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Biomedical subjects

D Y Li

Publications and source records attributed to D Y Li.

At least 55 records · Page 3Linked to original sources
PubMed1996

The role of prostaglandin receptors in regulating cerebral blood flow in the perinatal period.

Prostaglandins exert significant effects on the range of cerebral blood flow autoregulation. However, the newborn exhibits a narrow cerebral blood flow autoregulatory range compared to the adult, and this apparently contributes to the susceptibility of the newborn to major perinatal complications such as intraventricular cerebral haemorrhage. Reduced vasoconstriction in response to prostaglandins due to the fewer prostaglandin receptors, especially for PGE2 (EP) and PGF2 alpha (FP), seems to contribute in part to the narrower range of cerebral blood flow autoregulation in the newborn. Evidence suggests that high levels of prostaglandins in the perinatal period are responsible for the down-regulation of neurovascular EP and FP receptors. We review the pharmacology of prostaglandin receptors, in particular PGE2 and PGF2 alpha receptors, their ontogeny on the neural vasculature, the perinatal regulation of their expression, and how these changes relate to the control of neural blood flow autoregulation.

Cerebrovascular Circulation↗
PubMed1996

[The effects of LTA and plaque on the periodontal tissue of the Guinea pig]

40 Guinea pigs were divided into 4 groups.The gingival sulcus of 2 mandibular incisors were irrigated with LPS(Lipopolysaccharide),LTA (Lipoteichoicacid),PL(Subgingival plaque) and NS(Normal saline solution) respectively.2 animals were sacrificed in group of 5 successively at 1,2,3,6,8 week after irrigation.Microscopic examination demonstrated:Only a few penetration of inflammatory cells lay in the gingival tissue in NS control group.Significant infiltrate associated with evident crystal resorption were noted at 1st week and active remodeling took place at 4th,5th week in LPS group.Enhancing accumulations of plaque calculus with weak inflammation could be seen in LTA group.Not only accumulations of plaque and calculus but also penetration of inflammation with resorption of bone were seen in PL group.Their effects on the periodontal tissue of Guinea pig showed evident different.These findings served further expression the possible mechanisms of periodontal diseases.

Journal Article↗
PubMed1996

Inhibition of prostaglandin synthesis in newborn pigs increases cerebral microvessel prostaglandin F2 alpha and prostaglandin E2 receptors, their second messengers and vasoconstrictor response to adult levels.

We recently reported that the density of prostaglandin (PG) F2 alpha and E2 receptors (FP and EP) on the cerebral microvasculature of the newborn is less than on that of the adult animal. This study tests the hypothesis that higher levels of PGF2 alpha and PGE2 in the newborn than in the adult brain might down-regulate FP and EP and their functions in the cerebral microvasculature. Newborn pigs (1-2 days old) were treated with ibuprofen (40 mg/kg i.v.) every 6 h for 48 h; and cerebrovascular FP and EP density, receptor-coupled second messenger production and cerebral vasoconstrictor responses to PGF2 alpha and PGE2 were determined. The results showed that ibuprofen treatment in the newborn increased brain microvascular FP and EP densities to levels found in the brains of adult pigs. This up-regulation of prostaglandin receptors was also observed in isolated newborn brain microvessels incubated for 48 h with ibuprofen. PGF 2 alpha, fenprostalene (PGF2 alpha analog), PGE2, 17-phenyl trinor PGE2 (EP1 receptor subtype agonist) and M&B 28,767 (EP3 agonist) caused a significantly greater increase in inositol 1,4,5-triphosphate production in brain microvessels of ibuprofen-treated than in brain microvessels of saline-treated newborn pigs. The cerebral vasoconstrictor effects of PGF2 alpha, 17-phenyl trinor PGE2 and M&B 28,767 were also significantly increased in newborn pigs treated with ibuprofen to levels comparable to those of adults. However, the steady-state level of FP mRNA in cerebral microvasculature did not differ between saline-treated newborn, ibuprofen-treated newborn and adult pigs. It is concluded that the low FP and EP densities in newborn brain microvessels are a result of high levels of brain prostaglandins and that these receptors, receptor-coupled second messengers and cerebral vasoconstrictor responses to FP, EP1 and EP3 stimulation can be up-regulated to adult levels by decreasing endogenous prostaglandin production. The changes in receptor levels were not related to steady-state levels of receptor mRNA in brain microvessels.

