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Biomedical subjects

A Guo

Publications and source records attributed to A Guo.

At least 37 records · Page 2Linked to original sources

[Matrix metalloproteinase-1 and coronary atheroslerotic plaque rupture].

OBJECTIVE: To investigate the relationship between matrix metalloproteinase-1 (MMP-1) and coronary atherosclerotic plaque rupture, and the cellular source of MMP-1 within the plaques. METHODS: 42 cases, among which 20 died of acute myocardial infarction, 10 with unstable angina history and 12 with stable angina history but died of other diseases, were selected. All the branch of coronary arteries were examined, parts of the segments were selected for immunohistochemical staining, 5 markers against alpha-smooth muscle actin, CD20, CD45RO, CD68 and MMP-1 were performed. RESULTS: Plaque rupture and thrombosis were found in almost all the cases of acute myocardial infarction and unstable angina. But in the cases of stable angina, the majority of the plaques were stable ones. The expression of MMP-1 in the ruptured plaques were stronger than the unruptured ones (t = -8.07, P < 0.05); Positive relationship was also noted between the expression of CD68 and MMP-1 (r = 0.75, P < 0.05). CONCLUSION: Macrophages are capable of degrading extracellular matrix by secreting MMP-1; Enhanced secretion of MMP-1 within the coronary atherosclerotic plaques has significant relationship with plaque rupture.

Angina, Unstable↗

[Aortic calcification and matrix metalloproteinases].

OBJECTIVE: To study the relationship between arterial calcification and matrix metalloproteinases including MMP-1 and MMP-3. METHODS: 15 human aorta specimens from autopsies were stained with HE to identify calcification. Immunohistochemical method was used to determine the secretion of MMP-1 and MMP-3. RESULTS: Among the 15 aorta specimens, calcification was found in 10 and no calcification in the remaining 5. There was no significant difference in the percentage of MMP-1 positive cells between two groups, with 83.8% +/- 5.2% in calcified specimens vs 84.0% +/- 7.5% in non calcified ones. 9 of the 10 calcified aortas were positive for MMP-3 staining. Serial sections showed that the localization of positivity was in concordance with calcified regions. The 5 normal aortas were MMP-3 negative. The difference between the two groups was significant. CONCLUSION: MMP-3 secretion relates closely with arterial calcification. And MMP-3 may participate in calcium minerali-zation in arteries. MMP-1 has no relation with arterial calcification.

Aorta↗

[Effect of 5,7-dihydroxytryptamine on the distribution pattern of calcitonin gene-related peptide in different motoneuron pools].

OBJECTIVE: The effect of 5,7-dihydroxytryptamine (5,7-DHT) on distribution pattern of calcitonin gene-related peptide (CGRP) in different motoneuron pools was studied in rats. METHODS: Cholera toxin B subunit coupled with colloidal gold (CB-Au) retrograde labeling combined with CGRP immunocytochemistry technique was mainly used. RESULTS: In control group, there was a different distribution pattern of CGRP-LI content in soleus motoneuron (SOL-Mn) and extensor digitorum longus motoneuron (EDL-Mn) pools. SOL-Mn pools had a higher ratio of neurons lacking CGRP-LI/weak CGRP-LI and a lower proportion of strongly CGRP-LI labeled ones. Comparing with control, there was a marked shift to increasing of CGRP-LI content in SOL-Mn pool and slight decrease in EDL-Mn pools 14 days after 5,7-DHT. All the SOL-Mns were CGRP-LI positive and the ratio of CGRP-LI strongly positive Mns significantly increased (P < 0.001) while 5,7-DHT did not increase the ratio of CGRP-LI strongly positive Mn in EDL-Mn pool. CONCLUSIONS: Except muscular motor activity, the different distribution pattern of CGRP-LI content in SOL-Mn and EDL-Mn pools is related to different 5-HT inputs. SOL-Mns may receive more 5-HT inputs.

5,7-Dihydroxytryptamine↗

[The role of 5'proximal fragment of POMC gene in the regulation of transcription in AtT20 cells].

