PURPOSE: The aims of this study were to investigate the frequencies and role of hepatitis B virus(HBV) precore and core promotor mutations in children with chronic hepatitis B infection. METHODS: Sera from 46 children with chronic hepatitis B infection were analyzed by direct sequencing of polymerase chain reaction product of HBV DNA. In this study, the patients were divided into vertical and non-vertical groups according to the mode of HBV transmission. Statistical analysis was performed by using Fisher's exact test. RESULTS: Forty-six adr type of HBV DNA were analyzed. The mutations in HBV precore region were observed in 12(26.1Yo) of 46 cases. The GA mutation of nucletide(nt) 1896 was observed in 5 cases(10.9Yo). The frequency of mutations in HBV precore region of the non-vertical group (6/16; 37.5Fo) was higher than that of the vertical group(6/30; 20M), but there was no statistical significance. The mutation in HBV core promotor region was observed in 40(87.0%) of 46 cases. The A-->T mutation of nt 1762 or G-->A mutation of nt 1764 were observed in 24(52.2%) of 46 cases, and 23 cases revealed combined mutation at both positions 1762 and 1764. The frequency of mutations in HBV core promotor region of the vertical group(28/30; 93.3Yo) was higher than that of the non-vertical group(12/16; 75.0M), but there was no statistical significance. The frequencies of mutations in HBV precore and core promotor regions of the HBeAg negative patients was higher than that of HBeAg positive patients, but there was no statistical significance. Also there were no significant correlations between the frequencies of mutations in HBV precore and core promotor regions and AST, ALT level or the level of HBV DNA. CONCLUSION: These observations suggest that mutations in HBV precore and core promotor regions were frequently detected in children with chronic hepatitis B infection. There were no statistical significant differences in the frequencies of mutations in HBV precore and core promotor regions between vertical and non-vertical transmission groups. (J Korean Pediatr Soc 2000; 43:779-791)
Child* ; DNA ; Hepatitis B e Antigens ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis B, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Polymerase Chain Reaction ; Promoter Regions, Genetic

PURPOSE: Hepatitis B virus(HBV) with various mutations has been reported. The aims of this study were to investigate the frequency and manifestation of HBV pre-S/S mutations in children with chronic hepatitis B infection. METHODS: Sera from 17 children with chronic hepatitis B infection were analyzed by direct sequencing of polymerase chain reaction amplification of HBV DNA. Results: Seventeen cases of adr type were analyzed. The deletions in HBV pre-S region were observed in 3(17.6%) of 17 cases. Of 3 deleted cases, 2 had an in-phase deletion in the pre-S1 region spanning 18 bp. Another case had a 18 bp and 3 bp deletions in the pre-S1 region. Many point mutations in HBV pre-S region were detected in all cases and these mutations were observed more frequently in the pre-S2 region than the pre-S1 region. Six point mutations in the pre-S1 region were observed. Eight point mutations in pre-S2 region were observed. Point mutations in the S region were detected in 14(82.4%) of 17 cases. Among these, mutations of the "a" determinant were detected in 4(23.5%) of 17 cases. Mutations at codon 130 and at codon 146 were noted in 2 cases. Combined mutations at codon 124, 126, 146 and at 130, 131, 136, 146 were noted in the other 2 cases. Mutations except "a" determinant region included at codon 3, 29, 73, 120, 184, 214, 226, 227. CONCLUSION: These observations suggest that deletion and point mutations in HBV pre-S1, pre- S2 regions and point mutations in HBV S region are frequent in the children with chronic hepatitis B infection.
Child* ; Codon ; DNA ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis B, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Point Mutation ; Polymerase Chain Reaction

OBJECTIVE: The aim of this study was to investigate the usefulness of serum ECP as a marker of the severity of asthma and extent of airway inflammation. METHOD: We investigated 108 patients suffering from bronchial asthma, who were classified as mild intermittent(n=19), mild persistent(n=27), moderate persistent(n=42), and severe persistent(n=20) and 10 healthy controls. Atopy was defined as those who showed >2+ responses on skin prick test. Serum ECP, peripheral blood eosinophil, sputum eosinophil, and PEFR were measured on the same date and meth~acholine PC20 were determined within 2 weeks. RESULTS: Serum ECP levels were 10.1+- 2.0 ug/L in controls, and 29.1+- 23.6 ug/L in asthmatic patients. According to symptom severity, serum ECP levels were 22.9 +- 15.6 ug/L, 28. 6 +- 24.1 ug/L, 29.5 +- 22.2 ug/L, and 34.6 +- 31.2 ug/L in mild intermittent, mild persistent, moderate persistent and severe persistent asthmatic patients, respectively and there were no significant differences among four groups(p>0.05). Serum ECP levels correlated with peripheral blood eosinophil counts(r=0.48, p<0.01), but not with sputum eosinophil, PEFR, and methacholine PC20 levels. There was no significant difference in serum ECP level between atopic and non-atopic asthma(p>0.05). CONCLUSION: Single measurevment of ECP level at clinic could not represent the severity of asthma.
Asthma* ; Eosinophil Cationic Protein* ; Eosinophils* ; Humans ; Inflammation ; Methacholine Chloride ; Peak Expiratory Flow Rate ; Skin ; Sputum

