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Biomedical subjects

S H Choi

Publications and source records attributed to S H Choi.

At least 163 records · Page 9Linked to original sources
PubMed1998

Life-threatening carboplatin hypersensitivity during conditioning for autologous PBSC transplantation: successful rechallenge after desensitization.

Carboplatin hypersensitivity has rarely been reported in patients receiving repeated cycles of therapy, but has not been reported in transplant settings. We report a case of carboplatin hypersensitivity during conditioning for autologous PBSC transplantation. The patient suddenly developed chest tightness, hemoptysis, hypoxia and hypotension, resulting in a transient myocardial ischemia. The pathophysiologic mechanism for the event seemed to be non-immune-mediated direct histamine release given the lack of prior exposure to platinum. Contrary to advice not to continue further treatment with carboplatin by some authors, we successfully desensitized the patient and subsequently gave more carboplatin as a part of conditioning. Awareness of carboplatin as one of the causes of hypersensitivity may help avoid further problems either by substitution or desensitization, along with premedications.

Antineoplastic Agents↗
PubMed1998

Distribution of Xanthomonas oryzae pv. oryzae DNA modification systems in Asia.

The presence or absence of two DNA modification systems, XorI and XorII, in 195 strains of Xanthomonas oryzae pv. oryzae collected from different major rice-growing countries of Asia was assessed. All four possible phenotypes (XorI+ XorII+, XorI+ XorII-, XorI- XorII+ and XorI- XorII-) were detected in the population at a ratio of approximately 1:2:2:2. The XorI+ XorII+ and XorI- XorII+ phenotypes were observed predominantly in strains from southeast Asia (Philippines, Malaysia, and Indonesia), whereas strains with the phenotypes XorI- XorII- and XorI+ XorII- were distributed in south Asia (India and Nepal) and northeast Asia (China, Korea, and Japan), respectively. Based on the prevalence and geographic distribution of the XorI and XorII systems, we suggest that the XorI modification system originated in northeast Asia and was later introduced to southeast Asia, while the XorII system originated in southeast Asia and moved to northeast Asia and south Asia. Genomic DNA from all tested strains of X. oryzae pv. oryzae that were resistant to digestion by endonuclease XorII or its isoschizomer PvuI also hybridized with a 7.0-kb clone that contained the XorII modification system, whereas strains that were digested by XorII or PvuI lacked DNA that hybridized with the clone. Size polymorphisms were observed in fragments that hybridized with the 7.0-kb clone. However, a single hybridization pattern generally was found in XorII+ strains within a country, indicating clonal maintenance of the XorII methyl-transferase gene locus. The locus was monomorphic for X. oryzae pv. oryzae strains from the Philippines and all strains from Indonesia and Korea.

DNA Restriction Enzymes↗
PubMed1998

Streptococcal histone-like protein: primary structure of hlpA and protein binding to lipoteichoic acid and epithelial cells.

In addition to its role in the nucleoid, the histone-like protein (HlpA) of Streptococcus pyogenes is believed to act as a fortuitous virulence factor in delayed sequelae by binding to heparan sulfate-proteoglycans in the extracellular matrix of target organs and acting as a nidus for in situ immune complex formation. To further characterize this protein, the hlpA genes were cloned from S. pyogenes, S. gordonii, S. mutans, and S. sobrinus, using PCR amplification, and sequenced. The encoded HlpA protein of S. pyogenes has 91 amino acids, a predicted molecular mass of 9,647 Da, an isoelectric point of 9.81, and 90% to 95% sequence identity with HlpA of several oral streptococci. The consensus sequence of streptococcal HlpA has 69% identity with the consensus sequence of the histone-like HB protein of Bacillus species. Oral viridans group streptococci, growing in chemically defined medium at pH 6.8, released HlpA into the milieu during stationary phase as a result of limited cell lysis. HlpA was not released by these bacteria when grown at pH 6.0 or below. S. pyogenes did not release HlpA during growth in vitro; however, analyses of sera from 155 pharyngitis patients revealed a strong correlation (P < 0.0017) between the production of antibodies to HlpA and antibodies to streptolysin O, indicating that the histone-like protein is released by group A streptococci growing in vivo. Extracellular HlpA formed soluble complexes with lipoteichoic acid in vitro and bound readily to heparan sulfate on HEp-2 cell surfaces. These results support a potential role for HlpA in the pathogenesis of streptococcus-induced tissue inflammation.

