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Z Pang

Publications and source records attributed to Z Pang.

At least 19 recordsLinked to original sources
PubMed2001

Enhanced excitatory synaptic transmission in spiny neurons of rat striatum after unilateral dopamine denervation.

The synaptic transmission and intrinsic membrane properties of spiny neurons in rat neostriatum were studied after unilateral dopamine depletion using in vivo intracellular recording and staining techniques. Two to four weeks after dopamine denervation, the spontaneous firing rate of spiny neurons increased and the spontaneous membrane potential fluctuation stayed at a more depolarized state for longer periods of time. The amplitude of cortically evoked initial excitatory postsynaptic potentials increased and a late excitatory postsynaptic potential that was occasionally found in control neurons was elicited from 23% of spiny neurons after dopamine denervation. No significant changes in intrinsic membrane properties of spiny neurons were observed after dopamine denervation. These results suggest that dopamine inhibits excitatory synaptic transmission of spiny neurons in naïve animals.

Animals↗
PubMed2001

Differential changes of synaptic transmission in spiny neurons of rat neostriatum following transient forebrain ischemia.

Spiny neurons in neostriatum are vulnerable to cerebral ischemia. To reveal the mechanisms underlying the postischemic neuronal damage, the spontaneous activities, evoked postsynaptic potentials and membrane properties of spiny neurons in rat neostriatum were compared before and after transient forebrain ischemia using intracellular recording and staining techniques in vivo. In control animals the membrane properties of spiny neurons were about the same between the left and right neostriatum but the inhibitory synaptic transmission was stronger in the left striatum. After severe ischemia, the spontaneous firing and membrane potential fluctuation of spiny neurons dramatically reduced. The cortically evoked initial excitatory postsynaptic potentials were suppressed after ischemia indicated by the increase of stimulus threshold and the rise time of these components. The paired-pulse facilitation test indicated that such suppression might involve presynaptic mechanisms. The inhibitory postsynaptic potentials in spiny neurons were completely abolished after ischemia and never returned to the control levels. A late depolarizing postsynaptic potential that was elicited from approximately 5% of the control neurons by cortical stimulation could be evoked from approximately 30% of the neurons in the left striatum and approximately 50% in the right striatum after ischemia. The late depolarizing postsynaptic potential could not be induced after acute thalamic transection. The intrinsic excitability of spiny neurons was suppressed after ischemia evidenced by the significant increase of spike threshold and rheobase as well as the decrease of repetitive firing rate following ischemia. The membrane input resistance and time constant increased within 6 h following ischemia and the amplitude of fast afterhyperpolarization significantly increased after ischemia. These results indicate the depression of excitatory monosynaptic transmission, inhibitory synaptic transmission and excitability of spiny neurons after transient forebrain ischemia whereas the excitatory polysynaptic transmission in neostriatum was potentiated. The facilitation of excitatory polysynaptic transmission is stronger in the right neostriatum than in the left neostriatum after ischemia. The suppression of inhibitory component and the facilitation of excitatory polysynaptic transmission may contribute to the pathogenesis of neuronal injury in neostriatum after transient cerebral ischemia.

Action Potentials↗
PubMed2001

[In vitro modulation of the invasive and metastatic potentials of human hepatocellular carcinoma by interlukin-2].

