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Biomedical subjects

Z Yang

Publications and source records attributed to Z Yang.

At least 829 records · Page 46Linked to original sources
PubMed1994

Dynamic changes of fibrinopeptides A and B in sera of burn patients and their effects on vascular endothelial cells.

In this study, dynamic changes of fibrinopeptides A and B (FPA, FPB) in sera of burns patients are determined with an HPLC method. On this basis detrimental effects of FPA and FPB on vascular endothelial cells (VEC) are observed in vitro. The main results are as follows: (1) FPA and FPB in 18 burn patients' sera increase at day 2 postburn, reach peaks at days 5-7 postburn, then decline after day 15 postburn, and return to the control levels at day 25 postburn. The fluctuations in FPA and FPB levels in burn patients' sera are parallel to the progress of burn illness. The measurements of FPA and FPB levels in burn patients' sera may be useful in evaluating patients' condition. (2) FPA and FPB are detrimental to the cultured VEC in vitro. Characteristics of their injurious effects are: specific, irreversible and dose dependent. FPA and FPB may play an important role in endothelial injury.

Adolescent↗
PubMed1993

Synthesis, characterization, and antioxidative activity of vitamin B6 rare earth (III) complexes.

A series of vitamin B6 pyridoxol rare earth (III) complexes Re(PN)5Cl3. 6H2O (PN = pyridoxol; Re = La, Ce, Pr, Nd, Sm, Eu, Gd, Ho, Er, Y) were synthesized and characterized by elemental analysis, molar conductance, TGA-DTA, IR, and 1HNMR spectroscopic techniques. The antioxidative activity of complexes was determined, using the suppression ratio of activated oxygen as an indicator. The results show that the complexes have the scavenger effects for activated oxygen.

Antioxidants↗
PubMed1993

Regulation of biosynthesis of the basic fibroblast growth factor binding domains of heparan sulfate by heparan sulfate-N-deacetylase/N-sulfotransferase expression.

Heparan sulfate-N-deacetylase/N-sulfotransferase catalyzes both the N-deacetylation and N-sulfation reactions that initiate the modification of the oligosaccharide backbone of heparan sulfate (HS). The glycosaminoglycan polymer appears to modulate the activity of growth factors by mediating their initial binding. To understand how the biosynthesis of these binding sites is regulated, a rat liver-derived cDNA encoding the above activities was overexpressed in a COS cell mutant (CM-15) that has reduced levels of the enzyme and binds poorly to immobilized basic fibroblast growth factor (bFGF). This resulted in increased synthesis of sulfated blocks of decasaccharide size or longer. These blocks exhibited high affinity binding to bFGF and contained a high content of 2-O-sulfated iduronate and at least five consecutive N-sulfated disaccharides. An increase in the synthesis of these high affinity blocks was not seen in transfected wild-type COS cells even though they showed a 4-fold increase of both enzyme activities, suggesting that once sufficient levels of highly sulfated blocks of saccharides with high affinity for bFGF are attained, no further synthesis of these domains occurs.

Amidohydrolases↗
PubMed1993

Tumor necrosis factor activation of the sphingomyelin pathway signals nuclear factor kappa B translocation in intact HL-60 cells.

Recent investigations suggest that tumor necrosis factor (TNF)-alpha may utilize the sphingomyelin pathway for signal transduction. Signaling in this system involves hydrolysis of sphingomyelin to ceramide by action of a neutral sphingomyelinase and stimulation of a ceramide-activated protein kinase (Dressler, K. A., Mathias, S., and Kolesnick, R. N. (1992) Science 255, 1715-1718). To clarify the role of this pathway in TNF action, the present studies assessed the effect of the sphingomyelin pathway on activation of nuclear factor kappa B (NF-kappa B), an event considered integral to the transfer of the TNF message to the cell nucleus. As shown previously, TNF (1 nM) induced a marked increase in nuclear NF-kappa B binding in human leukemia (HL-60) cells within 5 min, and elevated binding was detected for as long as 1 h. Addition of a maximally effective concentration of sphingomyelinase, 0.1 units.ml-1, induced a 50% reduction in sphingomyelin content by 5 min from a basal level of 560 pmol.10(6) cells-1 and a quantitative increase in ceramide levels from 89 pmol.10(6) cells-1. Sphingomyelinase 0.1 units.ml-1 also induced an increase in nuclear NF-kappa B binding within 5 min, an effect measurable for as long as 1 h. As little as 1 x 10(-5) units.ml-1 sphingomyelinase was effective and a maximal effect occurred with 1 x 10(-3) units.ml-1. A cell-permeable ceramide analog, C8-ceramide, which mimics biologic effects of TNF-alpha, also enhanced nuclear NF-kappa B activation within minutes. In contrast, addition of a phospholipase C or a synthetic diacylglycerol (DG) analog, 1,2-dioctanoylglycerol, failed to enhance nuclear NF-kappa B binding despite large increases in cellular DG content. Further, TNF-alpha induced elevation in ceramide content by 2 min to 185% of control but did not affect DG levels. These studies provide evidence that stimulation of the sphingomyelin pathway leads to NF-kappa B activation in HL-60 cells.