Animals↗
PubMed1995

Prostaglandin G/H synthase-2 is a major contributor of brain prostaglandins in the newborn.

In order to understand the molecular basis of the elevated cerebral prostaglandin levels in the newborn, we compared the expression of the mRNAs and proteins of prostaglandin G/H synthases (PGHS), PGHS-1 and PGHS-2, in various regions of the brain and the microvasculature of newborn (1-2-day-old) and juvenile (4-7-week-old) pigs and also measured the relative contribution of PGHS-2 to cerebral prostaglandin synthesis both in vivo and in vitro by using a novel inhibitor of PGHS-2, NS-398. Ribonuclease protection assays using total RNA isolated from various regions of the porcine brain revealed that, unlike PGHS-1 mRNA, PGHS-2 mRNA was abundantly expressed in the cortex and the microvasculature of the newborn compared with those of the juvenile animal. PGHS-2 immunoreactive protein comprised the majority of total PGHS enzyme in neonatal cerebral microvasculature due to a 2-3-fold lower expression of immunoreactive PGHS-1 protein. Inhibition of PGHS-2 by NS-398 decreased the rate of prostaglandin synthesis by purified cerebral microvessels of the newborn by approximately 65% and of juvenile pigs by 30%. The decrease in brain tissue prostaglandin concentrations following intravenous administration of NS-398 was greater in newborn pigs (> or = 90%) than in the juvenile animals (< or = 30%). Furthermore, NS-398 substantially reduced the net in vivo cerebrovascular production of prostaglandins in newborn pigs. Taken together, these results indicate that PGHS-2 is the predominant form of prostaglandin G/H synthase in the newborn brain and cerebral microvasculature and the main contributor to the brain prostaglandin levels in the newborn animal.

Aging↗
PubMed1995

Peroxide-cyclooxygenase interactions in postasphyxial changes in retinal and choroidal hemodynamics.

To test the role of reactive oxygen species and cyclooxygenase products in the retinal hemodynamic changes induced by asphyxia, we measured retinal (RBF) and choroidal blood flows (ChBF), malondialdehyde (MDA), prostaglandin E2 (PGE2), 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TxB2) in 1- to 3-day-old pigs treated with saline, the free radical scavengers U-74389F or high-dose allopurinol, the cyclooxygenase inhibitors ibuprofen or indomethacin, or the thromboxane synthase blocker CGS-13080 before and 5 and 60 min after a 5-min period of asphyxia. In saline-treated animals, RBF and ChBF increased 5 min after asphyxia and decreased at 60 min. The increases in RBF and ChBF at 5 min postasphyxia were slightly attenuated by cyclooxygenase blockers and free radical scavengers but not by thromboxane synthase inhibition, whereas all drugs prevented the decreases at 60 min. MDA, TxB2, PGE2, and 6-keto-PGF1 alpha increased 5 min after asphyxia; at 60 min, PGE2 and 6-keto-PGF1 alpha returned to nearly preasphyxial levels, but MDA and TxB2 continued to increase. Cyclooxygenase inhibition prevented the asphyxia-induced rise in MDA, and the free radical scavengers prevented that of prostanoids. In isolated eyecup preparations, H2O2 and cumene hydroperoxide constricted retinal arteries; this effect was blocked by cyclooxygenase and thromboxane synthase inhibitors. The data suggest that during oxidative stresses reactive oxygen species are generated from the cyclooxygenase pathway and, in turn, also activate the synthesis of thromboxane; the latter mediates the oxidative stress-induced ocular vasoconstriction that might trigger the neovascularization of retinopathy of prematurity.

