Biomedical subjects

X Bu

Publications and source records attributed to X Bu.

At least 37 records · Page 2Linked to original sources

PubMed2000

Expression and significance of urokinase-type plasminogen activator in human gliomas.

OBJECTIVE: To investigate the expression and clinical significance of urokinase type plasminogen activator (uPA) in human gliomas. METHODS: mRNA and protein expressions of uPA were examined by Northern blot hybridization and immunohistochemical method in 43 cases of gliomas and 5 cases of normal brain tissues and their relationship to clinical indexes was comprehensively analyzed. RESULTS: All tissues expressed the 2.5 kb transcript of uPA mRNA. The uPA mRNA level in high-grade gliomas was considerably higher than that in low-grade gliomas and normal brain tissues (P < 0.01). Levels of uPA mRNA expression in tumor tissues with recurrence during 18 postoperative months and a survival period less than 3 years, were significantly higher than counterparts (P < 0.01). uPA mRNA expression was strongly correlated with the microvessel quantity (MVQ) in gliomas (r = 0.56, P < 0.01). uPA protein was mainly distributed in tumor cells and endothelial cells of glioblastomas and anaplastic astrocytomas. CONCLUSION: Expression of uPA is associated with the malignant progression, invasion and angiogenesis of gliomas, and it may play a critical role in the recurrence and prognosis of gliomas.

Adolescent↗

PubMed2000

[A study of simian virus 40 infection and its origin in human brain tumors].

OBJECTIVE: To study the status of simian virus 40 (SV40) infection and its origin in human brain tumors. METHODS: Polymerase chain reaction (PCR) and Dot blot hybridization were used to detect SV40 DNA sequences in 516 human brain tumor tissues, 80 peripheral blood cells and 50 sperm fluids from healthy individuals, 100 human embryo tissues from artificial abortion, 30 normal brain tissues and two human glioma cell lines: SHG44 and BT325. RESULTS: SV40 DNA sequences were found in 36.4% of human brain tumors (188/516), 16.3% of healthy peripheral blood cells (13/80), 22.0% of healthy semen (11/50), 8.0% of human embryo tissues (8/100) and 6.7% of normal brain tissues (2/30). SV40 DNA sequences were also detected in SHG44 and BT325 cell lines. The positive rates of SV40 DNA in human brain tumors, peripheral blood cells and semen from healthy donors were significantly higher than those in human normal brain and embryo tissues (P < 0.05). CONCLUSIONS: (1) SV40 has a higher infection rate in human brain tumors, (2) SV40 is closely related to the etiopathogenesis of human brain tumors, (3) the ways of SV40 spread may due to both horizontal and diaplacental infections in human population.

Brain↗

PubMed2000

[Chemical study of Alpinia officinarum].

Seven compounds were isolated from Alinia officinarum Hance and were identified as beta-sitoterol, 1,7-diphenyl-5-ol-3-heptone, 1-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-5-ol-3-heptone, glandin, kaempferol-4'-methylether and 3,4-dihydroxylbenzoic acid by IR, 1HNMR, 13CNMR, FAB-MS and EA. Among these compounds, 3,4-dihydroxylbenzoic acid was the first time obtained from Alpinia officinarum Hance. Furthermore, 1-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-5-ol-3-heptone and a new compound 1,7-diphenyl-3,5-heptandiol-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-3,5-heptaxdiol were obtained from 1,7-diphenyl-5-ol-3-heptone and 1-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-5-ol-3-heptone via chemical reductions.

Alpinia↗

PubMed2000

[Audiological findings and mitochondrial DNA mutation in a large family with matrilineal sensorineural hearing loss].

OBJECTIVE: To explore audiological features of matrilineal non-syndromic deafness and its molecular mechanism. METHODS: A large family with 41 members having inherited deafness was studied. Complete history and the data of general and otolaryngological examinations were collected. All subjects were screened for mitochondrial DNA A1555G mutation by molecular analysis. Audiological evaluation included puretone audiometry, auditory brainstem responses and transiently evoked otoacoustic emissions. RESULTS: All subjects were in good health generally. Molecular analysis showed that all maternal relatives with or without hearing loss harbored the A1555G mitochondrial mutation. No mutation was found among spouses and paternal relatives. Audiological results showed notable symmetric bilateral sensorineural hearing loss in 17 of 20 maternal relatives, in which 5 cases had a progressive hearing loss in the recent 11 years. The age of appearance of hearing loss ranged from 1 to 50 years. CONCLUSION: All hearing-impaired subjects of this family had late-onset sensorineural hearing loss. Most of which were progressive. The A1555G mitochondrial mutation in the 12S rRNA gene is responsible for the disorder. Other factors, such as nuclear genes or environmental determinants, may influence the clinical expression of mutant mtDNA.

