Search PubMed⌕ Search

Biomedical subjects

S L Lee

Publications and source records attributed to S L Lee.

At least 163 records · Page 9Linked to original sources
PubMed1990

A study of police referrals to Woodbridge Hospital.

This is a retrospective study of 127 cases brought by the police under Section 32 of the Mental Health Act (1973). The aims of the study were to collect epidemiological data and to review the mental health provisions. Majority of the patients were Chinese, male, 20-39 age-group, single, unemployed, schizophrenic with previous admissions to Woodbridge Hospital. Aggressive behaviour and public nuisance were the commonest reasons for police interventions. Ninety percent of the patients required admissions to hospital. There was no apparent misuse of the Mental Health Act.

Adult↗
PubMed1989

Serotonin uptake and configurational change of bovine pulmonary artery smooth muscle cells in culture.

Although it is well known that endothelial cells transport serotonin (5-HT) from extracellular to intracellular locations, it has been generally assumed that smooth muscle cells do not accumulate 5-HT but, rather, respond to 5-HT through a receptor activity unrelated to uptake of this amine or via stimulation of endothelial-derived relaxing factor. In the present study smooth muscle cells (PASMC), isolated and cultured from bovine pulmonary artery, were evaluated for 5-HT uptake under a variety of conditions. 5-HT uptake was linear up to 15 min and the rate was seven- to eightfold higher than that by bovine pulmonary artery endothelial cells. There was intracellular metabolism of 5-HT to 5-hydroxyindoleacetic acid (5-HIAA). The uptake was inhibited by exposure to 4 degrees C, absence of Na+ from the medium, and agents such as imipramine, verapamil, ketanserin, and methiothepin. Like that of endothelial cells, 5-HT uptake by PASMC was stimulated by exposure of cells to anoxia for 24 hr. Unlike endothelial cells that showed no morphological changes, PASMC at early passage showed dendritic formation after 30-60 min exposure to 5-HT at a concentration as low as 10(-8) M. Although this configurational change in response to 5-HT was lost with passage of cells, transport of 5-HT by these cells was retained. The configurational change was blocked by agents that inhibited 5-HT uptake, such as imipramine, verapamil, ketanserin, and methiothepin; it was unaffected by inhibitors of protein kinase C, phospholipase C, and calmodulin or absence of Ca2+ from the medium. We conclude that PASMC, as well as endothelial cells, accumulate 5-HT; there appears to be a close relationship between 5-HT uptake and configurational change of early passaged PASMC in culture. The factor(s) required for the configurational change are absent in endothelial cells and lost during passage of PASMC.

Animals↗
PubMed1989

Altered sympathetic system and adrenoceptors during the development of cardiac hypertrophy.

Increasing experimental evidence suggests that the development of cardiac hypertrophy may involve the sympathetic system and associated receptor mechanisms. However, very little work has been done so far to understand changes in the sympathetic system and cardiac adrenoceptors soon after an increased work load is imposed on the heart. Accordingly rat hearts subjected to aortic banding-induced pressure overload were assessed 3, 7, and 14 days postoperatively. Sham-operated rats without aortic banding were used as a control group. Rats with aortic constriction had increases in heart rate, left ventricular systolic pressure, and total mechanical energy during the entire study period. The cardiac RNA level was increased without a significant increase in left ventricular mass on days 3 and 7 in aortic-banded animals; these results were associated with a decrease in the cardiac norepinephrine (NE) store and an increase in the plasma level of NE and dopamine beta-hydroxylase (DBH) activity. By day 14 a significant increase in left ventricular mass and the NE store were found; both plasma NE and DBH remained elevated. Catecholamines in other tissues such as the spleen and kidney were depleted in the banded group, whereas the dopamine level, particularly in the brain, was significantly higher during the entire study. Furthermore, the density of alpha-adrenoceptors was higher on day 3 of aortic banding, and a reciprocal correlation was evident between cardiac alpha- and beta-adrenoceptors on day 14; the density of beta-adrenoceptors was increased, whereas that of alpha-adrenoceptors was decreased in the banded group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Reduction of calcium channel antagonist binding sites by oxygen free radicals in rat heart.