3,4-Methylenedioxyamphetamine↗
PubMed1995

[Study on inspection method of anaerobes in periodontal pockets]

This paper used two methods only use non-selective medium(CDC) and together with seven selective mediums(VS CS BS AS FS ES LS) to inspect anaerobes in periodontal pockets.The results showed that Gram-negative anaerobes were the predominant microflora of periodontitis.The method of CDC together with selective mediums was founded much simpler and faster,more valuable than the method of only use non-selective medium.It is illustrated that CDC added antibiotics or chemicals to make selective mediums was prepared convenience and was suitable for growth of relative anaerobes.But it is still necessary to establish much more,more special, more reliable selective or identical mediums.

Journal Article↗
PubMed1995

[Rapid identification of anaerobes in periodontics with computer]

It has documented that anaerobe has played important roles in the progress of periodontitis.Recently,the detection of its pathogens has caught more and more attention.This study has sieved physiological and biochemical reactions of more than 80 species anaerobes related to periodontics,selected the reactions with identifying significances to form a system,and identify bacterium according to their differences of the results to the selected reactions.The results of each bacteria is expressed with decimal number.then transfer it into the decimal number.So the decimal number represents the results of the bacteria to the selected reactions and represents a certain bacteria.The profile that the bacterium correspond to the numbers is designed.When the bacteria is identified,on the basis of its Gram stain,morphology and oxygen-tolerance,using compling program,the computer with suggest the reactions to be finished.After the reactions have been completed,input the produced number to the species of the indentified bacteria will be known.

Journal Article↗
PubMed1995

Up-regulation of brain PGE2 and PGF2 alpha receptors and receptor-coupled second messengers by cyclooxygenase inhibition in newborn pigs.

We recently reported that brain synaptosomes of newborn pigs contained fewer PGE2 (EP) and PGF2 alpha (FP) receptors than adult tissues. In the present study we investigated whether this was the result of down-regulation of these receptors by high levels of PGE2 and PGF2 alpha in the brain of newborn animals. Newborn pigs (1-3 days old) were treated with ibuprofen (40 mg/kg) or indomethacin (5 mg/kg) i.v. every 4 hr for 24 hr to reduce prostaglandins to adult levels. At the end of the treatment, EP and FP receptor density and receptor-linked second messenger formation in brain synaptosomes were measured. It was found that ibuprofen and indomethacin treatment increased EP and FP receptor densities in brain synaptosomes of newborn animals to levels found in the adult; this up-regulation of EP receptors was prevented by EP receptor agonist, 16,16-dimethyl-PGE2, and the up-regulation of FP receptors was prevented by the FP agonist, fenprostalene. PGE2, butaprost (an agonist for EP2 receptor subtype mediating cAMP stimulation) and 11-deoxy-PGE1 (an agonist for EP2 and EP3 receptors) caused a comparable increase of cAMP in brain synaptosomes of ibuprofen-treated and adult animals, which was significantly greater than in those of vehicle-treated animals. Also, PGF2 alpha and its analog, fenprostalene, caused a much greater increase in IP3 production in brain synaptosomes of ibuprofen-treated than in vehicle-treated pigs. These findings suggest that the relatively low EP and FP receptor densities in newborn pigs are caused by the high levels of prostaglandins and that these receptors can be up-regulated by inhibiting prostaglandin synthesis.

16,16-Dimethylprostaglandin E2↗
PubMed1994

Ontogenic increase in PGE2 and PGF2 alpha receptor density in brain microvessels of pigs.