OBJECTIVE: Identification of the vital regions in 5'-flanking sequence of POMC gene in order to determine the characteristics of POMC gene promoter and provide the basis for stadying the effects of multiple hormones and other factors in the POMC gene expression. METHODS: Construction of four kinds of plasmid recombined by rat POMC gene promoter regions and eukarytic expression reporter gene vector pG12-Basic. Each kind of them was identified by restriction maps analysis and DNA sequencing. All recombinant plasmids were transfected into AtT20 cells respectively by using a lipofectamine-based method. Luciferase activity in each cell-lytate was measured by monolight 2010 luminometer. RESULTS: Four recombinant plasmids were constructed, including pGL2-POMC480 (rPOMC -480/+63), pGL2-POMC323 (rPOMC -323/+63), pGL2-POMC165 (rPOMC -165/+63). pGL2-POMC34 (rPOMC -34/+63) Among them, PGL2-POMC34 contains the core promoter which consist of TATA box at -31/-25 bp and transcription start site at +1 bp of POMC gene. It showed that, comparing with the pGL2-POMC34, the relative luciferase activity of pGL2-POMC165 was 2.1 +/- 0.3, pGL2-POMC323 was 3.3 +/- 0.3, pGL2-POMC480 was 3.7 +/- 0.5, and the positive control pGL2-promoter was 4.8 +/- 0.8. CONCLUSIONS: (1) A model system to study the direct effects of various ACTH secretagogues on the dynamics of the POMC gene promoter activity in vitro was established. (2) The studying of POMC promoter basal transcriptional activities identified that the POMC gene has a weak core promoter. The proximal sequence elements were concentrated in the fragment of -34/-165 bp, and the transcriptional activities need POMC 5' promoter -480 bp or a longer region.

Adrenal Cortex Neoplasms↗

Altered outward K(+) currents in Drosophila larval neurons of memory mutants rutabaga and amnesiac.

K(+) currents in cultured Drosophila larval neurons have been classified into four categories according to their inactivation time constants, relative amplitude, and response to K(+) channel blockers 4-AP and tetraethylammonium. The percentage (65%) of neurons displaying K(+) currents which were reduced to 30% in amplitude by 5 mM cyclic adenosine monophosphate (cAMP) analog 8-bromo-cAMP in both Drosophila memory mutants rutabaga (rut) and amnesiac (amn) was significantly larger than that (50%) in wild type. This initial characterization provides evidence for altered K(+) currents in both rut and amn mutants. Arachidonic acid, a specifical inhibitor of Kv4 family (shal) K(+) channels, was found to inhibit K(+) currents in cultured Drosophila neurons, suggesting the presence of shal channels in these neurons.

4-Aminopyridine↗

Accuracy of quantitative ventriculographic analysis at reduced frame rates.

OBJECTIVE: We measured the error in left ventricular (LV) volume and wall motion measurement from recording contrast ventriculograms at 15 frames/sec instead of 30 frames/sec. BACKGROUND: Angiograms are increasingly recorded at 15 frames/sec instead of 30 frames/sec to improve efficiency. However the resulting error in quantitative analysis has not been evaluated. METHODS: Contrast ventriculograms recorded at 30 frames/sec of 23 patients undergoing diagnostic studies were digitized from cine film. End diastolic volume (EDV), end systolic volume (ESV), ejection fraction, anterior wall motion, and inferior wall motion were measured from a full set recorded at 30 frames/sec and from two reduced data sets at 15 frames/sec generated from the even and odd numbered frames. Intraobserver variability was compared with the error due to frame rate reduction. RESULTS: The error due to frame rate reduction did not differ significantly from intraobserver variability (p > 0.1 for all), measuring 2.6 +/- 2.2 ml (r = 0.997) vs. 1.9 +/- 1.2 ml (r = 0.999), respectively for EDV, 2.4 +/- 1.8 ml (r = 0.991) vs. 2.1 +/- 1.7 ml (r = 0.994), respectively for ESV, and 0.2 +/- 0.2 percent (r = 0. 981) vs. 0.1 +/- 1.2 percent (r = 0.994), respectively for ejection fraction. The error and variability for wall motion were 0.3 +/- 0.3 SD (r = 0.928) vs. 0.2 +/- 0.1 SD (r = 0.946), respectively for the anterior wall and 0.2 +/- 0.2 SD (r = 0.963) vs. 0.2 +/- 0.1 SD (r = 0.968), respectively for the inferior wall. CONCLUSION: Imaging the LV at 15 frames/sec does not cause a significant error in measuring LV volume and function compared with imaging at 30 frames/sec. Cathet. Cardiovasc, Intervent. 48:18-21, 1999.

