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H Cui

Publications and source records attributed to H Cui.

At least 73 records · Page 4Linked to original sources
PubMed1998

Loss of imprinting in disease progression in chronic myelogenous leukemia.

The pathophysiologic role of the Philadelphia chromosome translocation in chronic myelogenous leukemia (CML) has been known for nearly 20 years. However, the most significant morbidity and mortality in CML are caused by progression to blast crisis, about which comparatively little is known at the molecular level. Genomic imprinting is a chromosomal modification leading to parental-origin-specific gene expression in somatic cells. Recently, we and others have described loss of imprinting (LOI) of the insulin-like growth factor-II gene (IGF2), leading to biallelic rather than monoallelic expression in a wide variety of solid tumors. We have now examined the imprinting status of IGF2 in samples from CML patients in stable phase, accelerated phase, and blast crisis. Five of six stable-phase patients showed normal imprinting, but LOI was found in all six cases of advanced disease (three accelerated phase, three blast crisis), which was statistically highly significant (P < .01). Thus, LOI represents a novel type of genetic alteration in CML that appears to be specifically associated with disease progression.

Blast Crisis↗
PubMed1998

[Detection of hemophilia A carriers by PCR analysis of hind III polymorphism in the factor VIII gene].

OBJECTIVE: To explore a scheme of using PCR analysis in the detection of carriers of Hind III polymorphism of factor VIII gene of hemophilia A. METHODS: Implicating intron 19 of the factor VIII gene of 6 patients with the hemophilia A and 207 unrelated X-chromosomes were amplified by PCR and were analysed by means of Amp-RFLPs of Hind III. RESULTS: The incidence of the polymorphic Hind III sites in the given population was found to be 0.29. The frequence of the Hind III heterozygotes in women calculated according to Hardy-Weinberg equation was 0.41, which proved to be informative enough for carrier detection and prenatal diagnosis of hemophilia A. 2 out of 6 families (33%)examined in this study were informative. CONCLUSION: The new scheme proved to be effective for hemophilia A carrier detection and prenatal diagnosis.

Deoxyribonuclease HindIII↗
PubMed1998

Potassium chloride inhibits proliferation of cerebellar granule neuron progenitors.

CNS neurogenesis involves a critical transition where neuronal progenitors exit the cell cycle and initiate terminal differentiation. Recent experiments have suggested that depolarization inhibits DNA synthesis in cortical progenitors. Depolarization of proliferating neuronal progenitors may thus activate mechanisms that prevent proliferation and allow the initiation of terminal differentiation. We present evidence that depolarizing concentrations of KCl (25-50 mM) reduce proliferation of developing postnatal cerebellar granule cells in culture. These studies show that KCl antagonizes the mitogenic response of granule cells to insulin-like growth factor-I (IGF-I) and that this reduction in proliferating cells is not the result of a selective cell death. We also examined the differentiation of granule cell cultures using Brn-5 expression as an early differentiation marker. In vivo Brn-5 expression occurs soon after developing granule cells exit the cell cycle and begin their final differentiation. In control cultures and cultures treated with high concentrations of KCl Brn-5 expression increased over 24-48 h of culture. Our results suggest depolarizing concentrations of KCl antagonize proliferation of cerebellar granule neuron progenitors however allow their continued differentiation.

Animals↗
PubMed1998

BDNF accelerates gene expression in cultured cerebellar granule neurons.

This study reports that in purified cultures of postnatal cerebellar granule cells, BDNF significantly accelerated GABAA receptor alpha 6 subunit (GABAA alpha 6) mRNA expression, a marker for terminally differentiated cerebellar granule neurons, and also accelerated p21cip1 expression. p21cip1 is a general cyclin-dependent kinase (Cdk) inhibitor that can inhibit progression through the cell cycle. Alternatively, the expression of p27kip1, another Cdk inhibitor closely related to p21cip1, is not modified by BDNF. In cultured granule cells, the increase in p21cip1 expression induced by BDNF occurred after dividing granule cells had left the cell cycle and thus was not required to direct granule neuron precursors out of the cell cycle. p21cip1 may have an alterative function during granule neuron terminal differentiation, separate from its ability to regulate cell cycle exit. This report shows that, in vitro, BDNF accelerates granule cell gene expression and may thus modulate cerebellar granule cell differentiation.

Animals↗
PubMed1998

Hypervariable allelic expression patterns of the imprinted IGF2 gene in tumor cells.