Acoustic Impedance Tests↗

PubMed2000

[Whole genome-wide scanning for a large pedigree with matrilineal deafness].

OBJECTIVE: To search responsible nuclear genes for matrilineal non-syndromic deafness. METHODS: Whole genome-wide scanning was performed to analyze the 365 short tandem repeats in a deaf pedigree with maternal inheritance using DNA pooling strategy. Frequencies of allele in one patient pool were compared with that in one unaffected relative pool as well as in one normal control pool. Linkage analysis was also conducted in some positive loci. RESULTS: Allele from 45 loci occurred more frequently in the patient pool than that in the unaffected relative pool and the control pool. No linkage was found from any candidate locus investigated. CONCLUSION: 45 positive loci obtained from this family may be as the candidate positions for matrilineal non-syndromic deafness.

Deafness↗

PubMed1999

The direct release of nitric oxide by gypenosides derived from the herb Gynostemma pentaphyllum.

Herbal medicines are increasingly being utilized to treat a wide variety of disease processes. Gypenosides are triterpenoid saponins contained in an extract from Gynostemma pentaphyllum and are reported to be effective in the treatment of cardiovascular diseases; however, the mechanism underlying the therapeutic effect is not known. We tested the hypothesis that gypenosides extracted from G. pentaphyllum elicit vasorelaxation through the direct release of endothelium-derived nitric oxide. Nitric oxide production in bovine aortic endothelial cells grown under standard tissue culture conditions was quantitated using a chemiluminescence method. Arterial vasomotion was assayed using isolated porcine coronary artery rings under standard isometric recording conditions. The extract of G. pentaphyllum at 0.1-100 microg/ml elicited concentration-dependent vasorelaxation of porcine coronary rings that was antagonized by the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester. Indomethacin had no significant effect on G. pentaphyllum-induced relaxation. The G. pentaphyllum extract elicited a concentration-dependent increase in nitric oxide production from cultured bovine aortic endothelial cells. At the concentrations utilized, there was no morphological evidence for cellular toxicity. These results demonstrate that extracts of G. pentaphyllum directly stimulate nitric oxide release, but not prostanoid production. Nitric oxide production in response to gypenosides may be one mechanism whereby this herbal medicine elicits its therapeutic effects.

Animals↗

PubMed1999

[Particle repositioning maneuver for benign paroxysmal positional vertigo of posterior semicircular canal].

OBJECTIVE: To determine the effectiveness of particle repositioning maneuver (PRM) for the treatment of benign paroxysmal positional vertigo (BPPV). METHODS: Thirty one patients with BPPV of the posterior semicircular canal treated between July 1996 and June 1998 were retrospectively analyzed. Patients received a single treatment of PRM based on the hypothesis that the vertigo and nystagmus of BPPV were due to debris floating in the long arm of the posterior canal (canalithiasis). Treatment outcome was classified as cure (asymptomatic), improvement reduction of symptoms > 50%, or no change. RESULTS: After a single treatment of PRM, complete remission of vertigo and nystagmus were found in 67.7% of the patients and improvement of the symptoms was found in 19.4% of the patients. The total improvement rate was 87.1%. CONCLUSION: The particle repositioning maneuver was effective for most of the patients with benign paroxysmal positional vertigo and can be recommended as the first-line treatment modality.

Adult↗

PubMed1998

Evidence for complex nuclear inheritance in a pedigree with nonsyndromic deafness due to a homoplasmic mitochondrial mutation.

The relationship between mitochondrial genotype and clinical phenotype is complicated in most instances by the heteroplasmic nature of pathogenic mitochondrial mutations. We have previously shown that maternally inherited hearing loss in a large Arab-Israeli kindred is due to the homoplasmic A1555G mutation in the mitochondrial 12S ribosomal RNA gene [Prezant et al., 1993: Nat Genet 4:289-294]. Family members with this mutation have phenotypes ranging from profound hearing loss to completely normal hearing, and we have shown that there is genetic and biochemical evidence for nuclear gene involvement in this family [Bu et al., 1993: Genet Epidemiol 9:27-44; Guan et al., 1996: Hum Mol Genet 5:963-971]. To identify such a nuclear locus, two candidate genes were excluded through linkage analysis and sequencing, and a genome-wide linkage search in family members who all have the identical homoplasmic mitochondrial mutation, but differ in their hearing status, was performed. In two stages a total of 560 polymorphic genetic markers was genotyped, and the data were analyzed under model-dependent and model-free assumptions. No chromosomal region was identified as a major contributor to the phenotypic expression of the mitochondrial mutation. Thus, in this simplified paradigm of a homoplasmic mitochondrial mutation in a single kindred who all live in the similar environment of a small village, the penetrance of the mitochondrial mutation appears to depend on the interaction of multiple nuclear genes.