Arachidonic Acid↗
PubMed1993

Molecular cloning and characterization of rho, a ras-related small GTP-binding protein from the garden pea.

The rho proteins, members of the ras superfamily of small GTP-binding proteins, play a central role in the modulation of cellular functions involving the actin cytoskeleton such as in the establishment of cell polarity and morphology. As a first step in elucidating signal transduction pathways leading to processes mediated by the actin cytoskeleton in plants, we initiated cloning and characterization of rho proteins from pea. One rho-related, partial cDNA clone of 167 bp was isolated utilizing a polymerase chain reaction-based cloning strategy, using degenerate primers that correspond to conserved domains within the rho proteins. A full-length cDNA was isolated by screening a pea cDNA library using the 167-bp cDNA as a probe. The Rho1Ps cDNA contains an open reading frame encoding a polypeptide (Rho1Ps) of 197 amino acids that shows 45-64% sequence identity to members of the rho family and about 30% identity to other members of the ras superfamily. In addition to the nucleotide-binding and GTPase domains, Rho1Ps shares conserved residues and motifs unique to the rho proteins. Purified Rho1Ps protein expressed in Escherichia coli retains specific GTP-binding activity. These data indicate that Rho1Ps encodes a small GTP-binding protein of the rho family. The Rho1Ps transcript is expressed in all organs of pea seedlings, being more abundant in root tips and apical buds. DNA gel blot analyses show that the rho proteins in pea are encoded by a multigene family.

Amino Acid Sequence↗
PubMed1993

Human T cell transcription factor GATA-3 stimulates HIV-1 expression.

A family of transcriptional activating proteins, the GATA factors, has been shown to bind to a consensus motif through a highly conserved C4 zinc finger DNA binding domain. One member of this multigene family, GATA-3, is most abundantly expressed in T lymphocytes, a cellular target for human immunodeficiency virus type 1 (HIV-1) infection and replication. In vitro DNase I footprinting analysis revealed six hGATA-3 binding sites in the U3 region (the transcriptional regulatory domain) of the HIV-1 LTR. Cotransfection of an hGATA-3 expression plasmid with a reporter plasmid whose transcription is directed by the HIV-1 LTR resulted in 6- to 10-fold stimulation of LTR-mediated transcription, whereas site specific mutation of these GATA sites resulted in virtual abrogation of the activation by hGATA-3. Further, deletion of the hGATA-3 transcriptional activation domain abolished GATA-dependent HIV-1 trans-activation, showing that the stimulation of viral transcription observed is a direct effect of cotransfected hGATA-3. Introduction of the HIV-1 plasmids in which the GATA sites have been mutated into human T lymphocytes also caused a significant reduction in LTR-mediated transcription at both the basal level and in (PHA- plus PMA-) stimulated T cells. These observations suggest that in addition to its normal role in T lymphocyte gene regulation, hGATA-3 may also play a significant role in HIV-1 transcriptional activation.

Animals↗
PubMed1993

[Mechanism of coronary bypass graft disease].

Clinical studies on the patency rate of different coronary bypass vessels suggest that biological properties importantly influence graft function. As regards function and patency of coronary bypass vessels, proliferative responses, antithrombotic properties, and vasomotion play important roles. Thrombotic processes are responsible for acute closure of grafts, particularly in the context of reduced endothelial function or surgical trauma to the endothelium. The internal mammary artery and gastroepiploic artery release significantly more factors with antithrombotic and antispastic properties, such as nitric oxide (the endogenous nitrovasodilator) and prostacyclin than the saphenous vein. Structural changes to bypass grafts are related to proliferation and migration of vascular smooth muscle cells. Vascular smooth muscle cells of the saphenous vein exhibit particularly pronounced proliferative responses to pulsatile stretch and platelet-derived growth factor, while cells obtained from the internal mammary artery respond poorly to these stimuli. These different biological properties of the endothelium and vascular smooth muscle cells may contribute importantly to the excellent patency rate of internal mammary artery grafts, while those constructed with the saphenous vein exhibit thrombotic occlusions and proliferative changes.