The IGF2 gene, which encodes a growth factor, is subject to genomic imprinting. The frequently observed loss of IGF2 imprinting in a variety of tumors has been suggested to contribute to neoplasia. Since these reports have not documented the imprinting status of IGF2 at the cellular level, it cannot be excluded that the imprinting status might vary within the tumor. The possibility that loss of IGF2 imprinting in neoplastic cells reflects random imprinting patterns, was therefore addressed. We show here that individual cell populations of the JEG-3 choriocarcinoma cell line display heterogenous imprinting patterns of both IGF2 and H19. In addition, a lack of correlation between IGF2 and H19 imprinting status suggests that any regional parental imprint has been functionally lost. This notion is reinforced by the observation that JEG-3 cell subclones display a range of promoter-specific IGF2 allele usage. Moreover, we observed that the imprinting status of H19 and IGF2 were differentially modulated in JEG-3-derived tumors generated in nude mice. The results suggest that allele-specific expression of IGF2 operates in the absence of a parental imprint. Finally, our observations urge caution with respect to the general interpretation of biallelic expression as 'loss of imprinting'.

Alleles↗
PubMed1998

Methylmercury antagonizes the survival-promoting activity of insulin-like growth factor on developing cerebellar granule neurons.

Methylmercury (MeHg), a widely distributed environmental toxicant, has a profound effect on the developing central nervous system. Human exposure to MeHg in utero has led to severe neurological abnormalities in children, including cognitive and motor dysfunction. The abnormalities appear to result from death of neurons and altered cytoarchitecture in the developing CNS. Death of cerebellar granule neurons occurs following both adult and in utero exposure to MeHg, indicating the vulnerability of these cells to the toxic action of MeHg. The studies reported here use purified cultures of developing mouse cerebellar granule neurons to evaluate whether MeHg directly acts on these developing neurons to inhibit their survival. These experiments show that, in purified cultures of cerebellar granule neurons maintained in medium containing insulin-like growth factor I (IGF-I) as the only added trophic factor, low micromolar concentrations of MeHg inhibit granule neuron survival. The reduction in survival produced by MeHg can be partially reversed by increasing the concentration of IGF-I, suggesting an antagonism between MeHg and IGF-I. Inhibition of phosphoinositide 3-kinase (PI3-K), an intracellular mediator of IGF-I's survival promoting action, can synergistically enhance MeHg's effect on survival. Further studies indicate that MeHg's inhibition of survival involves apoptotic death of granule neurons. This apoptosis appears to require activation of gene transcription and may involve an increase in expression of the immediate early transcription factor c-Jun. These studies suggest that MeHg can act on developing granule neurons to increase the expression of c-Jun and antagonize IGF-I's survival promoting activity.

Animals↗
PubMed1998

Loss of imprinting in normal tissue of colorectal cancer patients with microsatellite instability.

Loss of imprinting (LOI) is an epigenetic alteration of some cancers involving loss of parental origin-specific expression of imprinted genes. We observed LOI of the insulin-like growth factor-II gene in twelve of twenty-seven informative colorectal cancer patients (44%), as well as in the matched normal colonic mucosa of the patients with LOI in their cancers, and in peripheral blood samples of four patients. Ten of eleven cancers (91%) with microsatellite instability showed LOI, compared with only two of sixteen tumors (12%) without microsatellite instability (P < 0.001). Control patients without cancer showed LOI in colonic mucosa of only two of sixteen cases (12%, P < 0.001) and two of fifteen blood samples (13%, P < 0.001). These data suggest that LOI in tumor and normal tissue identifies most colorectal cancer patients with microsatellite instability in their tumors, and that LO! may identify an important subset of the population with cancer or at risk of developing cancer.

Colon↗
PubMed1998

Effects of N-methyl berbamine on delayed outward potassium current in isolated rat hepatocytes.

AIM: To study the effects of N-methyl berbamine (NMB) on the delayed outward potassium currents (Ik) in isolated rat hepatocytes. METHODS: With patch-clamp techniques and whole-cell recording method, holding potential -50 mV, command potential +30 to +140 mV, duration 900 ms. RESULTS: NMB reduced Ik in a concentration-dependent manner. When the concentrations of NMB were 20, 50, 400 nmol.L-1 and 50 mumol.L-1, the amplitude values of Ik were decreased to 3.6 +/- 0.4 (P > 0.05), 2.1 +/- 1.6 (P > 0.05), 3.7 +/- 1.6 (P < 0.05), 2.3 +/- 1.3 nA (P < 0.01) from 4.4 +/- 1.0 (n = 4), 2.5 +/- 1.8 (n = 4), 5.8 +/- 2.1 (n = 5), 4.6 +/- 1.3 (n = 6) nA of control, respectively. The inhibitory rates were 10%, 15%, 37%, and 51%, respectively. CONCLUSION: NMB was a K+ channel inhibitor.