Amino Acid Sequence↗
PubMed1998

Direct identification of Vibrio vulnificus in clinical specimens by nested PCR.

This study was performed to establish optimal nested PCR conditions and a high-yield DNA extraction method for the direct identification of Vibrio vulnificus in clinical specimens. We designed two sets of primers targeting the V. vulnificus hemolysin/cytolysin gene. The target of the first primer set (P1-P2; sense, 5'-GAC-TAT-CGC-ATC-AAC-AAC-CG-3', and antisense, 5'-AGG-TAG-CGA-GTA-TTA-CTG-CC-3', respectively) is a 704-bp DNA fragment. The second set (P3-P4; sense, 5'-GCT-ATT-TCA-CCG-CCG-CTC-AC-3', and antisense, 5'-CCG-CAG-AGC-CGT-AAA-CCG-AA-3', respectively) amplifies an internal 222-bp DNA fragment. We developed a direct DNA extraction method that involved boiling the specimen pellet in a 1 mM EDTA-0.5% Triton X-100 solution. The new DNA extraction method was more sensitive and reproducible than other conventional methods. The DNA extraction method guaranteed sensitivity as well, even when V. vulnificus cells were mixed with other bacteria such as Escherichia coli or Staphylococcus aureus. The nested PCR method could detect as little as 1 fg of chromosomal DNA and single CFU of V. vulnificus. We applied the nested PCR protocol to a total of 39 serum specimens and bulla aspirates from septicemic patients. Seventeen (94.4%) of the 18 V. vulnificus culture-positive specimens were positive by the nested PCR. Eight (42.1%) of the 19 culture-negative samples gave positive nested PCR results.

Base Sequence↗
PubMed1998

A method of cranioplasty using coralline hydroxyapatite.

INTRODUCTION: Current cranioplasty materials include autologous or homologous bone grafts, wire mesh and methyl methacrylate, either alone or in combination. However, each material has its own unique disadvantages. Although hydroxyapatite has been used extensively in other specialties as a bone substitute, the coralline form has rarely been used to repair cranial bone defects. Coralline hydroxyapatite, similar to that found in bone, provides a matrix on which living tissue can form and grow. Because it is an ideal bioimplant, a method of cranioplasty using coralline hydroxyapatite was employed. METHODS: The hydroxyapatite granules are mixed with Avitene and autologous blood to form a paste which can be contoured as needed. RESULTS: Over the past few years, we have used hydroxyapatite either alone or in combination with tantalum mesh in 19 pediatric patients for a variety of conditions. The cosmetic results were good to excellent. Furthermore, postoperative CT scans have documented bony substitution of the hydroxyapatite granules. Follow-up ranged from 1 to 43 months with a mean of 26 months. CONCLUSION: In neurosurgical procedures when a bone substitute is needed, hydroxyapatite is an effective alternative to other currently available materials.

Bone Substitutes↗
PubMed1998

Periodontal repair in dogs: effect of allogenic freeze-dried demineralized bone matrix implants on alveolar bone and cementum regeneration.