Heterogeneity in clinical features and pathogenesis of non-steroidal anti-inflammatory agent (NSAIDs) hypersensitivity have been reported. NSAIDs can cause bronchial constriction in asthmatics or hives and angioedema in patients with chronic urticaria, in which case causative drugs show cross-reactivity with other NSAIDs. Normal subjects without allergic diseases may develop urticaria angioedema or anaphylaxis after ingestion of a specific NSAID. In this type of reaction, cross-reactivity between causative drugs and other NSAIDs does not occur. We experienced a case of acetaminophen anaphylaxis without aspirin sensitivity in a 38-year-old male, which was confirmed by oral provocation test. An oral challenge with 150mg of acetaminophen induced urticaria in lower legs, and erythema, with febrile sensation in ears. With a dose of 600mg acetaminophen, urticaria developed in trunk and extremities with facial angioedema. An oral provocation test with 650mg of aspirin was well tolerated without any adverse reactions. We report acase of acetaminophen anaphylaxis, which occurred in a normal individual at a small dose(150mg) without cross-reactivity with aspirin. This type of reaction supports heterogenei~ty of NSAIDs hypersensitivity and it may be caused by an other mechanism, not by cyclooxygenase inhibition.
Acetaminophen* ; Adult ; Anaphylaxis* ; Angioedema ; Anti-Inflammatory Agents, Non-Steroidal ; Aspirin* ; Bronchoconstriction ; Ear ; Eating ; Erythema ; Extremities ; Humans ; Hypersensitivity ; Leg ; Male ; Population Characteristics ; Prostaglandin-Endoperoxide Synthases ; Sensation ; Urticaria

BACKGROUND/AIMS: In order to determine the relationship between the HBV precore mutant and the severity of liver disease in Korea, we performed liver biopsies in patients with HBV related chronic liver disease and compared the types of mutations and histologic findings in the same liver tissue simultaneously. METHODS: HBV DNA in liver tissues was amplified by polymerase chain reaction (PCR). The precore mutants were detected by PCR-SSCP(single strand conformation polymorphism), cloning the amplified PCR products and direct sequencing for them. RESULTS: 1. HBV DNA was detected in liver tissues of 28 cases among 30 patients with PCR. And with SSCP, the most cases were mixed type infections. 2. The HBV precore mutants were found in 12 cases among the total number of 28 cases(42.9%) and all mutations were G to A change at nucleotide 1896, creating a stop codon at codon 28. However, 10 cases among 12 mutants were associated with simultaneous another mutation at different positions or regions;9 cases at core gene region, 2 cases at nucleotide 1856(C to T change at codon 15), one case at core promoter, and one case with double mutations at nucleotide 1837 and 1846 respectively. Also, all HBV precore mutants were combined with wild type HBV sequence. 3. The relationship between HBV precore mutants and HBeAg status revealed that 4 cases from 13 HBeAg positive(30.8%) and 8 from 15 HBeAg negative or Anti-Hbe positive(53.3 %) were mutants. 4. In analysis of the types of mutants and histopathological findings of liver diseases, 6 among 15 chronic active hepatitis(40.0%), all 3 cases with hepatocellular carcinoma(100,0 %), 2 among 4 asymptomatic carriers with minimal histopathologic changes(50.0%) and a case with chronic lobular heaptitis(100.0%) showed precore region mutation. CONCLUSION: The patterns of HBV precore mutants in Korea could be summarized as followings. Firstly, most of the mutations are composed of G to A change at nucleotide 1896. Secondly, the most of the mutants at nuclmtide 1896 have been associated with simultaneous mutations at core promoter, core gene, and rarely at other positions, and manifested usua'ly mixed type viremic conditions. Thirdly, although precore mutation could be occurred in asymptomatic carrier, this type of mutation might be closely related with chronic or severe liver disease. However, it needs further investigations hereafter.
Biopsy ; Clone Cells ; Cloning, Organism ; Codon ; Codon, Terminator ; DNA ; Hepatitis B e Antigens ; Hepatitis B, Chronic* ; Hepatitis, Chronic* ; Humans ; Korea ; Liver Diseases ; Liver* ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational

