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T T Nguyen

Publications and source records attributed to T T Nguyen.

At least 235 records · Page 13Linked to original sources
PubMed1987

Bovine adrenal chromaffin granules are a site of synthesis of atrial natriuretic factor.

We have previously reported the existence of a peptide factor in the adrenal medulla which inhibits aldosterone secretion in cultured bovine zona glomerulosa cells. The acid extracts of chromaffin granules from bovine adrenal medulla were purified by a four step high performance liquid chromatography procedure. Two active fractions exhibited sequence homology with bovine atrial natriuretic factor ANF (Ser99-Tyr126) and its polypeptide precursor (Asn1-Tyr126). The occurrence of both precursor and mature forms of ANF within chromaffin granules indicates the endogenous character of ANF in the adrenal medulla and suggests the potential usefulness of cultured adrenal chromaffin cells for investigating the synthesis, maturation and secretion of atrial peptides.

Adrenal Medulla↗
PubMed1987

Oligo-[alpha]-deoxynucleotides covalently linked to an intercalating agent. Double helices with parallel strands are formed with complementary oligo-[beta]-deoxynucleotides.

An oligo-[alpha]-deoxynucleotide of sequence (5')d(TCTAAACTC) (3') was synthesized using the alpha-anomers of deoxynucleosides and its 5'-phosphate was covalently linked to a 9-amino acridine derivative via a pentamethylene linker. Two oligo-[beta]-deoxynucleotides containing the complementary sequence in either the 5'----3' or the 3'----5' orientation were synthesized using natural [beta]-deoxynucleosides. Complex formation was investigated by absorption and fluorescence spectroscopies. No change in spectroscopic properties was detected with the anti-parallel [beta] sequence. Absorption changes were induced in the visible absorption band of the acridine derivative at 2 degrees C when the acridine-substituted oligo-[alpha]-deoxynucleotide was mixed in equimolecular amounts with the complementary [beta]-sequence in the parallel orientation. Hypochromism was observed in the UV range. The fluorescence of the acridine derivative was quenched by the guanine base present in the second position of the complementary sequence. Cooperative dissociation curves were observed and identical values of melting temperatures were obtained by absorption and fluorescence. An increase in salt concentration stabilized the complex with a delta Tm of 8 degrees C when NaCl concentration increased from 0.1 to 1 M. These results demonstrate that an oligo-[alpha]-deoxynucleotide covalently linked to an intercalating agent is able to form a double helix with an oligo-[beta]-deoxynucleotide. The two strands of this [alpha]-[beta] double helix adopt a parallel 5'----3' orientation. The acridine ring is able to intercalate between the first two base pairs on the 5'-side of the duplex structure.

Base Sequence↗
PubMed1987

Transmitter releasing action of selegiline ((-)-deprenyl) from peripheral sympathetic nerves under different experimental conditions.

A high concentration of selegiline ((-)-deprenyl; 10(-4) M) potentiated low frequency (2 Hz) nerve stimulation-evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit in the presence of neuronal (cocaine, 3 X 10(-5) M) and extraneuronal (corticosterone, 5 X 10(-5) M) uptake blockers, and inhibited the postsynaptic response. The transmitter-releasing action of 10(-4) M selegiline was inhibited by a moderate increase of external K+ (23.6 mM). Excess K+ by itself abolished the nerve-evoked release of [3H]noradrenaline but did not increase the resting outflow of radioactivity. Excess Ca2+ (7.5 mM) increased the stimulation-evoked transmitter release. In the presence of excess Ca2+, selegiline (10(-4) M) was effective in increasing the [3H]noradrenaline release in response to nerve-stimulation. Excess Ca2+ partly antagonized the postsynaptic inhibitory action of selegiline. In Ca2+-free, 1 mM EGTA-containing Krebs solution both the nerve-evoked 3H release and the transmitter releasing action of selegiline were abolished in agreement with the 'Ca-hypothesis'. The voltage-dependent K+-channel blocker, 4-aminopyridine (10(-5) M), increased the nerve-stimulation-evoked release of tritium from arteries. If selegiline was also present in the perfusion medium the nerve-evoked transmitter release further increased. 4-Aminopyridine completely antagonized the inhibitory action of selegiline on the postsynaptic contraction.

