Biomedical subjects

W Tang

Publications and source records attributed to W Tang.

At least 307 records · Page 17Linked to original sources

PubMed1993

Nude mouse interim host model for human parathyroid grafts. Part IV. Human PTG xenograft rejection in a mouse B lymphocyte system.

An interim host model for human parathyroid gland (PTG) grafts has been established. In this experiment, the proliferation of mouse blood vessels and infiltration of mouse B lymphocytes into human PTG grafts were successively observed. The results showed that within 10 d of interim hosting, when PTG grafts were still nourished by permeable factors, scattered mouse B lymphocyte infiltration was already apparent. As time went by, B lymphocyte infiltration and IgG secretion became more obvious. At 60-90 d interim hosting, an intact human-mouse tissue "chimera" was formed. Thereafter, human PTG grafts were gradually fragmented and absorbed. The theoretical significance and clinical value of this rejection phenomenon are discussed.

Animals↗

PubMed1993

Comparison of parathyroid donor grafts.

We compared the degrees of cell maturity, antigenicity and secretory function of parathyroid tissues (PTG) from cadavers (C-PTG), 20-28 week fetuses (F-PTG) and PTG adenomas (A-PTG). In A-PTG, scattered or clustered immature cells were observed, but there were none in F-PTG and C-PTG tissues. A-PTG and C-PTG exhibited better secretory function than did F-PTG. No clear differences were found in HLA class I (ABC) antigen quantity among the three donor PTG tissues, but the amounts of HLA class II (DR) antigen in A-PTG and F-PTG were significantly lower than that in C-PTG. The results demonstrate that C-PTG, with its functional advantages, and F-PTG, with its relatively low antigenicity, can be used in clinical transplantation, while A-PTG tissues are not suitable for clinical transplantation on account of their immaturity and the possibility of carcinomatous change.

Adenoma↗

PubMed1993

Comparison of gastric luminal and gastric wall PCO2 during hemorrhagic shock.

Measurement of gastric wall PCO2 has emerged as a promising monitor of perfusion deficits during low-flow states of circulatory shock. In the present study, gastric luminal PCO2 measured with the gastric tonometer was compared with the PCO2, measured directly in the wall of the stomach during hemorrhagic shock in two groups of five Sprague-Dawley rats. One group was pretreated with the H2 blocker, ranitidine. During a 120-min interval of hemorrhage, tonometer PCO2 increased from 60 +/- 7 mmHg to 90 +/- 10 mmHg, and time-coincident gastric wall PCO2 from 52 +/- 5 mmHg to 131 +/- 14 mmHg. Following reinfusion of shed blood, tonometer PCO2 remained elevated for an interval exceeding 60 min, but gastric wall PCO2 returned to control levels within approximately 10 min. Ranitidine pretreatment did not alter the relationships between gastric wall PCO2 and tonometer PCO2. These observations indicate that gastric luminal PCO2 underestimates relatively rapid increases in gastric wall PCO2 during profound hemorrhagic shock in rats.

Animals↗

PubMed1992

Human embryonic zeta-globin chain expression in deletional alpha-thalassemias.

zeta-Globin chain expression in carriers of a number of deletional alpha-thalassemias is investigated by radioimmunoassay. In a few cases, zeta-globin mRNAs are also studied. zeta-Globin chains are detected in (--SEA/), (--MED/), and (--SPAN/) deletions, but not in six other deletional mutations. These results suggest that the DNA element capable of suppressing zeta-globin expression in adult erythroid cells is present within the (--SPAN/) deletion, while the DNA fragment between the 5' breakpoints of the (--SA/) and the (--SEA/) deletions may contain sequences necessary for augmenting zeta-globin expression in adult erythroid cells. Furthermore, zeta-globin chains are shown by an immunocytologic technique to be present in all circulating erythrocytes in carriers of the (--SEA/) and (--MED/) deletions. This simple immunocytologic test is highly sensitive and specific to detect adult carriers of either the (--SEA/) or (--MED/) deletions, and can be used for the detection of couples at risk of pregnancies involving fetuses with homozygous alpha-thalassemia.

