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Biomedical subjects

B Chen

Publications and source records attributed to B Chen.

At least 235 records · Page 13Linked to original sources
PubMed1999

Determination of zinc contents in rabbits with cerebral ischemia by NAA and ICP-AES.

Cerebral ischemia is an important cerebral vascular disease, and zinc is a necessary trace element for humans. In this work, a cerebral ischemia model of rabbit was established by operation. The samples of brain and serum in the animal models were collected. The Zn contents in the samples were determined by neutron activation analysis and inductively coupled plasma-atomic emission spectrometry. The results show the Zn contents in brain decreased 2 mo after cerebral ischemia, and Zn contents in serum decreased even more obviously. In addition, a positive correlation of Zn contents between left and right cerebral hemispheres was observed, and the positive correlation between brain and serum was also observed. A test of Chinese medicine was also carried out in the work. Two Chinese medicines were fed to rabbits with cerebral ischemia in the experiments. The results showed they probably can prevent the decrease of Zn contents in serum.

Animals↗
PubMed1999

Circadian rhythms in light-evoked responses of the fly's compound eye, and the effects of neuromodulators 5-HT and the peptide PDF.

Two sets of wide-field neurons extend neurites into the fly's optic lamina, where monopolar cells receive photoreceptor input. They exhibit immunoreactivity to antibodies raised against either 5-hydroxytryptamine or the crustacean peptide PDH, respectively. Both are proposed whole-field neuromodulators of vision, apparently regulating a circadian rhythm of monopolar cell size. Seeking functional correlates, we have re-examined the electroretinogram for circadian rhythmicity, and for responses to locally injected 5-hydroxytryptamine and peptide. Long-term electroretinogram recordings from Calliphora entrained to a light/dark cycle and then transferred to constant darkness, uncovered a gradual, modest increase during the subjective night in the electroretinogram's ON- and OFF-transients, from the lamina's monopolar cells. Five to twenty nl of 5-hydroxytryptamine (10(-3) mol.1(-1)) injected into the head haemolymph strongly enhanced the electroretinogram transients, an action reversed by 5-hydroxytryptamine antagonists. Injected into the eye, 5-hydroxytryptamine (10(-4) mol.1(-1)) had the opposite effect; the rapid onset there suggests direct action, whilst the opposing effect from haemolymph injection suggests a different receptor site. Pigment-dispersing hormone (2.2 x 10(-5) mol.1(-1)) injected into the haemolymph increased the electroretinogram transients along a biphasic course, with a slow partial recovery; injected into the eye, it lacked effect.

Animals↗
PubMed1999

Fluoxetine impairs the CYP2D6-mediated metabolism of propafenone enantiomers in healthy Chinese volunteers.

OBJECTIVE: To determine the effect of 20 mg/day fluoxetine on the pharmacokinetics of propafenone enantiomers and CYP2D6 activity by phenotyping with dextromethorphan. METHODS: Nine healthy Chinese volunteers (seven men and two women) were included in a two-phase study. Dextromethorphan (20 mg) was given before and after subjects took 20 mg/day fluoxetine for 10 days, and the dextromethorphan metabolic ratio was calculated to determine CYP2D6 phenotype. Pharmacokinetic studies of propafenone enantiomers after a single oral 400 mg dose before and after pretreatment with 20 mg/day fluoxetine for 10 days were also conducted in these subjects. Reversed-phase HPLC with precolumn derivatization was used to determine enantiomeric concentrations of propafenone in plasma. RESULTS: Mean CYP2D6 dextromethorphan metabolic ratios before and after fluoxetine therapy were 0.028 +/- 0.031 and 0.080 +/- 0.058, respectively (P = .001), indicating that a strong inhibition of CYP2D6 by fluoxetine activity was observed in Chinese subjects. Propafenone metabolism was also impaired significantly after fluoxetine treatment. The elimination half-life, peak concentration, and area under the curve from 0 hours to infinity of two enantiomers after fluoxetine therapy were significantly increased compared with those at baseline (P < .01), whereas oral clearance decreased from 75.01 +/- 17.69 L/h to 49.36 +/- 8.62 L/h for S-propafenone (P = .005) and from 107.62 +/- 33.82 L/h to 70.60 +/- 12.42 L/h for R-propafenone (P = .027). In addition, fluoxetine increased the peak concentration of S-propafenone by 39% and that of R-propafenone by 71% (P < .05). A significant increase of the time to reach peak concentration was observed only in the R-enantiomer and not in the S-enantiomer of propafenone after fluoxetine therapy. There were no differences in the percentage changes of PR and QRS intervals before or after fluoxetine pretreatment at the time observed (P > .05). CONCLUSION: We conclude that fluoxetine may cause significant inhibition of the CYP2D6 activity as determined by dextromethorphan phenotyping. This inhibition impairs the metabolism of propafenone enantiomers in Chinese subjects. Caution must be exercised when fluoxetine and propafenone are coadministered to avoid potential toxicity.