OBJECTIVE: To investigate the effects of interlukin-2 (IL-2) on the in vitro invasiveness and the expression of several cell surface antigens related to invasive and metastatic potentials of human hepatocellular carcinoma (HCC) QGY-7701 cell line. METHODS: QGY-7701 cells were incubated with high concentration of IL-2 or low concentration of IL-2 in different time. The expression of ICAM-1, CD(44) and HLA-I of the tumor cells was determined by fluorescence-activated cell sorter (FACS) analysis The tumor cell binding affinity to extracellular matrix components was measured by cell attachment assay. The degree of homotypic aggregation was quantified by cell aggregation assay. RESULTS: IL-2 treatment exhibited enhanced expression of ICAM-1 (from 8.3% to 20.5% after high concentration of IL-2 treatment and 17.3% after low concentration of IL-2 treatment) and HLA-I (from 9.8% to 25.4% and 22.1%, respectively after high and low concentration of IL-2 treatment), suppression of CD(44) (from 26.4% to 12.5% and 11.6%, respectively) on HCC cell line and decreased binding affinity to type IV collagen (from 23.5% to 12.4%, 32.3% to 13.8%, 45.7% to 19.6% at 20 min, 40 min and 60 min, respectively after high concentration of IL-2 treatment, and 9.6%, 12.5% and 17.9%, respectively after low concentration of IL-2 treatment) and fibronectin (from 18.6% to 14.1%, 31.2% to 18.4%, 44.5% to 20.5% at 20 min, 40 min and 60 min, respectively after high concentration of IL-2 treatment, and 14.6%, 17.1% and 18.9%, respectively after low concentration of IL-2 treatment) and the degree of homotypic aggregation (from 58.3% to 26.5%, 85.4% to 37.6%, 88.6% to 42.3% at 20 min, 40 min and 60 min, respectively after high concentration of IL-2 treatment, and 25.0%, 36.4% and 42.6%, respectively after low concentration of IL-2 treatment)of HCC cells. CONCLUSIONS: IL-2 may directly alter tumor properties associated with invasive and metastatic phenotypes of HCC cells, and can inhibit the invasive and metastatic potentials of HCC cells.

Carcinoma, Hepatocellular↗
PubMed2001

[Purification and characterization of 2-carbonyl reductase from marine bacteria Bacillus sp].

ANADPH-dependent 2-Oxoaldehyde reductase was isolated and purified from a marine bacteria Bacillus sp. The purification procedure involved ammonium sulfate fractionation and Q Sepharose FF, Hydroxyapatite, Sephadex G-100 column chromatographies. The specific activity of the purified enzyme was increased by 141.1 folds over crude extract and the recovery yield was 11.4%. 2-Oxoaldehyde compounds were found to be speciall good substrates. The optimum pH of the enzyme activity was 6.2-6.6. The Km coefficient for 3-deoxyglucosone was 2.5 mmol/L. The molecular weight of the enzyme was estimated to be 33 kD The enzyme activity is stable below 30 degrees C and pH 5.0-8.0. EDTA, beta-mercaptoethanol and dithiothreitol enhanced the enzyme activity. On the other hand, the enzyme activity was partially lost by idoacetic acid or N-ethylmaleimide.

Alcohol Oxidoreductases↗
PubMed2000

Cbln3, a novel member of the precerebellin family that binds specifically to Cbln1.

Precerebellin (Cbln1) is the precursor of the brain-specific hexadecapeptide cerebellin. Although cerebellin has properties of a conventional neuropeptide, its function is controversial because Cbln1 has structural features characteristic of circulating atypical collagens. Cbln1 is related to the three subunits of the complement C1q complex. Therefore, we hypothesized that Cbln1 participated in analogous heteromeric complexes with precerebellin-related proteins. Using LexA-Cbln1 as bait in a yeast two-hybrid screen, we isolated a cDNA encoding a novel Cbln1-related protein, designated Cbln3. The gene encoding cbln3 had the same intron-exon structure as cbln1 but mapped to a different mouse chromosome (14). The deduced amino acid sequence of Cbln3 was 55% identical to Cbln1 and also contained a C1q signature domain and signal sequence for secretion. In addition to binding avidly to Cbln3, Cbln1 also formed homomeric complexes. In contrast, Cbln3 homomeric association was weak. These interactions exhibited specificity because C1qB bound to neither Cbln1 nor Cbln3. Like cbln1, cbln3 was expressed in the cerebellum and dorsal cochlear nucleus in which it was detected in granule neurons. Because Cbln1 and Cbln3 are coexpressed in the brain and interact avidly, they may function as a secreted heteromeric complex in vivo.