1. The hypothesis that the relative vasoconstrictor ineffectiveness of prostaglandin E2 (PGE2) and PGF2 alpha on cerebral vessels of newborn pigs might be due to fewer receptors for these prostanoids was tested by comparing receptors for PGE2 (EP) and PGF2 alpha (FP) in cerebral microvessels from newborn and adult pigs. 2. Specific binding of [3H]-PGE2 and [3H]-PGF2 alpha to membranes prepared from brain microvessels showed that EP and FP receptor density (Bmax) in tissues from newborn animals was less than 50% of that determined in tissues from adults. By contrast, estimates of affinity (KD) were unchanged. 3. Specifically bound [3H]-PGE2 to brain microvessels from both the newborn and adult was displaced by AH 6809 (EP1-selective antagonist) by 80-90%, and only by approximately 30-35% by both 11-deoxy PGE1 (EP2/EP3 agonist) and M&B 28,767 (EP3 agonist); butaprost (EP2 agonist) was completely ineffective. 4. PGE2, 17-phenyl trinor PGE2 (EP1 agonist), PGF2 alpha and fenprostalene (PGF2 alpha analogue) caused significantly less increase in inositol 1,4,5-triphosphate (IP3) in brain microvessels from the newborn than in those from adult pigs. The stimulation of IP3 by PGE2 and 17-phenyl trinor PGE2 was almost completely inhibited by the EP1 antagonist, AH 6809. 5. PGE2, 11-deoxy PGE1 and M&B 28,767 produced small reduction of adenosine 3':5'-cyclic monophosphate (cyclic AMP) production in adult vessels but no effect in newborn tissues. 6. The lower density of EP and FP receptors in microvessels of newborn pigs compared to adults may explain the reduced ability of PGE2 and PGF2 alpha to stimulate production of IP3 in tissues from newborn animals. This in turn, may provide an explanation for previous observations demonstrating that these prostanoids elicit contraction of adult cerebral microvessels, but exert minimal effects on these vessels in newborn animals.

Animals↗
PubMed1994

Reduced responses of retinal vessels of the newborn pig to prostaglandins but not to thromboxane.

The upper blood pressure limit of retinal blood flow autoregulation is lower in the newborn than in the adult; this suggests an insufficient vasoconstrictor response in the newborn when perfusion pressure is increased. Because prostaglandins (PGs) have an important role in autoregulation of retinal blood flow, we compared the effects of PGE2, PGF2 alpha, carbacyclin (PGI2 analogue), and U46619 (thromboxane analogue), as well as that of agonists for the three different PGE2 receptor subtypes, 17-phenyl trinor PGE2 (EP1), butaprost (EP2), and M&B 28,767 (EP3), on the retinal vasculature of newborn and adult pigs, using isolated eyecup preparations. PGF2 alpha and PGE2 caused a markedly greater constriction of retinal arteries and veins of the adult than of the newborn animals. Further analysis of the response to PGE2, using receptor subtype agonists, revealed that the EP1 receptor agonist, 17-phenyl trinor PGE2, and the EP3 receptor agonist, M&B 28,767, caused a significant constriction of adult arteries and veins but produced minimal effects on newborn vessels; the EP2 receptor agonist, butaprost, caused a small and comparable dilation of newborn and adult arteries and veins. The PGI2 analogue, carbacyclin, caused a greater dilation of the adult than of the newborn arteries, but produced comparable dilation of veins from both newborn and adult animals. In contrast to the effects of PGF2 alpha and PGE2, the thromboxane analogue, U46619, as well as the alpha 1-adrenoceptor agonist, phenylephrine, significantly constricted newborn arteries and veins, and this effect was comparable with that observed on retinal vessels of the adult.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Ontogeny of positive inotropic responses to sympathomimetic agents and of myocardial adrenoceptors in rats.