Animals↗
PubMed1987

[3H]noradrenaline release from rabbit pulmonary artery: sodium-pump-dependent sodium-calcium exchange.

1. The release of [3H]noradrenaline ([3H]NA) from the isolated main pulmonary artery of the rabbit has been measured in the presence of neuronal (cocaine, 3 X 10(-5) M) and extraneuronal (corticosterone, 5 X 10(-5) M) uptake blockers. 2. K+ removal from the external medium increased the release of [3H]NA, an action transiently inhibited by Ca2+-free (+1 mM-EGTA) solution, i.e. after Ca2+ removal transmitter release was first abolished and then started to increase again after a delay lasting about 90-120 min. 3. Ca2+ readmission to arteries which had been kept in Ca2+- and 'K+-free' solution, markedly increased the [3H]NA release. The rate of transmitter release was dependent on the preceding perfusion period with 'K+-free' solution, being greater for longer exposure times. 4. When Ca2+ and K+ were readmitted together to K+-depleted and Na+-enriched preparations, the release of [3H]NA transiently increased. 5. If K+ was readmitted first, the subsequently applied Ca2+ was ineffective in producing transmitter release. 6. Different alkali metal ions (Rb+, Cs+ or Li+) were also readmitted as K+ substitutes together with Ca2+. In all cases the release of neurotransmitter transiently increased; however, the rate of release was dependent on the monovalent cation used. Thus, Rb+ ions were as effective as, Cs+ about one-third as effective as, and Li+ about one-fifth as effective as K+ in activating the Na+ pump. 7. It is concluded that in the absence of external Ca2+, and in response to Na+-pump inhibition, the release of Ca2+ from internal stores is responsible for the NA release observed. On readmission of Ca2+ the rate of transmitter release is dependent on the Na+ previously gained inside. Furthermore, the activity of the Na+ pump determines the rate of transmitter release through the Na-Ca exchange mechanism.

Animals↗
PubMed1987

Nonadrenergic modulation by clonidine of the cosecretion of catecholamines and enkephalins in adrenal chromaffin cells.

Cultured bovine chromaffin cells cosecrete catecholamines and enkephalins following cholinergic nicotinic stimulation. Initial reports on the inhibitory effect of clonidine on catecholamine secretion raised the possibility of a modulation of chromaffin cell function through a presynaptic adrenergic mechanism. The purpose of this work was to investigate the pharmacological characteristics of this inhibitory effect of clonidine on the cosecretion of catecholamines and enkephalins in 4-day-old cultured chromaffin cells. We observed that clonidine completely inhibits nicotine-stimulated secretion of both leucine-enkephalin and catecholamines with an IC50 of 34 microM. Treatment of chromaffin cells for 3 days with 100 nM reserpine leads to a 67% increase in nicotine-stimulated secretion of leucine-enkephalin without any effect on the IC50 of clonidine. In reserpine-treated chromaffin cells, norepinephrine (100 microM) inhibits only by 27% nicotine-stimulated secretion of leucine-enkephalin with an IC50 of 50 microM. Neither the alpha 2-adrenergic antagonist yohimbine nor the alpha 1-adrenergic antagonist prazosin could fully reverse the inhibitory effect of clonidine on leucine-enkephalin secretion at 10 nM. These results tend to rule out the role of alpha-adrenergic receptors in the mediation of clonidine inhibition of cosecretion in chromaffin cells.

Adrenal Medulla↗
PubMed1987

Analysis of the immunomodulatory properties of the secretin-glucagon family of peptides on mouse lymphoid cell functions and the demonstration of specific receptors on T cells.