Aging↗
PubMed2000

Phosphorescent oxygen sensors utilizing sulfur-nitrogen-phosphorous polymer matrixes: synthesis, characterization, and evaluation of poly(thionylphosphazene)-b-poly(tetrahydrofuran) block copolymers

We examine the use of thionylphosphazene-based block copolymers as matrixes for oxygen sensor applications. Poly(aminothionylphosphazene)-b-poly(tetrahydrofuran) (PATPy-PTHFx) block copolymers were prepared via reaction of ring-opened poly(chlorothionylphosphazene) with THF and subsequently with excess n-butylamine (to form PBATPy-PTHFx) or methylamine (to form PMATPy-PTHFx). The block copolymers were characterized by NMR, gel permeation chromatography, and differential scanning calorimetry. Films of PBATPy-PTHFx block copolymers containing platinum octaethylporphyrin or [Ru(dpp)3]Cl2 (dpp = 4,7-diphenyl-1,10-phenanthroline) as the oxygen-sensitive chromophore were prepared, and time-scan experiments were carried out to determine the diffusion coefficients, Do2, and solubilities, So2, of oxygen therein. Despite microphase separation, the data fit well to a simple Fick's law description of oxygen diffusion and gave Do2 values smaller than that for the n-butylamino-substituted PBATP635. For films freshly annealed above the melting point of PTHFx, the Do2 values were 35-50% (dye-dependent) larger than after aging 3 days at room temperature. Films with [Ru(dpp)3]Cl2 as the dye were evaluated as media for phosphorescent pressure-sensing. The dye-containing polymer films exhibit linear Stern-Volmer-like plots, even at high dye concentrations, as well as good photostability, and significantly higher sensitivity to oxygen quenching than simple mixtures of the analogous homopolymers.

Journal Article↗
PubMed2000

The effect of coriaria lactone on NMDA receptor mediated currents in rat hippocampal CA1 neurons.

To investigate the exact mechanism of epileptogenesis induced by coriaria lactone (CL), the effect of CL on NMDA receptor mediated current (IAsp) in rat hippocampal CA1 neurons was investigated by using nystatin perforated whole-cell patch clamp. 10(-6)-10(-4) mol/L Asp acted on NMDA receptors and elicited an inward current (IAsp) at a holding potential (VH) of -40 mV in presence of 10(-6) mol/L glycine and absence of Mg2+ extracellularly. CL enhanced NMDA receptor mediated current induced by Asp, but had no effect on threshold concentration, EC50, Hill coefficient as well as maximal-effect concentration and reversal potential of IAsp. The effect had no relationship with holding potential. These results showed that CL could enhance NMDA receptor mediated current to increase [Ca2+]i of neurons by acting on Gly site, thereby inducing epilepsy.

Animals↗
PubMed2000

[A histopathologic and immunohistochemical study of 68 cases of hemangioblastoma].

The aim of this study was to evaluate the histologic characteristics of hemangioblastoma (HB) and investigate the histogenesis of its stromal cells. Sixty-eight cases of hemangioblastoma were studied by light microscopy and thirty-three cases were examined by immunohistochemical stainning. Forty-eight of the 68 patients were males and 20 were females. The average age was 37. Fifty-two cases (76.6%) had been present for two months to one year before the diagnosis was made. Sixty cases (88.2%) arose in the cerebellum. Fifty cases (73.5%) appeared as cystic nodules. Histologically, the 68 cases of HB were further categorized into three subtypes: typical (30 cases), cellular (21 cases) and reticular (17 cases). In 33 cases, the stromal cell were positive for NSE, but negative for F-VIII, UEA-1, GFAP and EMA. In summary, there are three essential histologic categories of hemangioblastoma, and its stromal cells may well have the characters of neuroendocrine differentiation.

Adolescent↗
PubMed1998

6-Hydroxydopamine injections into the nigrostriatal pathway attenuate striatal malonate and 3-nitropropionic acid lesions.

The mitochondrial inhibitors malonate and 3-nitropropionic (3NP) acid are potent neurotoxins in vivo. Administration of these compounds results in neuronal loss similar to that seen in Huntington's disease. Although the mechanism of cell death produced by these compounds likely involves activation of N-methyl-D-aspartate receptors, it remains unclear why the striatum demonstrates regional susceptibility to the toxicity of these and other mitochondrial poisons. We hypothesized that dopamine, a weak neurotoxin that occurs in high concentrations in the striatum, may contribute to the neuronal damage caused by mitochondrial inhibition. We investigated whether depletion of striatal dopamine using the catecholaminergic toxin 6-hydroxydopamine would attenuate lesions induced by mitochondrial inhibition. We found that dopamine depletion reduced significantly the extent of histological damage in the striatum elicited by both intraparenchymal injections of 0.8 micromol malonate and 20 mg/kg systemic administration of 3NP. These data suggest that dopamine or one of its metabolites may contribute to mitochondrial toxin-induced cell death.

