Biomedical subjects

Y Guo

Publications and source records attributed to Y Guo.

At least 415 records · Page 23Linked to original sources

PubMed1998

[Construction and application of retroviral vector carrying green fluorescent protein].

OBJECTIVE: To construct retroviral vector carrying rapidly selective marker. METHODS: The recombination retroviral vector GCGFPPXSN was constructed by cloning the green fluorescent protein (GFP) cDNA into the retroviral vector containing putative internal ribosome entry sites GCXPXSN and transferred in ecotropic packaging cell line PE501 by electroporation method. The supernatants of the PE501GCGFPPXSN were used to infect the amphotropic packaging cell line PA317. The G418 resistant clones were selected in 4 weeks and were detectable by fluorescence microscopy or by fluorescence-activated cell sorting(FACS). RESULTS: A recombination retroviral vector GCGFPPXSN carrying rapidly selective marker GFP was constructed. GFP expression in packaging cell line PA317-GCGFPPXSN transferred by GCGFPPXSN was detected by fluorescence microscopy of FACS. PA317-GCGFPPXSN grew to a titer of 1.2 x 10(5) cpu/ml. By cocultivating retroviral vector producing cells and T lymphocytes, expression of GFP was observed in T lymphocytes 2 days after the end of the cocultivation. T lymphocytes expressing GFP were separated. CONCLUSION: The mammalian cell can be efficient gene transfected by retroviral vector carrying GFP. The use of GFP for cell marking represents an important advantage over conventional strategies which typically involve the use of neomycin resistance. GFP, in fact, allows a rapid in vitro selection of transduced cell by FACS. The selection requires only two-day culture with this retroviral vector, compared with 10-14 day culture with a classical retroviral vector.

Cell Line↗

PubMed1998

SP/W-5186, A cysteine-containing nitric oxide donor, attenuates postischemic myocardial injury.

The effects of SP/W-5186, a cysteine-containing nitric oxide (.NO) donor, on myocardial reperfusion injury were studied in a rabbit ischemia (45 min) and reperfusion (180 min) model. Five min before reperfusion, either low-dose (0.3 micromol/kg) or high-dose (1 micromol/kg) SP/W-5186 was given intravenously as a bolus. Administration of 0.3 micromol/kg SP/W-5186 did not change mean arterial blood pressure, heart rate or pressure-rate index. However, administration of low-dose SP/W-5186 exerted marked cardioprotective effects as evidenced by improved cardiac functional recovery (P <.05 vs. vehicle), decreased plasma creatine kinase concentration (P <. 01) and reduced infarct size (P <.01). Moreover, administration of SP/W-5186 significantly decreased platelet aggregation (P <.01 vs. vehicle), attenuated polymorphonuclear leukocyte (PMN) accumulation in myocardial tissue, inhibited PMN adhesion to endothelial cells and preserved endothelial function. Administration of high-dose SP/W-5186 resulted in a transient but significant decrease in mean arterial blood pressure and exerted more cardiac protection compared with low-dose treatment. However, the effects on platelet aggregation, PMN accumulation and PMN adhesion did not differ significantly between the two SP/W-5186 groups. Furthermore, administration of SP/W-6373, an analogue of SP/W-5186 that lacks the NO moiety, failed to exert any protective effects. These results demonstrate that NO released from SP/W-5186 significantly protected myocardial tissue from reperfusion injury. The primary mechanisms of the observed cardioprotection by SP/W-5186 involve inhibition of platelet aggregation, attenuation of PMN-endothelium interaction and preservation of endothelial function.

Animals↗

PubMed1997

Differential control of murine aldose reductase and fibroblast growth factor (FGF)-regulated-1 gene expression in NIH 3T3 cells by FGF-1 treatment and hyperosmotic stress.

Aldose reductase (AR) is an NADPH-dependent aldo-keto reductase implicated in cellular osmoregulation and detoxification. Two distinct murine genes have been identified that are predicted to encode proteins with significant amino acid sequence identity with mouse AR: mouse vas deferens protein and fibroblast growth factor (FGF)-regulated-1 protein (FR-1). Here we report that the AR and FR-1 genes are differentially regulated in NIH 3T3 fibroblasts. FGF-1 stimulation of quiescent cells induces both AR and FR-1 mRNA levels, but the effect on FR-1 mRNA expression is significantly greater. FGF-1 treatment also increases FR-1 protein expression, as determined by Western-blot analysis using FR-1-specific polyclonal antiserum. Calf serum stimulation of quiescent cells increases AR mRNA expression but not FR-1 mRNA expression. Finally, when NIH 3T3 cells are grown in hypertonic medium, AR mRNA levels are significantly increased whereas FR-1 mRNA levels are only slightly up-regulated. These results indicate that the AR and FR-1 genes are differentially regulated in murine fibroblasts by two different growth-promoting agents and by hyperosmotic stress. Therefore these structurally related enzymes may have at least some distinct cellular functions; for example, although both AR and FR-1 activity may be important for the metabolic changes associated with cellular proliferation, AR may be the primary aldo-keto reductase involved in cellular osmoregulation.