The ability of members of the secretin-glucagon family of peptides to modulate the responses of mouse lymphoid cells stimulated with Concanavalin A (Con A), Lipopolysaccharide (LPS) and alloantigens was determined. It was observed that vasoactive intestinal peptide (VIP) and peptide having NH2-terminal histidine and COOH-terminal Isoleucine (PHI) inhibited the incorporation of 3H-methyl-thymidine by cells stimulated with Con A (55% inhibition) or alloantigen-bearing cells (40% inhibition). Secretin was approximately 10,000 less effective as an immunomodulator. Other members of the neuropeptide family, including glucagon and gastric inhibitory peptide, were ineffective in affecting mitogenesis elicited by Con A (20% inhibition). Lipopolysaccharide stimulated spleen cells were refractory to modulation by all members of the secretin-glucagon family of peptides (less than 5% modulation). The inhibition measured was concentration dependent over the range of 10(-6) to 10(-16) M. A peptide fragment of VIP encompassing amino acid residues 10-28, although capable of modulating in vitro responses, was 30-50% less effective than intact VIP. In addition, a VIP specific binding assay for mouse lymphoid cells was described. The binding of 125I-VIP to lymph node cells was rapid, saturable and reversible. Apparent equilibrium was reached within 15 minutes and nonspecific binding, measured as 125I-VIP binding in the presence of an excess (2 x 10(-7) M) of native VIP, did not exceed 25% of the total binding. In competitive experiments using VIP related peptides, PHI but not gastric inhibitory peptide, glucagon or secretin was able to significantly inhibit 125I-VIP binding. PHI had only one-eighth of the competitive capacity of native VIP. Scatchard analyses indicated the existence of a single class of high affinity receptors on lymph node cells (KD = 3.46 nM; 26,000 sites/cell). 125I-VIP specific binding to purified T cells (14%) was markedly higher than to B cells (3% binding). Thymocytes bound less than 2% of the label and had relatively few VIP binding sites (8,000) as compared with purified T cells (45,000 sites/cell). There was variability in the ability of various T cells tumors and functional T cell clones to bind 125I-VIP. The role of VIP as a physiological modulator of T cell activation is discussed.

Animals↗
PubMed1987

[Specific IgM of cytomegaloviruses and primary infection in kidney transplant patients].

In 20 renal transplant recipients suffering from symptomatic CMV infection we looked if a specific IgM response was indicative of a primary infection. By an ELISA technique we investigated the specific IgG and IgM in a pair of sera taken at the time of the transplantation and later at the time of the CMV isolation. For 7 out of 8 patients exhibiting an IgM response in the late serum, the pretransplant serum did not contain either IgG or IgM specific antibodies. Therefore the specific IgM response was associated in 7 out of 8 patients with a primary CMV infection. Nevertheless in 6 other primary infected patients no specific IgM response was detected. Otherwise rheumatoid factors appeared in each primary infected patient developing a specific IgG response, with or without specific IgM response.

Antibodies, Viral↗
PubMed1986

The action of excess potassium and calcium on ouabain-evoked [3H]-noradrenaline release from the rabbit pulmonary artery.

[3H]-noradrenaline [( 3H]-NA) release from the main pulmonary artery of the rabbit has been measured in the presence of neuronal (cocaine, 3 X 10(-5) M) and extraneuronal (corticosterone, 5 X 10(-5) M) uptake blockers. Removal of K from the external medium increased the [3H]-NA release. In the absence of external K, ouabain (10(-4) M) further enhanced the neurotransmitter release. The 'K-free' stimulated [3H]-NA release was inhibited by an increase of external Ca (7.5 mM), an action antagonized by ouabain. After preperfusion of the preparations for 30 min with either excess K (23.6 mM) or excess Ca (7.5 mM), the ouabain-stimulated [3H]-NA release was inhibited by about 50%; the rates of inhibition did not differ significantly from each other. However, the characteristic initial delay before ouabain-evoked neurotransmitter release was shortened in excess K, and prolonged in excess Ca-containing solution. When both excess K and Ca were applied together 30 min before ouabain perfusion, the action of ouabain in releasing neurotransmitter was also inhibited but the rate of inhibition did not differ significantly from that seen when K or Ca were applied separately. The action of K in shortening the initial delay was partly antagonized by Ca. Excess Ca antagonized the inhibition of ouabain-stimulated [3H]-NA release caused by excess K when Ca and ouabain were applied together after 30 min preperfusion with excess K-containing solution. Again excess Ca failed to inhibit the ouabain-evoked neurotransmitter release if ouabain and excess K were applied together after excess Ca preperfusion (30 min). In both cases the initial delay of ouabain action was greatly shortened. 6 The results suggest a Na-Ca competition at the external activation site of the nerve terminal sodium-pump similar to that of Na-K competition. Furthermore it seems that there is a sort of K-Ca competition as well, suggested by the finding that excess Ca prevented the inhibition caused by excess K of ouabain-evoked noradrenaline release and vice versa.

