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Biomedical subjects

H S Lin

Publications and source records attributed to H S Lin.

At least 109 records · Page 6Linked to original sources
PubMed1984

Synaptic junctions between the adrenergic axon varicosity and the pinealocyte in the rat.

Intercellular relationships of sympathetic nerve fibers and cells in pineal glands of Long-Evans rats and yellow-bellied country rats (Rattus losea Swinhoe) were studied with conventional electron microscopy. Typical synapses were found between adrenergic axon varicosities and pinealocytes. The synaptic cleft was 20-30 nm thick and contained granular or filamentous material of moderate electron density. Some small granulated vesicles attached to, or fused with, the presynaptic axolemma, a feature suggesting an exocytotic release of the vesicle content. The occurrence of membranous cisternae or tubules in the synaptic nerve ending may connote the phenomenon of synaptic vesicle recycling. Beneath the postsynaptic pinealocyte plasmalemma there was a dense plaque corresponding to the postsynaptic density of neurons. Possible origins and functional significance of the synapse-making nerve fibers are also discussed.

Adrenergic Fibers↗
PubMed1984

Receptor-mediated binding and internalization of colony-stimulating factor (CSF-1) by mouse peritoneal exudate macrophages.

Colony-stimulating factor (CSF-1) purified from L-cell-conditioned medium is a haemopoietic growth factor that specifically stimulates the proliferation and differentiation of mononuclear phagocytes. Using radioactively labelled CSF-1 [( 125I]CSF-1), the presence of specific CSF-1 receptor has been identified in the cells of the mononuclear phagocytic series and their precursors only. To determine the fate of [125I]CSF-1 bound to peritoneal exudate macrophages (PEM) at 37 degrees C, we have examined the distribution of radioactivity as a function of time by quantitative electron microscopic autoradiography. At 0 degrees C, we have localized the initial step in the binding of [125I]CSF-1 to the plasma membrane and its invaginations of the mouse PEM. Approximately 16% of the macrophages were not labelled at this time point. When the temperature was raised to 37 degrees C, the labelled CSF-1 was internalized progressively by the cells in a time-dependent fashion. The proportion of grains associated with the phagolysosome compartment increased progressively, reaching a plateau by 40 min after warming up, while the relative areas of the surface membrane and its invaginations decreased in invaginated membrane. At 37 degrees C, incubation with unlabelled CSF-1 resulted in a "down-regulation' of the subsequent [125I]CSF-1-binding activity by PEM in a time- and dose-dependent fashion. The restoration of CSF-1-binding activity after CSF-1 induced down-regulation was inhibited by cycloheximide, a potent protein synthesis inhibitor. These data provide direct evidence that at 37 degrees C, saturable binding of CSF-1 to PEM is followed by internalization and cellular degradation of the ligand and possibly its receptor by phagolysosomes.

Animals↗
PubMed1984

Arachidonic acid metabolism in inflamed gingiva and its inhibition by anti-inflammatory drugs.

Prostaglandin (PG) synthetase inhibitors are tissue-selective. Therefore, the action of four nonsteroidal anti-inflammatory drugs (NSAID) was tested against PG synthesis from 14C-arachidonic acid by gingival homogenate. Suprofen and tolmetin sodium did not significantly inhibit PGs at any of the three concentration levels used (10(-7), 10(-5), 10(-3) M), whereas flurbiprofen and zomepirac sodium did significantly inhibit PG formation at millimolar concentration. The results, coupled with our previous study on indomethacin, piroxicam and ibuprofen open the way for future tests of NSAIDs in treatment of gingival inflammation and periodontal disease.

Anti-Inflammatory Agents↗
PubMed1984

Colony-stimulating factor (CSF-1): its enhancement of plasminogen activator production and inhibition of cell growth in a mouse macrophage cell line.