3T3 Cells↗

PubMed1997

Expression of two forms of glutamic acid decarboxylase (GAD67 and GAD65) during postnatal development of the cat visual cortex.

The postnatal development of GAD67 and GAD65 protein expression and of GAD67 positive neurons and GAD65 containing axon terminals in cat visual cortex was studied. Western blot analysis showed that the expression of both GAD67 and GAD65 increased to approximately two-thirds of the adult level during the first 5 postnatal weeks and gradually increased thereafter. In adult cats, immunohistochemistry showed that GABA and GAD67 containing neurons were found in all cortical layers. Faint cell body staining was seen with the antibody to GAD65, but it densely labeled puncta. In neonates, GABA and GAD67 immunoreactivity was most intense in two distinct bands, one superficial (Layer 1/Marginal zone), another deep (Layer VI/Subplate). Unlike in adults, GAD65 positive cell bodies were clearly evident in neonates and distributed similarly to, but less frequently than, GABA and GAD67. These GAD65 positive cells frequently had morphologies suggestive of embryonic cells and largely disappeared in older animals. During postnatal development, the neurochemical differentiation of GAD67 positive neurons and GAD65 positive axon terminals across visual cortical laminae followed an inside-outside developmental pattern, which reached adult levels after 10 weeks of age. These results suggest that postnatal development of the visual cortical GABA system involves three distinct processes: (A) a dying off of embryonic GABA cells which could play a role in formation of the cortical plate; (B) a period of relative quiescence of the VC GABA system in the first 5 postnatal weeks which could maximize excitatory NMDA effects during the rising phase of the critical period; (C) the prolonged postnatal maturation of the adult GABA system which could be involved in the crystallization of adult physiological properties and the disappearance of neural plasticity.

Aging↗

PubMed1997

Distribution of protein inhibitor of neuronal nitric oxide synthase in rat brain.

In neuronal cells, nitric oxide (NO) is synthesized by neuronal nitric oxide synthase (nNOS) and performs various functions including neurotransmission, modulation of nociception and long-term potentiation and memory. Recently, a novel 89-amino acid protein, designated PIN, has been shown to interact specifically with nNOS and inhibit nNOS dimerization. In this report, we investigated the distribution and the correlation of PIN with that of nNOS in various brain regions of rats. Amplified PIN cDNA from brain tissues revealed an open reading frame which is identical to that of human PIN. Northern blotting of brain RNA with PIN cDNA produced two transcripts, a major 0.9 kb and a minor 2.5 kb. Expression of PIN cDNA as a fusion protein in E. coli produced a 10 kDa protein which interacted specifically with pure nNOS in an overlay assay. Immunoblotting of rat brain regions with nNOS antibody demonstrated strong expression in the cerebellum, moderate expression in the cerebral cortex, midbrain, medulla and hippocampus with only weak expression in the spinal cord. By comparison, PIN expression was stronger in the cerebral cortex, midbrain, hippocampus and medulla compared with that of cerebellum and spinal cord. We conclude that PIN interacts strongly with nNOS and is constitutively expressed in various brain regions. The dissimilarity between nNOS and PIN expressions in various brain regions may explain the well known differences in NOS activity between these regions. Our results also suggest that PIN may serve other functions other than nNOS inhibition.

Amino Acid Sequence↗

PubMed1997

Estrogens attenuate neuronal injury due to hemoglobin, chemical hypoxia, and excitatory amino acids in murine cortical cultures.