In view of the importance of Ca2+-channels in controlling the entry of Ca2+ into the myocardium, this study was undertaken to examine the effects of oxygen free radicals on the binding of Ca2+-channel antagonists in rat heart by employing [3H]-nitrendipine as a ligand. Isolated heart membranes were incubated with xanthine + xanthine oxidase (a superoxide anion radicals generating system), hydrogen peroxide (an activated species of oxygen), or hydrogen peroxide + Fe2+ (a hydroxyl radicals generating system). The assay of the [3H]-nitrendipine binding activity revealed that the maximal number of binding sites (Bmax) were reduced in a time-dependent manner by superoxide radicals without any changes in the binding constant (Kd); a significant reduction of Bmax was seen after incubating membranes with xanthine + xanthine oxidase for a 10-min-period. Superoxide dismutase showed a protective effect on the superoxide radicals induced reduction in Bmax. Both hydrogen peroxide and hydroxyl radicals also depressed the Bmax for [3H]-nitrendipine binding without any significant change in Kd; catalase and mannitol showed protective effects on hydrogen peroxide or hydroxyl radicals induced depression in Bmax, respectively. These results indicate that oxygen free radicals may reduce the number of Ca2+-channels in the cell membrane and this change may contribute towards decreasing the voltage-dependent Ca2+ influx in the cardiac cell.

Animals↗
PubMed1989

Endothelial cell inhibition of hypoxia-induced stimulation of serotonin uptake by vascular smooth muscle cells.

Exposure of bovine pulmonary artery smooth muscle cells (SMC) to anoxia for 24 h resulted in an approximate twofold stimulation of serotonin (5-HT) uptake compared with SMC exposed to 20% O2. The stimulation of 5-HT uptake by exposure to anoxia was eliminated when bovine pulmonary artery endothelial cells (EC) were cocultured with SMC. Incubation with EC-conditioned medium produced similar inhibitory effects on 5-HT uptake of SMC exposed to anoxia, a result not seen with SMC-conditioned medium. The inhibitory effect of EC-conditioned medium on the anoxia-stimulated 5-HT uptake was concentration dependent and absent at a dilution of 1:16. The production of the inhibitor was time-dependent. The EC-derived inhibitory factor was heat-stable at 100 degrees C for as long as 10 min and was stable in a pH range from 5.0 to 10.0. Significant losses of inhibitory activity of EC-conditioned medium were observed after treatment with trypsin, pronase E, and proteinase K. The molecular weight on the inhibitory factor from EC-conditioned medium was estimated to be approximately 66,000 by size-exclusion chromatography. The data show that stimulated uptake of 5-HT by SMC under anoxic conditions is under regulation by a protein (or polypeptide) produced by EC.

Animals↗
PubMed1989

Hypoxia stimulates the release by bovine pulmonary artery endothelial cells of an inhibitor of pulmonary artery smooth muscle cell growth.

The proliferation of smooth muscle cells (SMC) seen in hypoxic pulmonary hypertension is a poorly understood phenomenon but may involve endothelial cell (EC)-SMC interaction. Using bovine pulmonary artery cells, we examined the effect of O2 tension and the role of EC or media conditioned by EC (ECCM) on SMC proliferation. We found no difference in SMC proliferation under 3%, 10%, and 20% O2. EC, co-cultured with SMC in 3% O2, inhibited SMC proliferation consistently by about 40% (versus SMC exposed to hypoxia but not to EC). In normoxia, the degree of inhibition was dependent on EC:SMC ratio. In separate experiments, media from EC exposed to 3% or 20% O2 had a mitogenic activity of 24% and 42%, respectively (compared to 100% mitogenic activity with 5% FCS), on serum-deprived SMC. On the other hand, when SMC were stimulated to grow with FCS, an inhibitory activity (IA) from ECCM on SMC proliferation was observed and was significantly greater in hypoxic versus normoxic ECCM (40% versus 21%, respectively). Amicon concentration showed that the IA was contained in the less than 10 kD fraction of ECCM. Preliminary characterization of this IA indicates that it is unlike any of the known inhibitors of SMC growth, such as lactic acid, prostaglandin derivatives, or heparan sulfate. We conclude that hypoxia causes pulmonary artery EC to release a unique inhibitor of SMC growth.

Animals↗
PubMed1989

Smooth muscle cell conditioned medium elevates angiotensin-converting enzyme of bovine pulmonary artery endothelial cells.

Conditioned medium obtained from bovine pulmonary artery smooth muscle cells (SMC) in culture was found to elevate angiotensin-I-converting enzyme (ACE) of bovine pulmonary artery endothelial cells (EC) by 2- to 3-fold upon incubation for 24 to 48 h. The elevation in ACE was time dependent and inhibited by 10(-6) M cycloheximide, making it likely that the elevation was related to new protein synthesis by EC. Conditioned medium from EC failed to produce the same effect. The stimulatory effect of SMC conditioned medium on EC ACE was uninfluenced by exposures to anoxia as compared with room air, either during conditioning of medium or while assaying the effect of conditioned medium on EC ACE. Inhibitors of prostaglandin metabolism and calcium transport failed to influence the stimulatory effect of SMC conditioned medium on EC ACE. The stimulatory effect on EC ACE by conditioned medium was additive to that produced by Ca2+ ionophore A23187 and 3-isobutyl-1-methylxanthine and, similar to baseline ACE, was inhibited by 3 x 10(-8) M ouabain. Thus, SMC produce a factor that regulates the level of EC ACE.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Interleukin-1 beta stimulates somatostatin biosynthesis in primary cultures of fetal rat brain.