Chromosome Mapping↗

PubMed1998

[The expression of plasminogen activator inhibitor-1 (PAI-1) gene in human astrocytomas].

OBJECTIVE: To investigate the expression of PAI-1 gene and its clinical significance in human astrocytomas. METHODS: The mRNA and protein expression of PAI-1 were examined with Northern blot hybridization and ABC immunohistochemical methods in 36 cases of astrocytomas. The correlation between PAI-1 expression with clinicopathologic factors were studied. RESULTS: All astrocytoma tissues expressed 3.0 kb and 2.2 kb transcripts of PAI-1 mRNA. The PAI-1 mRNA level in high grade astrocytomas were considerably higher than that in low grade astrocytomas (P < 0.01). Detectable levels of PAI-1 mRNA were not found in normal brain tissues. PAI-1 mRNA expression was positively correlated with necrosis (r = 0.51, P < 0.01), micro-blood vessel quantity (r = 0.33, P < 0.01) and brain edema (r = 0.27, P < 0.01) respectively. There was no correlation between PAI-1 mRNA expression and tumor size, sex or age of patients. Immunohistochemical staining for PAI-1 showed the distribution of PAI-1 protein was mainly in tumor cells of high grade astrocytomas, particularly in abundant areas of vascular proliferation and in remnant tumor cells surrounding necrotic foci, whereas it was only weakly expressed in low grade astrocytomas. CONCLUSION: The expression of PAI-1 gene was closely associated with grade, necrosis, angiogenesis and brain edema, which may provide a molecular marker for determining the malignant degree of astrocytoma.

Astrocytoma↗

PubMed1997

Identification of an endothelial cell-specific regulatory region in the murine endothelin-1 gene.

Endothelin-1 is a 21-amino acid peptide first characterized as a potent vasoactive compound synthesized by endothelial cells. Because of its high level cell-restricted pattern of expression, we have employed this gene as a model for investigating the DNA and protein elements that mediate endothelial cell-specific gene expression. In this study we have identified a complex positive regulatory region located at base pairs -364 to -320 in the murine endothelin-1 gene. This region consists of three functionally dependent elements, ETE-C, ETE-D, and ETE-E, which are all required for full activity. When a 43-base pair fragment containing these three elements was employed in heterologous promoter experiments, this sequence was capable of increasing transcriptional activity in an endothelial cell-specific fashion. None of the elements contains a recognized consensus sequence known to bind transcriptional regulatory proteins in higher eukaryotes; however, each element does appear to mediate protein binding. The combination of all three elements promotes binding of a protein complex that is endothelial cell-specific. This is the first evidence for an endothelial cell-specific DNA regulatory element and cognate binding proteins.

Animals↗

PubMed1997

Large-cage zeolite structures with multidimensional 12-ring channels

Zeolite type structures with large cages interconnected by multidimensional 12-ring (rings of 12 tetrahedrally coordinated atoms) channels have been synthesized; more than a dozen large-pore materials were created in three different topologies with aluminum (or gallium), cobalt (or manganese, magnesium, or zinc), and phosphorus at the tetrahedral coordination sites. Tetragonal UCSB-8 has an unusually large cage built from 64 tetrahedral atoms and connected by an orthogonal channel system with 12-ring apertures in two dimensions and 8-ring apertures in the third. Rhombohedral UCSB-10 and hexagonal UCSB-6 are structurally related to faujasite and its hexagonal polymorph, respectively, and have large cages connected by 12-ring channels in all three dimensions.

Journal Article↗

PubMed1997

Complex genetic contribution of the Apo AI-CIII-AIV gene cluster to familial combined hyperlipidemia. Identification of different susceptibility haplotypes.