The objective of this study was to evaluate alveolar bone and cementum regeneration following surgical placement of an allogenic, freeze-dried, demineralized bone matrix (DBM) cortical strip implant. Critical size, supraalveolar periodontal defects were surgically created around the second, third, and fourth mandibular premolar teeth in eight mongrel dogs. Contralateral jaw quadrants in six animals were randomly assigned to receive the DBM implant, or serve as surgical control. Two additional animals received bilateral DBM implants. Flaps were coronally advanced to submerge teeth and implants, and sutured. Three animals were exited from the study due to extensive early wound failure. Remaining animals were sacrificed at 8 weeks postsurgery. Histometric recordings included defect height, bone regeneration/DBM implant height, cementum regeneration height, root resorption, and ankylosis. Large areas of unresorbed DBM exhibiting fragmentation and empty osteocyte lacunae were observed adjacent to new bone formation, or bone formation was observed adjacent to or within the implant, often exhibiting ankylosis. Cementum regeneration appeared enhanced in shelter of the DBM implant. Histometric recordings (mean+/-SD) for DBM and control defects, respectively, were: defect height, 4.8+/-0.2 mm and 4.4+/-0.2 mm; bone regeneration/DBM implant height, 4.0+/-1.3 mm and 1.2+/-0.6 mm; cementum regeneration height, 1.4+/-0.4 mm and 0.7+/-0.2 mm; root resorption, 0.5+/-0.3 mm and 1.2+/-0.3 mm; and ankylosis, 0.5+/-0.2 mm and 0.1+/-0.1 mm without statistically significant differences between experimental conditions (N=3). Within the limitations of this study, the histologic observations suggest that surgical implantation of allogenic, freeze-dried DBM cortical strip implants may have a potential to support cementum regeneration, possibly by providing conditions for guided tissue regeneration, however, alveolar regeneration appears unpredictable.

Alveolar Bone Loss↗
PubMed1998

Periodontal repair in intrabony defects treated with a calcium sulfate implant and calcium sulfate barrier.

THIS RANDOMIZED, CONTROLLED, CLINICAL STUDY was designed to evaluate outcome following surgical implantation of an allogeneic, freeze-dried, demineralized bone matrix-calcium sulfate (DBM+CS) composite with a CS barrier in intrabony periodontal defects. Twenty-six patients contributing 26 deep intrabony defects completed the study. Thirteen patients received the DBM+CS implant. Thirteen patients received gingival flap surgery alone (GFS; control). Clinical outcome was assessed at 6 and 12 months postsurgery. At 12 months postsurgery, probing depth (PD) reduction (mean +/-SD) for the DBM+CS and GFS group was to 4.3+/-0.5 and 3.0+/-1.3 mm; clinical attachment gain was to 2.9+/-0.8 and 1.7+/-1.5 mm; and probing bone level gain was to 2.9+/-1.4 and 1.2+/-1.2 mm, respectively. There were no apparent differences between evaluations at 6 and 12 months postsurgery. Clinical improvements were significantly different from presurgery for both groups at both observation intervals (P < 0.01). There were no significant differences between groups in PD reduction and clinical attachment gain. Probing bone level gain was significantly greater in the DBM+CS group compared to controls (P < 0.05). In summary, surgical implantation of DBM+CS with a CS barrier resulted in reduced PD and improved attachment levels comparable to that achieved by gingival flap surgery alone. However, gain in probing bone levels in deep intrabony periodontal pockets assessed by clinical parameters was greater than that observed by gingival flap surgery alone. These changes were noted at both 6 and 12 months after surgery. This regenerative technique needs further biologic evaluation before being generally accepted.

Adult↗
PubMed1998

Effect of a calcium sulfate implant with calcium sulfate barrier on periodontal healing in 3-wall intrabony defects in dogs.

This controlled, split-mouth, preclinical study was designed to evaluate outcome following surgical implantation of an allogeneic, freeze-dried demineralized bone matrix-calcium sulfate (DBM+CS) composite with a CS barrier in 3-wall intrabony periodontal defects in 4 dogs. Control conditions included surgical implantation of DBM or CS and gingival flap surgery (GFS) alone. Three-wall intrabony defects (4x4x4 mm) were surgically created at the mesial and distal aspect of the maxillary and mandibular first and third premolars, respectively. Maxillary and mandibular defects each received 1 of the 4 experimental conditions. Experimental conditions were rotated between defect sites in subsequent animals. Block sections of the defects were collected at sacrifice 8 weeks postsurgery and processed for histometric analysis. Histometric defect height (means +/- SD) for the DBM+CS, DBM, CS, and GFS groups amounted to 4.2 +/- 0.5, 4.3 +/- 0.7, 4.0 +/- 0.2, and 4.1 +/- 0.2 mm, respectively. Connective tissue adhesion (connective tissue contact to the root without apparent cementum formation) amounted to 0.4 +/- 0.3, 0.4 +/- 0.3, 0.5 +/- 0.2, and 1.6 +/- 0.5 mm for the DBM+CS, DBM, CS, and GFS groups, respectively; the DBM+CS, DBM, and CS groups being significantly different from the GFS group (P < 0.05). Cementum regeneration amounted to 3.0 +/- 0.3, 3.1 +/- 0.4, 2.5 +/- 0.4, and 1.6 +/- 0.3 mm for the DBM+CS, DBM, CS, and GFS groups, respectively; the DBM+CS, DBM, and CS groups being significantly different from the GFS group (P < 0.05). Alveolar bone regeneration amounted to 2.7 +/- 0.4, 2.7 +/- 0.3, 1.8 +/- 0.5, and 0.7 +/- 0.1 mm for the DBM+CS, DBM, CS, and GFS groups, respectively; the DBM+CS, DBM, and CS groups being different from the GFS group (P < 0.05), and the DBM+CS and DBM groups being different from the CS group (P < 0.05). None of the DBM-containing implants provided evidence of bone metabolic activity. In summary, surgical implantation of DBM and CS, alone or in combination, may result in significantly improved regeneration of alveolar bone and cementum in this preclinical model. Observed regeneration is likely unrelated to a biologic activity inherent in DBM. Rather it appears that space-providing properties of the implants supported observed regeneration.