Adult↗

Selective visual attention in a neurocomputational model of phase oscillators.

In order to understand the dynamic property of covert selective visual attention, which is different from the proposed mechanism of the spotlight metaphor, a two-layered network of phase oscillators was developed. The first layer is related to the hippocampus and controls attention focus formation. The second layer is related to the visual cortex, and each cortical oscillator in it simulates an assembly of cells coding for a particular stimulus in the sense of feature binding. Selective visual attention is interpreted as the result of the emergent synchronization of hippocampus oscillators and a part of cortical oscillators. Numerical experiments are presented to illustrate attention focus formation and attention shifting from one set of stimuli to another. From a neurocomputational point of view, our results demonstrate that attention is an emergent property of the dynamical cell assemblies responding to the whole visual field.

Attention↗

Immunocytochemical localization of the vanilloid receptor 1 (VR1): relationship to neuropeptides, the P2X3 purinoceptor and IB4 binding sites.

The vanilloid receptor (VR1) protein functions both as a receptor for capsaicin and a transducer of noxious thermal stimuli. To determine the expression and targetting of this protein, we have generated antisera against both the amino and carboxy termini of VR1. Within the dorsal root and trigeminal ganglia of rats, VR1-immunoreactivity (VR1-ir) was restricted to small and medium sized neurons. VR1-ir was transported into both the central and peripheral processes of these primary afferent neurons, as evidenced by: (i) the presence of VR1-ir in nerve fibres and terminals in lamina I and lamina II of the superficial dorsal horn, and the association of VR1-ir with small diameter nerve fibres in the skin and cornea; (ii) the reduction of VR1-ir in the spinal cord after dorsal rhizotomy; and (iii) the accumulation of VR1-ir proximal to sciatic nerve ligation. At the ultrastructural level, VR1-ir was associated with plasma membranes of neuronal perikarya in dorsal root ganglia and nerve terminals in the dorsal horn. VR1-ir was also seen in nerve fibres and terminals in the spinal trigeminal nucleus and nucleus of the solitary tract. Within a large proportion of dorsal root ganglion neurons and the terminals of their axons, VR1-ir was colocalized with staining for the P2X3 purinoceptor, and with binding sites for the lectin IB4. Surprisingly, VR1-ir did not coexist substantially in nerve fibres and terminals that contain substance P and calcitonin gene-related peptide, suggesting complex mechanisms for the release of these neuropeptides in response to capsaicin application.

Animals↗

Ineffectiveness of burst suppression therapy in mitigating perioperative cerebrovascular dysfunction. Multicenter Study of Perioperative Ischemia (McSPI) Research Group.