Positive inotropic efficacies (maximal increase in contractile force) and potencies of the alpha-adrenoceptor agonist methoxamine and beta-adrenoceptor agonist isoprenaline were determined on electrically driven (1 Hz) ventricular strips from rats aged 0.5, 1, 2, 3, 6, and 10 (adult) weeks. The inotropic response to methoxamine significantly decreased after 2 weeks of age. The inotropic potency of isoprenaline was slightly but significantly lower at all ages than at 0.5 weeks of age. Up to 2 weeks of age, the maximal inotropic effect of methoxamine was comparable with that of isoprenaline, thereafter it was but markedly less. Phenylephrine behaved like methoxamine, and noradrenaline like isoprenaline. The effect of methoxamine was antagonized by prazosin but not by propranolol; the reverse was true for isoprenaline. Injections at birth of triiodothyronine and dexamethasone exerted minimal effects on the inotropic responses to methoxamine and isoprenaline. Chemical sympathectomy with 6-hydroxydopamine caused supersensitivity to the inotropic effects of isoprenaline but produced subsensitivity to responses to methoxamine at 1 week; effects of methoxamine at 3 and 6 weeks of age were not altered by sympathectomy. No significant differences in alpha 1- or beta 1-adrenoceptor densities or affinities in ventricular membranes from 7-day-old and adult rats were found. It is concluded that the positive inotropic responses to sympathomimetic amines decline with age, the decline is most marked in the case of alpha 1-adrenoreceptor- mediated effects, and these changes do not appear to be due to a decrease in the number or affinity of alpha 1- and beta 1-adrenoceptors.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1994

[Effect of high calcium intake on blood pressure and intracellular pH, Na(+)-H+ exchange activity in stroke-prone spontaneously hypertensive rats].

Effect of high calcium (3%) intake on blood pressure and intracellular pH, Na(+)-H+ exchange activity, cytosolic free calcium concentration in stroke-prone spontaneously hypertensive rats (SHRSP-Ca) is compared with sex-, ag-matched SHRSP and WKY rats without high calcium intake. The results showed that high calcium intake significantly suppressed increase in blood pressure and decreased cytosolic free calcium concentration after it was given to SHRSP-Ca for 6 weeks, while plasma calcium was increased. The intracellular pH tended to be in the normal range of WKY rats. Na(+)-H+ exchange activity was slightly decreased. Correlationship between blood pressure and intracellular pH, Na(+)-H+ exchange activity and cytosolic free calcium concentration were discussed.

Animals↗
PubMed1994

Free radicals in retinal and choroidal blood flow autoregulation in the piglet: interaction with prostaglandins.

PURPOSE: To study the role of free radicals in autoregulation of retinal blood flow (RBF) and choroidal blood flow (ChBF) and the contribution of the cyclooxygenase pathway in free radical formation during blood pressure changes in 1- to 3-day-old pigs. METHODS: Blood pressure was adjusted by inflating balloon-tipped catheters placed at the aortic isthmus and the aortic root to induce hypertension and hypotension, respectively. Blood flow was measured using the microsphere technique. Also, the effects of peroxides on retinal artery diameter were studied on eyecup preparations using time-frame photography processed by digital imaging. RESULTS: Blood gases and intraocular pressure (13 +/- 1 mm Hg) remained stable throughout the experiments. In control animals, RBF was constant only between 30 and 75 mm Hg of ocular perfusion pressure and ChBF increased as a function of ocular perfusion pressure (tau = 0.58, P < 0.01). Inhibition of peroxidation with the free radical scavenger 21-aminosteroid U74389F (2.5 mg/kg) widened the range of RBF and ChBF autoregulation (ocular perfusion pressure from 30 to 131 mm Hg). Hypertension caused an increase in the products of peroxidation, malondialdehyde, and hydroperoxides, as well as in prostaglandin E2, prostaglandin F2 alpha, and 6-keto-prostaglandin F1 alpha in the retina and choroid of control animals; these changes were inhibited by the free radical scavengers U74389F (2.5 mg/kg) and high-dose allopurinol (140 mg/kg) as well as by the cyclooxygenase inhibitors ibuprofen (40 mg/kg) and indomethacin (5 mg/kg). In isolated eyecup preparations, H2O2 and cumene hydroperoxide dilated retinal vessels, and this effect was completely blocked by indomethacin. CONCLUSIONS: These findings indicate that free radicals play a major role in setting the upper limit of RBF and ChBF autoregulation of the newborn animal. In addition, there exists a positive feedback interaction between free radicals and cyclooxygenase activity in ocular tissues, such that during hypertension the cyclooxygenase pathway is an important producer of free radicals and in turn is also activated by them.