Familial combined hyperlipidemia (FCH) is a common genetic lipid disorder in Western societies. In a recent report (Dallinga-Thie, G.M., X.D. Bu, M. van Linde-Sibenius Trip, J.I. Rotter, A.J. Lusis, and T.W.A. de Bruin. J. Lipid Res., 1996, 36:136-147) we have studied three restriction enzyme polymorphisms: XmnI, and MspI sites 5' of the apo AI gene and SstI site in the 3' untranslated region of exon 4 of the apo CIII gene in 18 FCH pedigrees, including 18 probands, 178 hyperlipidemic relatives, 210 normolipidemic relatives, and 176 spouses. DNA variations in the apo AI-CIII-AIV gene cluster had a modifying effect on plasma triglycerides, LDL cholesterol, and apolipoprotein CIII levels. In this study, combinations of haplotypes were analyzed to further characterize their interactions and effect on the expression of severe hyperlipidemia in FCH subjects. A specific combination of haplotypes with one chromosome carrying the X1M1S2 (1-1-2) haplotype and the other the X2M2S1 haplotype (2-2-1) was significantly more frequent in hyperlipidemic relatives (6%) than in normolipidemic relatives (3%) and spouses (0.5%). Associated with this combination of haplotypes were significantly elevated plasma cholesterol (P < 0.0001), triglycerides (P < 0.0001), and apo CIII (P < 0.001) levels when compared to the wild type combination of haplotypes 1-1-1/1-1-1. The only spouse with this specific combination of haplotypes showed a severe hyperlipidemic phenotype, similar to FCH. Furthermore, nonparametric sibpair linkage analysis revealed significant linkage between these markers in the gene cluster and the FCH phenotype (MspI P = 0.0088, SstI P = 0.044, and XMS haplotype P = 0.037). The present findings confirm that the apo AI-CIII-IV gene cluster contributes to the FCH phenotype, but this contribution is genetically complex. An epistatic interaction between different haplotypes of the gene cluster was demonstrated. The S2 allele on one haplotype was synergistic to the X2M2 allele on the other haplotype in its hyperlipidemic effect. Therefore, two different susceptibility loci exist in the gene cluster, demonstrating the paradigm of complex genetic contribution to FCH.

Adult↗

PubMed1997

[Microsatellite instability in nephroblastoma and its relationship to clinicopathological variables].

OBJECTIVE: To study the relationship between microsatellite instability (MSI) and clinicopathological variables in nephroblastoma. METHODS: 2 microsatellite repeat sequences AR (chromosome X), UT762(chromosome 21) were examined in normal and tumor pairs from 50 nephroblastoma patients by PCR and denatured polyacrylamide gel electrophoresis. RESULTS: The MSI positive for AR and UT loci were 14/50 and 10/50 respectively in nephroblastoma. MSI positive for both AR and UT occurred in 2 cases. According to NTWS-III categorization, stage I & II belong to early stage and stage III & IV belong to late stage, the MSI for this series were 16/38 and 6/12 for early and late stages. According to the NWTI-II categorization, the MSI of this series for favorable and non-favorable histology were 71% and 33% respectively. CONCLUSIONS: Analysis of MSI may have some significance in discriminating the malignant status of nephroblastoma.

Chromosomes, Human, Pair 21↗

PubMed1997

[Expression of p53 in nephroblastoma and neuroblastoma].

We studed on the expression of p53 in 48 nephroblastomas and 32 neuroblastomas wit, immunohistochemical method of avidinbiotinperoxidase complex. 11 of the nephroblastomas were positive and all neuroblastomas were negative. Statistical analysis revealed that abnormal expression of p53 was significantly correlated with NWTS--II classification, NWTS--III clinical pathology stages and metastasis of nephroblastoma. The results indicate that abnormal expression of p53 is not only involved in the development, but also in the differentiation and metastasis of nephroblastoma. Therefore, detection of p53 expression may have significant clinical importance in the evaluation of prognosis of nephroblastoma. However, the absence of expression of p53 in neuroblastomas suggests that the inactivation of this gene does not play a significant role in the tumor's occurring and progression.

Child↗

PubMed1996

Quantitative trait locus mapping of human blood pressure to a genetic region at or near the lipoprotein lipase gene locus on chromosome 8p22.