Chromosome Deletion↗

PubMed1992

Identification of a membrane-associated 1-0-alkyl-2-arachidonoyl-sn-glycero-3-phosphocholine hydrolyzing phospholipase A2 in guinea pig 1 epidermis. Implications in the cutaneous biosynthesis of platelet-activating factor.

A membrane-associated 1-0-alkyl-2-arachidonoyl-GPC hydrolyzing phospholipase A2 was identified in guinea pig epidermis. It is regio-specific (associated with the particulate microsomal fraction) and specific for the hydrolysis of 1-0-alkyl-2-arachidonoyl-sn-glycero-3-phosphocholine. It is sensitive to low calcium concentrations suggesting that it may be activated by increasing intracellular calcium. Since ether-linked phospholipids are known to exist in the epidermis, further understanding of the properties of this 1-0-alkyl-arachidonoyl-hydrolyzing PLA2 may allow us to control the generation of 1-0-alkyl-2-lyso-sn-glycero-3-phosphocholine, a key substrate for the generation of the platelet-activating factor in the tissue.

Animals↗

PubMed1992

Characterization of a polyclonal anti-peptide antibody to the angiotensin II type-1 (AT1) receptor.

A polyclonal antibody has been prepared against a synthetic peptide corresponding to amino acids 14-23 of the angiotensin II type-1 (AT1) receptor. The antibody is of high titer and mono-specific. Western blot analysis of membranes from rat liver, kidney, and adrenal gland showed that the antibody specifically recognizes a protein band of MW 70,000 whose amounts are highest in the liver, followed by kidney and adrenals. In addition, a relatively less prominent band of MW 95,000 was also detected. The relative distribution of this protein correlates well with the values obtained for [3H]-DuP753 binding and AT1 receptor mRNA.

Adrenal Glands↗

PubMed1992

Dietary intake of concentrated gamma-linolenic acid (GLA)-enriched oil suppresses cutaneous level of dihomo-gamma-linolenic acid (DGLA): possible in vivo inhibition of microsomal elongation of GLA to DGLA.

The dietary supplementation of normal guinea-pig diet with moderate levels of vegetable oils containing gamma-linolenic acid (GLA) is associated with elevation of epidermal levels of dihomo-gamma-linolenic acid (DGLA) and 15-hydroxyeicosatrienoic acid (15-lipoxygenase product of DGLA). However, supplementation of diet with higher level (70%) of GLA (GLA-70) resulted in marked decrease of epidermal level of DGLA. This nutritional observation prompted us to investigate in vitro the effects of varying concentrations of polyunsaturated fatty acids (PUFAs) on rat liver microsomal chain elongation of GLA into DGLA. Our data revealed that low concentrations of GLA (less than 100 microM) are stimulatory on the chain elongation while higher concentrations (greater than 100 microM) are inhibitory. The 18-carbon linoleic acid (precursor of GLA) was also markedly inhibitory at high concentrations. Interestingly, the longer chain 20-carbon n-3 PUFAs: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) exerted negligible effect. The results suggest that increased systemic presence of free PUFAs, such as may occur in vivo after dietary intake of high n-6 PUFA-containing vegetable oils, may explain the decreased level of DGLA in the epidermal tissue.

8,11,14-Eicosatrienoic Acid↗

PubMed1992

Post-transcriptional regulation by interferon-alpha of epsilon-globin production in human erythroleukemia K-562 cells.

Treatment of human K-562 erythroleukemia cells with interferon-alpha (IFN-alpha) resulted in a six-fold increase in the production of epsilon-globin, a component of embryonic hemoglobin, but in a two-fold or less augmentation of the production of other globin species. There was no comparable increase in the production of epsilon-globin mRNA following IFN treatment. We did, however, observe a shift in the cytoplasmic location of the epsilon-globin mRNA from the messenger ribonucleoprotein (mRNP) to the polysome fraction after IFN-alpha addition. No such shift was noted in the location of the mRNA for A gamma-globin, the major globin product of K-562 cells, which was always present in the polysome fraction. These results are significant with respect to the mechanisms of cellular regulation and differentiation induced by IFNs.

