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H L Zhang

Publications and source records attributed to H L Zhang.

At least 37 records · Page 2Linked to original sources

Hypoxia alters the subcellular distribution of protein kinase C isoforms in neonatal rat ventricular myocytes.

Cardiac myocytes coexpress multiple protein kinase C (PKC) isoforms which likely play distinct roles in signaling pathways leading to changes in contractility, hypertrophy, and ischemic preconditioning. Although PKC has been reported to be activated during myocardial ischemia, the effect of ischemia/hypoxia on individual PKC isoforms has not been determined. This study examines the effect of hypoxia on the subcellular distribution of individual PKC isoforms in cultured neonatal rat ventricular myocytes. Hypoxia induces the redistribution of PKC alpha and PKC epsilon from the soluble to the particulate compartment. This effect (which is presumed to represent activation of PKC alpha and PKC epsilon) is detectable by 1 h, sustained for up to 24 h, and reversible within 1 h of reoxygenation. Inhibition of phospholipase C with tricyclodecan-9-yl-xanthogenate (D609) prevents the hypoxia-induced redistribution of PKC alpha and PKC epsilon, whereas chelation of intracellular calcium with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) blocks the redistribution of PKC alpha, but not PKC epsilon; D609 and BAPTA do not influence the partitioning of PKC alpha and PKC epsilon in normoxic myocytes. Hypoxia, in contrast, decreases the membrane association of PKC delta via a mechanism that is distinct from the hypoxia-induced translocation/activation of PKC alpha/PKC epsilon, since the response is slower in onset, slowly reversible upon reoxygenation, and not blocked by D609 or BAPTA. The hypoxia-induced shift of PKC delta to the soluble compartment does not prevent subsequent 4-beta phorbol 12-myristate-13-acetate-dependent translocation/activation of PKC delta. Hypoxia does not alter the abundance of any PKC isoform nor does it alter the subcellular distribution of PKC lambda. The selective hypoxia-induced activation of PKC isoforms through a pathway involving phospholipase C (PKC alpha/PKC epsilon) and intracellular calcium (PKC alpha) may critically influence cardiac myocyte contractility, gene expression, and/or tolerance to ischemia.

Animals↗

Catalytic oxidation of uric acid at the polyglycine chemically modified electrode and its trace determination.

Cyclic voltammetry was undertaken to investigate the electrochemical behavior of uric acid at a polyglycine modified electrode. The modified electrode shows catalytic ability for the oxidation of uric acid, reducing the overpotential by 250 mV in pH 7.0 phosphate buffer solution. The enhanced voltammetric response can be used to determine uric acid. The linear range is between 5.0 x 10(-8) and 4.5 x 10(-6) M with a detection limit as low as 5.0 x 10(-9) M. The relative standard deviation is 1.4% (8 runs) at a concentration of 50 microM uric acid. The catalytic effect of the modified electrode resulted in the voltammetric resolution of the overlapping of uric acid and ascorbic acid. This allows the simultaneous detection of uric acid and ascorbic acid in the same sample.

Catalysis↗

Antioxidative compounds isolated from safflower (Carthamus tinctorius L.) oil cake.

Seven antioxidative serotonin derivatives were isolated from safflower (Carthamus tinctorius L.) oil cake. Their structures were established as N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]ferulamide (1), N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]-p-coumaramide (2), N,N'-[2,2'-(5,5'-dihydroxy-4,4'-bi-1H-indol-3,3'-yl)diethyl]- di-p-coumaramide (3), N-[2-[3'-[2-(p-coumaramido)ethyl]-5,5'-dihydroxy- 4,4'-bi-1H-indol-3-yl]ethyl]ferulamide (4), and N,N'-[2,2'-(5,5'-dihydroxy-4,4'-bi-1H-indol-3,3'-yl)diethyl]- diferulamide (5), N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]- p-coumaramide (6), and N-[2-[5-(beta-D-glucosyloxy)-1H-indol-3-yl)ethyl]ferulamide (7). Antioxidative activities of the compounds were measured by the ferric thiocyanate method and the alpha,alpha-diphenyl-beta-picrylhydrazyl (DPPH) method, and compounds 1-5 were found to have relatively strong antioxidative activity.

Antioxidants↗

[Effects of ginkgo leave concentrated oral liquor in treating asthma].

OBJECTIVE: To determine the effects of Ginkgo leave concentrated oral liquor (GLC) on airway inflammation. METHODS: Airway hyperreactivity and clinical symptoms and pulmonary functions of asthma patients were determined. RESULTS: In contrast to placebo group, GLC significantly reduced airway hyperreactivity (P < 0.05) and improved clinical symptoms (P < 0.05), pulmonary functions (P < 0.05) of the asthmatic patients. CONCLUSION: GLC is an effective drug of anti airway inflammation.