A growing body of evidence supports the hypothesis that estrogens may be beneficial in Alzheimer's disease and other neurodegenerative processes. Less is known of their therapeutic potential in acute CNS insults. In this study, we assessed the effect of estrogens in three injury paradigms that may be relevant to CNS hemorrhage, trauma, and ischemia. Supraphysiologic concentrations of 17beta-estradiol, estrone, or equilin attenuated neuronal loss due to prolonged exposure to the pro-oxidant hemoglobin, with complete protection at 10 microM. Most of this effect persisted despite concomitant treatment with the antiestrogen ICI 182,780 or the protein synthesis inhibitor cycloheximide. In contrast, the non-estrogenic steroid methylprednisolone, which is currently in clinical use in spinal cord injury, reduced neuronal loss by only about 30%. High concentrations of equilin or estrone also attenuated the submaximal neuronal injury induced by 3.5-4.5 h exposure to the cytochrome oxidase inhibitor sodium azide, with near complete protection at 30 microM. Estrogens had a weaker and somewhat variable effect on pure excitotoxic injury, reducing neuronal loss due to 24 h kainate exposure by about half, and due to 24 h NMDA exposure by 15-65%; similar neuroprotection was provided by the antioxidant 21-aminosteroid U74500A. These results suggest that estrogens may be beneficial in acute CNS injuries associated with oxidative and excitotoxic stress. Investigation of high dose estrogen therapy in in vivo models of CNS hemorrhage, trauma, and ischemia is warranted.

Animals↗

PubMed1997

KLP38B: a mitotic kinesin-related protein that binds PP1.

We have identified a new member of the kinesin superfamily in Drosophila, KLP38B (kinesin-like protein at 38B). KLP38B was isolated through its two-hybrid interaction with the catalytic subunit of type 1 serine/threonine phosphoprotein phosphatase (PP1). We demonstrate that recombinant KLP38B and PP1 associate in vitro. This is the first demonstration of direct binding of a kinesin-related protein to a regulatory enzyme. Though most closely related to the Unc-104 subfamily of kinesin-related proteins, KLP38B is expressed only in proliferating cells. KLP38B mutants show cell proliferation defects in many tissues. KLP38B is required for normal chromatin condensation as embryos from KLP38B mutant mothers have undercondensed chromatin at metaphase and anaphase. This is the first time that a kinesin-related protein has been shown to have such a role. Incomplete lethality of a strong KLP38B allele suggests partial redundancy with one or more additional kinesin-related proteins.

Amino Acid Sequence↗

PubMed1997

Role of mast cell histamine in the formation of rat paw edema: a microdialysis study.

We determined the endogenous histamine concentration in the subplantar space of rat hind paws using an in vivo microdialysis technique. A microdialysis probe was implanted into the rat hind paw and the histamine content in dialysates was measured by high performance liquid chromatography-fluorometry. In wild type (+/+) rats, the histamine output (basal level 25.7 +/- 0.9 pmol/ml) increased 115-, 199- and 426-fold rapidly after subplantar injection of compound 48/80 at doses of 0.5, 5 and 50 microg/paw, respectively. In genetically mast cell-deficient (Ws/Ws) rats, the basal level of histamine was one third of that obtained from +/+ rats, and was not increased by compound 48/80 injection. With this treatment, marked, dose dependent, but relatively gradual development of the paw edema was found in +/+ rats. However, no edema formation was observed in Ws/Ws rats. Histological observations showed neither mast cells nor edema to be present in the paw skin of Ws/Ws rats. These findings indicate the critical role of histamine as a trigger for the development of edema in vivo. In addition, Ws/Ws rats will provide important information as to the roles of mast cells in the inflammatory response.

Animals↗

PubMed1997

Fibroblast growth factor-1 induction of delayed-early mRNA expression in NIH 3T3 cells is prolonged by heparin addition.

Fibroblast growth factor (FGF)-1, also known as acidic FGF, is a multifunctional heparin-binding protein that is mitogenic for a wide variety of cell types cultured in vitro and a potent angiogenic agent in vivo. These cellular responses are mediated via high-affinity binding to a family of four membrane-spanning tyrosine kinase receptors. FGF-1-stimulated mitogenesis is potentiated by heparin, a sulfated glycosaminoglycan. In this study, we examined the effect of exogenous heparin on FGF-1-inducible gene expression in murine NIH 3T3 cells using both wild-type FGF-1 and FGF-1/glu132, an FGF-1 mutant with a reduced apparent affinity for heparin. The induction levels and temporal expression kinetics of two immediate-early response mRNAs (early growth response gene-1, thrombospondin-1) as well as two delayed-early response mRNAs (proliferin, ornithine decarboxylase) were monitored by Northern blot hybridization analysis. We found that although FGF-1 alone can promote the initial induction of these four mRNAs, heparin coaddition is necessary for prolonged delayed-early mRNA expression. This heparin effect occurs when cells are stimulated with wild-type FGF-1 but not with FGF-1/glu132. Furthermore, FGF-1 and heparin must be added together at the initial time of mitogen stimulation and they must remain present in the cell culture medium for a minimum period of 8 h to promote sustained delayed-early mRNA expression. These findings are consistent with the proposal that heparin promotes a long-term FGF-1:FGFR interaction which is required for sustained delayed-early gene expression and a full mitogenic response.