CSF-1 is a hemopoietic growth factor that specifically causes the proliferation and differentiation of mononuclear phagocytic cells. J774 cells are a monocyte precursor-like macrophage cell line. This transformed macrophage cell line exhibits specific 125I-CSF-I-binding activity similar to that of normal murine macrophages, although its survival and growth is independent of CSF-1. At 0 degrees C, saturation of binding sites was achieved at 240 pM 125I-CSF-1. At 37 degrees C, the bound 125I-CSF-1 was rapidly internalized and degraded by the target cells with a T1/2 of approximately 30 min; degradation was inhibited by the addition of NH4Cl. The addition of CSF-1 to cultures caused dose-dependent inhibition rather than stimulation of [3H]thymidine uptake by J774 cells. Whereas CSF-1 stimulated the clonal growth of normal mouse peritoneal exudate macrophages, it inhibited the clonal growth of J774 cells in agar cultures. Furthermore, CSF-1 exhibited a concentration-dependent enhancement of the production of plasminogen activator (PA) by J774 cells. The enhanced production of PA was detected 6 hr after the addition of CSF-1 and was inhibited by the simultaneous addition of the anti-inflammatory drug. It appears that the effects of CSF-1 on cell proliferation and PA production by CSF-1 receptor-bearing cells are mediated by distinct intracellular pathways albeit through the same receptor.

Animals↗
PubMed1983

Enzyme-linked immunoadsorbent assay for detection of colony-stimulating factor (CSF-1).

An enzyme-linked immunoadsorbent assay (ELISA) has been developed for the quantitative measurement of L-cell colony-stimulating factor (CSF-1). According to this method, purified antigen (CSF-1) was allowed to adsorb to polystyrene or polyvinyl microtiter wells, which were then incubated with specific rat anti-CSF-1 antiserum with or without standard antigen or unknown test samples. The amount of antibody bound to the solid phase was then quantitated by enzyme (horseradish peroxidase)-conjugated rabbit anti-rat immunoglobulin antibody. This assay has a sensitivity comparable to that of the bioassay (approximately 5 U) and can be carried out in a single day.

Animals↗
PubMed1983

Tumor-promoting phorbol esters inhibit the binding of colony-stimulating factor (CSF-1) to murine peritoneal exudate macrophages.

L-cell colony-stimulating factor (CSF-1) is a sialoglycoprotein of molecular weight 70,000 daltons that specifically stimulates macrophage colony formation by single committed cells from normal mouse bone marrow and by various classes of more differentiated tissue-derived mononuclear phagocyte colony-forming cells (Stanley et al., 1978). CSF-1 interacts with target cells by direct and specific binding to membrane receptors (CSF-1 receptors) that are present only on cells of the mononuclear phagocyte series and their precursors. We studied the effect of tumor-promoting phorbol esters on the binding of 125I-labeled CSF-1 (125I-CSF-1) to murine peritoneal exudate macrophages (PEM). Biologically active TPA (12-O-tetradecanoyl phorbol-13-acetate) inhibits the binding of 125I-CSF-1 to its receptor on PEM. This inhibition exhibits temperature, time, and concentration dependence. At 37 degrees C, maximum inhibition occurred at about 10(-7) M; inhibition was 50% at 5 X 10(-9) M. At 0 degrees C, the inhibitory activity of TPA is diminished. The action of TPA on PEM is transient. Treated cells recover their 125I-CSF-1-binding activity whether TPA is later removed or not. The process of recovering CSF-1-binding activity is completely blocked by the addition of cycloheximide. When several phorbol derivatives were tested for their inhibitory activities, only biologically active phorbol esters were found to possess such activities. Furthermore, the inhibitory activities of various phorbol esters are proportional to their tumor-promoting activities. Inhibition appears to be due to a reduction in the total number of available CSF-1 receptors rather than a decrease in receptor affinity.

Animals↗
PubMed1983

Pharmacokinetic profile of a new anticonvulsant, stiripentol, in the rhesus monkey.