Alkaloids↗
PubMed1998

[Effect of zinc on cadmium-induced fetal damage].

The effect of different zinc level on cadmium (Cd)-induced fetal damage was studied in pregnant rats. Seventy Waster rats were divided into five groups: zinc 30 mg/kg diet, zinc deficiency (3.2 mg/kg), zinc deficiency with Cd 2.0 mg/kg, zinc 30 mg with Cd 2.0 mg and zinc 227 mg with Cd 2.0 mg. The pregnant rats were killed on the 20 th day of gestation. Blood samples were taken and all the fetuses were examined. The result showed that zinc deficiency could induce fetus absorption or malformation, which were increased significantly in zinc dificient plus Cd rats. Fetuses can be protected if high dose of zinc (227 mg/kg) is given. The occurrence of fetus absorption and malformation decreased and survival increased in compared with the nonsupplemented group. The results suggested that fetal malformations can be induced by zinc deficiency, and being worse when Cd is added. Zinc supplementation can offset to some extent the toxic effect of Cd.

Abnormalities, Drug-Induced↗
PubMed1998

[Effects of noradrenaline on delayed outward potassium current in isolated rat hepatocytes].

Heretofore no reports are available on the outward potassium currents in rat hepatocytes. Using whole-cell patch clamp technique, the effects of noradrenaline and other reagents on the delayed outward potassium current (IK) in isolated rat hepatocytes were investigated. The experimental results showed that the magnitude of IK was 2.85 +/- 1.21 nA at a command potential of +140 mV from a holding potential of -50 mV. Noradrenaline decreased IK distinctly. Isoprenaline and acetylcholine showed no effect on IK in isolated rat hepatocytes.

Adrenergic alpha-Agonists↗
PubMed1998

[Clinical effect of tianma-cuzhi granules on senile vascular dementia].

OBJECTIVE: To assess the clinical efficacy of Tianma-cuzhi Granules (TMC) in treating senile vascular dementia(VaD) of the "sthenia of liver-yang" type. METHOD: TMC were given to thirty VaD patients three times a day of 0.5 g/bageach. The treatment course was one month and the patients finished two consecutive courses. RESULTS: TMC could markedly increase the mini-mental state examination (MMSE) and Hamilton depression scale(HDS) marks of VaD patients, and also contribute to improving certain indexes especially in abnormal cases. CONCLUSION: TMC have certain effects on senile VaD.

Aged↗
PubMed1998

[Determination of content of radix Paeoniae Rubar(Chishao)801 in rabbit's plasma by HPLC].

A HPLC method was used to determine the content of Radix Paeoniae Rubar (Chishao)801 in rabbit's plasma, using Nucleosil C18 column, methanol, water and glacial acetic acid (48:50:2) as mobile phase ethye 4-hydroxybenzoate as internal standard, and UV-detector(lambda max: 275 nm, AUFS: 0.02). The average recovery was 96.70%(C: 2.5 micrograms/ml) and 98.86%(C: 5 micrograms/ml) respectively. The lowest determination limit was 0.1 microgram/ml. The method is simple, accurate, sensitive and reliable.

Animals↗
PubMed1998

[The comparison on growth rate and photopigments of filaments of Spirulina platensis strain Z with different morphology].

The line-shaped filaments Sp-Z(L) were isolated and cultured from Spirulina platensis Sp-Z. The growth rate of Sp-Z(L) was only 64% as much as that of Sp-Z when the light intensity was 4000 Lux. The contents (x 10(-3) g/g dry weight) of chlorophylls, carotenoids and phycobilins of Sp-Z(L) and Sp-Z were 20.6, 0.343, 5.00 and 24.1 0.297, 4.46, respectively. Moreover, as to the absorption spectra of the three photopigments of Sp-Z(L), red shifts were observed. Therefore, after the spiral Sp-Z breeded or changed into Sp-Z(L), The contents of carotenoids and phycobilins raised 23% and 12%, respectively, but the contents of chlorophylls dropped 14.5%, and the growth rate dropped 36% too. The results probably showed that the decrease of chlorophylls was one of the main reasons that caused the remarkable decrease of the growth rate of Sp-Z(L).

Carotenoids↗
PubMed1997

Inactivation of H19, an imprinted and putative tumor repressor gene, is a preneoplastic event during Wilms' tumorigenesis.