3T3 Cells↗

PubMed1997

Regulation of cerebellar nitric oxide production in response to prolonged in vivo hypoxia.

The aim of this study was to assess the influence of prolonged in vivo hypoxia on cerebellar nitric oxide (NO) production. Conscious rats were exposed to 10% O2 (balanced N2) for 12 or 48 hr (arterial PO2 between 35 and 39 mmHg). The animals were then killed, and the cerebella were quickly frozen. NO production was measured in vitro by monitoring the conversion of L-[3H]arginine to L-[3H]citrulline. Protein and mRNA expressions of the neuronal (nNOS) and endothelial (ecNOS) isoforms of nitric oxide synthases were assessed by using immunoblotting and semiquantitative reverse transcription-polymerase chain reaction, respectively. We also measured mRNA expression of GTP cyclohydrolase I, the rate-limiting enzyme in the synthesis of NOS cofactor, tetrahydrobiopterin, and mRNA and protein expressions of argininosuccinate synthase and argininosuccinate lyase, essential enzymes for the recycling of L-citrulline to L-arginine. Prolonged in vivo hypoxia resulted in a time-dependent increase in cerebellar nitric oxide synthase activity and a significant rise in mRNA and protein expressions of nNOS isoform; however, ecNOS protein expression declined significantly. There was also a rise in mRNA expression of GT cyclohydrolase I; however, neither mRNA nor protein expression of argininosuccinate synthase and argininosuccinate lyase changed significantly in hypoxic animals. These results suggest that prolonged hypoxia increases cerebellar NO formation as a result of upregulation of cerebellar nNOS expression, whereas ecNOS expression declines. We propose that cofactor availability for NO production may also increase during hypoxia because of upregulation of GTP cyclohydrolase I expression. Recycling of L-citrulline to L-arginine, however, remains unchanged.

Animals↗

PubMed1997

Down-regulation of protein and mRNA expression for transforming growth factor-beta (TGF-beta1) type I and type II receptors in human prostate cancer.

Transforming growth factor-beta (TGF-beta1) is a potent negative regulator of cell growth that transduces signals through interactions with type I and II receptors. Abnormal expression and mutational alterations of these receptors have been observed in several human malignancies. In this study, we investigated the expression of the two types of TGF-beta1 receptors, R-I and R-II, in a normal human prostate, primary prostate adenocarcinoma and lymph nodes with metastatic deposits. Expression of receptor proteins was examined by immunohistochemical analysis in paraffin-embedded prostatic tissue sections, and mRNA expression was determined by Northern blot and RT-PCR analysis. Uniformly strong immunoreactivity for both TGF-beta receptor proteins, R-I and R-II, was exclusively localized to the prostatic glandular epithelium of normal prostates. In contrast, tumor epithelial cells in primary and metastatic prostatic cancer specimens exhibited a weak heterogeneous immunoreactivity for both R-I and R-II receptors; 25% of primary prostatic tumors and 45% of the lymph nodes with metastases were totally negative for R-I and R-II expression, while the rest exhibited a significantly reduced immunoreactivity for both types of receptors compared to the normal prostate (p < 0.05). Moreover, there was a significant decrease in the expression of R-I and R-II mRNA, in all 20 primary prostatic tumors and 4 lymph nodes positive for metastases, indicating that the decreased protein expression was due to down-regulation of gene expression for the two receptors. Our findings imply that decreased expression of TGF-beta1 type I and type II receptors might be involved in prostate tumorigenesis.

Activin Receptors, Type I↗

PubMed1997

CTLA-4-B7 interaction is sufficient to costimulate T cell clonal expansion.

