PubMed Health⌕ Search

Biomedical subjects

M T Lin

Publications and source records attributed to M T Lin.

At least 19 recordsLinked to original sources
PubMed1992

(2S-[2 alpha,3 alpha,3a beta,6 beta(R*),7 alpha, 7a alpha])-6-(3-benzyloxy-2-propyl)-2-hydroxy-2,3,7-trimethylhexahydro-4H- furo [3,2-c]pyran-4-one, a rearrangement product of pyranone derivatives in the tirandamycin A series.

The six- and five-membered heterocyclic rings are cis-fused and adopt twist-boat and half-chair conformations, respectively. The average bond distances are: Csp3-Csp3 1.520 (6), Csp3-Csp2 1.494 (6), C-Cbenz 1.360 (10) and Csp3-O 1.425 (5) A; the C = O and Csp2-O bond lengths are 1.214 (5) and 1.324 (5) A, respectively.

Aminoglycosides↗
PubMed1992

Plasmin and the regulation of tissue-type plasminogen activator biosynthesis in human endothelial cells.

Plasmin inhibited the biosynthesis of tissue-type plasminogen activator (tPA) antigen by human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. The amount of tPA antigen found in the 24-h conditioned medium of cells treated with 100 nM plasmin for 1 h was 20-30% of that in the control group. However, in contrast to tPA, such treatment led to a 3-fold increase in plasminogen activator inhibitor (PAI) activity, whereas the amount of PAI type 1 antigen was unchanged. The effects of plasmin on HUVEC were binding- and catalytic activity-dependent and were specifically blocked by epsilon-aminocaproic acid. Microplasmin, which has no kringle domains, was less effective in reducing tPA antigen biosynthesis or enhancing PAI activity in HUVEC. Kringle domains of plasmin affected neither tPA antigen nor PAI activity of the cells. Other proteases including chymotrypsin, trypsin, and collagenase at comparable concentrations did not have a significant effect on the biosynthesis of tPA antigen or PAI activity of HUVEC. Thrombin stimulated the biosynthesis of tPA and PAI-1 antigens by HUVEC. Thrombin also stimulated an increase in the protein kinase activity in HUVEC, whereas plasmin inhibited the protein kinase activity of the cells. It is possible that plasmin regulates the biosynthesis of tPA in HUVEC through the signal transduction pathway involving protein kinase.

Aminocaproic Acid↗
PubMed1992

Cerebral ischemia is the main cause for the onset of heat stroke syndrome in rabbits.

During the onset of heat stroke, rabbits displayed hyperthermia (42.8 degrees C), and decreased cerebral perfusion pressure and decreased cerebral blood flow (as reflected by a prolonged cerebral circulation time) compared to those of normothermic rabbits. On the other hand febrile rabbits, during the fever plateau did not show the above responses, although they had a similar level of hyperthermia (42.4 degrees C). The data support the concept that cerebral ischemia is the main cause for the onset of the heat stroke syndrome.

Animals↗
PubMed1992

Epidermal growth factor enhances a microsomal 12-lipoxygenase activity in A431 cells.