BACKGROUND: Cerebral injury is among the most common and disabling complications of open heart surgery. Attempts to provide neuroprotection have yielded conflicting results. We assessed the potential of propofol-induced burst suppression during open heart surgery to provide cerebral protection as determined by postoperative neuropsychologic function. METHODS: Two hundred twenty-five patients undergoing valve surgery were randomized to receive either sufentanil or sufentanil plus propofol titrated to electroencephalographic burst suppression. Blinded investigators performed neurologic and neuropsychologic testing at baseline, postoperative day (POD) 1 (neurologic testing only), PODs 5-7, and PODs 50-70. Neuropsychologic tests were compared with the results of 40 nonsurgical patients matched for age and education. RESULTS: Electroencephalographic burst suppression was successfully achieved in all 109 propofol patients. However, these patients sustained at least as many adverse neurologic outcomes as the 116 controls: POD 1, 40% versus 25%, P = 0.06; PODs 5-7, -18% versus 8%, P = 0.07; PODs 50-70, -6% versus 6%, P = 0.80. No differences in the incidence of neuropsychologic deficits were detected, with 91% of the propofol patients versus 92% of the control patients being impaired at PODs 5-7, decreasing to 52 and 47%, respectively, by PODs 50-70. No significant differences in the severity of neuropsychologic dysfunction, depression, or anxiety were noted. CONCLUSIONS: Electroencephalographic burst suppression surgery with propofol during cardiac valve replacement did not significantly reduce the incidence or severity of neurologic or neuropsychologic dysfunction. The authors' results suggest that neither cerebral metabolic suppression nor reduction in cerebral blood flow reliably provide neuroprotection during open heart surgery. Other therapeutic approaches must be evaluated to address this important medical problem.

Adult↗

Interactions of a nonpeptidic drug, valacyclovir, with the human intestinal peptide transporter (hPEPT1) expressed in a mammalian cell line.

The results of previous work performed in our laboratory using an in situ perfusion technique in rats and rabbit apical brush border membrane vesicles have suggested that the intestinal uptake of valacyclovir (VACV) appears to be mediated by multiple membrane transporters. Using these techniques, it is difficult to characterize the transport kinetics of VACV with each individual transporter in the presence of multiple known or unknown transporters. The purpose of this study was to characterize the interaction of VACV and the human intestinal peptide transporter using Chinese hamster ovary (CHO) cells that overexpress the human intestinal peptide transporter (hPEPT1) gene. VACV uptake was significantly greater in CHO cells transfected with hPEPT1 than in cells transfected with only the vector, pcDNA3. The optimum pH for VACV uptake was determined to occur at pH 7.5. Proton cotransport was not observed in hPEPT1/CHO cells, consistent with previously observed results in tissues and Caco-2 cells. VACV uptake was concentration dependent and saturable with a Michaelis-Menten constant and maximum velocity of 1.64 +/- 0.06 mM and 23.34 +/- 0.36 nmol/mg protein/5 min, respectively. A very similar Km value was obtained in hPEPT1/CHO cells and in rat and rabbit tissues and Caco-2 cells, suggesting that hPEPT1 dominates the intestinal transport properties of VACV in vitro. VACV uptake was markedly inhibited by various dipeptides and beta-lactam antibiotics, and Ki values of 12.8 +/- 2.7 and 9.1 +/- 1.2 mM were obtained for Gly-Sar and cefadroxil at pH 7.5, respectively. The present results demonstrate that VACV is a substrate for the human intestinal peptide transporter in hPEPT1/CHO cells and that although transport is pH dependent, proton cotransport is not apparent. Also, the results demonstrate that the hPEPT1/CHO cell system has use in investigating the transport kinetics of drugs with the human intestinal peptide transporter hPEPT1; however, the extrapolation of these transport properties to the in vivo situation requires further investigation.

Acyclovir↗

[Morphometric study of inflammatory cells and smooth muscle cells in coronary plaques and their relation with plaque stability].

OBJECTIVE: To compare the content of inflammatory cells and smooth muscle cells in stable and unstable coronary plaques in order to clarify the role of these cells in the vulnerability of plaques. METHODS: Hearts from 12 postmortem acute myocardial infarction cases were studied. The epicardial coronary arteries were dissected en bloc, fixed, decalcified, cut at 4 mm intervals and routinely processed for HE sections. 163 stable plaques (with no or only little lipid core) and 163 unstable plaques (with lipid core size > 40% of plaque area) were studied immunohistochemically using monoclonal antibodies specific for macrophages (CD68), T lymphocytes (UCHL-1) and smooth muscle cells (actin). Computor aided planimetry was used to measure the positive area of different cells. RESULTS: The content of macrophage and T lymphocytes in unstable plaques were significantly higher than that in stable plaques (P < 0.05). CONCLUSIONS: Stable plaques and unstable plaques not only had different lipid core size but also had different inflammatory cell and smooth muscle cell content. The larger the lipid core and the more macrophages and T lymphocytes in the fibrous cap, the more unstable the plaque. The lipid core and inflammatory cells (including macrophages and T lymphocytes) are the two major determinants of the vulnerability of coronary plaques.