Animals↗
PubMed1998

[Research on risk factors of 5 types of viral hepatities among population with high risk behaviors].

Epidemiological and serological survey on five types of viral hepatities (hepatitis A-hepatitis E) was conducted from October 1994 to December 1996 among 119 labourers returned from abroad, including 55 female prostitutes, 86 medical workers, 88 STD patients and 88 paid blood donors. HAV infection rates for all of the 5 groups were above 83%. HBV infection rate showed significantly different (chi 2 = 3.86, P < 0.05) between medical workers (53.49%) and the control group (30.43%). A significant difference (chi 2 = 5.36, P < 0.05) between HBV infection among prostitutes (52.73%) and control group (26.67%) was also noticed. In all the five groups, none was found to be anti-HDV positive. The HEV infection rates for the medical workers, prostitutes, blood donors, returned labourers and STD patients were 1.16%, 3.64%, 2.27%, 5.88% and 6.82%, whereas the anti-HCV positive rates were 1.16%, 3.64%, 0.00%, 0.00% and 1.14%, among them respectively.

Adult↗
PubMed1998

Oxidative and malondialdehyde modification of low-density lipoprotein: a comparative study of binding and degradation by macrophages and endothelial cells.

Comparative study of oxidatively modified low-density lipoprotein (Ox-LDL) and malondialdehyde-modified low-density lipoprotein (MDA-LDL) is important for further understanding the biological properties of Ox-LDL, such as its toxic effects, immunogenicity and multiplicity of scavenger receptor binding. In this study, the characteristics of Ox-LDL and MDA-LDL binding and degradation were compared. The results show that when their degree of modification (as determined by relative electrophoretic mobility) was similar, the binding and degradation of Ox-LDL by the macrophage cell line P388D1 were greater than those of MDA-LDL. The binding and degradation of Ox-LDL by macrophages and human umbilical vein endothelial cells increased with the degree of modification. In addition, Ox-LDL or MDA-LDL could competitively inhibit binding of labelled Ox-LDL or labelled MDA-LDL to their respective macrophage receptors, and could partially inhibit each other.

Animals↗
PubMed1997

Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid: acute excitotoxic necrosis and delayed apoptosis.

Impaired energy metabolism may play an important role in neuronal cell death after brain ischemia and in late-onset neurodegenerative diseases. Both excitotoxic necrosis and apoptosis have been implicated in cell death induced by metabolic impairment. However, the factors that determine whether cells undergo apoptosis or necrosis are not known. In the present study, metabolic impairment was induced by 3-nitropropionic acid (3-NP), a suicide inhibitor of succinate dehydrogenase. Treatment of cultured rat hippocampal neurons with 3-NP resulted in two types of cell death with distinct morphological, pharmacological, and biochemical features. A rapid necrotic cell death, characterized by cell swelling and nuclear shrinkage, could be completely prevented by the NMDA receptor antagonist MK-801 (10 microM) and dose-dependently potentiated by low micromolar levels of extracellular glutamate. A slowly evolving apoptotic death, characterized by nuclear fragmentation, was not attenuated by MK-801 but was prevented by cycloheximide (1 microg/ml). The combination of MK-801 and cycloheximide resulted in an almost complete protection against 3-NP-induced cell death. DNA fragmentation, detected by the terminal deoxynucleotidyl transferase-mediated dUTP-X 3' nick end-labeling technique, was a late event in apoptosis and also occurred after necrotic cell death. ATP depletion was an early event in the 3-NP-induced neuronal degeneration, and the decline in ATP was exacerbated by glutamate. We conclude that 3-NP triggers two separate cell death pathways: an excitotoxic necrosis as a result of NMDA receptor activation and a delayed apoptosis that is NMDA receptor-independent. Mildly elevated levels of extracellular glutamate shift the cell death mechanism from apoptosis to necrosis.

Animals↗
PubMed1997

Amyloid beta-peptide impairs glucose transport in hippocampal and cortical neurons: involvement of membrane lipid peroxidation.