12-Hydroxyeicosatetraenoic acid (12-HETE) is formed from arachidonic acid either by 12-lipoxygenase or by a cytochrome P450 monooxygenase. 12-Lipoxygenase is generally localized in the soluble cytosolic fraction, and the cytochrome P450 monooxygenase is a microsomal enzyme. In this study, 12-HETE biosynthesis and the regulation of 12-HETE biosynthesis by epidermal growth factor (EGF) in A431 cells were investigated. 12-HETE was biosynthesized from arachidonic acid by the microsomal fraction of A431 cells, but not by the cytosolic fraction. The formation of 12-HETE was inhibited by 5,8,11,14-eicosatetraynoic acid, nordihydroguaiaretic acid, and caffeic acid. Nordihydroguaiaretic acid at 10(-4) M and 5,8,11,14-eicosatetraynoic acid at 10(-5) M almost completely inhibited its formation. However, the formation of 12-HETE was not affected by the presence of an NADPH-generating system, carbon monoxide, or SKF 525A. The biosynthetic 12-HETE was analyzed by chiral stationary phase high performance liquid chromatography and was highly enriched in (12S)-HETE. We therefore concluded that the enzyme responsible for the formation of (12S)-HETE in the microsomes of A431 cells is a 12-lipoxygenase. The microsomal 12-lipoxygenase of A431 cells belongs to the "leukocyte-type" enzyme as determined by substrate specificity and enzyme kinetics studies. The microsomal 12-lipoxygenase oxygenated linoleic acid much faster than the cytosolic platelet 12-lipoxygenase and is a "self-catalyzed inactivation" enzyme. Treatment of cells with 50 ng/ml EGF significantly induced microsomal 12-lipoxygenase activity. The lag period for the expression of the stimulatory effect of EGF on 12-lipoxygenase activity was approximately 10 h. The stimulatory effect of EGF on 12-lipoxygenase activity was completely blocked by treatment with 35 microM cycloheximide, indicating a requirement for de novo protein biosynthesis. Furthermore, the presence of the endogenous inhibitor of 12-lipoxygenase (which masked (12S)-HETE biosynthesis in intact cells) was identified in the cytosolic fraction of A431 cells. The putative inhibitor was enzyme-selective. It inhibited the leukocyte-type 12-lipoxygenase, but not the "platelet-type" enzyme.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1992

Stimulation of the nigrostriatal dopamine system inhibits both heat production and heat loss mechanisms in rats.

The effects of stimulating the pars compacta of the substantia nigra (SNC) on thermoregulation were assessed in normal rats, in rats with chemical lesion of the SNC dopamine (DA) pathways and in rats with striatal DA receptor blockade. Electrical stimulation of the SNC produced hypothermia, decreased metabolism and/or cutaneous vasoconstriction in rats at ambient temperatures (Ta) below 22 degrees C, as well as hyperthermia and cutaneous vasoconstriction in rats at Ta of 30 degrees C. Microinjection of an excitotoxic amino acid (kainic acid) at the same brain sites also produced the same thermal responses. In vivo voltammetric studies revealed that electrical or chemical stimulation of the SNC produced an increase in striatal DA release. The enhanced striatal DA release induced by SNC stimulation was attenuated in rats after selective destruction of the nigrostriatal DA pathway by administration of 6-hydroxydopamine into the medial forebrain bundle. In addition, the magnitude of the thermal responses produced by the SNC stimulation in the cold was attenuated by selective bilateral destruction of the nigrostriatal DA pathways or selective blockade of the striatal DA produced by intrastriatal infusion of haloperidol, a DA receptor antagonist. The results indicate that stimulation of the SNC inhibits both heat production and heat loss mechanisms in the rat.

Animals↗
PubMed1992

Spinal 5-HT pathways and the antinociception induced by intramedullary clonidine in rats.

The possible involvement of spinal 5-hydroxytryptamine (5-HT) pathways in antinociception induced by microinjection of clonidine into the ventrolateral surface of the medulla oblongata was investigated in rats. Microinjection of clonidine (10-20 micrograms), but not yohimbine (1 microgram) or 0.9% saline, into the lateral medulla prolonged the hot plate latency in rats. This clonidine-induced antinociception was abolished by intramedullary injection of the alpha 2-adrenoceptor antagonist, yohimbine. Selective destruction of spinal 5-HT neurons produced by intraspinal injection of 5,7-dihydroxytryptamine (5,7-DHT; 10 micrograms) or postsynaptic blockade of spinal 5-HT receptors produced by intrathecal injection of cyproheptadine (1 microgram; a mixed 5-HT1/5-HT2 antagonist) also abolished clonidine-induced antinociception. Rats given 5,7-DHT intraspinally or cyproheptadine intrathecally showed a decrease in hot plate latency as compared with the controls. In anesthetized rats, the 5-HT release from the thoracic spinal cord was enhanced by microinjection of clonidine into the lateral medulla. This enhanced spinal 5-HT release evoked by intramedullary injection of clonidine was abolished by pretreatment of rats with intraspinal injection of 5,7-DHT. These results indicate that 5-HT pathways to the spinal cord mediate the antinociceptive effect induced by microinjection of clonidine into the ventrolateral surface of the medulla oblongata in rats.