Alveolar Bone Loss↗
PubMed1998

Prevalence and risk factors of urinary stones in Koreans.

To estimate the prevalence of urinary stone disease in Koreans, and to determine the inter-relationships between urinary stone disease and various epidemiological factors, 1,521 controls and 1,177 cases with urinary stones were evaluated. Of special interest in this study were: 1) proportion of past urinary stone history among controls; 1.9% 2) the point prevalence rate of urinary stones among controls; 0.2% 3) the recurrence rate of urinary stones (the proportion of past history of urinary stone) among cases; 56.8% 4) high incidences (76.3%) in the thirties to the fifties among cases 5) the risk factors for urolithogenesis; obesity [higher than 25 of BMI (body mass index, weight/height2)], more than 10 year-experience as a production worker, past stone history, familial stone history, low physical activity (< 2,000 Kcal/day), and low intake of fruit. However, the well-known risk factors for urinary stones; over intake of meat or fish and milk or dairy products, perspiration, amount and kind of drinking water, and stress unexpectedly were not significantly different between the controls and the cases.

Adolescent↗
PubMed1998

Hepatitis G virus infection in hemodialysis and continuous ambulatory peritoneal dialysis patients.

To determine the prevalence and clinical relevance of HGV infection in dialysis patients, we performed a cross-sectional study of 61 HD patients and 79 Continuous Ambulatory Peritoneal Dialysis (CAPD) patients. HGV-RNA was identified by reverse-transcription (RT) polymerase chain reaction (PCR) assay with primers from the 5'-untranslated region of the viral genome. The prevalence of HGV infection was similar in HD and CAPD patients (9.8% vs. 12.7%), while that of HCV infection was significantly higher in HD patients compared to CAPD patients (16.4% vs. 1.3%, p < 0.05). The mean age (49.2 +/- 13.4 vs. 46.7 +/- 13.0 years), male to female ratio (2.4:1 vs. 1.3:1), history of transfusion (62.3% vs. 49.4%), history of hepatitis (27.9% vs. 26.6%), mean ALT level during the previous 6 months (22.4 +/- 37.9 vs. 14.0 +/- 7.4 IU/L), and the prevalence of HBsAg (8.2% vs. 6.3%) showed no difference between HD and CAPD patients. In both HD and CAPD patients, the presence of HGV RNA was not related to age, sex, duration of dialysis, history of transfusion, history of hepatitis, or to the presence of HBV or HCV markers. There was no significant difference in the clinical and biochemical data between patients with isolated HGV infection (n = 12) and patients without viremia (n = 106). The clinical feature of patients coinfected with HGV and HBV (n = 2), or HGV and HCV (n = 2) seemed to be similar to those of patients with isolated HBV (n = 8) or HCV (n = 9) infection. In conclusion, the prevalence of HGV infection was not different between HD and CAPD patients, and HGV infections did not seem to be associated with clinically significant hepatitis. The routes of HGV transmission, other than transfusion or contamination during HD procedure, were suspected.