Actins↗

[The effect of interleukin-1 beta on cell growth of normal mouse pituitary cells and ACTH secreting adenoma].

OBJECTIVE: To investigate whether IL-1 beta could affect the cell proliferation of normal pituitary cells and ACTH secreting adenoma cells. METHODS: Normal mouse pituitary cells were cultured in mininum essential medium-D-valine medium, a cultures virtually free of fibroblasts. AtT20 cells were also cultured as an ACTH secreting adenoma model. MTT method was used to study 10(-9) mol/L-10(-13) mol/L IL-1 beta effect on both normal and adenoma cells growth. RESULTS: (1) In the primate cells culture of normal mouse pituitary, IL-1 beta failed to influence cell growth during a period of 72 hours (n = 9, P > 0.05). This finding can not confirm that IL-1 beta has no effect on pituitary cell growth, because of the variety of cell types in pituitary. (2) In the AtT20 cells, 10(-9) mol/L-10(-13) mol/L IL-1 beta stimulated cell proliferation significantly after 48 and 72 hours culturing respectively (n = 9, P < 0.05, P < 0.01). CONCLUSIONS: These results suggested that IL-1 beta might be partially in involved in modulating pituitary adenoma cells growth.

Adenoma↗

Treatment of irritable bowel syndrome with Chinese herbal medicine: a randomized controlled trial.

CONTEXT: Irritable bowel syndrome (IBS) is a common functional bowel disorder for which there is no reliable medical treatment. OBJECTIVE: To determine whether Chinese herbal medicine (CHM) is of any benefit in the treatment of IBS. DESIGN: Randomized, double-blind, placebo-controlled trial conducted during 1996 through 1997. SETTING: Patients were recruited through 2 teaching hospitals and 5 private practices of gastroenterologists, and received CHM in 3 Chinese herbal clinics. PATIENTS: A total of 116 patients who fulfilled the Rome criteria, an established standard for diagnosis of IBS. INTERVENTION: Patients were randomly allocated to 1 of 3 treatment groups: individualized Chinese herbal formulations (n = 38), a standard Chinese herbal formulation (n = 43), or placebo (n = 35). Patients received 5 capsules 3 times daily for 16 weeks and were evaluated regularly by a traditional Chinese herbalist and by a gastroenterologist. Patients, gastroenterologists, and herbalists were all blinded to treatment group. MAIN OUTCOME MEASURES: Change in total bowel symptom scale scores and global improvement assessed by patients and gastroenterologists and change in the degree of interference in life caused by IBS symptoms assessed by patients. RESULTS: Compared with patients in the placebo group, patients in the active treatment groups (standard and individualized CHM) had significant improvement in bowel symptom scores as rated by patients (P=.03) and by gastroenterologists (P=.001), and significant global improvement as rated by patients (P=.007) and by gastroenterologists (P=.002). Patients reported that treatment significantly reduced the degree of interference with life caused by IBS symptoms (P=.03). Chinese herbal formulations individually tailored to the patient proved no more effective than standard CHM treatment. On follow-up 14 weeks after completion of treatment, only the individualized CHM treatment group maintained improvement. CONCLUSION: Chinese herbal formulations appear to offer improvement in symptoms for some patients with IBS.

Adolescent↗

Direct evidence for peptide transporter (PepT1)-mediated uptake of a nonpeptide prodrug, valacyclovir.