Administration, Oral↗
PubMed1999

Opioid receptor upregulation in mu-opioid receptor deficient CXBK and outbred Swiss Webster mice.

Chronic in vivo treatment with opioid antagonists increases opioid receptor density and the potency of opioid agonists without altering receptor mRNA levels. To determine if basal receptor density affects opioid receptor upregulation, we examined the effect of chronic naltrexone treatment on mu-opioid receptor density and mRNA in two mice strains that differ in mu-opioid receptor density. CXBK mice (mu-opioid receptor deficient) and outbred Swiss Webster mice were implanted s.c. with a placebo or 15 mg naltrexone pellet for 8 days, the pellets removed and 24 hr later opioid receptor density (mu, delta) and receptor mRNA level (mu) determined in whole brain; or morphine dose-response studies conducted. In placebo-treated CXBK mice, mu-opioid receptor density was approximately 40% less than in Swiss Webster mice, although mu-opioid receptor mRNA abundance was similar in both strains. In placebo-treated CXBK mice, morphine potency was approximately 6-fold less than Swiss Webster mice. Naltrexone treatment increased morphine potency (1.7-fold) and mu- (approximately 90%) and delta- (approximately 20-40%) opioid receptor density in CXBK and Swiss Webster mouse brain similarly. Mu-opioid receptor mRNA was unchanged by naltrexone treatment in either strain. There was no difference in the basal or naltrexone-treated whole brain G(i alpha2) protein levels in CXBK or Swiss Webster mouse. These data indicate that a deficiency in mu-opioid receptors does not alter the regulation of opioid receptors by opioid antagonists in vivo, and suggest that adaptive responses to chronic opioid antagonist treatment are independent of opioid receptor density.

Analgesics↗
PubMed1999

Influence of calcium ions on the structure and stability of recombinant human deoxyribonuclease I in the aqueous and lyophilized states.

The effect of calcium ions on the structure and stability of recombinant human DNase I (rhDNase) in the aqueous and solid (lyophilized) states was investigated. Fourier transform infrared (FTIR) spectroscopy was used to examine the overall secondary structure, while chemical stability was monitored in terms of deamidation and soluble aggregate formation at 40 degrees C. The exogenous calcium was removed by EGTA. This process can remove all but approximately one calcium ion per protein molecule. Analysis of the FTIR spectra in the amide III region in either the aqueous or lyophilized state demonstrated that removal of exogenous Ca2+ by EGTA-treatment had little effect on the secondary structure (and lyophilization-induced rearrangement thereof). For the aqueous solution, circular dichroism was used as an independent technique and confirmed that there was no large overall change in the secondary or tertiary structure upon the removal of calcium. The primary degradation route for the aqueous protein was deamidation. For the EGTA-treated protein, there was also severe covalent aggregation, e.g., formation of intermolecular disulfides facilitated by the cleavage of Cys173-Cys209. The aggregates exhibited a markedly different secondary structure compared to the native protein. For instance, the beta-sheet band observed at ca. 1620 cm-1 wavenumber in the amide I second derivative spectra was increased. Enzymatic activity was completely lost upon aggregation, consistent with the cleavage of the aforementioned native disulfide. For the protein lyophilized in the presence of Ca2+, there was no increase in deamidated species during solid-state storage; however, some aggregation was observed. For the lyophilized EGTA-treated protein, aggregation was even more pronounced, and there was some loss in enzymatic activity upon reconstitution. Thus, the removal of calcium ions by EGTA-treatment decreased the stability of rhDNase in both the aqueous and solid states even though no large overall calcium-induced structural changes could be observed by the techniques used in this study.