A deficit in glucose uptake and a deposition of amyloid beta-peptide (A beta) each occur in vulnerable brain regions in Alzheimer's disease (AD). It is not known whether mechanistic links exist between A beta deposition and impaired glucose transport. We now report that A beta impairs glucose transport in cultured rat hippocampal and cortical neurons by a mechanism involving membrane lipid peroxidation. A beta impaired 3H-deoxy-glucose transport in a concentration-dependent manner and with a time course preceding neurodegeneration. The decrease in glucose transport was followed by a decrease in cellular ATP levels. Impairment of glucose transport, ATP depletion, and cell death were each prevented in cultures pretreated with antioxidants. Exposure to FeSO4, an established inducer of lipid peroxidation, also impaired glucose transport. Immunoprecipitation and Western blot analyses showed that exposure of cultures to A beta induced conjugation of 4-hydroxynonenal (HNE), an aldehydic product of lipid peroxidation, to the neuronal glucose transport protein GLUT3. HNE induced a concentration-dependent impairment of glucose transport and subsequent ATP depletion. Impaired glucose transport was not caused by a decreased energy demand in the neurons, because ouabain, which inhibits Na+/K(+)-ATPase activity and thereby reduces neuronal ATP hydrolysis rate, had little or no effect on glucose transport. Collectively, the data demonstrate that lipid peroxidation mediates A beta-induced impairment of glucose transport in neurons and suggest that this action of A beta may contribute to decreased glucose uptake and neuronal degeneration in AD.

Adenosine Triphosphate↗
PubMed1997

Differential gene expression in SV40-mediated immortalization of human fibroblasts.

Normal human diploid fibroblasts (HF) have a limited life span, undergo senescence, and rarely, if ever, spontaneously immortalize in culture. Introduction of the gene for T antigen encoded by the DNA virus SV40 extends the life span of HF and increases the frequency of immortalization; however, immortalization requires both T-dependent and T-independent functions. We previously generated independent SV40-transformed non-immortal (pre-immortal) HF cell lines from which we then obtained immortal sublines as part of a multifaceted approach to identify functions responsible for immortalization. In this study we undertook a search for cellular mRNAs which are differentially expressed upon immortalization. A lambda cDNA library was prepared from a pre-immortal SV40-transformed HF (HF-C). We screened the library with a subtracted probe enriched for sequences present in HF-C and reduced in immortal AR5 cells. A more limited screen was also employed for sequences overexpressed in AR5 using a different strategy. Alterations in the level of mRNAs in AR5 encoding functions relevant to signal transduction pathways were identified; however, most cDNAs encoded novel sequences. In an effort to clarify which of the altered mRNAs are most relevant to immortalization, we performed Northern analysis with RNA prepared from three paired sets of independent pre-immortal and immortal (4 cell lines) SV40-transformants using eight cloned cDNAs which show reduced expression in AR5. Three of these were reduced in additional immortal cell lines as well; one, J4-4 (unknown function) is reduced in all the immortal cell lines tested; a second, J4-3 (possible PP2C type phosphatase) is reduced in 2 of the 3 matched sets; and a third, J2-2 (unknown function) is reduced in 2 unrelated immortal cell lines. Although the roles of these genes are as yet unclear, their further analysis should extend our understanding of the molecular bases for immortalization. In particular, the patterns of expression of J4-4 and J4-3 strongly suggest that they are involved in the process of immortalization and/or can serve as target genes for assessing regulators of gene expression in this process.

Cell Line, Transformed↗
PubMed1997

Impairment of glucose and glutamate transport and induction of mitochondrial oxidative stress and dysfunction in synaptosomes by amyloid beta-peptide: role of the lipid peroxidation product 4-hydroxynonenal.

