regulated in the gastric cancer cell lines established from malignant ascites compared to those from primary tumors. This comprehensive molecular profiling of human gastric cancer should be useful for elucidating the genetic events associated with human gastric cancer.

Base Sequence↗

[Relevancy between liver injury, serum HBV-DNA, and intrahepatic HBcAg in young male chronic HBV carriers].

BACKGROUND/AIMS: Although the viral load is correlated with HBcAg, liver injury was not correlated to viral load in HBeAg positive patient. We aimed to study the inter-relationship of clinical parameters such as the level of HBV-DNA, the level of aminotransferase, intrahepatic expression of HBcAg and severity of histological liver damage in the young male chronic HBV carriers according to HBeAg status. METHODS: The study group included 85 young male patients (mean age: 19.8) with biopsy-proven chronic hepatitis B (HBeAg-positive group: n=60, HBeAg-negative group: n=25). RESULTS: Serum levels of HBV-DNA and the expression of intrahepatic HBcAg in the HBeAg-positive group were significantly higher than in the HBeAg-negative (p<0.001), but fibrosis score was lower (p<0.01). Serum levels of HBV-DNA positively correlated with lobular activity, portal/periportal activity, biochemical activities in the HBeAg-negative group but negatively correlated in the HBeAg-positive group. There were no significant differences in histological activity according to the pattern of expression of intrahepatic HBcAg in both groups. The lobular activity correlated positively with biochemical activity in both groups, and portal/periportal activity correlated with biochemical activity only in the HBeAg-positive group. CONCLUSIONS: There are close correlations among liver injury, intrahepatic expression of HBcAg, and detectable HBV-DNA in the young male chronic HBV carriers with HBeAg-negativity, but in the HBeAg-positive group, the correlations are diversified.

Adolescent↗