Calcium↗
PubMed1999

Phenylpropanol derivatives from morina chinensis

Seven new phenylpropanol derivatives, named morinins A-G (1-7), along with five known compounds, 4-O-methylcinnamyl alcohol, 4-O-methylcinnamyl methyl ether, 4-O-methylcinnamyl acetate, p-methoxybenzaldehyde, and 4-O-methyl-(E)-coniferyl alcohol, have been isolated from the roots of the medicinal Chinese plant, Morina chinensis. Their structures were determined on the basis of spectral data, especially 2D NMR and HRMS.

Journal Article↗
PubMed1999

The influence of CYP2D6 activity on the kinetics of propafenone enantiomers in Chinese subjects.

AIMS: To determine role of CYP2D6 activity in the pharmacokinetics of propafenone (PPF) enantiomers in native Chinese subjects. METHODS: Sixteen extensive metabolizers (EMs) and one poor metabolizer (PM), whose phenotype had been previously assessed with dextromethorphan metabolic phenotyping, were enrolled. Blood samples (0 approximately 15 h) were taken after oral administration of a single dose (400 mg) of racemic-propafenone hydrochloride. A reverse-phase h.p.l.c. method with pre-column derivatization was employed to quantitate enantiomeric concentrations of propafenone in plasma. RESULTS: For the EM subjects, S-PPF was less rapidly metabolized and had higher peak plasma concentrations than R-PPF (413+/-143 vs 291+/-109 ng ml-1, P<0.001). The AUC was markedly higher for S-PPF than for R-PPF (2214+/-776 vs 1639+/-630 microg h l-1, P<0.001), whereas the clearance of S-PPF was significantly lower than that of R-PPF (96.0+/-39.0 vs 138+/-78 l h-1, P<0.01). There were no differences in t1/2, and Cmax between the two isomers (P >0.05). In the one PM subject, not only did S-PPF appear to undergo less rapid metabolism than R-PPF, but the subject also showed 2 approximately 3 fold differences in Cmax, CL and AUC compared with EMs. The correlation coefficients (rs ) between dextromethorphan metabolic ratio (lg MR) and pharmacokinetic parameters (Cmax, CL and AUC) were 0.63, -0.87, 0.87 for S-PPF and 0. 57, -0.73, 0.86 for R-PPF, respectively. CONCLUSIONS: Our results suggest that CYP2D6 activity contributes to the pharmacokinetic variability of propafenone enantiomers in Chinese subjects.

Administration, Oral↗
PubMed1999

Structure of the GM2A gene: identification of an exon 2 nonsense mutation and a naturally occurring transcript with an in-frame deletion of exon 2.

Deficiency of the GM2 activator protein, encoded by GM2A, results in the rare AB-variant form of GM2 gangliosidosis. Four mutations have been identified, but the human gene structure has been only partially characterized. We report a new patient from a Laotian deme whose cells are deficient in both GM2-activator mRNA and protein. However, reverse transcription (RT)-PCR detected some normal-sized cDNA and a smaller cDNA species, which was not seen in the RT-PCR products from normal controls. Sequencing revealed that, although the patient's normal-sized cDNA contained a single nonsense mutation in exon 2, his smaller cDNA was the result of an in-frame deletion of exon 2. Long PCR was used to amplify introns 1 and 2 from patient and normal genomic DNA, and no differences in size, in 5' and 3' end sequences, or in restriction-mapping patterns were observed. From these data we developed a set of four PCR primers that can be used to identify GM2A mutations. We use this procedure to demonstrate that the patient is likely homozygous for the nonsense mutation. Other reports have associated nonsense mutations with dramatically reduced levels of mRNA and with an increased level of skipping of the exon containing the mutation, thus reestablishing an open reading frame. However, a recent article has concluded that, in some cases, the latter observation is caused by an artifact of RT-PCR. In support of this conclusion, we demonstrate that, if the competing, normal-sized cDNA is removed from the initial RT-PCR products, from both patient and normal cells, by an exon 2-specific restriction digest; a second round of PCR produces similar amounts of exon 2-deleted cDNA.

Base Sequence↗
PubMed1999

Espin contains an additional actin-binding site in its N terminus and is a major actin-bundling protein of the Sertoli cell-spermatid ectoplasmic specialization junctional plaque.

