PubMed Health⌕ Search

Biomedical subjects

B Gu

Publications and source records attributed to B Gu.

At least 37 records · Page 2Linked to original sources
PubMed1999

Gene therapy for human hepatocellular carcinoma with cytosine deaminase gene and prodrug flucytosine.

AIM: To investigate the antitumor effects of cytosine deaminase (CD) gene in combination with prodrug flucytosine (Flu, 5-fluorocytosine) on human hepatocellular carcinoma. METHODS: CD gene was transduced into human hepatocellular carcinoma cell line SMMC7721 with retroviral method and the cytotoxicity of Flu on the tumor cells was assayed in vitro with clonogenic techniques. The xenograft tumor model in nude mice was used to study in vivo therapeutic effects of CD gene/Flu system against human hepatocellular carcinoma. RESULTS: CD gene/Flu system had significant antitumor activities on human hepatocellular carcinoma cells in vitro and in nude mice. The antitumor activities of Flu 500 mg.kg-1 on hepatocellular carcinoma xenografts in nude mice were more potent than those of 5-fluouracil 10 mg.kg-1. CD gene/Flu system possessed bystander killing effects on hepatocellular carcinoma xenografts in nude mice. CONCLUSION: The experiment demonstrates the potential value of the CD gene/Flu system in the treatment of human hepatocellular carcinoma.

Animals↗
PubMed1999

[Expression of recombinant inserting mutants of HBsAg in vitro and its antigenic analysis].

OBJECTIVE: To study the immunological characteristics of two inserting variants of HBsAg as further to elucidate the role of inserting mutants in the development of HBsAg-negative chronic hepatitis B. METHODS: The inserting mutants of HBsAg were constructed by PCR-mediated mutagenesis in vitro. Epstein-Barr virus vector pCEP4 and retrovirus vector PXT1 carrying the mutant genes of HBsAg were transfected into mammalian cells. The affinity of polyclonal and monoclonal antibodies against HBsAg for mutant antigens were studied by ELISA and western blot. RESULTS: Two insertions were introduced into s gene, and a six nucleotide insertion introduced two aminoacids (Arg and Ala) between codons 122 and 123 of the s polypeptide, whereas a nine nucleotide insertion introduced three aminoacids(Arg, Gly and Ala) between codons 123 and 124. These s genes were subcloned into two eukaryotic expression vectors (pCEP4 and PXT1), and the recombinant eukaryotic expression plasmids had been constructed, which could express s polypeptide in mammalian cells. Cell lines expressing wild-type or mutant-type HBsAg stably were obtained after transfection of these vectors into mammalian cells. Two two inserting variants failed to react with polyclonal and monoclonal antibodies against HBsAg by ELISA and Western blot. CONCLUSION: The insertions may result in a conformational change of the s protein, and affect its antigenicities, suggesting that the inserting mutations may be critical for immunoescape of HBV and in part responsible for chronicity of HBsAg-negative patients.

Epitopes↗
PubMed1999

[Study on spectral emission characteristics of infrared lamps].

The spectral characteristics at wavelength ranges of 0.35-0.85 microm and 1.72-16.7 microm (5800-600 cm(-1)) for both domestic and imported infrared lamps used in scientific research, industry, medical service, home electrical appliance etc. have heen studied and compared. This paper has provided the theoreical and experimental bases for their applications and improvement in designs, technology of manufacture, quality and performance.

English Abstract↗
PubMed1998

Adenosine triphosphate-induced shedding of CD23 and L-selectin (CD62L) from lymphocytes is mediated by the same receptor but different metalloproteases.

CD23 is a transmembrane protein expressed on the surface of B-lymphocytes that binds IgE, CD21, CD11b, and CD11c. High concentrations of soluble CD23 and L-selectin are found in the serum of patients with B-chronic lymphocytic leukemia (B-CLL). Because extracellular adenosine triphosphate (ATP) causes shedding of L-selectin via activation of P2Z/P2X7 receptors expressed on B-CLL lymphocytes, we studied the effect of ATP on shedding of CD23. ATP-induced shedding of CD23 at an initial rate of 12% of that for L-selectin, whereas the EC50 for ATP was identical (35 micromol/L) for shedding of both molecules. Furthermore, benzoylbenzoyl ATP also produced shedding of CD23 and L-selectin with the same agonist EC50 values for both (10 micromol/L). Inactivation of the P2Z/P2X7 receptor by preincubation with oxidized ATP abolished ATP-induced shedding of both molecules. Moreover, KN-62, the most potent inhibitor for the P2Z/P2X7 receptor, inhibited ATP-induced shedding of both CD23 and L-selectin with the same IC50 (12 nmol/L). Ro 31-9790, a membrane permeant zinc chelator that inhibits the phorbol-ester-stimulated shedding of L-selectin, also inhibited shedding of CD23 from B-CLL lymphocytes. However, the IC50 for this inhibition by Ro31-9790 was different for L-selectin and CD23 (83 v 6 micromol/L, respectively). Although L-selectin was completely shed by incubation of cells with phorbol-ester, CD23 was not lost under these conditions. The data show that extracellular ATP induces shedding of L-selectin and CD23 from B-CLL lymphocytes by an action mediated by the P2Z/P2X7 receptor. However, different membrane metalloproteases seem to mediate the shedding of L-selectin and CD23.