Antibodies, Monoclonal↗

PubMed1992

Atrial natriuretic peptide receptor subtypes in rat neuronal and astrocyte glial cultures.

We have compared the levels and subtypes of atrial natriuretic peptide (ANP) receptors in astrocyte glial and neuronal cultures prepared from the hypothalamus and brain stem of 1-day-old rats. Astrocyte glial cultures contain approximately twice the number of ANP receptors, as measured by 125I-ANP specific binding, compared with neuronal cultures. Rat ANP-(99-126), rat brain natriuretic peptide (BNP32), C-type natriuretic peptide (CNP-22), atriopeptin I, and [des-Gln18,Ser19,Gly20,Leu21, Gly22]atrial natriuretic factor-(4-23)-NH2[C-ANF-(4-23)] all competed strongly for 125I-ANP binding in both culture types, with inhibitory constant values ranging from 0.47 to 8.07 nM. The presence of ANP-C receptors (clearance type) in both cell types is indicated from the strong competition of 125I-ANP specific binding by C-ANF-(4-23). The potency profiles for stimulation of guanosine 3',5'-cyclic monophosphate levels by these peptides were ANP = BNP much greater than CNP-22 greater than atriopeptin I in astrocyte glia and CNP-22 much greater than BNP32 greater than ANP greater than atriopeptin I in neuronal cultures. These results indicate that both types of culture contain guanylate cyclase-coupled ANP receptors, with astrocytes containing predominantly the ANP-A subtype and neurons predominantly the ANP-B subtype.

Animals↗

PubMed1992

Angiotensin II stimulation of plasminogen activator inhibitor-1 gene expression in astroglial cells from the brain.

In this study, we investigated the mechanism of angiotensin II (Ang II) induced secretion of plasminogen activator inhibitor-1 (PAI-1) from astroglial cells prepared from 21-day-old rat brain. Competition-inhibition experiments with the use of selective antagonists for Ang II receptor subtypes indicated that astroglial cells contain chiefly Ang II type 1 (AT1) receptors. The interaction of Ang II with AT1 receptors resulted in a time- and concentration-dependent stimulation of PAI-1 gene expression. A maximal, 20-fold induction of PAI-1 messenger RNA (mRNA) steady-state levels was observed with 10 nM Ang II. This effect of Ang II was blocked by DuP753, an AT1 receptor antagonist, but not by PD123177, an AT2 receptor antagonist. Raise in PAI-1 mRNA levels was followed by an elevation in PAI-1 concentration in culture media reaching its maximum after 24 h. Interaction of Ang II with AT1 receptors also resulted in a time- and concentration-dependent stimulation of inositol phospholipid (IP) hydrolysis. A maximal, 3- to 5-fold stimulation of IP hydrolysis was observed with 10 nM Ang II. The time course experiments indicated that Ang II-induced stimulation of IP hydrolysis precedes the stimulation of PAI-1 mRNA. This suggested that activation of phospholipase C, IP hydrolysis system and possibly protein kinase C (PKC) may mediate Ang II's effect on PAI-1 mRNA. Direct stimulation of PKC by phorbol ester, phorbol 12,13-dibutyrate (PDB), resulted in a time- and concentration-dependent elevation of PAI-1 mRNA levels, similar to that caused by Ang II (maximal stimulation of 20-fold with 100 nM PDB for 4 h). This effect was totally blocked by the protein kinase C inhibitor, H7. In addition, Ang II stimulation of PAI-1 mRNA was also blocked by H7. In contrast, Ang II did not elevate PAI-1 mRNA levels in astroglial cultures from neonatal rat brains. However, treatment of neonatal cultures with PDB increased levels of this mRNA species. These observations indicate that the coupling of AT1 receptors with IP hydrolysis and PKC activation may be important for Ang II stimulation of PAI-1 gene expression. The lack of Ang II's effect on PAI-1 mRNA in neonatal astroglia may be explained either by a low coupling efficiency between AT1 receptors and the second messenger system, or by a low AT1 to AT2 receptor level ratio.