Adolescent↗

The role of the carboxyl-terminal amino acid residues in Escherichia coli DNA topoisomerase III-mediated catalysis.

The role that the carboxyl-terminal amino acids of Escherichia coli DNA topoisomerase I (Topo I) and III (Topo III) play in catalysis was examined by comparing the properties of Topo III with those of a truncated enzyme lacking the generalized DNA binding domain of Topo III, Topo I, and a hybrid topoisomerase polypeptide containing the amino-terminal 605 amino acids of Topo III and the putative generalized DNA binding domain of Topo I. The deletion of the carboxyl-terminal 49 amino acids of Topo III decreases the affinity of the enzyme for its substrate, single-stranded DNA, by approximately 2 orders of magnitude and reduces Topo III-catalyzed relaxation of supercoiled DNA and Topo III-catalyzed resolution of DNA replication intermediates to a similar extent. Fusion of the carboxyl-terminal 312 amino acid residues of Topo I onto the truncated molecule stimulates topoisomerase-catalyzed relaxation 15-20-fold, to a level comparable with that of full-length Topo III. However, topoisomerase-catalyzed resolution of DNA replication intermediates was only stimulated 2-3-fold. Therefore, the carboxyl-terminal amino acids of these topoisomerases constitute a distinct and separable domain, and this domain is intimately involved in determining the catalytic properties of these polypeptides.

Amino Acid Sequence↗

Two types of ATP-sensitive potassium channels in rat portal vein smooth muscle cells.

1. Single-channel recordings were made from single, enzymatically isolated smooth muscle cells of rat portal vein by the patch-clamp technique. 2. Unitary potassium currents were identified through two types of K-channels with conductances in 60:130 mM K-gradient of 50 and 22 pS; these are referred to as LK and MK channels respectively. 3. The LK channels became extremely active if isolated patches were created into nucleotide-free solution; activity was inhibited by ATP applied to the inner surface of the patch with a half maximal inhibition (Ki) of 11-23 microM. Channel activity declined and disappeared with time and could be regenerated by a brief application of Mg-ATP or a nucleoside diphosphate such as UDP (in the presence of Mg). LK channel activity was rarely stimulated by levcromakalim and not by pinacidil (K-channel openers, KCOs) but was blocked by glibenclamide. 4. Activity of MK channels declined if isolated patches were created into nucleotide free solution; activity reappeared if UDP or ATP alone (in the presence of Mg) was applied; pinacidil or levcromakalim in the presence of ATP or UDP further increased channel activity which was blocked by glibenclamide. 5. The LK channel inhibited by ATPi is very similar in its conductance and other properties to the KATP channel described in tissues other than smooth muscle, in its conductance and properties the MK channel resembles the KNDP channel we have previous described as present in other smooth muscles and opening in responses to KCOs.

Adenosine Triphosphate↗

Endothelin-dependent actions in cultured AT-1 cardiac myocytes. The role of the epsilon isoform of protein kinase C.

The consequences of endothelin receptor activation were examined in atrial tumor myocytes derived from transgenic mice (AT-1 cells). Endothelin-1 (endothelin) stimulates phosphoinositide hydrolysis in a dose-dependent manner. Endothelin also induces the rapid and transient translocation of protein kinase C (PKC)-epsilon immunoreactivity from the soluble to the particulate cell fraction. The subcellular distributions of PKCalpha and PKCzeta (also expressed by AT-1 cells) are not influenced by endothelin. Using quantitative fluorescence microscopy with fura 2, we examined the effects of endothelin on intracellular calcium. In electrically driven myocytes, endothelin induces a rapid and transient increase in the amplitude of the calcium transient. This is blocked by both phorbol 12-myristate 13-acetate (PMA) pretreatment to downregulate PKC and the PKC inhibitor chelerythrine, arguing that PKCepsilon plays a critical role in endothelin receptor-dependent increases in intracellular calcium. Endothelin also stimulates mitogen-activated protein kinase (MAPK). MAPK activation is markedly attenuated by pretreatment with PMA or pertussis toxin (PTX, to activate susceptible G protein alpha subunits); it is completely prevented by combined pretreatment with PMA and PTX. In contrast, it is not attenuated by chelation of intracellular calcium with BAPTA. These findings indicate that the pathway for endothelin receptor stimulation of MAPK involves PKCepsilon and PTX-sensitive G protein(s). Thus, these studies identify a functional role for PKCepsilon as a mediator of endothelin receptor-dependent increases in cytosolic calcium and MAPK activity in AT-1 cells. Accordingly, the AT-1 cell system should provide a uniquely useful model to identify the intracellular targets for PKCepsilon and investigate their function in the regulation of intracellular calcium homeostasis and the induction of the growth response in cardiac myocytes.