The espins are actin-binding and -bundling proteins localized to parallel actin bundles. The 837-amino-acid "espin" of Sertoli cell-spermatid junctions (ectoplasmic specializations) and the 253-amino-acid "small espin" of brush border microvilli are splice isoforms that share a C-terminal 116-amino-acid actin-bundling module but contain different N termini. To investigate the roles of espin and its extended N terminus, we examined the actin-binding and -bundling properties of espin constructs and the stoichiometry and developmental accumulation of espin within the ectoplasmic specialization. An espin construct bound to F-actin with an approximately threefold higher affinity (K(d) = approximately 70 nM) than small espin and was approximately 2.5 times more efficient at forming bundles. The increased affinity appeared to be due to an additional actin-binding site in the N terminus of espin. This additional actin-binding site bound to F-actin with a K(d) of approximately 1 microM, decorated actin stress fiber-like structures in transfected cells, and was mapped to a peptide between the two proline-rich peptides in the N terminus of espin. Espin was detected at approximately 4-5 x 10(6) copies per ectoplasmic specialization, or approximately 1 espin per 20 actin monomers and accumulated there coincident with the formation of parallel actin bundles during spermiogenesis. These results suggest that espin is a major actin-bundling protein of the Sertoli cell-spermatid ectoplasmic specialization.

Actins↗
PubMed1999

Mapping of a hypovirus p29 protease symptom determinant domain with sequence similarity to potyvirus HC-Pro protease.

Hypovirus infection of the chestnut blight fungus Cryphonectria parasitica results in a spectrum of phenotypic changes that can include alterations in colony morphology and significant reductions in pigmentation, asexual sporulation, and virulence (hypovirulence). Deletion of 88% [Phe(25) to Pro(243)] of the virus-encoded papain-like protease, p29, in the context of an infectious cDNA clone of the prototypic hypovirus CHV1-EP713 (recombinant virus Deltap29) partially relieved virus-mediated suppression of pigmentation and sporulation without altering the level of hypovirulence. We now report mapping of the p29 symptom determinant domain to a region extending from Phe(25) through Gln(73) by a gain-of-function analysis following progressive repair of the Deltap29 deletion mutant. This domain was previously shown to share sequence similarity [including conserved cysteine residues Cys(38), Cys(48), Cys(70), and Cys(72)] with the N-terminal portion of the potyvirus-encoded helper component-proteinase (HC-Pro), a multifunctional protein implicated in aphid-mediated transmission, genome amplification, polyprotein processing, long-distance movement, and suppression of posttranscriptional silencing. Substitution of a glycine residue for either Cys(38) or Cys(48) resulted in no qualitative or quantitative changes in virus-mediated symptoms. Unexpectedly, mutation of Cys(70) resulted in a very severe phenotype that included significantly reduced mycelial growth and profoundly altered colony morphology. In contrast, substitution for Cys(72) resulted in a less severe symptom phenotype approaching that observed for Deltap29. The finding that p29-mediated symptom expression is influenced by two cysteine residues that are conserved in the potyvirus-encoded HC-Pro raises the possibility that these related viral-papain-like proteases function in their respective fungal and plant hosts by impacting ancestrally related regulatory pathways.

Ascomycota↗
PubMed1999

Infectious cDNA clone of hypovirus CHV1-Euro7: a comparative virology approach to investigate virus-mediated hypovirulence of the chestnut blight fungus Cryphonectria parasitica.

We report the construction of a full-length infectious cDNA clone for hypovirus CHV1-Euro7, which is associated with reduced virulence (hypovirulence) of the chestnut blight fungus Cryphonectria parasitica. Field strains infected with CHV1-Euro7 are more virulent and exhibit less severe phenotypic changes (hypovirulence-associated traits) than strains infected with the prototypic hypovirus CHV1-EP713, for which the first infectious cDNA clone was developed. These differences exist even though the two hypoviruses show extensive sequence identities: 87 to 93% and 90 to 98% at the nucleotide and amino acid levels, respectively. The relative contributions of viral and host genomes to phenotypic traits associated with hypovirus infection were examined by transfecting synthetic transcripts of the two hypovirus cDNAs independently into two different virus-free C. parasitica strains, EP155 and Euro7(-v). Although the contribution of the viral genome was clearly predominant, the final magnitude and constellation of phenotypic changes were a function of contributions by both genomes. The high level of sequence identity between the two hypoviruses also allowed construction of viable chimeras and mapping of the difference in symptom expression observed for the two viruses to the open reading frame B coding domain. Implications of these results for engineering enhanced biological control and elucidating the basis for hypovirus-mediated attenuation of fungal virulence are discussed.

Ascomycota↗
PubMed1999

Characterization of the thyroxine-binding site of thyroxine-binding globulin by site-directed mutagenesis.