Stiripentol is a new anticonvulsant drug derived from phenyl-l-pentene-ol. One of its metabolites resulting from opening of the methylenedioxy ring also possesses anticonvulsant activity. This study undertook to define the overall pharmacokinetic profile of stiripentol in rhesus monkey prior to its efficacy evaluation. The experimental design included six treatments (three intravenous doses of 40, 80, and 120 mg; one oral dose of 80 mg; and two intraperitoneal doses of 80 and 120 mg) administered to five chaired rhesus monkeys in a randomized fashion. Sixteen plasma samples were obtained over 7 h and urine was collected for 24 h. A high-performance liquid chromatography assay was developed for the determination of stiripentol in plasma and urine (C8 reverse phase column and UV detection, lambda = 254 nm). The intravenous data revealed multiexponential behavior and therefore noncompartmental methods were used to describe the pharmacokinetics of stiripentol. Values for plasma clearances (L/h/kg) were 1.10 +/- 0.07 (40 mg), 0.92 +/- 0.08 (80 mg), and 0.86 +/- 0.15 (120 mg). The decrease in clearance with dose provided evidence of nonlinearity. The average mean residence time was 1.09 +/- 0.03 h. The average volume of distribution at steady state was 1.03 +/- 0.3 L/kg. The bioavailabilities obtained for the oral and intraperitoneal doses were consistent with first-pass effect predictions: 0.3 (oral), 0.32 (i.p. 80 mg), and 0.34 (i.p. 120 mg). The free fraction determined by equilibrium dialysis was less than 1%. The fraction of dose excreted unchanged in urine ranged between 0 and 3%. The metabolite with anticonvulsant activity could not be detected in plasma with any of the modes of administration. However, it was found in urine and accounted for 2% of the dose. The fraction metabolized by glucuronidation was 34.8 +/- 9.1%. The percentages of total amount of glucuronide excreted in the intervals 0-2, 2-4, 4-8, and 8-24 h were 70.6 +/- 6.2, 10.1 +/- 5.4, 13.6 +/- 5.1, and 5.7 +/- 3.1%. These findings suggested that the terminal phase was not associated with elimination but rather with drug distribution.

Animals↗
PubMed1983

Relative conversion of arachidonic acid through lipoxygenase and cyclooxygenase pathways by homogenates of diseased periodontal tissues.

The present study shows that 14C-arachidonic acid metabolism in gingiva of patients with periodontal disease is mainly via the lipoxygenase pathway. In two pools of gingival tissue homogenates, the lipoxygenase products contained 22.65% and 23.38%, while the prostaglandins (PGs), products of the cyclooxygenase pathway, contained only 4.85% and 3.98% of the total radioactivity incubated. 12-hydroxy-eicosatetraenoic acid (12-HETE), a lipoxygenase product, was detected as a major metabolite of arachidonic acid in gingiva.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

The effect of non-steroidal anti-inflammatory drugs on the metabolism of 14C-arachidonic acid by human gingival tissue in vitro.

We investigated the effect of non-steroidal anti-inflammatory drugs on prostaglandins (PGs) and 12-hydroxyeicosatetraenoic acid (12-HETE) formation by inflamed human gingival tissues. Gingival tissue homogenates were incubated with 14C-arachidonic acid in the presence of indomethacin, piroxicam, or ibuprofen, and the organic solvent extracts were chromatographed on silica gel plates with standards for radiometric assay. There was a significant negative trend between the doses (10(-7)-10(-3) M) of each of indomethacin, piroxicam, and ibuprofen, and the amounts of PGF2 alpha, PGE2, PGD2, and 15-keto-PGE2 produced. All three drugs have a significant inhibitory effect on PGs and 12-HETE production at 10(-3) M when compared with the control. The rank order effectiveness of the drugs, at 10(-3) M, on PG inhibition was indomethacin greater than piroxicam greater than ibuprofen, and on 12-HETE inhibition was indomethacin greater than ibuprofen greater than piroxicam.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

Lipopolysaccharide inhibits the binding of colony-stimulating factor (CSF-1) to murine peritoneal exudate macrophages.

These studies demonstrate the potent effect of bacterial endotoxin (LPS) on the inhibition of iodinated colony-stimulating factor- (125I-CSF-1) binding by murine peritoneal exudate macrophages (PEM) from C3H/An and C57BL/6 mice. As small an amount as 0.1 ng/ml LPS is sufficient to cause a significant inhibitory effect; this effect is temperature-, time- and concentration-dependent. LPS, however, causes minimal or no inhibition of 125I-CSF-1-binding by PEM from LPS-resistant C3H/HeJ mice. Inhibition of 125I-CSF-1-binding does not appear to be a result of a direct occupancy by LPS of CSF-1 receptors present on the cell membrane and is most likely due to a progressive loss of available CSF-1-binding sites. The effect can be neutralized by the addition of the antibiotic polymyxin B, which binds to the lipid A portion of LPS. The action of LPS on PEM is transient; treated cells recover their 125I-CSF-1-binding activity whether or not LPS is later removed. The restoration of 125I-CSF-1-binding activity can be blocked completely by the addition of cyclohexamide. These findings suggest the rapid, LPS-induced disappearance of CSF-1 receptors from the cell surface may be related to the activation of macrophages by LPS.