T cell costimulation, particularly by the B7 family members B7-1 and B7-2, plays a critical role in regulating T cell-mediated immunity. Two molecules on T cells, CD28 and CTLA-4, are known to bind to B7. It has been suggested that CD28-B7 interaction promotes T cell response, whereas B7-CTLA-4 interaction downregulates T cell clonal expansion. However, the proposed responses of individual receptors to B7 have not been verified directly. Here, we report that B7-1 promotes clonal expansion of CD28-deficient T cells, and that the CD28-independent costimulatory activity is mediated by CTLA-4, as it is completely blocked by intact and Fab of anti-CTLA-4 mAb. In addition, a mutant B7-1 molecule, B7W88 >A, which has lost binding to CD28 but retained significant CTLA-4 binding activity, promotes T cell clonal expansion. Furthermore, while presence of CD28 enhances T cell response to B7-1, such response is also completely blocked by anti-CTLA-4 mAb. Taken together, our results demonstrate that B7-CTLA-4 interaction promotes T cell clonal expansion, and that optimal T cell response to B7 is achieved when both CD28 and CTLA-4 interact with B7. These results establish an important function of CTLA-4 in promoting T cell activation, and suggest an alternative interpretation of the function of CTLA-4 in T cell activation.

Abatacept↗

PubMed1997

Hyperpolarization- and depolarization-activated Ca2+ currents in Paramecium trigger behavioral changes and cGMP formation independently.

Using 5% ethanol as a deciliating agent, 20 mm colchicine to prevent reciliation and 1 mm amiloride to affect ion fluxes in Paramecium we examined the compartmentation and function of Ca2+ fluxes employing the biosynthesis of cGMP and the stereotypic swimming behavior as indicators for Ca2+ entry. As a function of extracellular Ca2+ Paramecia responded to colchicine and amiloride with a short-lived ciliary augmentation (fast swimming) which indicated hyperpolarization, and formation of cGMP, i.e., the reported hyperpolarization-activated Ca2+ inward current in the somatic membrane is coupled to intracellular generation of cGMP. This is comparable to the coupling of the depolarization-activated, ciliary Ca2+ inward current and ciliary cGMP formation.Ethanol-deciliated cells and ethanol-treated, yet ciliated control cells did not respond to a depolarization with backward swimming or formation of cGMP. Both responses recovered with similar kinetics. A persistent effect of an ethanol exposure on the axonemal apparatus or on guanylyl cyclase activity of ciliated control cells was excluded using permeabilized cells and cell-free enzyme, respectively. Further, in the presence of 20 mm colchicine ethanol-treated cells only recovered the depolarization-dependent avoiding reaction whereas the formation of cGMP remained depressed, i.e., the drug dissected both responses. Similarly, ethanol exposure of Paramecia did not affect the fast swimming response towards the hyperpolarizing agent amiloride whereas the cGMP formation was abrogated and recovered over a period of 7 hr, i.e., amiloride dissected the hyperpolarization-elicited behavioral response from the intracellular cGMP formation. The data demonstrate that in Paramecium depolarization- and hyperpolarization-stimulated behavioral responses and cGMP formation are not coupled. The behavioral changes are triggered by smaller Ca2+ inward currents than the formation of intracellular cGMP.

Amiloride↗

PubMed1997

Poly(ethylene glycol)-conjugated surfactants promote or inhibit aggregation of phospholipids.

The calcium-induced aggregation of dilauroyl phosphatidic acid (DLPA) suspensions, with or without added poly(ethylene oxide) (PEO)-conjugated surfactants containing 4 to 30 ethylene oxide subunits, were monitored by turbidity measurement and quasi-elastic light scattering (QLS). The aggregation was inhibited (protected) by the incorporated PEO surfactant for most samples, while a window for promotive effect was found for samples with low surface coverage by the PEO moiety of the incorporated surfactant. Promotion occurs only when the aggregation is slow and at a low level. The promotion is explained by the synergistic effect of PEO and divalent calcium cations when the steric repulsion is weak. The promotion/protection crossover is a display between the PEO/calcium synergistic effect and the steric repulsion.

Calcium↗

PubMed1997

Effects of functional endoscopic sinus surgery on maxillary sinus mucosa.