Angiotensin II↗

PubMed1992

Angiotensin-II induction of plasminogen activator inhibitor-1 gene expression in astroglial cells of normotensive and spontaneously hypertensive rat brain.

Angiotensin-II (AII) stimulates plasminogen activator inhibitor-1 (PAI-1) gene transcription, translation, and protein secretion from astroglial cells derived from normotensive [Wistar-Kyoto (WKY)] rat brain, an effect mediated by AII type 1 (AT1) receptors. Since abnormal expression of the brain AII system has been demonstrated in spontaneously hypertensive (SH) rats, we investigated the regulation of PAI-1 gene expression by AII in astroglial cells from the brains of these animals. AII caused an increase in PAI-1 gene expression in SH rat astroglia in a manner similar to that observed in WKY-derived cultures. However, both the basal and AII-stimulated levels of PAI-1 mRNA in SH rat astroglia were only 20% of those observed in WKY rat astroglial cultures. Consequently, there was a significant reduction in the de novo synthesis and secretion of PAI-1 from astroglia of SH rat brain. The reduced synthesis and secretion of PAI-1 from SH rat brain astroglia was associated with lower numbers of AT1 receptors in these cells. However, the steady state levels of AT1 receptor mRNA were comparable in both WKY and SH rat astroglia. This reduction in AII-modulated PAI-1 levels in SH rat astroglia is consistent with a proposed role of these interactions in the development of hypertension in these animals.

Angiotensin II↗

PubMed1992

Extracorporeal circulation as an alternative to open-chest cardiac compression for cardiac resuscitation.

Open-chest direct cardiac compression represents a more potent but highly invasive option for cardiac resuscitation when conventional techniques of closed-chest cardiac resuscitation fail after prolonged cardiac arrest. We postulated that venoarterial extracorporeal circulation might be a more effective intervention with less trauma. In the setting of human cardiac resuscitation, however, controlled studies would be limited by strategic constraints. Accordingly, the effectiveness of open-chest cardiac compression was compared with that of extracorporeal circulation after a 15-min interval of untreated ventricular fibrillation in a porcine model of cardiac arrest. Sixteen domestic pigs were randomized to resuscitation by either peripheral venoarterial extracorporeal circulation or open-chest direct cardiac compression. During resuscitation, epinephrine was continuously infused into the right atrium, and defibrillation was attempted by transthoracic countershock at 2-min intervals. Systemic blood flows averaged 198 ml.kg-1.min-1 with extracorporeal circulation. This contrasted with direct cardiac compression, in which flows averaged only 40 ml.kg-1.min-1. Coronary perfusion pressure, the major determinant of resuscitability on the basis of earlier studies, was correspondingly lower (94 vs 29 mm Hg). Extracorporeal circulation, in conjunction with transthoracic DC countershock and epinephrine, successfully reestablished spontaneous circulation in each of eight animals after 15 min of untreated ventricular fibrillation. This contrasted with the outcome after open-chest cardiac compression, in which spontaneous circulation was reestablished in only four of eight animals (p = .038). We conclude that extracorporeal circulation is a more effective alternative to direct cardiac compression for cardiac resuscitation after protracted cardiac arrest.

Acidosis↗

PubMed1992

[Changes in T cell subsets and the expression of receptors of transferrin and interleukin-2 in chronic active hepatitis].

The changes of T-cell subsets and expression of transferrin receptor (TFR) and interleukin-2 receptor (IL 2 R) of peripheral blood lymphocyte from patients with chronic active hepatitis (ACH) and chronic serious hepatitis (CSH) were studied. The results showed that T3+ cells were decreased. (P less than 0.01) and T8+ cells were significantly increased (P less than 0.01) in patients with CAH and CSH. TH/TS ratio was markedly decreased in both groups of patients (P less than 0.01). The data also showed that TFR and IL 2 R were in a state of high-expression in resting T-cell, but no obvious changes could be found in the expression of receptor of PHA-stimulated T cells of patients, as compared the controls. The results suggested that some inhibitory factor may be present in the serum of CAH and CSH patients.