Adenosine Triphosphate↗
PubMed1998

[Detection of CBF beta-MYH11 fusion transcript and inv(16)(p13;q22) in acute myelomonocytic leukemia(M4) by RT-PCR and FISH].

OBJECTIVE: To study the clinical significance of inv(16) and CBF beta-MYH11 fusion gene in the diagnosis and prognosis for M4Eo. METHODS: CBF beta-MYH11 fusion transcripts and inv (16) were analyzed by reverse-transcriptase polymerase chain reaction(RT-PCR) and fluorescence in situ hybridization(FISH), respectively, in acute myelomonocytic leukemia(M4) with or without eosinophilia. RESULTS: In fifteen cases tested, one case of M4Eo and one of 9 M4 without eosinophilia were found to have CBF beta-MYH11 fusion transcript. Follow-up of the M4Eo patient showed residual PCR positivity 2 months after complete remission. CONCLUSION: The data suggest that screening by both RT-PCR and FISH should be performed in all AML-M4 regardless of morphologic features to allow accurate diagnosis and prognosis of M4 patients.

Adolescent↗
PubMed1998

[Surgical treatment of epispadias].

OBJECTIVE: To analyse the surgical treatment of 124 cases of epispadias (incomplete 27 cases, complete 21 and complex 76). METHOD: Leadbetter's operation was used for anti-incontinence. Urethral tightening was used in 4 cases of complete female epispadias. Penile straightening was adopted for incomplete epispadias and penile lengthening for complete and complex male epispadias. RESULT: In 97 cases of urinary incontinence, complete continence was achieved in 73. CONCLUSION: The orthopedic effects of external genitals were satisfactory.

Adolescent↗
PubMed1998

[Studies on complex chromosomal translocation and their relevance to clinical prognosis in acute promyelocytic leukemia].

OBJECTIVE: To study the relationship between the complex chromosome translocation in acute promyelocytic leukemia(APL, M3) and clinical therapy and prognosis. METHODS: Chromosome translocation and PML-RAR fusion transcript in three APL patients were studied by using karyotypic analysis, fluorescence in situ hybridization and reverse transcriptase/polymerase chain reaction. RESULTS: The findings revealed that all these cases had PML/RAR A gene rearrangement. Apart from the chromosomes 15 and 17 involved in the translocation, other multiple chromosomes including 5, 11, 16, 22 were also implicated in complex translocations, which to some extent seemed to be related with clinical prognosis. CONCLUSION: This study provides additional information for monitoring clinical therapy and prognostic evaluation.

Adult↗
PubMed1996

[Anti-reflux ureterocysto-reimplantation in treatment of ectopic ureters: report of 51 cases].

From 1974 to 1994, anti-reflux ureterocysto-reimplantation was performed on 51 children (1 boy, 50 Girls) aged from 10 months to 13 years. The follow-up duration of 45 cases was 3 months to 14 years. The clinical symptoms of frequency of urination, lumbago and repeatedly fever, etc, were not observed except urinary incontinence in 2 cases. The results showed that ureterocysto-reimplantation is simple and traumatic. Some important aspects such as preoperative location and intraoperative identification of the unilateral or bilateral ectopic ureters were analyzed.

Adolescent↗
PubMed1995

Relationship between TATA-binding protein and herpes simplex virus type 1 ICP4 DNA-binding sites in complex formation and repression of transcription.