Coronary Artery Bypass↗
PubMed1993

Four years' experience with the treatment of all-trans retinoic acid in acute promyelocytic leukemia.

A retrospective analysis was done on 43 patients with acute promyelocytic leukemia (APL) at our hospital from June 1987 to August 1992. All-trans retinoic acid was used to induce these patients to differentiation. In the early period of induction there were risks of severe hemorrhage, which was the main cause of early death. Treatments combined with platelets and heparin or aminomethylbenzoic (PAMBA) were given to patients with abnormal coagulation. As a result only 4 out of 43 patients died of intracranial bleeding at 4-12 days when their white blood cell (WBC) counts peaked. The combination of retinoic acid (RA) and HA chemotherapy could reduce hyperleukocytosis during the RA induction course. None of 7 patients died at early stage with this treatment combination. Our studies showed that it could predict the onset of remission at early stage through observations on the successive changes of karyotypes and morphology of the bone marrow and peripheral blood cells. Our studies also showed that the growth of CFU-F could be inhibited by RA. We think that it may play a role in the RA-induced differentiation. In 4 years of follow-up the overall leukemia-free survival (LFS) was 80% with a relapse rate of 45%. Thirty-five patients out of 43 cases were still alive in remission, and one was alive in relapse. All 11 out of 43 patients relapsed within 3 years, but the relapses occurred later, after 3 years duration of remission (P < .01). Retinoic acid failed to induce 5 patients who relapsed with the continuation treatment of RA and chemotherapy alternatively. In order to overcome the resistance to RA, the continuation treatment of simple chemotherapy had been administered following CR. Two cases achieved remission in this way. The difference of resistant events to RA reached significance between these 2 groups of different continuation treatment.

Adolescent↗
PubMed1993

Metallothionein I reduction of cytochrome c.

Using absorption spectroscopy we have found that metallothionein I at concentrations as low as 1 microM reduces ferricytochrome c. This reduction is more potent than that of another abundant intracellular thiol, glutathione. Also, oxidation of ferricytochrome c which had been reduced by metallothionein I occurs more slowly than when the reductant was glutathione. Over a pH range of 6 through 9 there is no variation in the initial rate of metallothionein I reduction of ferricytochrome c. These data demonstrate a potent interaction between metallothionein I and ferricytochrome c.

Animals↗
PubMed1993

Maximum-likelihood estimation of phylogeny from DNA sequences when substitution rates differ over sites.

Felsenstein's maximum-likelihood approach for inferring phylogeny from DNA sequences assumes that the rate of nucleotide substitution is constant over different nucleotide sites. This assumption is sometimes unrealistic, as has been revealed by analysis of real sequence data. In the present paper Felsenstein's method is extended to the case where substitution rates over sites are described by the gamma distribution. A numerical example is presented to show that the method fits the data better than do previous models.

Animals↗
PubMed1993

Different effects of angiotensin-converting enzyme inhibition in human arteries and veins.

The renin-angiotensin system (RAS) participates in the regulation of vascular tone; its effects were studied in human internal mammary artery (IMA) and saphenous vein (SV) suspended in organ chambers for isometric tension recording. The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (10(-7) M) markedly augmented endothelium-dependent relaxations to bradykinin in SV (concentration shift: 10-fold; n = 6; p < 0.005), but not in IMA; in both blood vessels, it had no effect on endothelium-dependent relaxations to acetylcholine. The contractions to angiotensin I (Ang I; 10(-7) M) were markedly inhibited by enalaprilat (10(-7) M) in SV (control: 34 +/- 6% of 100 mM KCl; treatment: 18 +/- 6%; n = 7; p < 0.05) but not in IMA (control: 33 +/- 4%; treatment: 30 +/- 6%; n = 7; NS) and abolished by the Ang II receptor antagonist DuP 753 (10(-7) M) in both blood vessels. Ang II (10(-7) M) induced more pronounced contractions than Ang I in IMA (63 +/- 4%) and SV (63 +/- 5%; n = 5-6; p < 0.05 vs. Ang I), which was markedly inhibited by DuP 753 (10(-7) M; IMA: 21 +/- 5%; SV: 32 +/- 5%; p < 0.05). Thus, in SV but not IMA, ACE inactivates bradykinin and thereby blunts endothelium-dependent relaxations to the peptide and converts Ang I to Ang II.