Interleukin-1 (IL-1), a secretory product of activated macrophages and many other cell types, is an important mediator of the acute phase reaction to infection and to endotoxin administration. Previous reports that GH and TSH secretion are decreased following injection of endotoxin or IL-1 led us to test the hypothesis that IL-1 acts by releasing increased amounts of somatostatin (SS), a hypothalamic factor inhibitory of both GH and TSH release. Primary cultures of dispersed fetal rat diencephalic cells were found to contain increasing amounts of immunoreactive SS in both cells and media after addition of recombinant human IL-1 beta. This increase was detectable at 24 hours and continued for up to 6 days, the longest time interval tested. Increased content of SS peptide was accompanied by marked increases in SS mRNA. These changes were dose-related, the lowest effective dose being 10(-10) M. In contrast to the long term response, exposure of the cells to IL-1 beta for one hour had only minimal stimulating effects on somatostatin release. These data indicate that IL-1 beta is neurotrophic for the somatostatinergic neuron, an action that may be responsible at least in part, for the neuroendocrine response to infection.

Animals↗
PubMed1989

Effects of exogenous vasoconstrictors on coronary vascular resistance and prostacyclin production of the quiescent heart: the inhibitory effect of aspirin.

The in situ heart is exposed to blood-borne vasoconstrictor agents (e.g., vasopressin) which, if unopposed, may cause radically increased coronary vascular resistance (CVR). Release of endogenous vasodilator, such as prostacyclin (PGI2), is a possible mitigating mechanism. We investigated the ability of the heart to maintain CVR within a narrow range when exposed to exogenous vasoconstrictors. The isolated rat heart was perfused at constant flow rate (5-6 ml/min) with oxygenated Krebs-Ringer bicarbonate solution (37 degrees C, pH 7.4), and was rendered quiescent by a local injection of lidocaine to the atrio-ventricular node. Changes of perfusion pressure, indicating changes of CVR, were monitored and the cardiac effluent was collected for analysis of 6-keto PGF1 alpha and thromboxane B2 (stable metabolites of PGI2 and thromboxane A2, respectively) by radioimmunoassay. Hearts were infused with four different vasoconstrictors (i.e., serotonin, vasopressin, angiotensin II and the thromboxane A2/PGH2 mimetic, U46619). There was a linear relationship between the dose-dependent increase in CVR and PGI2 production in serotonin, U46619 and vasopressin-infused quiescent heart. Vasoconstriction induced by angiotensin II was not dose-dependent and was unrelated to PGI2 production. Thus, PGI2 is produced in response to coronary vessel constriction, presumably to mitigate the constriction. No detectable thromboxane B2 was released by any of these vasoconstrictors. Partial inhibition (approximately 50%) of PGI2 production by aspirin (5.6 microM) treatment resulted in a paradoxically decreased vasoconstriction except at the lowest level of serotonin and vasopressin. Aspirin (1 mM) greatly reduced PGI2 production (approximately 90%) but the fall in CVR persisted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Activation of heart sarcoplasmic reticulum Ca++-stimulated adenosine triphosphatase by insulin.

Although insulin is known to elicit a positive inotropic effect in cardiac muscle preparations, very little is known concerning the mechanism of this action. In view of the crucial role played by the sarcoplasmic reticular (SR) calcium transport in cardiac contractile events, the effects of insulin on the pig heart SR were investigated. Insulin activated the SR Ca++-stimulated adenosine triphosphatase (ATPase) in a concentration-dependent manner (0.1 mU to 1 U/ml); maximal activation (125%) was seen at 0.1 to 1 U/ml of insulin. Kinetic studies revealed that the insulin-induced activation was due to an increase in the apparent Vmax of Ca++-stimulated ATPase without any alteration in the Km. Insulin was found to bind with SR membranes in a specific manner and this binding was rapid, saturable and displacable. The dose-related increase in the activation of Ca++-stimulated ATPase was related linearly (r = 0.98) to binding of insulin with SR membranes; 50% activation of Ca++-stimulated ATPase was found to occur at 13.5 fmol of insulin binding per mg of SR protein. When insulin was allowed to dissociate by a 100-fold dilution of the insulin-receptor complex, the activity of SR Ca++-stimulated ATPase also declined gradually. Furthermore, proteolytic digestion on the membrane with trypsin (3 micrograms/mg of protein) decreased both insulin binding as well as the increase in Ca++-stimulated ATPase activity by about 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1989

Measurement of boar sperm motility by the trans-membrane migration method.