Animals↗
PubMed1986

[3H]noradrenaline-releasing action of vinpocetine in the isolated main pulmonary artery of the rabbit.

Vinpocetine (10(-6)-3 X 10(-5) M) increased both the resting and the nerve stimulation-evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3 X 10(-5) M; corticosterone, 5 X 10(-5) M), and inhibited the nerve stimulation-evoked postsynaptic response. The resting transmitter releasing action of vinpocetine increased in the absence of cocaine. Exogenously applied (-)noradrenaline [(-)NA] (10(-6) M) or clonidine (10(-6) M) inhibited the vinpocetine (3 X 10(-5) M)-potentiated [3H]NA release and contracted the circular muscle. The clonidine-induced contraction was abolished by 10(-7) M prazosin. The inhibitory action of (-)-NA on vinpocetine-potentiated [3H]NA release was partly antagonized by 3 X 10(-7) M yohimbine, a preferential alpha 2-adrenoceptor blocker. In Ca-free Krebs solution containing 1 mM EGTA the neurotransmitter releasing action of vinpocetine was abolished, however, its stimulating action on the resting [3H]NA outflow was not changed. In Na-pump-inhibited arteries (K-free solution), where both the resting and the nerve stimulation-evoked release of neurotransmitter had already been increased, vinpocetine further enhanced the nerve stimulation-evoked release of [3H]NA. It is concluded that vinpocetine may have alpha 2- and alpha 1-adrenoceptor blocking action, as well as a tyramine-like effect. The presynaptic neurotransmitter releasing action of vinpocetine is presumably the consequence of its inhibitory action on the Ca-pump which is suggested by the finding that in K-free solution vinpocetine was able to enhance further the release of neurotransmitter.

Animals↗
PubMed1985

Oligonucleotides covalently linked to intercalating agents. Influence of positively charged substituents on binding to complementary sequences.

A pentamethylene chain was used to covalently link the 3'-phosphate of oligothymidylates to the 9-amino group of an acridine derivative. Positively charged substituents were further attached to the 3'-phosphate group to form 3'-phosphotriesters. These molecules form specific complexes with poly(rA) which involve the formation of a number of A X T base pairs equal to that of thymines in the oligonucleotide. Absorption changes induced in the acridine absorption bands are similar to those expected upon intercalation of the acridine dye between A X T base pairs. The acridine covalently linked to the 3'-phosphate strongly stabilizes the complexes formed with poly(rA) as compared with the corresponding unsubstituted oligodeoxynucleotide. The presence of a positively charged substituent on the 3'-phosphate together with the acridine dye further enhances the interaction. The effect of salt concentration on complex stability depends on the number of negatively charged phosphate groups of the oligodeoxynucleotide and on the nature of the substituents borne by the 3'-phosphate group. When the oligothymidylate is substituted by an acridine dye, the stability of the poly(rA) complexes increases when salt concentration increases. If an additional positively charged substituent is present on the 3'-phosphate group, stability decreases when salt concentration increases for the shortest oligonucleotide (trimer) and increases with longer oligonucleotides. Thermodynamic parameters have been calculated from the concentration dependence of melting temperatures.

Base Sequence↗
PubMed1985

Glucocorticoid resistance is a dominant trait in hybrids between cytolytic T-lymphocyte lines and AKR thymomas.