Xenopus laevis oocytes were used as a gene expression system to characterize the carrier-mediated transport of valacyclovir (vacv), the L-valine ester prodrug of the acyclic nucleoside acyclovir (acv). A significant increase in the uptake of [3H]vacv by Xenopus laevis oocytes injected with human intestinal peptide transporter (hPepT1) cRNA compared to the uptake by water injected oocytes indicated that vacv was translocated by hPepT1. Vacv uptake was found to be concentration dependent, saturable (K(m) = 5.94 +/- 1.91 mM and Jmax = 1.68 +/- 0.25 nmoles/hr/oocyte), pH dependent, and inhibited by various known substrates of hPepT1 but not by acv, valine or pentaglycine. Vacv also inhibited the uptake of 14C-glycylsarcosine, a known substrate of hPepT1, in a concentration-dependent manner (Ki = 4.08 +/- 1.02 mM). These results demonstrate that human intestinal peptide transporter hPepT1 has broad specificity since it recognizes vacv as a substrate even though it lacks a typical peptide bond.

Acyclovir↗

Conditioned visual flight orientation in Drosophila melanogaster abolished by benzaldehyde.

To study learning and memory of Drosophila melanogaster in the flight simulator, single flies are trained in an operant conditioning paradigm to avoid a course towards visual objects that are associated with heat. The results demonstrate that normal flies (wild-type "Berlin") can quickly learn to avoid the heat-associated objects and retain the memory. This allows us to further explore a recently communicated long-term effect of preimaginal benzaldehyde (BAL) influence on the association of visual objects with the aversive odor of BAL. Here we show that flies, exposed to BAL in the embryonic, larval or adult stage, do not accompany by a similar indifference to heat shocks. The flies are successfully trained to avoid the heat-associated visual patterns. It shows that the learning acquisition is not affected during the operant conditioning in the flight simulator. Neither object perception nor object discrimination is altered after exposure to BAL, as is shown by Fourier analysis. However, the test results after training show that exposure to BAL interferes directly with memory formation in Drosophila. It takes at least two generations of growth on the noncontaminated medium that the strain recovers fully from BAL-induced amnesia. The BAL treatment seems not only to affect the associative memory formation, but in addition the flies' development in general, as is indicated by prolonged developmental time. However, the impaired memory after BAL treatment in different stages seems to have nothing to do with an influence of BAL on the cAMP-level.

Adaptation, Physiological↗

Characterization of the regional intestinal kinetics of drug efflux in rat and human intestine and in Caco-2 cells.

PURPOSE: The aim of the present study was to investigate the transport kinetics of intestinal secretory processes in the jejunum, ileum and colon of rats and humans and in Caco-2 cells, in vitro. METHODS: Etoposide, vinblastine sulphate and verapamil hydrochloride were chosen as model substrates since they have been reported to undergo efflux in various other tissues. The concentration dependence, inhibition, directionality, temperature dependence, proton/sodium dependence, and ATP dependence of efflux were studied using side-by-side diffusion chambers and brush border membrane vesicles (BBMVs). Intestinal tissue from rats and humans and Caco-2 cells (passage no. 26) were used. Directional steady state effective permeabilities were calculated from drug appearance in the apical (AP) or basolateral (BL) chambers. Kinetic studies were carried out by investigating substrate efflux at concentrations ranging from 0.2 microns to 1000 microns. Since substrate efflux may be a result of more than one transporter, the hybrid efflux Km (Michaelis-constant), Pc (carrier-mediated permeability), and Pm (passive permeability) were determined as a function of intestinal region. Inhibitor studies were performed using quinidine (0.2mM), a mixed inhibitor of P-glycoprotein (Pgp) and Multidrug Resistance-Associated Protein (MRP), and Leukotriene C4 (100 nM), an inhibitor of MRP and the canalicular multispecific organic anion transporter (cMOAT). Temperature dependent efflux was determined by investigating the BL to AP transport at temperatures ranging from 3 degrees C to 37 degrees C. Energies of activation (Ea) were determined from an Arrhenius analysis. Sodium, proton, and ATP dependence were determined using BBMVs. Immunoquantitation of Pgp, MRP and Lung Resistance Protein (LRP) in Caco-2 cells were carried out using Western blot analysis. RESULTS: Active efflux of all substrates was observed in all regions of rat and human intestine and in Caco-2 cells. Directionality was observed with BL to AP transport exceeding AP to BL transport. The BL to AP/AP to BL permeability ratio, the efflux ratio, ranged from 1.4 to 19.8. Ileal efflux was significantly higher (p < 0.001) than in other regions. Kinetic studies revealed that hybrid efflux Km values ranged from 4 to 350 microns. In some cases, efflux was not saturable due to the solubility limits of the compounds utilized in this study. In presence of inhibitors, efflux ratios approached 1. BL to AP transport was temperature dependent in rat ileum for all substrates. Each of the intestinal efflux was found to be 11.6, 8.3, and 15.8 kcal/mole for etoposide, vinblastine and verapamil, respectively, suggesting an active, energy-dependent efflux mechanism. Substrate efflux was not sodium or proton dependent but was dependent on ATP. Using Western blot analysis the presence of Pgp, MRP, and LRP was demonstrated in Caco-2 cells and the amount of each transport protein varied as a function of passage number. CONCLUSIONS: Using multiple putative efflux substrates, the current results demonstrate that intestinal efflux was regionally dependent, mediated by multiple efflux transporters, the Km's were in the micro-molar range, and involved an energy dependent mechanism(s).