Animals↗
PubMed1993

Fewer PGE2 and PGF2 alpha receptors in brain synaptosomes of newborn than of adult pigs.

PGE2 and PGF2 alpha decrease cerebral metabolism in the adult but increase it in the newborn. The present study was done using synaptosomes from newborn and adult pigs to find out whether these diverse cerebral effects of prostanoids are a consequence of newborn synaptosomes containing fewer or no EP2 receptors for PGE2 (mediating cAMP increase and in turn cerebral metabolism decrease) and PGF2 alpha receptors [mediating IP3 (inositol 1,4,5-triphosphate) increase and in turn cerebral metabolism decrease]. It was found that maximum binding values (fmol/mg protein) of [3H]PGE2 and [3H]PGF2 alpha were, respectively, only 11.6 +/- 0.8 and 8.6 +/- 1.4 on newborn synaptosomes compared with 41.8 +/- 1.8 and 31.2 +/- 4.8 on adult tissues. EP1 receptors were virtually absent in newborn and adult preparations. Practically all the PGE2 receptors on newborn synaptosomes were EP3 subtype, whereas adult brain synaptosomes contained both EP2 and EP3 subtypes; this was indicated by the ability of M&B 28,767, a specific EP3 receptor agonist, to cause 100% displacement of [3H]PGE2 binding to synaptosomes of the newborn but only 51% in the case of the adult. Also, PGE2, 11-deoxy PGE1 (a nonselective EP2 and EP3 agonist) and M&B 28,767 (an EP3 agonist) caused comparable decreases in cAMP formation in synaptosomes from the newborn, whereas in those from the adult, PGE2 and 11-deoxy PGE1 increased and M&B 28,767 decreased cAMP production. PGF2 alpha markedly increased IP3 synthesis in synaptosomes of the adult but not of the newborn.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1992

The v-sis oncogene product but not platelet-derived growth factor (PDGF) A homodimers activate PDGF alpha and beta receptors intracellularly and initiate cellular transformation.

The v-sis oncogene product p28v-sis and the platelet-derived growth factor (PDGF) B chain share 92% homology with each other and over 50% homology with the PDGF A chain. Exogenously added homodimers of PDGF A and PDGF B and of p28v-sis are potent mitogens but only PDGF B and p28v-sis induce transformation when endogenously expressed with a strong promoter. Because exogenous PDGF AA and PDGF BB both initiate a full mitogenic response, understanding the mechanisms underlying the difference in their transforming potential may clarify how growth factor genes act as oncogenes. In this work, we compared cells expressing high levels of PDGF A and v-sis. We observed that transformation by v-sis correlated directly with the rapid degradation (t1/2 approximately 20 min) of the alpha and beta PDGF receptors, with a failure of either the alpha or beta receptor to be fully processed and with the association of high levels of phosphatidylinositol (PI) 3-kinase with immunoprecipitates of the PDGF receptors. In contrast, in cells expressing essentially equal levels of PDGF A, transformation was not detected, alpha and beta PDGF receptor processing was normal, and association of PI 3-kinase with receptors in immunoprecipitates was not found above control values. The ability of v-sis to autoactivate PDGF receptors within processing compartments and to initiate activation of the PI 3-kinase signaling pathway coupled with the failure of PDGF A to activate its receptor intracellularly and to induce transformation when endogenously expressed at high levels suggests that the internal autoactivation of PDGF receptors may be essential for transformation by v-sis.

3T3 Cells↗