Genetic evidence shows that the parent of origin-dependent expression patterns of the Igf2 and H19 genes is coordinated in mouse, such that H19 controls the activity of Igf2 in cis. Equally compelling evidence for a similar situation in humans is absent, although the frequently observed activation of the maternal IGF2 allele (ie., loss of imprinting) in Wilms' tumors has been attributed to the silencing of the maternal H19 locus. We show here that loss of H19 activity is generally a preneoplastic event, which may be linked with an overgrowth lesion that has been proposed to be permissive for tumor formation. Although our results document one instance in which a postneoplastic loss of H19 activity correlates with loss of IGF2 imprinting at the cellular level, it appears that inactivation of H19 is more generally independent of loss of imprinting of IGF2, at least in our specimens. Our results imply that inactivation of H19 correlates with blastema overgrowth and can be independent of a regulatory role with respect to IGF2 imprinting status in cis.

Alleles↗
PubMed1997

Expression of the POU transcription factor Brn-5 inhibits proliferation of NG108-15 cells.

The POU domain transcription factors are a subgroup of homeodomain proteins that appears to control cellular phenotypes. The expression of the POU protein Brn-5 occurs selectively in postmitotic CNS neurons. Ectopic expression of Brn-5 in dividing NG108-15 cells reduces the level of RNA encoding the proliferating cell nuclear antigen (PCNA). This ectopic expression also inhibits DNA synthesis as measured by the incorporation of bromodeoxyuridine (BrdU). Thus, Brn-5 may inhibit the continued proliferation of these cells. A potential function of Brn-5 may be to suppress the action of proliferative signals in postmitotic neurons and thus prevents them from reentering the cell cycle.

Cell Differentiation↗
PubMed1997

Proteasome regulation of activation-induced T cell death.

Lactacystin, a microbial metabolite that inhibits protease activity only in the proteasome, was used to study the role of the proteasome in the activation-induced cell death (AICD) of T cells. Lactacystin induces DNA fragmentation and apoptosis in a T cell hybridoma (DO.11. 10) in a dose-dependent manner. Between 1 and 10 microM, the mildly cytotoxic lactacystin inhibited the AICD of DO.11.10 cells cultured in anti-CD3-coated wells. Degradation of IkappaBbeta and the translocation of the NF-kappaB (p50/RelA) into the nucleus, which occurred at 1.5 hr after anti-CD3 activation, were inhibited by lactacystin. Lactacystin did not inhibit the expression of nuclear transcription factor Oct-1. The activation-induced expression of the immediate-early gene, Nur77, and the T cell death genes, CD95 (Fas) and CD95 ligand (FasL), were inhibited. Functional expression of FasL cytotoxicity and the increase of cell surface Fas were also inhibited. Lactacystin must be added within 2 hr of activation to efficiently block AICD. In addition, lactacystin failed to inhibit the killing of DO.11.10 by FasL-expressing allo-specific cytotoxic effector cells. These observations strongly suggest a direct link between the proteasome-dependent degradation of IkappaBbeta and the AICD that occurs through activation of the FasL gene and up-regulation of the Fas gene.

Acetylcysteine↗
PubMed1997

Proteasome regulation of Fas ligand cytotoxicity.

The role of NF-kappa B in regulating FasL-mediated cytotoxicity was investigated by using lactacystin. Lactacystin is a microbial metabolite known to inhibit only the protease activity of the proteasome, which is required for NF-kappa B translocation. When activated by immobilized anti-CD3 monoclonal antibody, hybridoma T cells (5D5) degraded I kappa B beta, translocated NF-kappa B into the nucleus, transcribed immediate-early genes and the Fas ligand (FasL) gene, and expressed FasL-mediated cytotoxicity. Lactacystin strongly blocked I kappa B beta degradation and the translocation of NF-kappa B (p50/RelA heterodimer), but had little effect on the expression of the transcription factors, Oct-1 and AP-1. Moreover, lactacystin did not inhibit the nuclear translocation of NF-ATp whereas cyclosporin A inhibited the translocation of both NF-kappa B and NF-ATp. The expression of c-myc and nur77, two immediate-early genes implicated in FasL gene activation, was blocked by lactacystin. Subsequently, the expression of FasL gene and FasL-mediated cytotoxicity was inhibited. LLnL, a well-known peptide aldehyde which inhibits the protease activities of the proteasome and cysteine proteases, also inhibited NF-kappa B translocation and FasL-mediated cytotoxicity. However, these events were not inhibited by the highly specific cysteine protease inhibitor E64. These observations provide further evidence that FasL cytotoxicity is regulated by the proteasome. Furthermore, lactacystin must be added early in order to efficiently inhibit the induction of FasL cytotoxicity, indicating that the early events are critical for FasL gene activation. Our study integrates the proteasome-dependent I kappa B degradation and NF-kappa B translocation into a T cell activation cascade which results in FasL gene activation and the expression of FasL-mediated cytotoxicity.

Acetylcysteine↗