By screening several cytolytic T-lymphocyte lines, AKR thymomas, and CTL X AKR thymoma hybrids from two different crosses for their sensitivity to the glucocorticoid (GC) analog dexamethasone (dex), we have found that CTL lines and cytolytically active, IL-2-dependent (CTL-like) hybrids are resistant to the cytostatic or cytolytic effects of dex; AKR thymomas and thymoma-like hybrids (cytolytically inactive, IL-2-independent), however, are sensitive to these effects of the drug. The GC resistance behaves like a dominant trait in these crosses. Although they are resistant to GC, the CTL lines and the CTL-like hybrids do contain functional hormone receptors and macrophage-activating factor (MAF) release by the CTL lines and CTL-like hybrids is inhibited by dex.

Animals↗
PubMed1985

Presynaptic autoinhibition during rest and sodium-pump inhibition in isolated rat portal vein preparation.

In the presence of cocaine and corticosterone low-frequency (2 Hz) nerve stimulation evoked release of [3H]noradrenaline measured from isolated rat portal vein preparation. In normal Krebs solution exogenously applied l-noradrenaline (3 X 10(-8)-10(-6) M) significantly reduced the nerve-evoked [3H]noradrenaline release. The IC50 value of L-noradrenaline proved to be 1.8 X 10(-7) M. Yohimbine (3 X 10(-7) M) maximally blocked the alpha 2-adrenoceptors and enhanced nerve-evoked [3H]noradrenaline release. In the presence of 5.9 mM external K+, ouabain up to 10(-4) M did not affect either the resting or the stimulation-evoked release of radioactivity from tissues. In the absence of external K+ both the resting and the nerve-evoked release of [3H]noradrenaline increased markedly. When K+ was readmitted to preparations which had been kept in K+-free solution both the resting and the stimulation-evoked [3H]noradrenaline release were greatly reduced temporarily. In K+-free solution L-noradrenaline (10(-6) M) and yohimbine (3 X 10(-7) M) failed to significantly alter the nerve-evoked release. However, 3 X 10(-6) M yohimbine in K+-free solution significantly increased the stimulation-evoked release of [3H]noradrenaline. It is concluded that presynaptic alpha 2-adrenoceptor-mediated "negative feed-back" is present in rat portal vein preparations which can be inhibited by the preferential alpha 2-adrenoceptor blocker, yohimbine. However, if the Na+-pump is inhibited (which by itself enhanced the transmitter release), presynaptic autoinhibition is more pronounced, since a high concentration of yohimbine is required to block it.

Animals↗
PubMed1984

Nucleotide sequence of the repressor gene of the TN10 tetracycline resistance determinant.

The Tn10 tetR gene encodes the repressor that regulates transcription of the Tn10 tetracycline resistance determinant. We have determined the DNA sequence of the tetR gene and a 905 base pair region immediately 3' to tetR. The tetR gene is located on a 701 base pair HincII restriction fragment. Deletions at either end of this region eliminate synthesis of the wild-type TetR protein in E. coli minicells, and eliminate TetR activity as measured by repression of beta-galactosidase synthesis in tetA-lacZ operon fusion strains. Taken together, the DNA sequence and the genetic data indicate that tetR encodes a 207 amino acid protein with a calculated molecular weight of 23,328. This value is in good agreement with estimates of 23,000-25,000 based on electrophoretic mobility in SDS-polyacrylamide gels. There is 47% amino acid sequence homology between the deduced sequences of the Tn10 and RP1/Tn1721 TetR proteins. There is, in addition, significant amino acid sequence homology between an NH2-terminal region of the Tn10 TetR repressor and the DNA recognition regions of other DNA-binding proteins.

Amino Acid Sequence↗
PubMed1984

The inhibitory action of PGF2 alpha on release of [3H]noradrenaline enhanced by alpha 2-adrenoceptor blockade, sodium-pump inhibition and 4-aminopyridine in the main pulmonary artery of the rabbit.