Acetylcholine↗
PubMed1993

Protein farnesyltransferase in plants. Molecular cloning and expression of a homolog of the beta subunit from the garden pea.

Protein farnesyltransferase is a heterodimeric enzyme that attaches a farnesyl moiety to C-terminal cysteine residues. Both the alpha and beta subunits have recently been cloned and sequenced from yeast and rat. Degenerate oligonucleotides, corresponding to conserved regions of the beta subunit, were used as primers for the polymerase chain reaction to amplify cDNA synthesized from total cellular RNA from the apical buds of pea (Pisum sativum L.) seedlings. The 171-bp fragment obtained encodes an open reading frame of 57 amino acids showing 65% identity to the rat protein farnesyltransferase beta subunit. Using this fragment to screen a pea cDNA library, one full-length cDNA clone, designated PsFTb, was obtained that contains an open reading frame encoding a polypeptide of 419 amino acids. The predicted amino acid sequence exhibits 48 and 40% identity to the rat and yeast beta subunits, respectively, indicating that this cDNA encodes a pea homolog of the beta subunit of farnesyltransferase. Gel blot hybridizations show that PsFTb is likely to be encoded by a single-copy gene and is expressed as a transcript of approximately 1.7 kb. During photoregulated leaf development in continuous white light, PsFTb transcript levels within apical buds decline by approximately 5-fold.

Alkyl and Aryl Transferases↗
PubMed1993

The adenylyl cyclase-cyclic AMP system modulates morphological and functional development of hypothalamic beta-endorphin neurons in culture.

In rats, opioidergic beta-endorphin (beta EP1-31) is produced and released from neurons of arcuate nuclei in the hypothalamus. Although the neuropeptide has been implicated in sexual maturation and stress-induced reproductive dysfunction, the intra-hypothalamic regulation of beta EP neurons remains unclear. Employing long-term monolayer cultures of neonatal rat hypothalamic cells, we report here that 4 days of treatment with 10 microM forskolin increased approximately 3-fold (P < 0.01) the proportion of immunoreactive (ir)-beta EP positive neurons bearing neurites. In addition, treatment of forskolin also enhanced ir-beta EP release (634 +/- 59 pg/well; mean +/- SE, n = 4, P < 0.01) by 14-fold and ir-beta EP content (119 +/- 13 pg/well; P < 0.01) by 2-fold above that of vehicle-treated cultures; in both instances, the EC50 and the Emax of forskolin were approximately 10 microM and 100 microM, respectively. The forskolin-stimulated release of ir-beta EP was mimicked by cholera toxin and (Bu)2cAMP treatment in a dose-related manner, but not by pertussis toxin. Although by itself 3-isobutyl-1-methyl-xanthine (100 microM) only doubled ir-beta EP secretion, it markedly potentiated the stimulatory effect of forskolin. This forskolin-induced stimulation was reversible and in cultures re-exposed to the same drug within the first 24 h period, there was a marked increase in the stimulated release of ir-beta EP (P < 0.05); re-challenge of forskolin at later stages, however, induced a smaller but significant secretion of ir-beta EP (P < 0.01) compared to that of vehicle-treated control cultures. Sephadex G-50 gel chromatographic profile of the media prepared from forskolin-treated cultures revealed a major ir-beta EP peak of 3 K M(r). High-performance liquid chromatography analysis showed that ir-beta EP of the 3 K M(r) species was eluted with a retention time similar to that of synthetic rat beta EP1-31. We thus conclude that the adenylyl cyclase-cAMP system plays an important role in the modulation of beta EP1-31 production and release from hypothalamic beta EP neurons in culture. Furthermore, the functional responsiveness and the morphological development of these neurons are affected, at least in part, by the intrinsic activity of the adenylyl cyclase-cAMP system.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Effects of acute hypoxia on intracranial dynamics in unanesthetized goats.