The principal transport protein for T4 in human blood, thyroxine-binding globulin (TBG), binds T4 with an exceptionally high affinity (Ka = 10(10) M(-1)). Its homology to the superfamily of the serpins has recently been used in the design of chimeric proteins, providing experimental evidence that an eight-stranded beta-barrel domain encompasses the ligand-binding site. We have now characterized the T4 binding site by site-directed mutagenesis. Sequence alignment of TBG from several species revealed a phylogenetically highly conserved stretch of amino acids comprising strands 2B and 3B of the beta-barrel motif. Mutations within this region (Val228Glu, Cys234Trp, Thr235Trp, Thr235Gln, Lys253Ala, and Lys253Asp), designed to impose steric hindrance or restriction of its mobility, had no significant influence on T4 binding. However, binding affinity was 20-fold reduced by introduction of an N-linked glycosylation site at the turn between strands 2B and 3B (Leu246Thr) without compromising the proper folding of this mutant as assessed by immunological methods. In most other serpins, this glycosylation site is highly conserved and has been shown to be crucial for cortisol binding of corticosteroid-binding globulin, the only other member of the serpins with a transport function. The ligand-binding site could thus be located to a highly aromatic environment deep within the beta-barrel. The importance of the binding site's aromatic character was investigated by exchanging phenylalanines with alanines. Indeed, these experiments revealed that substitution of Phe249 in the middle of strand 3B completely abolished T4 binding, while the substitution of several other phenylalanines had no effect.

Amino Acid Sequence↗
PubMed1999

Plasma viral load and CD4 lymphocytes predict HIV-associated dementia and sensory neuropathy.

OBJECTIVE: To determine the predictive value of plasma HIV RNA and CD4 lymphocytes for HIV-associated dementia and sensory neuropathy. METHODS: A total of 1,604 AIDS-free HIV seropositive men from the Multicenter AIDS Cohort Study were followed over a 10-year period (1985 to 1995). HIV-associated dementia and sensory neuropathy were diagnosed according to standard definitions. Baseline samples were used to measure plasma HIV RNA levels with a branched DNA assay and levels of beta2-microglobulin, CD4 lymphocyte counts, and hemoglobin levels. RESULTS: Seventy-seven patients with HIV-associated dementia and 213 patients with sensory neuropathy were identified. Baseline HIV RNA levels above 3,000 copies/mL and CD4 counts below 500 cells/mm3 were predictive of both neurologic outcomes, but neither hemoglobin, body mass index, nor beta2-microglobulin were independently predictive. After adjusting for age and level of education, individuals with baseline plasma HIV RNA >30,000 copies/mL had a relative hazard for dementia 8.5 times (p < 0.001) that of those with <3,000 copies/mL, and those with CD4 counts <200 cells/mm3 had a 3.5-fold (p = 0.003) greater hazard relative to those with CD4 counts >500 cells/mm3. Individuals with HIV RNA >10,000 copies/mL had a 2.3-fold (p = 0.008) greater hazard of sensory neuropathy than those with <500 copies/mL, and men with <750 CD4 cells/mm3 had a 1.4-fold (p = 0.03) greater hazard than those with >750 CD4 cells/mm3. CONCLUSIONS: High levels of systemic HIV replication may "drive" the initiation of neurologic disease; effective suppression of HIV may reduce the incidence of dementia and neuropathy. Levels of plasma HIV RNA and CD4 counts, determined before the initiation of antiretroviral therapy, were predictive of HIV-associated dementia and sensory neuropathy.

AIDS Dementia Complex↗
PubMed1999

Recombinant expression and characterization of dentin matrix protein 1.

Dentin matrix protein 1 (DMP1) is an extracellular matrix noncollagenous protein (NCP) initially isolated from dentin and now found to be present in calcified tissues like calvaria and long bone. The characteristic feature of DMP1 is that it contains a large number of acidic domains and has properties which implicate it as a key participant in regulating matrix mineralization. The level of DMP1 in the tissue is sparse and it is not easily isolated from dentin because it copurifies with other dentin NCPs. The exact function of DMP1 is not known and this is due to the inherent difficulty of obtaining enough protein from the mineralized tissues. In order to understand the physiologic role for DMP1 during the formation of mineralized tissues we have produced milligram quantities of recombinant DMP1 in E. coli. The objective of this work was: (1) to prepare unmodified apoprotein so that it could be used for studying the function of DMP1; and (2) to prepare polyclonal antibody against the recombinant DMP1 antigen. The DMP1 polyclonal antibody did not cross-react with other NCPs present in dentin or with bone acidic glycoprotein-75 (BAG-75) present in the bone matrix, confirming the specificity of this antibody and thus making it a valuable tool to determine the in vivo function of DMP1.