The herpes simplex virus (HSV) regulatory protein, infected-cell polypeptide 4 (ICP4), represses the transcription of promoters that have binding sites for ICP4 located near the transcription start site. It also been shown that ICP4 binds such promoter DNA cooperatively with the TATA-binding protein (TBP) and TFIIB to form a tripartite protein-DNA complex (C. Smith, P. Bates, R. Rivera-Gonzales, B. Gu, and N. A. DeLuca, J. Virol. 67:4676-4687, 1993). In this study, we analyzed the effects of position and orientation of the ICP4-binding site relative to the TATA box in the ICP4 promoter on transcriptional repression by ICP4 and on the ability of ICP4 to form tripartite complexes with TBP and TFIIB. The results of theis parallel study provide a strong correlation between tripartite complex formation and repression. Both tripartite-complex formation and transcriptional repression were efficient when the ICP4-binding site was downstream of the TATA box, within a short distance and in proper orientation. In addition, both tripartite-complex formation and repression were partially sensitive to the stereoaxial positioning of the ICP4-binding site relative to the TATA box. As a preliminary characterization of the tripartite complex, circular permutation analysis was performed to assess the distortion of the proximal promoter region in the tripartite complex. As previously reported, both TBP and ICP4 independently could bend DNA and the relative magnitude by which each of these proteins bent DNA in the tripartite complex was preserved. The results of this study suggest that the formation of tripartite complexes on a promoter is part of the mechanism of repression and that simple blocking as a sole result of ICP4 binding is not sufficient for full repression.

Base Sequence↗
PubMed1995

Repression of activator-mediated transcription by herpes simplex virus ICP4 via a mechanism involving interactions with the basal transcription factors TATA-binding protein and TFIIB.

Infected-cell polypeptide 4 (ICP4) of herpes simplex virus is both a transcriptional activator and a repressor. It has been previously demonstrated that both SP1-activated transcription and USF-activated transcription are repressed by ICP4 without affecting basal transcription (B. Gu, R. Rivera-Gonzalez, C. A. Smith, and N. A. DeLuca, Proc. Natl. Acad. Sci. USA 90:9528-9532, 1993; R. Rivera-Gonzalez, A. N. Imbalzano, B. Gu, and N.A. DeLuca, Virology 202:550-564, 1994). In this study, it was found that ICP4 repressed the activation function of two other activators, VP16 and ICP4 itself, in vitro. ICP4 inhibited transcription by interfering with the formation of transcription initiation complexes without affecting transcription elongation. Repression of activator function required that an ICP4 DNA binding site was present in one orientation within approximately 45 bp 3' to the TATA box. DNA binding by ICP4 was necessary but not sufficient for repression. ICP4 has been shown to form tripartite complexes cooperatively with the TATA box-binding protein and TFIIB on DNA containing an ICP4 binding site and a TATA box (C. A. Smith, P. Bates, R. Rivera-Gonzalez, B. Gu, and N. DeLuca, J. Virol. 67:4676-4687, 1993). A region of ICP4 that enables the molecule to form tripartite complexes was also required in addition to the DNA binding domain for efficient repression. Moreover, repression was observed only when the ICP4 binding site was in a position that resulted in the formation of tripartite complexes. Together, the data suggest that ICP4 represses transcription by binding to DNA in a precise way so that it may interact with the basal transcription complex and inhibit some general step involved in the function of activators. The steps or interactions involved in transcriptional activation that are inhibited by ICP4 are discussed.

Base Sequence↗
PubMed1995

Induction of transcription by a viral regulatory protein depends on the relative strengths of functional TATA boxes.

The mechanisms by which viral regulatory proteins activate the cellular transcription apparatus without binding to specific DNA elements are not fully understood. Several lines of evidence suggest that activation by one such regulatory protein, herpes simplex virus ICP4, could be mediated, at least in part, by TFIID. To test this model, we replaced the TATA box of the ICP4-responsive viral thymidine kinase gene with functional TATA boxes that displayed different apparent affinities for TATA-box-binding protein as measured by DNase I footprinting. We measured the effects of these TATA boxes on ICP4 induction by constructing ICP4-deficient recombinant viruses containing the different TATA alleles and comparing their expression in cells lacking or expressing ICP4. Overall, ICP4 induced weak TATA boxes (those that displayed low apparent affinity for TATA-box-binding protein and low basal expression) the most (18- to 41-fold) and strong TATA boxes the least (7- to 10-fold). Therefore, ICP4 induction correlated inversely with TATA box strength. Using a reconstituted in vitro transcription assay, we determined that the relative levels of induction by ICP4 of the different TATA alleles were similar to those measured in vivo, suggesting that ICP4 was the only viral protein required for induction. These results fit a model in which ICP4 acts in part to enhance binding of TFIID to the TATA box. We compare and contrast these results with those observed with the viral regulatory proteins adenovirus E1a and simian virus 40 large T antigen and the cellular coactivator PC4.

Base Sequence↗