The conventional microscopic methods for evaluating sperm motility of domestic animals are mostly inadequate due to their subjectivity and lack of precision. Recently, a trans-membrane migration method, originally developed for the examination of human sperm motility, has substantially overcome these problems. This study investigated the applicability of the method to boar sperm motility measurement. The apparatus used was simple and consisted only of syringe plungers, poriferous membranes, and modified multi-well culture plates. It measured the proportion of sperm in the semen that moved across the membrane after incubation at 37 degrees C for 3 hr. The sperm motility as measured by this method correlated well with that measured by direct microscopic examinations. The measurement was more reliable using an 8-microns instead of a 5-microns pore-size membrane. The method was found to work equally well for the sperm motility measurement of the semen with a sperm concentration between 1.5 x 10(8)/ml and 6.0 x 10(8)/ml. The results indicate that this method is a simple, objective, quantitative, and reproducible design for the measurement of boar sperm motility.

Animals↗
PubMed1989

[A carotid resection in cervical tumors without a vascular reconstruction].

From 1979 to 1988, 15 cases, consisting of 12 carotid body paragangliomas, 1 vagal body paraganglioma, 1 aneurysm of the internal carotid artery, and 1 recurrent metastatic carcinoma of the neck, were given a simple carotid resection without a vascular reconstruction, since the lesions were fixed to the carotid artery. The collateral cerebral cross-flow was promoted preoperatively with the use of compressing exercises of the carotid artery and controlled by computerized rheoencephalography. There was no operative mortality, though a transient postoperative cerebral complication did occur in one female patient, from which she recovered in one month. Of this series of 15 patients, one died from a malignant lesion and 14 survived for 3 months to 9 years without cerebrovascular complications.

Adolescent↗
PubMed1988

Structure of the gene encoding rat thyrotropin releasing hormone.

The gene encoding the hypothalamic peptide thyrotropin releasing hormone (TRH) was isolated from two rat genomic bacteriophage libraries. Southern blot analysis indicates that the gene is present as a single copy in the rat genome. The transcriptional unit is 2.6 kilobases in size and contains three exons interrupted by two introns of approximately 750 and 450 base pairs. Exon 1 encodes the 5'-untranslated region of the mRNA, exon 2 encodes the signal sequence and the majority of the amino-terminal peptide, and exon 3 encodes the remainder of the amino-terminal peptide, five copies of the TRH sequence, the carboxyl-terminal peptide, and the 3'-untranslated region of the mRNA. The general structure of the TRH gene resembles that of three other polypeptide hormone genes, preproopiomelanocortin, preproenkephalin A, and preproenkephalin B. Further sequence analysis revealed that characteristic promoter elements are present in the 5'-flanking region of the TRH gene. In addition, sequence homologies with the glucocorticoid receptor binding site, the GC box hexanucleotide, and a portion of the flanking region of the thyroid stimulating hormone beta-subunit gene were also identified. These upstream sequences may be important for the regulation of TRH gene expression.

Amino Acid Sequence↗
PubMed1988

High prevalence of serum antibodies to reverse transcriptase in HIV-1-infected individuals.

The HIV immunoblot profiles of 700 HIV-antibody-positive sera were examined to determine the frequency of antibody reactivity with p66/p51, the reverse transcriptase of HIV. We report a remarkably high seroprevalence of antibodies to p66/p51, detected in 79% of the sera. Only gp41 is recognized more frequently in these assays. The level of anti-p66/p51 seroreactivity varies only slightly among the clinical stages of HIV infection.

AIDS-Related Complex↗
PubMed1987

Verapamil inhibits serotonin uptake of endothelial cells in culture by a mechanism unrelated to Ca2+ channel blockade.

Verapamil inhibited Na+-dependent uptake of serotonin (5-HT) by bovine pulmonary artery endothelial cells in culture both exposed to room air and stimulated by prior exposure to anoxia. The effect of verapamil occurred even in the absence of Ca2+ from the assay medium. Although absence of Ca2+ from the medium moderately reduced 5-HT uptake, stimulation of uptake was nevertheless observed for cells previously exposed to anoxia. Verapamil altered the Km, but not the Vmax, of 5-HT uptake. There was no change in 45Ca2+ uptake or release by cells previously exposed to anoxia as compared to those exposed to room air and verapamil did not influence 45Ca2+ fluxes by either set of cells. It is concluded that verapamil inhibits 5-HT uptake by endothelial cells through a mechanism other than Ca2+ channel blockade; the results are consistent with competitive inhibition of a 5-HT carrier. The stimulatory effect of anoxia on 5-HT uptake does not occur through a change in Ca2+ fluxes.

Animals↗