Female↗
PubMed1997

Expression and mutational analysis of the DCC, DPC4, and MADR2/JV18-1 genes in neuroblastoma.

Loss of heterozygosity (LOH) on chromosome 18q21 is found frequently in various human cancers. Three candidate tumor suppressor genes, DCC (deleted in colorectal carcinomas), DPC4 (deleted in pancreatic carcinomas, locus 4), and MADR2/JV18-1 (MAD-related gene 2), have been cloned and identified from this chromosome region. We have reported recently that LOH on chromosome 18q is observed frequently in neuroblastoma. Alterations of DCC are involved in many human tumors. DPC4 and MADR2/JV18-1 are recently demonstrated to be altered in pancreatic and colorectal cancers, respectively. To confirm if inactivation of the DCC, DPC4, and MADR2/JV18-1 genes is involved in the pathogenesis of neuroblastoma and to clarify the mechanism of inactivation, we analyzed the expression of DCC, DPC4, and MADR2/JV18-1 in neuroblastoma cell lines and primary tumors by reverse transcription-PCR and investigated the mutations in the coding regions of these genes by PCR/reverse transcription-PCR single-strand conformation polymorphism. We found that 12 of 25 (48%) cell lines and 14 of 32 (44%) primary tumors, including 3 with 18q LOH, had absent or reduced expression of DCC mRNA. Expression was more likely to be reduced in advanced (67%) than in early stage neuroblastomas (24%) (P = 0.036), suggesting that inactivation of the DCC gene plays an important role in the progression of neuroblastoma. Altered expression of DPC4 was found in six (24%) cell lines and six (19%) tumors. MADR2/JV18-1 expression was reduced or absent only in four (16%) cell lines and three (9%) tumors. Mutations of the DCC genes were examined in 25 of 29 exons in neuroblastoma cell lines, and those exons in which mutations were found were further examined in primary tumors. We found missense mutations of AAC (Asn) to AGC (Ser) at DCC codon 176 in one cell line and ACC (Thr) to ATC (Ile) at codon 1105 in one cell line and tumor, respectively; polymorphisms of CGA (Arg) to GGA (Gly) at codon 201 and TTT (Phe) to TTG (Leu) at codon 951 in most of the cell lines and tumors; and a silent mutation of GAG (Glu) to GAA (Glu) at codon 118 in four cell lines and five primary tumors. We did not identify any mutations in the DPC4 and MADR2/JV18-1 genes in neuroblastoma. Our results suggested that mutations of the DCC gene may be involved in the pathogenesis of neuroblastomas but failed to account for the relatively high frequency of the altered expression, implying that other mechanisms are responsible for the inactivation of the DCC gene in neuroblastoma. Low frequency of reduced or absent mRNA expression and lack of mutations in DPC4 and MADR2/JV18-1 genes suggested a limited role for these two genes in neuroblastoma.

Cell Adhesion Molecules↗
PubMed1997

Actual half-life of alpha-fetoprotein as a prognostic tool in pediatric malignant tumors.

In a retrospective study, the prognostic value of monitoring the decay of alpha-fetoprotein (AFP) was assessed. Serum AFP was determined serially in 18 children with malignant germ-cell or hepatic tumors: 7 endodermal sinus tumor, 3 embryonal carcinoma, 5 malignant teratoma, 2 hepatoblastomas, and 1 hepatocellular carcinoma. The actual half-life (AHL) of AFP was computed after surgical resection of the tumor. In group 1, which had complete resection and no recurrence during follow-up (n = 13), the AHL of AFP was 4.0 +/- 0.9 days. In group 2, which had incomplete resection or recurrence during follow-up (n = 5), the AHL of AFP was 24.8 +/- 20 days, significantly longer than that of group 1 (P = 0.0026). The increased AHL of AFP indicated residual active tumor after surgical resection. The AHL of AFP may be more sensitive than serial monitoring of AFP in detecting preclinical recurrence after surgical resection of AFP-secreting tumors. Treatment strategies can be based on AFP clearance, and prospective clinical trials are warranted.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Alterations of the tumour suppressor gene DCC in neuroblastoma.