OBJECTIVE: To compare the preoperative and postoperative changes on ciliary surface of maxillary sinus mucosa in patients treated with functional endoscopic sinus surgery. DESIGN: The maxillary mucosa of both the superolateral wall and the ostium were sampled during the operation and 6 to 12 months (mean duration, 7.6 months) after the operation. Ciliary surface was determined using scanning electron microscopy in combination with an image analyzer and was expressed in terms of ciliary area, which is the percentage of mucosal surface occupied by cilia. SETTING: The samples were taken at a hospital-based clinic. An electron microscopic study was performed at Mie University School of Medicine, Mie, Japan. PATIENTS: Sixteen patients (20 maxillary sinuses) undergoing functional endoscopic sinus surgery for treatment of chronic sinusitis. RESULTS: The mean (+/-SD) ciliary area before the surgery was 60.7%+/-28.8% and 39.9%+/-21.5% in the superolateral wall of the maxillary sinus and the ostium of the maxillary sinus, respectively. The ciliary area of the superolateral wall was significantly higher than that of the ostium (P<.001). The mean (+/-SD) postoperative ciliary area value was 74.3%+/-22.6% in the superolateral wall and 51.3%+/-16.1% in the ostium. These postoperative values were significantly higher than the preoperative values (P<.001). CONCLUSIONS: This study showed that the maxillary sinus mucosa in chronic sinusitis is capable of regeneration, and the damaged ciliated epithelium could return toward normal with the improvement of ventilation and drainage of the maxillary sinus following functional endoscopic sinus surgery.

Adolescent↗

PubMed1997

Quantitation of in vivo gene delivery by restriction enzyme PCR generated polymorphism.

The Multiple intestinal neoplasia (Min) mouse develops multiple polyps in the intestine, due to a heterozygous mutation of the Apc locus. Our laboratory has been introducing normal human adenomatous polyposis coli (APC) gene into the Min mouse through liposome enema to prevent or reverse polyp formation. We have quantitated the amount of normal human APC gene delivered in vivo by a restriction enzyme site specific quantitative PCR. Adult Min and BALB/C mice were treated with lipofectant and human APC complementary DNA (cDNA) plasmid. Min colonic DNA was amplified using primers for Apc nucleotide 2524F (5'2524-TCTCGTTCTGAGAAAGACAGAAGCT) and 2679R (5"2679-TGATACTTCTTCCAAAGCTTTGGCTAT). Highlighted primer sequences were purposely different so as to generate two HindIII restriction enzyme sites in the presence of normal mouse Apc (Apc+). Genomic DNA from untreated Min colonic epithelium revealed two bands: 144 bp for ApcMin and 123 bp for Apc+. BALB/C DNA was amplified using primers flanking a region within the APC gene containing a HindIII site on the human APC, which is absent in the murine APC (Apc). Min's DNA extracted 24 hr after treatment demonstrated a plasmid content of 3% due to a relative increase in the Apc+ (123 bp) band. Six weeks of treatments increased delivery to 10%. APC gene therapy of colonic epithelium can be quantitatively measured through restriction enzyme quantitative PCR. Long-term treatment further increases gene delivery. PCR generated polymorphism is a reliable and reproducible technique to initially optimize transfection conditions and ultimately quantitate efficacy in an in vivo gene delivery model.

Adenomatous Polyposis Coli↗

PubMed1997

The cure of acute Babesiasis perroncitoi in swine.

From June to August in 1988, a total of 64 pure-bred Landrace, Yorkshire (large white) and Inner Mongolian Black Swine from a farm in Huhehot were affected with a disease, 13 died. The pathogen was confirmed primarily to be Babesia perroncitoi. The drugs used for treatment were Berenil and Acaprin. The intramuscular dose for Berenil was 3 mg per kilogram weight. The subcutaneous dose for Acaprin was 0.8 mg per kilogram weight. All of which had satisfactory results. In the same season in the second year and the third year, the disease was also reported, but all sick animals were cured.

Animals↗

PubMed1997

Aortic plaque as a potential cause for cerebral ischemia.

The purpose of this study was to determine the prevalence, clinical significance, and embolic potential of thoracic aortic plaque in patients with cerebral ischemia and to further study the correlation of aortic plaque with carotid or heart disease. We used transesophageal echography (TEE) to evaluate potential source of emboli in aortic arch and heart, and duplex in carotid artery. A atherosclerotic lesion of aortic arch was defined as normal (0), mild plaque (1), moderate plaque (2) and protruding plaque or mobile plaque (3). 75 of 100 patients were found to have atherosclerotic lesion in aortic arch. 16 of 75 patients over degree 2 exhibited no pathologic finding of heart or carotid and 4 of 16 patients were classified as degree 3. The pathologic findings of heart and carotid were significantly correlated with aortic plaque. Age, diabetes, CAD were also significantly correlated with aortic plaque. Aortic atherosclerosis was common in cerebral ischemia. Aortic plaque might be responsible for not only some unexplained embolic events, but also for some of the embolic stroke in patient who have carotid artery or heart disease. Age, diabetes, CAD might be important risk factors in the development of atherosclerotic lesion in the aortic arch.

Adolescent↗