5,7-Dihydroxytryptamine↗
PubMed1992

Chemotactic and mitogenic activities of granulosa cells in developing follicles.

Chemotactic and mitogenic activities of granulosa cells in developing follicles were studied. Immature rats were subcutaneously injected with 20 IU of pregnant mare's serum gonadotrophin and killed at various intervals after injection. The ovaries were removed and granulosa cells were isolated and cultured in a serum-free medium supplemented with insulin, transferrin and hydrocortisone. Chemotactic and mitogenic activities in the conditioned medium were determined. Our results demonstrated that in addition to mitogenic activity, chemotactic activity was also expressed in the conditioned medium of granulosa cells. Both activities increased with the maturity of follicles. A gel filtration analysis revealed that there were two peaks showing both mitogenic and chemotactic activities with a molecular size smaller than 5000. These peaks had various sensitivities to heat and trypsin treatment. In addition, the active component of both peaks was organic solvent-extractable. A thin-layer chromatography analysis indicated that the lipid component was not prostaglandin, estradiol or hydrocortisone.

Analysis of Variance↗
PubMed1992

Reduction of blood PO2 decrease and PCO2 increase during asphyxia by paramedian reticular nucleus in cats.

Effects of activation of paramedian reticular nucleus (PRN) on the systemic arterial blood pressure (SAP), heart rate, renal nerve activity (RNA), and changes of the partial pressure of the arterial blood oxygen (PO2) and carbon dioxide (PCO2) during asphyxia were studied in cats anesthetized with chloralose (40 mg/kg) and urethane (400 mg/kg). During a 35-s period of asphyxial anoxia, SAP and RNA increased while heart rate decreased significantly. The arterial blood PO2 decreased by 64.6 +/- 4.7% while the PCO2 increased by 54.6 +/- 6.3%. Electrical stimulation of PRN produced a mild to moderate decrease of the SAP, heart rate, and RNA, but arterial PO2 and PCO2 did not change significantly. When PRN was stimulated simultaneously with asphyxia, increases of SAP and RNA and changes of blood gases subsequent to asphyxia reduced significantly. Arterial PO2 decreased only 54.0 +/- 4.9% while the PCO2 increased 39.4 +/- 10.5% (p < 0.01). Similar effects were observed in the venous blood from inferior vena cava. In addition, when the arteriovenous difference of PO2 and PCO2 was compared, simultaneous PRN stimulation during asphyxia produced a higher PO2 reserve (66.3%) and less PCO2 production (-7%) than without PRN stimulation; PO2 54.2%, PCO2 (-2.9%). The results suggest that PRN is a structure that can exert inhibition over a wide spectrum of body functions; not only autonomic system but probably also metabolism.

Animals↗
PubMed1992

Cytoprotective effect of reduced glutathione in hydrogen peroxide-induced endothelial cell injury.

The kinetic effects of hydrogen peroxide (H2O2) on cultured endothelial cells isolated from bovine carotid artery were studied. The cytoprotective effects of glutathione (GSH) on H2O2-induced cell injury were also investigated. H2O2-induced a dose- and time-dependent cell injury in cultured endothelial cells. H2O2-induced cell injury was blocked by simultaneous treatment by catalase, but not by superoxide dismutase. H2O2 also induced endogenous PGI2 biosynthesis, and the maximum PGI2 production was reached after 1 h treatment. Stimulation of PGI2 production was parallel with arachidonate release from H2O2-treated cells. However the prostaglandin biosynthesis enzyme activity in cells was inhibited by H2O2 treatment. When the cells were treated with GSH, the intracellular GSH reached a plateau after 3 h treatment. Both H2O2-induced cell injury and PGI2 production were significantly inhibited by the 3 h pretreatment with GSH. The cytoprotective effect of GSH was completely inhibited by buthionine sulfoximine which is a specific inhibitor of gamma-glutamylcysteine synthetase. The results indicate that the cytoprotective effect of GSH on H2O2-induced cell injury in cultured bovine carotid artery endothelial cells depends on the increase in intracellular GSH content.