The deleted in colorectal carcinoma (DCC) gene, a candidate tumour suppressor, might be inactivated in a number of human cancers. In order to evaluate the possible role of DCC alterations in the pathogenesis of neuroblastoma, we examined 25 neuroblastoma cell lines and 16 primary tumours, including 6 samples with loss of heterozygosity (LOH) at the DCC locus for DCC mRNA expression, by using the reverse transcriptase-polymerase chain reaction (RT-PCR) technique. The level of DCC expression was significantly reduced or undetectable in 12 of 25 (48%) cell lines and 7 of 16 (44%) primary tumours, suggesting that inactivation of the DCC gene is involved in the development of neuroblastoma. Three of the 6 tumours with LOH at the DCC locus revealed reduced DCC mRNA expression, indicating that LOH at the DCC locus might have affected the levels of DCC mRNA. We also screened for mutations in 4 exons of the DCC gene in 12 cell lines by using PCR-single strand conformation polymorphism (PCR-SSCP) analysis. Point mutations were not found except a polymorphic change at codon 201. The mechanism for inactivation of the DCC gene will be further investigated.

Genes, DCC↗
PubMed1997

Thermal-death times of opaque and translucent morphotypes of Vibrio vulnificus.

Thermal-death times were determined for Vibrio vulnificus strains with different morphotypes. Opaque strains showed higher D values (times required to reduce the viable population of a given strain by 90%) than translucent strains. Z values (absolute values of the temperature required to reduce 1 log scale of D values) were also significantly higher in opaque morphotypes (2.4 to 2.5 degrees C) than in translucent ones (1.7 to 2.1 degrees C). These results indicate that the morphotype is related to the organism's susceptibility to heat.

Bacteriological Techniques↗
PubMed1997

Tumor necrosis factor beta is a major source of antibody-activated effector cells in the killing of virally infected target cells.

We have extended our previous work on cross-linking CD4 molecules using specific monoclonal-antibody-induced antigen-nonspecific major-histocompatibility-complex unrestricted killing by CD4+ T cells of virally infected target cells. The killing activity of antibody-activated CD4+ T cells was completely blocked by herbimycin A, a protein tyrosine kinase (PTK) inhibitor, but not by bisindolylmaleimide, a protein kinase C inhibitor. Herbimycin-A-treated human or bovine peripheral blood CD4+ T cells lacked PTK activity and failed to kill virally infected target cells even after cross-killing of CD4 molecules. The cross-linking of CD4 molecules failed to induce effector cell proliferation or the transcription of TNF-beta. The upregulation of TNF-beta was induced by incubating antibody-activated effector cells with bovine herpesvirus type 1 (BHV-1)-infected D17 target cells for 10 h. Anti-TNF-beta antibody partially abolished (13-44%) direct effector-cell-mediated antiviral cytotoxicity. However, this antibody neutralized 70-100% of antiviral activity of effector and target cell culture supernatants against BHV-1-infected D17 cells. The inhibition level of the antiviral activity by the antibody was dependent on the effector:target cell ratio. These results support the hypothesis that increased p56lck enzyme activity in effector cells transduces a signal critical for effector cell recognition of viral glycoproteins expressed on the target cells. Following target cell recognition, lytic cytokines were produced that are known to participate in target cell killing. A better understanding of the killing activity displayed by CD4+ T lymphocytes following surface receptor cross-linking activity displayed by CD4+ T lymphocytes following surface receptor cross-linking will give insight into the mechanisms of cytotoxic activity directed toward virally infected cells.

Animals↗
PubMed1997

Gadolinium chloride inhibition of rat hepatic microsomal epoxide hydrolase and glutathione S-transferase gene expression.