Amino Acid Sequence↗
PubMed1999

Expression of membrane-associated macrophage colony-stimulating factor (M-CSF) in Hodgkin's disease and other hematologic malignancies.

We have identified a membrane-bound form of M-CSF (m-M-CSF) from an established human leukemic J6-1 cell line. To further understand its biological significance, we studied the expression of this membrane-associated growth factor in the lymph nodes of lymphoma patients and bone marrow smears from patients with hematologic diseases by immunohistochemical staining using anti-M-CSF MAb. We detected a high incidence of m-M-CSF expression in 75% (9/12) of the lymph node sections from patients with Hodgkin's Disease (HD). The antigens were detected primarily in large clusters of mononuclear Hodgkin's cells and the extracellular matrix (EM) surrounding them. In one HD patient with abundant multinucleated Reed-Sternberg (R-S) cells, all of them were intensely stained with anti-M-CSF MAb. In non-Hodgkin's lymphomas (NHL), the incidence (17.6 %) of m-M-CSF expression was lower (3/17). Yet, no m-M-CSF antigens were detected in the lymph nodes from six cases of non-hematologic malignancies and other diseases. A high response also was detected in bone marrow smears obtained from patients with hematologic malignancies, which include myeloid leukemias (32.5%), lymphomas with bone marrow metastasis (50%) and myelodysplastic syndromes (MDS) (37.5 %). By comparison, only 6.8 % of bone marrow smears from non-malignant hematologic diseases and 2.7% of lymphoid leukemias showed positive staining with anti-M-CSF MAb. Our results showed that high expression of m-M-CSF antigens is linked to some types of lymphomas, especially HD. and myeloid leukemias, and may play a role in the development of these hematologic malignancies.

Adult↗
PubMed1999

Association of human herpesvirus 6 with the demyelinative lesions of progressive multifocal leukoencephalopathy.

Progressive Multifocal Leukoencephalopathy (PML) is a primary demyelinating disease of the central nervous system occurring almost exclusively in individuals with impaired cell-mediated immunity. The JC polyoma virus has been accepted as the etiologic agent ofPML. Using a two-step in-situ polymerase chain reaction procedure to amplify and detect genomic DNA of human herpesvirus-6 (HHV6) in formalin-fixed paraffin-embedded archival brain tissues, a high frequency of infected cells was consistently detected in PML white matter both within and surrounding demyelinative lesions and HHV6 genome was found mainly within oligodendrocytes. Lesser amounts of HHV6 genome were detected in most normal, AIDS, and other neurological disease control tissues. Immunocytochemistry for HHV6 antigens showed actively infected nuclei of swollen oligodendrocytic morphology only within the demyelinative lesions of PML but not in adjacent uninvolved tissue. In addition, no HHV6 antigens were detectable in control tissues including brains of individuals with HIV-1 encephalopathy but without PML. Double immunohistochemical staining for JC virus large T antigen and HHV6 antigens demonstrated co-labeling of many swollen intralesional oligodendrocytes in the PML cases. The evidence suggests that HHV6 activation in conjunction with JC virus infection is associated with the demyelinative lesions of PML.

AIDS Dementia Complex↗
PubMed1999

Vaccinia virus-mediated expression of wild-type p53 suppresses glioma cell growth and induces apoptosis.

The use of vaccinia virus vectors for cancer gene therapy may become a powerful method to achieve efficient anti-tumor effects. We used recombinant vaccinia virus expressing wild-type p53 (rVV-p53) to examine the biological effects of exogenous tumor suppressor p53 in human (U-373MG, U-87MG, LN-Z308) and rat glioma cells (9L, C6) in vitro. All glioma cell lines infected with rVV-p53 exhibited growth inhibition and underwent apoptosis as demonstrated by morphological studies using nuclear staining and flow cytometry. The key role of p53 in cell growth inhibition was confirmed as measured by colony forming efficiency. Growth inhibition and apoptosis were independent of the endogenous p53 status of the glioma cell lines.

Animals↗