Deposits of amyloid beta-peptide (A beta), reduced glucose uptake into brain cells, oxidative damage to cellular proteins and lipids, and excitotoxic mechanisms have all been suggested to play roles in the neurodegenerative process in Alzheimer's disease. Synapse loss is closely correlated with cognitive impairments in Alzheimer's disease, suggesting that the synapse may be the site at which degenerative mechanisms are initiated and propagated. We report that A beta causes oxyradical-mediated impairment of glucose transport, glutamate transport, and mitochondrial function in rat neocortical synaptosomes. A beta induced membrane lipid peroxidation in synaptosomes that occurred within 1 h of exposure; significant decreases in glucose transport occurred within 1 h of exposure to A beta and decreased further with time. The lipid peroxidation product 4-hydroxynonenal conjugated to synaptosomal proteins and impaired glucose transport; several antioxidants prevented A beta-induced impairment of glucose transport, indicating that lipid peroxidation was causally linked to this adverse action of A beta. FeSO4 (an initiator of lipid peroxidation), A beta, and 4-hydroxynonenal each induced accumulation of mitochondrial reactive oxygen species, caused concentration-dependent decreases in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction, and reduced cellular ATP levels significantly. A beta also impaired glutamate transport, an effect blocked by antioxidants. These data suggest that A beta induces membrane lipid peroxidation, which results in impairment of the function of membrane glucose and glutamate transporters, altered mitochondrial function, and a deficit in ATP levels; 4-hydroxynonenal appears to be a mediator of these actions of A beta. These data suggest that oxidative stress occurring at synapses may contribute to the reduced glucose uptake and synaptic degeneration that occurs in Alzheimer's disease patients. They further suggest a sequence of events whereby oxidative stress promotes excitotoxic synaptic degeneration and neuronal cell death in a variety of different neurodegenerative disorders.

Aldehydes↗
PubMed1997

Oxidative and malondialdehyde modification of low-density lipoprotein: a comparative study.

Low-density lipoprotein (LDL) was modified with copper ions (Cu2+) and malondialdehyde (MDA), and the differences were compared. The results show that both oxidative and MDA modification produce a decrease in free amino groups in LDL and enhance its electrophoretic mobility on agarose gel, and that these observations are linked. However, differences produced by the two forms of modification were observed. Oxidative modification of LDL involves free radical-mediated lipid peroxidation which produces large amounts of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes. In addition, vitamin E was reduced considerably and cholesterol lowered, and apolipoprotein B (apo B) fragmentation and aggregation were seen. Similar changes were not seen with MDA modification which does not involve lipid peroxidation. Fluorescence emission spectra of both forms of modified LDL show that emission intensity increases gradually as the modification progresses, but maximum emission wavelength and spectrum patterns are not the same. These findings may be of some significance in the study of the antigenicity, scavenger receptor multiplicity and toxic effects of modified LDL.

Copper↗
PubMed1996

Neuronal loss and cytoskeletal disruption following intrahippocampal administration of the metabolic inhibitor malonate: lack of protection by MK-801.

Impaired energy metabolism may contribute to the pathogenesis of late-onset neurodegenerative disorders such as Alzheimer's disease by increasing neuronal vulnerability to excitotoxic damage through the NMDA receptor. The effects of metabolic impairment on the striatum have been extensively examined, but relatively little is known regarding the vulnerability of the hippocampus. To examine the effect of metabolic impairment on the hippocampal formation, malonate (0.25-2.5 mumol), a reversible inhibitor of succinate dehydrogenase, was administered by stereotaxic injection into the hippocampus of male Sprague-Dawley rats. Neuronal loss was assessed by Nissl stain, and immunocytochemistry was used to examine cytoskeletal disruption. Malonate produced a dose-dependent lesion in which CA1 pyramidal neurons were most vulnerable, followed by CA3 and dentate gyrus. Cytoskeletal alterations included the loss of microtubule-associated protein 2 (MAP2) and dendritic MAP1B immunoreactivity, whereas axonal MAP1B and tau proteins were relatively spared. Spatially and temporally correlated with the loss of MAP2 was an increase in the immunoreactivity of calpain-cleaved spectrin. A similar pattern of neuronal damage and cytoskeletal disruption was produced by intrahippocampal injection of quinolinate (0.1 mumol), an NMDA agonist. Although these results are consistent with the hypothesis that metabolic impairment results in excitotoxic death, MK-801 (dizocilipine maleate), a noncompetitive NMDA receptor antagonist, did not attenuate the lesions produced by malonate but was effective against quinolinate. The results suggest that NMDA receptor activation is not required for malonate-induced damage in the hippocampal formation.

Animals↗