The effects of gadolinium chloride, a Kupffer cell toxicant, on the constitutive and inducible expression of hepatic microsomal epoxide hydrolase (mEH) and glutathione S-transferase (GST) genes were examined in rats. Northern blot analysis showed that treatment of rats with GdCl3 caused suppression of mEH and GST gene expression. mEH mRNA levels were decreased in a time-dependent manner after a single injected dose of GdCl3 (10 mg/kg, iv), resulting in 95, 55, 17, 36, and 69% of the levels in untreated animals at 6, 12, 18, 24, and 48 hr after treatment, respectively. A maximal reduction in GST Ya, Yb1/2, and Yc1 mRNA levels was also noted at 18 hr after treatment with GdCl3, followed by a gradual return to levels in untreated rats at later time points. Whereas treatment of rats with thiazole, allyl disulfide, propyl sulfide, oltipraz, or clotrimazole caused 2-13-fold increases in mEH mRNA levels at 18 hr after treatment, concomitant GdCl3 treatment caused 30-70% reductions in the increases in mEH mRNA levels. The chemical-inducible mRNA levels for GST Ya, Yb1/2, and Yc1 were also significantly inhibited by GdCl3 at 18 hr after treatment. Rats treated with GdCl3 (10 mg/kg/day, iv) for 3-5 consecutive days exhibited 40-90% decreases in mEH, GST Ya, and GST Yb1/2 mRNA levels, relative to control, whereas the Yc1 mRNA level was suppressed at early times and returned to levels in untreated animals at day 5 after treatment. The mRNA levels for mEH and GST Ya in rats treated daily with both allyl disulfide (25 mg/kg, po) and GdCl3 for 3 consecutive days were 20-30% of those in rats treated with allyl disulfide alone. Western immunoblotting showed that mEH and GST Ya protein expression was decreased at 1-3 days after consecutive daily treatment with GdCl3. Whereas treatment of rats with GdCl3 at a dose of 1 mg/kg suppressed constitutive hepatic mEH gene expression by 85% at 18 hr, rats treated with CaCl2 (10 mg/kg, iv) in combination with GdCl3 (1 mg/kg, iv) showed 45% suppression of the mEH mRNA level, compared with untreated animals. GdCl3-induced suppression was also significantly reversed for GST Ya mRNA by excessive CaCl2 administration. These results demonstrate that GdCl3 effectively inhibits constitutive and inducible mEH and GST expression, with decreases in their mRNA levels. GdCl3 suppression of detoxifying enzyme expression may be associated with its blocking of intracellular Ca2+ influx, which affects signaling pathways for the expression of the genes.

Animals↗
PubMed1996

Cloning and characterization of a cDNA for rat CD30 homolog and chromosomal assignment of the genomic gene.

CD30 is a member of the tumor necrosis factor receptor superfamily, which is expressed on some activated lymphocytes, virus-infected cells and transformed lymphocytes. To facilitate our understanding of biological functions and functional domains, we isolated rat cDNA clones encoding the rat homolog of human CD30 from a cDNA library of a rat T-cell line, TARL-2. The nucleotide sequence of the cDNA showed 73% homology with that of human CD30. The deduced rat CD30 protein consisted of 493 amino acids with an M(r) of 59 160 and contained a single transmembrane domain. It lacked the second repeat of the cysteine-rich motif in the extracellular domain found in human CD30. The amino acid sequence showed 51.8 and 61.2% identity with the cysteine-rich and the cytoplasmic domains, respectively. In the cytoplasmic domain, however, the amino acid sequence was highly conserved in about 100 residues near the C-terminus showing 77.7% identity, whereas the rest of the cytoplasmic domain showed 45.2% identity. This conservation suggests the functional importance of this region. Comparison with the recently reported mouse CD30 revealed 83.7% conservation of the amino acid sequence and a common structure of the extracellular domain which lacks the second cysteine-rich motif. Northern blots revealed a 3.4-kb mRNA in the PHA-activated spleen cells and human T-cell leukemia virus type 1 (HTLV-1)-infected rat T-cell lines, whereas smaller transcripts of 2.3 kb were found in the lung. A rabbit polyclonal antibody raised against GST-fusion protein of the cytoplasmic domain detected bands with an apparent M(r) of 80 kDa and 100- 110 kDa expressed in TARL-2 and spleen cells. Transient overexpression of rat CD30 in TARL-2 cells activated HIV LTR in a NF-kappa B site-dependent manner, indicating that CD30 signals activate NF-kappa B. The chromosomal location of the gene was identified by fluorescence in situ hybridisation at 5q36.2, and appeared to correspond to human 1p36, where human CD30 has been mapped. The identification and characterization of the rat counterpart of human CD30 will facilitate studies of the biological function of this molecule.

Amino Acid Sequence↗