Animals↗

Escherichia coli DNA topoisomerase III is a site-specific DNA binding protein that binds asymmetrically to its cleavage site.

The binding of DNA topoisomerase III (Topo III) to a single-stranded DNA substrate containing a strong cleavage site has been examined. The minimal substrate requirement for Topo III-catalyzed cleavage has been determined to consist of 7 bases; 6 bases 5' to the cleavage site and only 1 base 3' to the site. Nuclease P1 protection experiments indicate that the enzyme also binds to its substrate asymmetrically, protecting approximately 12 bases 5' to the cleavage site and only 2 bases 3' to the cleavage site. A catalytically inactive mutant of Topo III shows the same protection pattern as the active polypeptide, indicating that Topo III is a site-specific binding protein as well as a topoisomerase. Consistent with this view, an oligonucleotide containing a cleavage site is a more effective inhibitor and is bound more efficiently by Topo III than an oligonucleotide without a cleavage site.

Base Sequence↗

The carboxyl-terminal residues of Escherichia coli DNA topoisomerase III are involved in substrate binding.

The nucleic acid-binding domain of Escherichia coli DNA topoisomerase III (Topo III) has been identified using a selection procedure designed to isolate inactive Topo III polypeptides. Deletion of this binding domain, contained in the carboxyl terminus of Topo III, results in a drastic reduction in the ability of the enzyme to bind to single-stranded DNA and RNA substrates. Successive truncation of the enzyme within this region results in the gradual loss of nucleic acid binding activity and in a gradual change in the mechanism of Topo III-catalyzed relaxation of negatively supercoiled DNA. The reduction of nucleic acid binding activity of the truncated polypeptides does not result in a loss of cleavage site specificity for the enzyme, suggesting that other amino acids are involved in the positioning of the nucleic acid within the nicking/closing site of the topoisomerase.

Amino Acid Sequence↗

Cytotoxic cyclolignans from Koelreuteria henryi.

Chemical investigation of the cytotoxic fraction of Koelreuteria henryi resulted in the isolation of three cyclolignans. A new cyclolignan, named koelreuterin-1 was elucidated as furo[3',4':6,7]naphtho[2,3-d]-1,3-dioxol-6(8H)-one,5-(7-methoxy-1, 3- benzodioxol-5-yl)[1]. Two known cyclolignans were characterized as austrobailignan-1 [2] and austrobailignan-2 [3]. The structure elucidation of 1 was based on extensive 1H- and 13C-nmr spectral analyses. Further chemical conversion of 2 to 3 and oxidative transformation of 2 to 1 unambiguously confirmed the structure of 1. The cytotoxicity and tubulin polymerization inhibitory activity of 1-3 are discussed.

4-Butyrolactone↗

[The expression of 67-KD laminin receptor (LN-R) gene in PG tumor cells with high metastatic potential].

The expression level of 67-KD LN-R mRNA was observed in high-metastatic PG tumor cells and low-metastatic PAa tumor cells based on the cDNA fragments of 67-KD LN-R amplified by PCR technique and the specific cDNA probe prepared by random primer labeling method. Results showed that the transcripts were homologous in size, about 1.7kb, in PG and PAa tumor cells. The 67-KD LN-R mRNA level was higher in PG than that in PAa tumor cells, and gene amplification was also more marked in PG tumor cells. After treated with 67-KD LN-R monoclonioal antibody (50, 100 and 400 micrograms/ml) for 48 hours, LN-R mRNA of PG tumor cells decreased significantly. It is suggested that 67-KD LN-R may play important roles in metastatic processes of PG tumor cells.

Base Sequence↗

[Sites of analgesic action of 3,15-diacetylbenzoylaconine].

In the rat hot plate test, vocalization induced by electric stimulation, tail flick test, and the mouse acetic acid writhing test, 3, 15-diacetylbenzoylaconine (DABA) ip exhibited a dose-dependent analgesic activity. Intrathecally (ith) administered DABA (527, 1186 micrograms.kg-1) had no analgesic action. Microinjection of DABA 35-75 micrograms.kg-1 or 20 micrograms into the cerebral ventricle (icv) or the periaqueductal gray (PAG) exerted a remarkable analgesic activity, which was abolished after bilateral lesions of locus coeruleus (LC). Microinjection of DABA (20 micrograms) into LC failed to produce apparent analgesic action. These results suggested that the sites of analgesia of DABA were mainly at the central supraspinal structures, and PAG was one of the primary sites, while LC was one of the intermediate links.