PURPOSE: The aims of this study were to investigate the frequencies and role of hepatitis B virus(HBV) precore and core promotor mutations in children with chronic hepatitis B infection. METHODS: Sera from 31 children with chronic HBV infection were analyzed by direct sequencing of polymerase chain reaction amplification of HBV DNA. RESULTS: Twenty-nine adr type were analyzed. The mutations in HBV precore region were observed in 8(27.6%) of 29 cases. The G->A mutation of nucleotide 1896(A1896; stop codon) were observed in 4 cases(13.8%). The mutations in HBV core promotor region were observed in 27 (93.1%) of 29 cases. The G(1764)->A mutation(A1764) was observed in 14 cases(48.3%), and among these 12 cases combined with a A to T change at nucleotide 1762(T1762). The mutations in HBV precore region were obsereved in 4(21%) of 19 cases of HBeAg positive group and 9(90%) of 10 cases of HBeAg negative group. A1896 mutation was observed in 2 cases in both HBeAg positive and negative group, respectively. The mutations in HBV core promotor region were observed in 18(94.7%) of 19 cases of HBeAg positive group and 9(90%) of 10 cases of HBeAg negative group. T1762 mutation were observed in 6(31.6%) of 19 cases of HBeAg positive group and 6(60%) of 10 cases of HBeAg negative group(P=0.14). A1764 mutation was obsereved in 7 (36.8%) of 19 cases of HBeAg positive group and 7(70%) of 10 cases of HBeAg negative group (P=0.089). A1896 mutation was observed in 2(18.2%) of 11 cases in increased AST/ALT group and 2(11.1%) of 18 cases in normal AST/ALT group. A1764 and T1762 mutations were higher (61.1%) in AST/ALT increased group than those(27.3%) in AST/ALT normal group, but there was no statistical significance(P=0.077). CONCLUSION: Mutations in the precore and core promotor regions can be frequently detected in children with chronic HBV infection. T1762 and A1764 mutations were observed more frequently in HBeAg negative group and in AST/ALT increased group but there was no statistical significance.
Child* ; DNA ; Hepatitis B e Antigens ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis B, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Polymerase Chain Reaction ; Promoter Regions, Genetic

No abstract available.
Central Nervous System Infections* ; Central Nervous System*

No abstract available.
Female ; Fetal Heart* ; Heart Rate, Fetal* ; Meconium* ; Pregnancy

The purpose of this experiment was to determind whether the gold electrodeposit on Pd-Ag and Ni-Cr alloys influences on the shear bond strength between veneering resin and silicoated metal surface. All the metal specimens were sandblasted with 250microneter aluminum oxide and followed by silicoating and resin veneering. According to the metal surfaces to be veneered, experimental groups were divided into five. Group Prec : Gold alloy without gold coating Group Semi : Pd-Ag alloy without gold coating Group Base : Ni-Cr alloy without gold coating Group Semi-G : Pd-Ag alloy with gold coating Group Base-G : Ni-Cr alloy with gold coating All specimens were thermocycled 1,000 times at temperature of 5degrees C to 55degrees C. The effects of gold electrodeposit on the shear bond strength between resin and metal interface were measured and fractured surface of the resin veneered metal was examined under the scaning electron microscope. The following results were obtained 1. The shear bond strength between resin and metal was 64.51+/-11.11Kg/cm2in Prec group, 62.77+/-11.23Kg/cm2in Base group and 58.97+/-9.20 Kg/cm2in Semi Group. There was no significant difference among the groups. 2. The bond strength in groups Semi-G and Base-G decreased about 17%, compared to the non-gold-electrodeposit groups(Semi, Base). 3. In groups of non electrodeposit(Prec, Semi, Base), fracture occurred at the interface between alloy and resin, while fracture interface was observed between gold coating and resin in group Semi-G, and between metal substrate and gold coating in group Base-G resp[ectively.
Alloys* ; Aluminum Oxide

No abstract available.
Female ; Pregnancy ; Pregnancy, Ectopic*