Adenosine Triphosphate↗

Characterization of a tobacco epoxide hydrolase gene induced during the resistance response to TMV.

A clone encoding a putative soluble epoxide hydrolase (EH-1), an enzyme which converts epoxides to diols, was isolated by differential screening of a cDNA library prepared from tobacco mosaic virus (TMV)-infected tobacco leaves. To confirm that EH-1 encodes an epoxide hydrolase, the recombinant EH-1 protein produced in bacteria was shown to have high epoxide hydrolase activity in vitro. Infection of resistant but not susceptible tobacco cultivars induced the accumulation of EH-1 transcripts in both the inoculated and uninoculated, systemic leaves. EH-1 expression was also induced in the inoculated and systemic tissues of TMV-infected NahG plants, which are unable to accumulate salicylic acid (SA). However, EH-1 expression in the inoculated leaves of NahG plants was delayed, whilst in the systemic leaves the induction was both later and weaker, compared to that observed in wild-type plants. Furthermore, exogenously applied SA or its functional analog 2,6-dichloroisonicotinic acid (INA) caused a rapid and transient accumulation of EH-1 transcripts, whereas an inactive SA analog did not. Thus, the induction of EH-1 gene expression appears to be regulated by both SA-independent and SA-dependent pathways. Since EH-1 was expressed only in TMV-resistant tobacco after infection, and the encoded enzyme is thought to help metabolize toxic compounds, we propose that EH-1 may play a role in protection from oxidative damage associated with defense responses. It may also play a role in generating signals for activation of certain defense responses.

Amino Acid Sequence↗

[Morphologic discrepancies of coronary atherosclerotic lesions between patients with stable and unstable angina plus acute myocardial infarction].

OBJECTIVE: To compare the morphological difference of coronary atherosclerotic plaques in patients with stable angina(SA), unstable angina (UA) and acute myocardial infarction (AMI). METHODS: 101 autopsy cases of patients with SA, UA and/or AMI were studied using routine histological and immunohistochemical staining. RESULTS: Coronary atherosclerotic plaques in SA patients were mainly the fibrous plaques with no or just very small necrotic cores; rich in smooth muscle cells and collagen fibers, less foamy cells (stable plaque), low incidence of plaque rupture (14% only) and no thrombosis found. The atherosclerotic plaques in UA and AMI patients were mainly the atheroma (unstable plaque) with large necrotic core (> 40%), thin fibrous cap, less smooth muscle cells and abundant foamy cells. The incidences of plaque rupture were 76% and 82%, thrombosis 81% and 91% respectively in 58 cases of UA and 22 cases of AMI, and the incidence of UA is statistically significant in comparing with that of the SA group (P < 0.001). CONCLUSION: In SA group, stable plaque was the main finding, plaque rupture and thrombosis rare. While in UA and AMI patients, unstable plaques predominant with a high incidence of plaque rupture and thrombosis which were the leading cause of acute coronary events.

Angina Pectoris↗