Aconitine↗

[Stimulation of low dose radiation on hematopoietic system].

We observed the changes of CSF secretion from lung cells and thymocytes and the number of G-CSF receptors on bone marrow cells (BMC) in mice after single whole-body X-irradiation in the dose range of 25-250 mGy. The results showed that the CSF secretion from lung cells increased only after 75 mGy (P < 0.05). The response of thymocytes to low dose radiation was more sensitive and the increase of secretion reached its maximum at the dose of 50 mGy and was still higher than normal after dose up to 250 mGy X-rays (P < 0.05 or P < 0.01). The reaction equilibrium of 125I-G-CSF binding to BMC at 37 degrees C was obtained in 60 minutes, and the maximum binding (Bmax) to 3 x 10(6) BMC was 15.1 pmol, the dissociation constant(Kd) was 78.6 pmol, and the number of G-CSF receptors per cell was estimated to be about 3,100. The number of G-CSF receptors on BMC in mice 48 hours after exposure to dose of 50, 75 and 100 mGy X-rays increased significantly, being 161%, 169% and 342% of control, respectively. The results demonstrated that not only CSF production from lung cells and thymocytes was stimulated, but also the expression of G-CSF receptors on BMC was enhanced, the two factors acting together resulting in hematopoietic stimulation after low dose whole-body irradiation.

Animals↗

The lysine analog L-oxalysine is an inhibitor of RNA synthesis.

1. The lysine analog L-4-oxalysine was found to be a potent inhibitor of RNA synthesis in Candida albicans. 2. The compound was a weak inhibitor of protein synthesis and DNA synthesis was not affected. 3. The inhibition of RNA synthesis was reversed by L-lysine but not D-lysine. 4. The decrease in the level of newly synthesized RNA in cells treated with L-oxalysine was due to inhibition of de novo synthesis rather than to degradation of RNA.

Amino Acids↗

Toxicity of oxalysine and oxalysine-containing peptides against Candida albicans: regulation of peptide transport by amino acids.

A lysine antimetabolite, L-4-oxalysine [H2NCH2CH2OCH2CH(NH2)COOH], and oxalysine-containing di-, tri-, tetra- and pentapeptides inhibited growth of Candida albicans H317. Micromolar amounts of amino acids were found to overcome ammonium repression of the di- and tripeptide transport system(s) in strain H317. Several amino acids increased the toxicity of oxalysine-containing di- and tripeptides for C. albicans with little or no increase in toxicity of oxalysine or oxalysine-containing tetra- and pentapeptides. L-Lysine completely reversed the toxicity of oxalysine by competing with the transport of oxalysine into the cells. In contrast, L-lysine increased the toxicity of oxalysine-containing di- and tripeptides, but had no effect on the toxicity of oxalysine-containing tetra- and pentapeptides. Incubation of cells with L-lysine for 4 h resulted in a 15-fold increase in the rate of transport of radiolabelled dileucine, indicating that increased sensitivity of C. albicans to some toxic peptides in the presence of L-lysine may be attributed to an increased rate of transport of these peptides. Our results indicate that the dipeptide and tripeptide transport system(s) of C. albicans are regulated by micromolar amounts of amino acids in a similar fashion to the regulation of peptide transport in Saccharomyces cerevisiae and that multiple peptide transport systems differentially regulated by various nitrogen sources and amino acids exist in C. albicans.

Amino Acid Sequence↗

Mechanical and electrophysiologic changes in rat cardiac allografts during immunologic rejection.

We studied the relationship between immunologic rejection and changes in contractility of isolated perfused papillary muscle, using heterotopically transplanted rat hearts. Rejection assessed by mononuclear cell infiltration was associated with depressed twitch amplitude and lower rates of tension development and relaxation. The relationship between maximum developed tension and [Ca2+]o was attenuated in muscle from the rejecting allografted heart, as compared with muscle of normal or isografted hearts. To determine the effects of rejection on ventricular electrophysiologic properties, we recorded transmembrane action potentials in isolated ventricular myocardium. We found that in rejecting allografted hearts the resting potential, action potential amplitude, and maximum upstroke velocity of phase zero were significantly reduced compared with normal and isografted hearts. The attenuation in the mechanical and electrophysiologic properties was largely prevented by treating the transplanted rat with anti-lymphocyte-globulin on days 0, 1, and 2 after transplantation. In summary, the present study demonstrates that immunologic rejection of the heterotopically allotransplanted rat heart is associated with marked attenuation of both mechanical and electrophysiologic properties of the ventricular myocardium.

Action Potentials↗