Animals↗
PubMed1992

Inactivation of the retinoblastoma gene in acute myelogenous leukaemia.

To investigate the role of retinoblastoma susceptibility (RB) gene inactivation in leukaemogenesis, we evaluated 36 bone marrow specimens of acute leukaemia for RB protein expression by immunoprecipitation and Western blot analysis. 15 patients had no detectable RB protein at initial screening. However, nine of them were subsequently excluded due to evidence of protein degradation. Of 27 valid cases, six (22%) were repeatedly shown to lack expression of the RB protein with three different anti-RB antibodies. Five were patients with acute myelogenous leukaemia (AML) and one, mixed-lineage acute leukaemia. The RB inactivation was noted more frequently in AML (5/18, 28%) than in acute lymphoid leukaemia (0/7, 0%). By karyotyping, none of these six patients exhibited cytogenetic changes involving chromosome 13q14, the RB locus. There is no correlation between inactivation of the RB gene and FAB subtypes or cytogenetic changes. Four patients achieved complete remission with standard chemotherapy for 6, 12, 20 and 26+ months, respectively. Southern and Northern blot analyses further indicated that the RB genes were grossly intact and the level of RB transcripts did not decrease in the majority of these six patients. These results suggest that the absence of RB products in some of acute leukaemia might be regulated at the post-transcriptional level, and it imposes no significant effect on treatment response and prognosis.

Adolescent↗
PubMed1992

Microcomputer-aided system for electrocardiograms and blood pressure analysis during drug-induced transient periods.

In the current experiments, we have developed a microcomputer-aided system for amplitude and duration parameter analysis of electrocardiogram (ECG) and blood pressure (BP) waveforms during the drug-induced transient period. Both ECG and BP are monitored, amplified and recorded using standard techniques. For studying the parameter variation trend, the time course of each parameter was produced. Based on these requirements, the present system combined data acquisition, data selection, data analysis, graph plotting and some experimental techniques to meet the need. Generalized human ECG and arterial BP waveforms were used in this system to expand its usable ranges. From the time course graph plotting, the variation trend of each parameter during each drug-induced transient period was obtained thereafter. The main advantages of this system include: (1) transient analysis--the system is suitable for complete and precise parameter analysis of human and animal ECG and BP in the drug-induced transient period; (2) ease of construction--the simplified hardware interface and IBM PC-AT compatible system make this system easy to be constructed; (3) ease of operation--modular data acquisition, processing and analysis procedures make this system easy to be operated; (4) high expansion potential--the modular hardware interface and modular software procedure make this system easy to be expanded; (5) wide utility--the system can be applied to any other research areas which involve the parameter analysis of ECG and BP.

Animals↗
PubMed1992

Effects of adrenoceptor agonists and antagonists on cardiovascular functional parameters in rats.