The effects of acute hypoxia on intracranial dynamics were studied in six unanesthetized goats that were subjected to hypobaric hypoxia at a simulated 4,000-m high altitude for 2 h. Another six nonhypoxic goats served as control group for cerebral water content (CWC). In this study, we measured cerebral blood flow (CBF) by electromagnetic flowmeter, intracranial pressure (ICP) through an intraventricular catheter, and CWC by a wet-to-dry weight technique for a given volume of brain tissue. Intracranial compliance was calculated from a pressure-volume index derived from the change in intraventricular pressure after a subarachnoid injection of saline. During acute hypoxia CBF increased from 146.0 +/- 10.60 to 185.3 +/- 7.83 ml x min-1.100 g-1, ICP increased from 15.4 +/- 1.82 to 27.4 +/- 3.84 cmH2O, and CWC increased from 78.7 +/- 0.30 to 79.5 +/- 0.16%, but intracranial compliance decreased from 0.65 +/- 0.28 to 0.36 +/- 0.19 ml/cmH2O. The data suggest that acute hypoxia results in a significant disturbance of intracranial dynamics, which may be one of the important pathophysiological mechanisms of high-altitude cerebral edema and acute mountain sickness.

Acute Disease↗
PubMed1993

Calcium antagonists differently inhibit proliferation of human coronary smooth muscle cells in response to pulsatile stretch and platelet-derived growth factor.

BACKGROUND: Vascular smooth muscle cell proliferation is the key event of coronary artery disease. Mechanical forces, in particular, pulsatile stretch and platelet-derived growth factor, may play an important role. METHODS AND RESULTS: Vascular smooth muscle cells were cultured from the media of human left descending coronary arteries obtained from organ donors using the explant method. To study effects of pulsatile stretch on vascular smooth muscle cell proliferation, a computer-controlled in vitro pulsatile stretch device was used. Cells were seeded onto Flex I culture plates with deformable membranes and exposed to pulsatile stretch (60 cycles per minute) and/or growth factors. Proliferation of smooth muscle cells was determined by 3H-thymidine incorporation. Pulsatile stretch markedly stimulated 3H-thymidine incorporation of coronary smooth muscle cells (180 +/- 15 to 432 +/- 27 cpm/10(5) cells; P < .05) after 24 hours and increased cell number after 6 days (10.3 +/- 0.7 x 10(4)/mL; P < .05). Platelet-derived growth factor-AB (0.01 to 10 ng/mL) concentration-dependently stimulated 3H-thymidine incorporation in coronary smooth muscle cells (EC50, 0.1 ng/mL) and had additive effects with pulsatile stretch. The Ca2+ antagonist verapamil (10(-7) to 10(-5) M) concentration-dependently inhibited proliferation stimulated by platelet-derived growth factor back to control levels (P < .05 to .01) but not that induced by pulsatile stretch. CONCLUSIONS: Pulsatile stretch and platelet-derived growth factor are potent stimuli for proliferation of coronary smooth muscle cells. The selective inhibitory effect of a Ca2+ antagonist on smooth muscle cell proliferation stimulated by platelet-derived growth factor but not by pulsatile stretch may explain why the drugs have only modest antiatherogenic effects in patients with coronary artery disease.

Cell Division↗
PubMed1993

Recombinant platelet-derived growth factor B gene expression in porcine arteries induce intimal hyperplasia in vivo.

Platelet-derived growth factor (PDGF) B chain induces cell proliferation in vitro and is associated with arterial lesions that cause cardiovascular disease. However, it has been difficult to document the biological response to PDGF B gene expression in arteries in vivo. To determine the biologic effects of this growth factor in vivo, we have introduced an eukaryotic expression vector plasmid encoding recombinant PDGF B by direct gene transfer into porcine iliofemoral arteries using DNA liposome complexes. The presence of PDGF B plasmid DNA and expression of recombinant mRNA were confirmed by polymerase chain reaction analysis, and recombinant PDGF protein was demonstrated by immunohistochemistry. Intimal thickening was observed in porcine arteries 21 days following transfection with the recombinant PDGF B gene compared with arteries transduced with a control gene, E. coli beta-galactosidase. An eightfold increase in intimal to medial ratio was present in PDGF B gene transfected arteries compared with control transfected arteries (P = 0.001). This study suggests that expression of a recombinant PDGF B gene in vivo can play a role in the induction of intimal hyperplasia, which can lead to cardiovascular diseases.

Animals↗