Biomedical subjects

X J Liu

Publications and source records attributed to X J Liu.

At least 55 records · Page 3Linked to original sources

PubMed1999

Microglial and astrocyte chemokines regulate monocyte migration through the blood-brain barrier in human immunodeficiency virus-1 encephalitis.

The numbers of immune-activated brain mononuclear phagocytes (MPs) affect the progression of human immunodeficiency virus (HIV)-1-associated dementia (HAD). Such MPs originate, in measure, from a pool of circulating monocytes. To address the mechanism(s) for monocyte penetration across the blood-brain barrier (BBB), we performed cross-validating laboratory, animal model, and human brain tissue investigations into HAD pathogenesis. First, an artificial BBB was constructed in which human brain microvascular endothelial and glial cells-astrocytes, microglia, and/or monocyte-derived macrophages (MDM)-were placed on opposite sides of a matrix-coated porous membrane. Second, a SCID mouse model of HIV-1 encephalitis (HIVE) was used to determine in vivo monocyte blood-to-brain migration. Third, immunohistochemical analyses of human HIVE tissue defined the relationships between astrogliosis, activation of microglia, virus infection, monocyte brain infiltration, and beta-chemokine expression. The results, taken together, showed that HIV-1-infected microglia increased monocyte migration through an artificial BBB 2 to 3.5 times more than replicate numbers of MDM. In the HIVE SCID mice, a marked accumulation of murine MDM was found in areas surrounding virus-infected human microglia but not MDM. For human HIVE, microglial activation and virus infection correlated with astrogliosis, monocyte transendothelial migration, and beta-chemokine expression. Pure cultures of virus-infected and activated microglia or astrocytes exposed to microglial conditioned media produced significant quantities of beta-chemokines. We conclude that microglial activation alone and/or through its interactions with astrocytes induces beta-chemokine-mediated monocyte migration in HAD.

AIDS Dementia Complex↗

PubMed1999

Differential distribution of urocortin- and corticotropin-releasing factor-like immunoreactivities in the rat brain.

Urocortin, a novel 40 amino acid neuropeptide, is a member of the corticotropin-releasing factor family. With 45% homology to corticotropin-releasing factor, urocortin binds with similar affinity to the corticotropin-releasing factor- and corticotropin-releasing factor-2 receptors and may play a role in modulating many of the same systems as corticotropin-releasing factor. To assess whether urocortin and corticotropin-releasing factor are localized in the same regions of the brain, we compared the distribution of urocortin- and corticotropin-releasing factor-like immunoreactivities in the rat central nervous system. Polyclonal antibodies to rat corticotropin-releasing factor and rat urocortin were generated and utilized to map the distribution of corticotropin-releasing factor- and urocortin-like immunoreactivities throughout the rat forebrain and brainstem. Characterization of the antibodies by radioimmunoassay showed no cross-reactivity with related peptides. Male Sprague-Dawley rats were treated with colchicine for 18-24 h. Following colchicine treatment, the rats were perfused with paraformaldehyde-lysine-periodate fixative and their brains removed. Serial coronal sections were taken throughout the rat brain and processed for either corticotropin-releasing factor- or urocortin-like immunoreactivity. Urocortin-like immunoreactivity shows a discrete localization within several regions including the supraoptic nucleus, the median eminence, Edinger-Westphal nucleus and the sphenoid nucleus. This is in contrast to the more abundant corticotropin-releasing factor-like immunoreactivity. Regions containing high levels of corticotropin-releasing factor immunoreactivity include the lateral septum, paraventricular nucleus of the hypothalamus, median eminence and locus coeruleus. There are a few regions that contain both urocortin-immunoreactive and corticotropin-releasing factor-immunoreactive cells, such as the supraoptic nucleus and the hippocampus. Therefore, urocortin and corticotropin-releasing factor appear to have different distribution patterns which may be indicative of their respective physiological functions.