The effects of intravenous administration of adrenoceptor agonists and antagonists on electrocardiographic or blood pressure (BP) functional parameters were assessed in urethane-anesthetized rats. The responses of cardiovascular functional parameters produced by these drugs included: (1) isoproterenol decreased the duration of a whole BP cycle (Wd), duration of the diastolic wave (Dd), peak amplitude of the systolic wave (SYa), amplitude of the diastolic notch (DNa), amplitude of the diastolic wave (DWa), pulse pressure (dp) and mean arterial pressure (mp) but increased the heart rate (HR) accompanied by prolonged R-R (RR) or P-P interval (PP) (2) propranolol decreased SYa, DNa, dp, mp, HR, the amplitude of the P wave (Pa) and amplitude of the S wave (Sa) but increased the duration of the QRS wave, P-R interval, duration of the R wave (Rd) and duration of the P wave (Pd); (3) adrenaline decreased HR (accompanied by prolonged RR and PP), Rd, Pa and amplitude of the T wave (Ta) but increased Pd, Wd, Dd, DNA, the time interval between aortic valve opening and closure (Dw), dp, mp, amplitude of the Q wave and amplitude of the R wave (Ra); (4) noradrenaline decreased HR (accompanied by prolonged RR and PP) and Pa but increased Wd, Pd, SYa, DNa, Dw, dp, mp, Ra and Ta; (5) phenylephrine decreased HR (accompanied by prolonged RR and PP) and Pa but increased Wd, Dd, DNa, mp and Ra; (6) phentolamine decreased SYa, DNa, DWa, Dw, dp and mp. This study illustrates the utility of the automated electrocardiogram (ECG) and BP analysis system for investigation of adrenoceptor agonists and antagonists. The use of this methodology not only reproduced most of cardiovascular functional parameter effects produced by these drugs using the conventional methodology but also realizes some new information about the drug-induced ECG or BP waveform effects.

Adrenergic alpha-Agonists↗
PubMed1992

Ganoderma tsugae mycelium enhances splenic natural killer cell activity and serum interferon production in mice.

Effects of the water-soluble extract of Ganoderma tsugae mycelium (GT), its alcohol-insoluble subfraction (GTI), and its alcohol-soluble subfraction (GTS) on splenic natural killer (NK) cell activity and serum interferon (IFN) production were assessed in mice. Intraperitoneal administration of GT (4-200 mg/kg) or GTI (1-50 mg/kg), but not GTS, augmented the NK cytotoxic activity in a dose-dependent manner in C3H/HeN mice. This augmentation of splenic NK cytolytic activity was not mouse-strain-dependent. The serum IFN titers of mice were also elevated after i.p.-doses of GTI. The GTI-induced serum IFN was reduced by either IFN-(alpha+beta) antiserum or IFN-gamma monoclonal antibody in vitro. The treatment with antiserum neutralizing IFN-(alpha+beta) resulted in a 70% reduction of GTI-induced IFN, while monoclonal antibody against mouse IFN-gamma, moderately neutralized the GTI-induced IFN (50%). These results demonstrated that both the splenic NK activity and serum IFN [IFN-(alpha+beta) and IFN-gamma] titers are elevated by Ganoderma tsugae mycelium extracts in mice.

Animals↗
PubMed1992

Localization of the sympathetic postganglionic neurons innervating cardiac coronary artery with horseradish peroxidase in monkeys.

Localization of the sympathetic postganglionic neurons innervating the cardiac coronary arteries in monkeys was investigated by using retrograde axonal transport of horseradish peroxidase (HRP). HRP was applied to the main trunk of the left and right coronary arteries, and to the terminal branches of the ventral and dorsal descending vessels of the left and right coronary arteries, respectively. The animals were sacrificed 84-96 hours later and perfused via the left ventricle. The paravertebral sympathetic ganglia from the superior cervical, middle cervical and stellate ganglia to the T9 ganglia, and nodose ganglia were removed and processed for HRP identification. After HRP was applied into the main trunk of the right coronary artery, and into the main trunk and the terminal branches of the descending vessels of the left coronary artery, the HRP-labeled sympathetic neurons were localized predominantly in the right superior cervical ganglion, and next in the left superior cervical ganglia. However, labeled cells were found in the stellate ganglia bilaterally. After HRP applications to the terminal branches of the dorsal descending vessels of the right coronary artery, HRP-labeled cells were mainly present in the left superior cervical ganglion and next in the right superior cervical ganglion. Some labeled cells were found in the middle cervical and stellate ganglia. No labeled cell was found in ganglia below the second thoracic ganglia on either side in these four groups.