Large concentrations of prostaglandin PGF2 alpha inhibited the stimulation (2 Hz) evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit (the inhibition caused by 3 X 10(-5) M PGF2 alpha was 62%). Furthermore, PGF2 alpha inhibited the release evoked by stimulation when it was enhanced by different procedures. During blockade of presynaptic alpha 2-adrenoceptors by 3 X 10(-7) M yohimbine, which by itself enhanced the overflow of [3H]NA in response to stimulation, the inhibitory action of PGF2 alpha was more pronounced (78.2%). In tissue in which the Na+-pump was inhibited (K+-free treatment) where the overflow of 3H was markedly increased, PGF2 alpha exerted nearly equal inhibition of transmitter release to that observed in control experiments (64.3%). The inhibitory effect of PGF2 alpha on the stimulation-evoked release of [3H]NA was less pronounced (32.1%) in the presence of 10(-4) M 4-aminopyridine (a blocker of K+-channels).

4-Aminopyridine↗
PubMed1984

[3H]noradrenaline release evoked by selegiline ((-)-deprenyl) in the isolated main pulmonary artery of the rabbit.

High concentrations of selegiline[-)-deprenyl) (greater than 10(-5) M) enhanced the nerve stimulation (2 Hz)-evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit. This facilitation of stimulation-evoked [3H]noradrenaline release by selegiline was reduced by exogenous (-)-noradrenaline, an agonist of presynaptic alpha 2-adrenoceptors. This inhibitory action of (-)-noradrenaline was partly antagonized by yohimbine, a selective alpha 2-adrenoceptor blocker. When the stimulation-evoked [3H]noradrenaline release had already been increased by inhibition of Na+-pump (K+-free solution), selegiline further enhanced the nerve-evoked release of labelled neurotransmitter.

Animals↗
PubMed1984

Spontaneous [3H]noradrenaline release from the main pulmonary artery of the rabbit induced by sodium-pump inhibition.

Inhibition of Na pump either by ouabain (10(-4) M) or by K removal increased the [3H]noradrenaline [( 3H]NA) release from the isolated main pulmonary artery of the rabbit in the presence of neuronal (cocaine, 3 X 10(-5) M) and extraneuronal (corticosterone, 5 X 10(-5) M) uptake blockers. The ouabain-evoked [3H]NA release began after a delay of about 30 min and peaked after 66 min of ouabain application. Both times were shortened by omission of K from the external medium. About 90% of ouabain-evoked [3H]NA release proved to be external Ca concentration ([Ca]o) dependent and the peak effect was delayed by about 80 min in Ca-free (+ 1 mM EGTA) solution. In the presence of external Ca (2.5 mM) the [3H]NA-releasing effect of 'K-free' treatment was much less pronounced than that of 10(-4) M ouabain, the initial delay in transmitter release was shorter (10-15 min) and the peak effect developed earlier (at 42 min). On readmission of K the [3H]NA release recovered quickly to the original value. Ca removal did not antagonize the transmitter release observed in K-free solution, but the peak release was delayed by about 90 min. A low concentration of ouabain (10(-5) M) failed to produce transmitter release in the presence of normal external K, but markedly increased the release in K-free solution. The release was much bigger than the sum of their separate effects, and the rate of rise was faster than when 10(-4) M ouabain was applied in normal solution. Excess Ca (7.5; 15 mM) inhibited the [3H]NA release observed in K-free solution. 7.5 mM-Ca also delayed the transmitter-releasing action of 10(-4) M ouabain, an effect antagonized by omission of K from the external medium. The mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP, 10(-5) M) significantly increased the [3H]NA release in Ca-free, 1 mM EGTA-containing solution, and enhanced the effects of ouabain (10(-4) M). The Ca ionophore A23187 (10(-5) M) also significantly increased the [3H]NA release in the absence of external Ca and in the presence of 1 mM EGTA. Again, in the presence of A23187 the effects of 10(-4) M ouabain in releasing neurotransmitter were enhanced. When CCCP and A23187 were applied together in Ca-free, EGTA solution the [3H]NA releasing action of ouabain was still apparent. Veratridine (10(-4) M) enhanced the transmitter release in the absence of external Ca in a tetrodotoxin (TTX)-sensitive manner.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