CD4-CD8 Ratio↗

PubMed1992

Cardiac anaphylaxis in the Sprague-Dawley rat.

Anaphylactic shock was induced in pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats that had been sensitized 21 days earlier to crystallized ovalbumin. The sensitization was confirmed by passive cutaneous anaphylaxis test. Antigen challenge produced an immediate reduction in mean aortic pressure from 168 to 67 mm Hg within 1 minute after intravenous injection of ovalbumin. Plasma histamine increased from 4.5 to 128 ng/ml within 5 minutes after injection of antigen. There were no changes in airway or esophageal pressures after antigen challenge. Left ventricular diastolic pressure was increased, and contractility, as measured by the rate of change of left ventricular pressure (dP/dt), was decreased over an interval exceeding 90 minutes. When isolated, constant flow--perfused hearts from sensitized Sprague-Dawley rats were challenged with antigen, decreases in left ventricular function were observed associated with decreased positive and negative maximum rate of change of left ventricular pressure (dP/dtmax). This experimental model in the rat therefore demonstrated selective myocardial impairment with reduced inotropism and lusitropism after anaphylaxis.

Anaphylaxis↗

PubMed1991

Angiotensin II receptor subtypes are coupled with distinct signal-transduction mechanisms in neurons and astrocytes from rat brain.

Both neurons and astrocytes contain specific receptors for angiotensin II (AII). We used selective ligands for the AT1 and AT2 types of AII receptors to investigate the expression of functional receptor subtypes in astrocyte cultures and neuron cultures from 1-day-old (neonatal) rat brain. In astrocyte cultures, competition of 125I-labeled AII (125I-AII) specific binding with AT1 (DuP753) or AT2 (PD123177, CGP42112A, [Phe(p-NH2)6]AII) selective receptor ligands revealed a potency series of AII greater than DuP753 much greater than CGP42112A greater than [Phe(p-NH2)6]AII greater than PD123177. These results suggest a predominance of the AT1 receptor subtype in neonatal astrocytes. Also, in astrocyte cultures, AII stimulated increases in inositolphospholipid hydrolysis that were significantly reduced by the AT1 receptor antagonist DuP753 but not altered by the AT2 receptor antagonist PD123177. In neonatal neuron cultures, competition of 125I-AII specific binding with the above ligands revealed a potency series of CGP42112A = AII greater than [Phe(p- NH2)6]AII greater than PD123177 much greater than DuP753. 125I-AII specific binding to neonate neuronal cultures was reduced 73-84% by 1 microM PD123177, and the residual 125I-AII specific binding was eliminated by DuP753. Also, in neuron cultures, AII induced decreases in basal cGMP that were completely blocked by PD123177 or CGP42112A but not by DuP753. Our results suggest that astrocyte cultures from neonatal rat brains contain predominantly AT1 receptors that are coupled to a stimulation of inositophospholipid hydrolysis. In contrast, neuron cultures from neonatal rat brain contain mostly AT2 receptors that are coupled to a reduction in basal cGMP levels, but a smaller population of AT1 receptors is also present in these neurons.

Angiotensin II↗

PubMed1991

Phorbol ester inhibits 13-cis-retinoic acid-induced hydrolysis of phosphatidylinositol 4,5-bisphosphate in cultured murine keratinocytes: a possible negative feedback via protein kinase C-activation.