Animals↗

PubMed1999

Growth induction of hepatic stimulator substance in hepatocytes through its regulation on EGF receptors.

The cytosolic liver-specific growth factor-hepatic stimulator substance (HSS) has been shown to be able to amplify the rat hepatocyte proliferation responded to EGF. In order to get more insight into the mechanism, the regulatory effect of HSS on EGF-receptor (EGF-R) and the receptor phosphorylation at molecular level was studied. HSS partially purified from weanling rat liver was given to cultured hepatocytes and its influence on EGF-R specific binding and internalization as well as mRNA expression were investigated. The results showed that preincubation of hepatocytes with HSS could lead to an increase in [125I]-EGF binding to its receptors and inhibit EGF-induced receptor down-regulation. Furthermore, the over-expression of EGF-R mRNA stimulated by HSS was seen during 2-12 h after the incubation. Additionally, it was demonstrated with human hepatoma SMMC-7721 cells in Western blot that the EGF-R expression and the receptor autophosphorylation were increased with dose/time-dependency after HSS treatment. These results strongly suggest that the mechanism of HSS action on hepatocyte growth might be related to its modulation on EGF-R and receptor-mediated signaling transduction.

Animals↗

PubMed1999

Postnatal profiles of glycogenolysis and gluconeogenesis are modified in rat pups by maternal dietary glucose restriction.

Because glucose is an important metabolic fuel during perinatal development, the effect of restriction of maternal dietary glucose on the developmental profile of neonatal glucoregulatory pathways was investigated. Pregnant rats were fed isoenergetic diets (0, 12, 24 or 60% glucose) and offspring were killed at seven postpartum time periods: 0-2, 4-6, 12-16 and 24 h, and 3, 6 and 15 d. Failure of the most restricted pups (0%) to survive 24 h was explained by persistent hypoglycemia resulting from the following: 1) insufficient tissue glycogen reserves at birth; 2) lower liver glycogen mobilization; 3) delayed phosphorylase a induction; and 4) low phosphoenolpyruvate carboxykinase (PEPCK) gene expression, all of which occurred despite the lower insulin:glucagon ratio. Differences in liver glycogen stores, which had been exhausted in all dietary groups by 16 h, could not account for the high d 1 pup mortality in the moderately restricted (12 and 24% glucose) groups. However, a certain metabolic distress was suggested because these moderately restricted neonates had significantly higher liver PEPCK gene expression at 12-16 h but significantly lower plasma glucose at 24 h. The high d 3 mortality, confirmed by analysis of deviance, was not supported by significant differences in any of the measured glucoregulatory indices. We conclude that dietary glucose during pregnancy is required for neonatal survival; its restriction not only lowers tissue glycogen reserves, but can disrupt the normal gene expression of liver PEPCK and the neonatal profile of phosphorylase a activity. Importantly, these observations show that the development of neonatal glucoregulatory mechanisms is modified by the availability of maternal dietary glucose.

Aging↗

PubMed1999

RHO-associated protein kinase alpha potentiates insulin-induced MAP kinase activation in Xenopus oocytes.

We recently identified Xenopus Rho-associated protein kinase alpha (xROKalpha) as a Xenopus insulin receptor substrate-1 binding protein and demonstrated that the non-catalytic carboxyl terminus of xROKalpha binds Xenopus insulin receptor substrate-1 and blocks insulin-induced MAP kinase activation and germinal vesicle breakdown in Xenopus oocytes. In the current study we further examined the role of xROKalpha in insulin signal transduction in Xenopus oocytes. We demonstrate that injection of mRNA encoding the xROKalpha kinase domain or full length xROKalpha enhanced insulin-induced MAP kinase activation and germinal vesicle breakdown. In contrast, injection of a kinase-dead mutant of xROKalpha or pre-incubation of oocytes with an xROKalpha inhibitor significantly reduced insulin-induced MAP kinase activation. To further dissect the mechanism by which xROKalpha may participate in insulin signalling, we explored a potential function of xROKalpha in regulating cellular Ras function, since insulin-induced MAP kinase activation and germinal vesicle breakdown is known to be a Ras-dependent process. We demonstrate that whereas injection of mRNA encoding c-H-Ras alone induced xMAP kinase activation and GVBD in a very low percentage (about 10%) of injected oocytes, co-injection of mRNA encoding xROKalpha and c-H-Ras induced xMAP kinase activation and germinal vesicle breakdown in a significantly higher percentage (50-60%) of injected oocytes. These results suggest a novel function for xROKalpha in insulin signal transduction upstream of cellular Ras function.