Animals↗
PubMed1982

Binding, internalization and degradation of colony-stimulating factor by peritoneal exudate macrophages.

Iodinated colony-stimulating factor produced by L-cells (125I-CSF-1) binds specifically to murine peritoneal exudate macrophages. At 37 degrees C, the cell-bound 125I-CSF-1 was internalized and degraded very rapidly, with the appearance of radioactive iodotyrosine in the medium. At 0 degree C, the cell-bound 125I-CSF-1 was not internalized and degraded, nor did it dissociate from the membrane. The internalization and degradation at 37 degrees C could be blocked or reduced by the presence of phenylglyoxal, methylamine and NH4Cl. The chemical nature of the CSF-1 binding site is polypeptide as judged by its sensitivity to trypsin treatment. After the binding and degradation of unlabeled CSF-1, the exudate cells were no longer able to rebind freshly added 125I-CSF-1, indicating the removal of CSF-1 binding site. The binding capacity of these cells, however, could be restored by prolonged incubation at 37 degrees C but not at 0 degrees C in culture medium containing fetal calf serum.

Animals↗
PubMed1982

Mechanical and neurological response of cat spinal cord under static loading.

The force/deformation relationship of the exposed spinal cord of cats was studied when the force was gradually applied posteriorly at T10. A linear elastic behavior was identified for deformation less than 0.5 mm, but it was not observed when the static force was no longer supported by the dural sheath. Nonlinear force/deformation, along with a strong hysteresis during a cycle of compression and decompression. The mechanical behavior remained practically the same in a repeated loading if the deformation was less than 2 mm. The motor function of cats did not recover after the cord had been compressed to 4 mm. The associated static force was about 15% of the dynamic force producing the same deformation.

Animals↗
PubMed1982

Testosterone inhibits prostaglandin formation by human gingival connective tissue: relationship to 14C-arachidonic acid metabolism.

The relationship between various concentrations of the male sex steroid, testosterone, and the formation of radioactive prostaglandins (PGs) from 14C-arachidonic acid by human gingival homogenate has been investigated. There were statistically significant (combined) linear and quadratic trends between hormone treatment at concentrations of 10(-9), 10(-7), 10(-5) and 10(-3)M and the amounts of PGF2, PGE2, PGD2 and 15-keto-PGE2 formed. The mean amount of each PG formed at the various concentrations of testosterone was statistically significantly less than the corresponding control level. The results indicate that testosterone, at the dose levels tested, is inhibitory to the cyclooxygenase pathway of arachidonic acid metabolism in gingiva.

Arachidonic Acid↗
PubMed1982

Effects of hydrocortisone acetate on pulmonary alveolar macrophage colony-forming cells.

We investigated the effect of prolonged monocytopenia induced by daily injections of hydrocortisone acetate on the number of alveolar cells and alveolar macrophage colony-forming cells (AL-CFC) in mice. We did not observe an appreciable reduction in the number of either alveolar macrophages of AL-CFC under this experimental condition, which markedly inhibited the blood monocyte concentration over 10 days. These results suggest the existence of a mechanism by which the number of alveolar macrophages, including AL-CFC, can be maintained without a continuous migration of blood monocytes into alveolar spaces.

Administration, Topical↗
PubMed1982

The relationship between the concentration of female sex steroids and prostaglandins production by human gingiva in vitro.

The relationship between various concentrations of estradiol-17 beta and progesterone, alone and in combination, and the formation of radioactive prostaglandins (PGs) from 14C-arachidonic acid by gingival homogenate has been investigated. There was a statistically significant negative linear trend between each of the hormone treatments at concentrations of 10(-9), 10(-7), 10(-5) and 10(-3)M and the amounts of 6-keto-PGF1a, PGF2a, PGE2, PGD2 and 15-keto-PGE2 formed. Each of estradiol-17 beta and progesterone at 10(-9) and 10(-7)M exerted stimulatory effect, whereas at higher concentrations they had an inhibitory effect on all PGs tested. These observations suggest that the concentration of female sex hormones is an important factor in regulating PG biosynthesis by gingival tissue.

6-Ketoprostaglandin F1 alpha↗