The incubation of double-labelled [( 14C]-glycerol and [3H]-myoinositol) keratinocytes with 13-cis retinoic acid induced the transient and simultaneous release of [3H]-inositol trisphosphate ([3H]-InsP3) and [14C]-diacylglycerol ([14C]-DAG) indicating that a possible mode of action of this retinoid on murine keratinocytes may be at least in part the early transient release of the two putative messengers (InsP3 and DAG) from phosphatidylinositol-4,5 bisphosphate (PtdIns4, 5P2). In contrast, the preincubation of the keratinocytes with 12-O-tetradecanoylphorbol-13-acetate (TPA) prior to incubation with 13-cis-RA suppressed the 13-cis-RA-induced release of [3H]-InsP3 and [14C]-DAG. The specificity of the TPA effect was established by the lack of effect of the biologically inactive 4 alpha-phorbol 12, 13-didecanoate. Furthermore, the incubation of the TPA-primed keratinocytes with 13-cis-RA caused a delayed and sustained accumulation of [14C]-DAG. An exploration of the source of this late release of [14C]-DAG revealed that this [14C]-DAG was released from non-inositol containing phospholipids, particularly, phosphatidylcholine. This latter DAG released in the TPA-primed cells correlated with the translocation of the cytoplasmic protein kinase C (PKC) activity to the membrane associated PKC activity. Taken together, these results suggest that alteration of PKC activity, presumably induced by DAG released from non-inositol phospholipids, may play a major role in the TPA-induced negative feedback inhibition of 13-cis RA-induced hydrolysis of keratinocyte PtdIns4, 5P2.

Animals↗

PubMed1991

Antineoplastic ether-linked phospholipid induces differentiation of acute myelogenous leukemic KG-1 cells into macrophage-like cells.

The culture of a human acute myelogenous leukemic cell line (KG-1) with a synthetic ether-linked phospholipid: 1-0-octadecyl-2-0-methylglycerol phosphocholine (ET-18-OCH3), suppressed the growth of the KG-1 cells while the variant subline, (KG-1a cells) similarly treated was unresponsive. The growth inhibition of the KG-1 cells was accompanied by morphological changes into cells of the monocyte/macrophage lineage. Histochemically, the ET-18-OCH3-treated KG-1 cells increase 17-fold in the nonspecific esterase activity when compared to control non-treated cells, whereas they responded negatively in the assay for the reduction of soluble nitroblue tetrazolium into insoluble blue formazan deposits (a marker for cells of the granulocytic lineage). Taken together, our data revealed that the synthetic ether-lipid inhibited the growth of the KG-1 acute myelogenous leukemic cells while inducing the differentiation of these cells into cells of the monocyte/macrophage-lineage. These effects of the synthetic ether lipid raise the possibility that naturally occurring ether-linked phospholipids may likewise function in vivo to modulate hyperproliferative processes and thus warrant further explorations.

Antineoplastic Agents↗

PubMed1991

Dietary supplementation with ethyl ester concentrates of fish oil (n-3) and borage oil (n-6) polyunsaturated fatty acids induces epidermal generation of local putative anti-inflammatory metabolites.

Clinical reports have attributed the amelioration of chronic inflammatory skin disorders to the presence of certain polyunsaturated fatty acids (PUFA) in dietary oils. To test the hypothesis of a local modulatory effect of these PUFA in the epidermis, the basal diet of normal guinea pigs was supplemented with ethyl esters of either fish oil [rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] or borage oil [rich in gamma-linolenic acid (GLA)]. Our data demonstrated that dietary oils influence the distribution of PUFA in epidermal phospholipids and the epidermal levels of PUFA-derived hydroxy fatty acids. Specifically, animals supplemented with ethyl esters of fish oil markedly incorporated EPA and DHA into epidermal phospholipids, which paralleled the epidermal accumulation of 15-hydroxyeicosapentaenoic acid (15-HEPE) and 17-hydroxydocosahexaenoic acid (17-HDoHE). Similarly, animals supplemented with esters of borage oil preferentially incorporated dihomogammalinolenic acid (DGLA), the epidermal elongase product of GLA, into the epidermal phospholipids, which also was accompanied by epidermal accumulation of 15-hydroxyeicosatrienoic acid (15-HETrE). By factoring the epidermal levels of the 15-lipoxygenase products and their relative inhibitory potencies, we evolved a measure of the overall potential of dietary oils to exert local anti-inflammatory effect. For example, the leukotriene inhibition potentials (LIP) of both fish oil and borage oil were greatly enhanced when compared to controls. Thus, the altered profiles of epidermal 15-lipoxygenase products generated from particular dietary oils may be responsible, at least in part, for reported ameliorative effects of oils on chronic inflammatory skin disorders.

Animals↗