Resistance to insulin-mediated glucose disposal is a common finding in patients with non-insulin-dependent diabetes mellitus (NIDDM), as well as in nondiabetic individuals with hypertension. In an effort to identify the generic loci responsible for variations in blood pressure in individuals at increased risk of insulin resistance, we studied the distribution of blood pressure in 48 Taiwanese families with NIDDM and conducted quantitative sib-pair linkage analysis with candidate loci for insulin resistance, lipid metabolism, and blood pressure control. We found no evidence for linkage of the angiotensin converting enzyme locus on chromosome 17, nor the angiotensinogen and renin loci on chromosome 1, with either systolic or diastolic blood pressures. In contrast, we obtained significant evidence for linkage or systolic blood pressure, but not diastolic blood pressure, to a genetic region at or near the lipoprotein lipase (LPL) locus on the short arm of chromosome 8 (P = 0.002, n = 125 sib-pairs, for the haplotype generated from two simple sequence repeat markers within the LPL gene). Further strengthening this linkage observation, two flanking marker loci for LPL locus, D8S261 (9 cM telomeric to LPL locus) and D8S282 (3 cM centromeric to LPL locus), also showed evidence for linkage with systolic blood pressure (P = 0.02 and 0.0002 for D8S261 and D8S282, respectively). Two additional centromeric markers (D8S133, 5 cM from LPL locus, and NEFL, 11 cM from LPL locus) yielded significant P values of 0.01 and 0.001, respectively. Allelic variation around the LPL gene locus accounted for as much as 52-73% of the total interindividual variation in systolic blood pressure levels in this data set. Thus, we have identified a genetic locus at or near the LPL gene locus which contributes to the variation of systolic blood pressure levels in nondiabetic family members at high risk for insulin resistance and NIDDM.

Adult↗

PubMed1996

AP1 enhances polyomavirus DNA replication by promoting T-antigen-mediated unwinding of DNA.

An early step in the initiation of polyomavirus DNA replication is viral large-T-antigen-mediated unwinding of the origin. We report that components of the AP1 transcription factor, Fos and Jun, interact with T antigen in vitro to enhance unwinding of the viral origin. This provides a biochemical basis for the capacity of AP1 to activate viral DNA replication in vivo.

Antigens, Viral, Tumor↗

PubMed1996

Short-term recombinant human growth hormone treatment increases growth rate in achondroplasia.

To investigate the effect of recombinant hGH treatment on the growth rate and proportion of individuals with achondroplasia and hypochondroplasia, we studied 15 individuals with these common skeletal dysplasias. The study lasted 24 months and included 6 months of observation, 12 months of hGH therapy (0.04 mg/kg.day), and 6 months of posttreatment growth rate determination. In achondroplasia, the mean growth rate during the hGH treatment (5.3 +/- 1.6 cm) was significantly increased compared with that during the pretreatment (4.0 +/- 1.0 cm.yr, P < 0.01)) and posttreatment periods (3.1 +/- 1.3 cm; P < 0.001). In the 4 children with hypochondroplasia, the growth rate during hGH treatment was 7.0 +/- 2.4 cm/yr and 4.9 +/- 1.5 cm/yr during the pre- and posttreatment periods, respectively. In achondroplasia, there was a significant increase in growth rate of only the lower segment (from 1.1 +/- 1.6 cm/yr to 3 +/- 1.2 cm/yr, P < 0.02). There was no significant acceleration in the growth of the upper segment and of the scanogram measurements of the long bones. No untoward effects were noted. Recombinant hGH increases short-term growth velocity in children with achondroplasia/hypochondroplasia. Unexpectedly, this treatment does not seem to have a lesser effect on limbs than on trunk growth rate and, therefore, during 1 yr of treatment, does not increase body disproportion.

Achondroplasia↗

PubMed1996

Erythropoietin stimulates phosphorylation of eIF-4E and identification of a 37-kD phosphoprotein that binds mRNA caps in erythroblasts.

To explore the mechanism of erythropoietin action on differentiation of erythroblasts, we have examined its effect on regulating phosphorylation of the 25-kD mRNA cap binding protein (eIF-4E). Erythroblasts from the spleens of mice infected with the anemia strain of Friend virus (FVA cells) were studied. Erythropoietin stimulated phosphorylation of eIF-4E in FVA cells within 30 minutes, and this effect was maximal at 60 minutes. Phosphoamino acid analysis and tryptic phosphopeptide map analysis of eIF-4E isolated from both control and erythropoietin-treated cells identified a predominant phosphopeptide containing phosphoserine. However, when cells were incubated with 1 muM okadaic acid, eIF-4E was phosphorylated on both serine and threonine residues and three additional tryptic phosphopeptides were detected. We also identified a 37-kD phosphoprotein (pp37) that bound specifically to the m7GTP cap structure and coimmunoprecipitated with eIF-kD protein was phosphorylated on both serine and threonine residues. These results indicate that phosphorylation of eIF-4E is a target in erythropoietin-initiated signal transduction events and that this phosphorylation precedes observable effects of erythropoietin on macromolecular biosynthesis. Although of pp37 remains to be studied, it may represent a developmentally regulated mRNA cap binding protein.

Anemia↗