Animals↗

PubMed1999

[Cadmium concentrations in hair, urine and blood among residents in a cadmium-polluted area, Nagasaki, Japan: a 18-year follow-up after soil replacement].

In 1981, the soil of cadmium (Cd)-polluted rice fields was replaced with new soil in Kashine, a Cd-polluted district located on Tsushima Island, Nagasaki Prefecture, Japan. Consequently, the average dietary Cd intake among the inhabitants decreased from 215 micrograms/day in 1969 to 106 micrograms/day in 1983. The authors investigated the health status of Kashine inhabitants before and after the reduction of Cd intake. Concentrations of beta 2-microglobulin in urine (U-beta 2-mg) and Cd in urine (U-Cd), hair (H-Cd) and blood (B-Cd) were measured on 35 inhabitants in 1979 and 1996. The geometric mean of U-beta 2-mg concentration for 9 subjects with U-beta 2-mg levels > or = 1,000 micrograms/g creatinine (microgram/g cr) in 1979 increased by approximately 2.5-fold in 1996. Meanwhile there was little change in the geometric mean for 26 subjects with U-beta 2-mg levels < 1,000 micrograms/g cr in 1996. It was concluded that renal tubular dysfunction among Cd-exposed inhabitants was irreversible and progressive, even after dietary Cd intake decreased. The geometric mean of U-Cd concentration decreased significantly from 11.0 micrograms/g cr in 1979 to 6.3 micrograms/g cr in 1996. The decrease in U-Cd concentrations was significantly greater among inhabitants with U-beta 2-mg levels > or = 1,000 micrograms/g cr than among those with U-beta 2-mg levels < 1,000 micrograms/g cr (p = 0.03). From these results, it was considered that the level of U-Cd was more decreased by the presence of renal tubular dysfunction. The geometric mean of H-Cd concentration decreased significantly from 109.1 micrograms/kg in 1979 to 55.1 micrograms/kg in 1996. However, it was unclear whether the decrease of H-Cd depended on the decrease of dietary Cd intake, decrease of body burden or both, because U-Cd concentrations also decreased by approximately 43% during this period. H-Cd concentration was weakly and positively correlated with U-Cd (r = 0.38-0.44), an indicator of body burden of Cd. These results suggested that H-Cd concentration was influenced by the body burden of this metal. The geometric mean of B-Cd concentration in 33 inhabitants was 5.7 micrograms/l in 1996. The geometric mean was significantly greater in subjects with initial U-beta 2-mg levels > or = 1,000 micrograms/g cr than in those with U-beta 2-mg levels < 1,000 micrograms/g cr. A close positive correlation was found between B-Cd concentrations and U-Cd (r = 0.70, p < 0.01). It was suggested that the body burden influenced the levels of B-Cd as well as U-Cd, many years after Cd exposure had decreased.

Adolescent↗

PubMed1999

Effects of ligustrazine, tanshinone II A, ubiquinone, and idebenone on mouse water maze performance.