Animals↗
PubMed1992

Effect of copper ion on collagenase release. Its implication in corneal vascularization.

The involvement of leukocytes in corneal neovascularization has been known for a long time. Recent observations suggest that collagenase from leukocytes may be a common mediator for prostaglandin E1 (PGE1)- and copper-induced corneal neovascularization. This study was designed to investigate the effect of copper ion on collagenase activity from leukocytes and other sources and leukocyte infiltration in the corneal angiogenic process induced by PGE1. These results demonstrated that collagenase production from leukocytes was stimulated in a dose-dependent manner by copper ion but not by PGE1. Copper chloride 0.2 mM produced the highest stimulation. Copper ion had no effect on collagenase release from corneal fibroblasts and capillary endothelium. There were more polymorphonuclear leukocytes (PMN) in the prostaglandin E1 treated corneas than in the control. The time-course study showed that the appearance of PMN reached a peak on day 2 and new vessel growth could not be identified until day 4. These results supported an earlier suggestion that leukocytes play a role in corneal neovascularization and further suggested that copper in corneal neovascularization can stimulate the release of collagenase from leukocytes.

Alprostadil↗
PubMed1992

Successful treatment of cytomegalovirus pneumonitis with ganciclovir and high-dose intravenous immunoglobulin in a bone marrow transplant recipient.

A 35-year-old man with acute lymphoblastic leukemia in second remission received an allogeneic bone marrow transplant from an HLA-compatible sibling donor. Unfortunately, cytomegalovirus (CMV) pneumonitis was histologically documented on Day +72. Combination therapy with ganciclovir (9-[2-hydroxy-1-(hydroxy-methyl) ethoxymethyl] guanine) and high-dose intravenous immunoglobulin (IVIG) was started immediately. The treatment comprised a three-week induction course (ganciclovir, 2.5 mg/kg q8h and IVIG, 500 mg/kg qod) and a seven-week fixed-dose maintenance course (ganciclovir 5 mg/kg thrice a week for 20 doses and IVIG 500 mg/kg twice a week for eight doses). The pneumonia resolved gradually, and he was free from symptoms within two weeks. The only significant side effect was moderately severe myelosuppression which was reversible after discontinuation of ganciclovir. The patient had a relapse of leukemia on Day +186, but there was no recurrence of CMV pneumonitis. This result confirms that such combination therapy is effective in the treatment of CMV pneumonitis in a patient with a bone marrow transplant.

Adult↗
PubMed1992

Effects of intra-raphe injection of amino acids on cardiovascular function in rats.

The effects of microinjection of an excitatory amino acid (glutamate, 10 micrograms) or several inhibitory amino acids (taurine 10 micrograms, GABA 10 ug or glycine 10 ug) into the dorsal raphe region on cardiovascular function were assessed in rats under pentobarbital sodium. Intra-raphe administration of glutamate, but not saline, caused an increase in the mean arterial pressure. By contrast, intra-raphe administration of taurine, GABA or glycine, but not saline, caused a decrease in both the mean arterial pressure and the heart rate. The glutamate-induced hypertension or both the hypotension and the bradycardia induced by taurine, GABA or glycine was antagonized by pretreatment with intra-raphe injection of a serotonergic receptor antagonist (1 ug cyproheptadine). In addition, the vasopressor and bradycardia responses to an intravenous dose of epinephrine (2.5 ug/kg) were assessed in saline-treated rats and amino acid-treated rats. Intra-raphe injection of glutamate produced a significant decrease in reflex bradycardia compared to the controls. On the other hand, administration of taurine, GABA or glycine into the dorsal raphe region led to an enhancement of epinephrine-induced bradycardia. Again, the reduction or the facilitation of the epinephrine-induced bradycardia following administration of these amino acids was antagonized by pretreatment with cyproheptadine. The results suggest that the serotonergic receptor mechanisms in the dorsal raphe region play a role in the elaboration or modulation of the cardiovascular responses to amino acids (including glutamate, taurine, GABA and glycine).

Amino Acids↗