AIM: To observe the effects of four drugs, ligustrazine (Lig), tanshinone II A (Tan), ubiquinone (Ubi) and idebenone (Ide), on learning and memory of mouse. METHODS: Mouse water maze was used to evaluate nootropic effect. RESULTS: In comparison with the defective model (only scopolamine 3 mg.kg-1, Tan 20 mg.kg-1, ig) shortened the escape latency dramatically from (36 +/- 19) s to (11 +/- 5) s (P < 0.01) and reduced errors from 7 +/- 5 to 1.5 +/- 1.3 (P < 0.05). Ubi 20 mg.kg-1 ig decreased the escape latency from (37 +/- 18) s to (17 +/- 12) s and errors from 8 +/- 5 to 2.1 +/- 2.7 (P < 0.01). Ide 120 mg.kg-1 (ig) reduced the errors from 8 +/- 6 to 3.4 +/- 2.9 (P < 0.05), but had no remarkable effect on the escape latency. Lig did not exhibit marked effect on the deficit. CONCLUSION: Tan, Ubi, and Ide improved scopolamine-caused spatial performance defects in mouse.

Abietanes↗

PubMed1998

Characterization of [125I-Tyr0]-corticotropin releasing factor (CRF) binding to the CRF binding protein using a scintillation proximity assay.

We describe the characterization of high affinity [125I-Tyr0]-human CRF binding to purified recombinant human CRF-binding protein (CRF-BP) using a scintillation proximity assay (SPA). For this stable nonseparation technique developed in 96 well microtiter plates, biotinylated CRF-BP is captured by streptavidin-coated SPA beads for the detection of bound [125I-Tyr0]-CRF. Unbound [125I-Tyr0]-CRF represented little or no signal in the assay. Total binding observed was greater than 5000 cpm with a nonspecific signal of < 100 cpm determined in the presence of excess unlabeled human CRF. A comparison of the SPA method with a charcoal precipitation method confirmed that the biotinylation procedure did not adversely affect affinity of the CRF-BP for [125I-Tyr0]-CRF. Saturation binding analysis yielded an apparent equilibrium dissociation constant (Kd) of 208 +/- 5.0 pM (+/- S.D., n = 3). An inhibition constant (Ki) for unlabeled CRF was calculated to be 0.22 +/- 0.03 nM (+/- S.D., n = 8) and a pharmacological profile for eight CRF-related neuropeptides gave a rank potency similar to previously reported results. Finally, the assay variability was assessed with intra- and inter-plate coefficients of variation which were less than 5% each.

Animals↗

PubMed1998

Effect of intravenous infusions of 12-O-tetradecanoylphorbol-13-acetate (TPA) in patients with myelocytic leukemia: preliminary studies on therapeutic efficacy and toxicity.

Studies by several investigators have shown that 12-0-tetradecanoylphorbol-13-acetate (TPA) is an extraordinarily potent stimulator of differentiation of cultured human promyelocytic leukemia cells in vitro. In the present study, TPA was administered to humans by i.v. infusion without irreversible toxicity, and it was shown to have pharmacological activity for the treatment of myelocytic leukemia in patients refractory to cytosine arabinoside (Ara C), retinoic acid, and other antileukemic drugs. Marked decreases in bone marrow myeloblasts as well as temporary remission of disease symptoms were observed when TPA was administered alone or in combination with vitamin D3 and Ara C. Additional studies with TPA after the determination of optimum dosing regimens are needed to determine whether long-lasting or permanent remissions of myelocytic leukemia can be achieved. Transient and reversible side effects were observed after a 1-mg i.v. dose of TPA, but these adverse effects became less intense or disappeared when a lower dose of TPA was used. The results of this study indicate a therapeutic effect of TPA in patients with myelocytic leukemia.

Adult↗

PubMed1998

A rho-associated protein kinase, ROKalpha, binds insulin receptor substrate-1 and modulates insulin signaling.

Insulin receptor substrate-1 (IRS-1) is phosphorylated on multiple tyrosine residues by ligand-activated insulin receptors. These tyrosine phosphorylation sites serve to dock several Src homology 2-containing signaling proteins. In addition, IRS-1 contains a pleckstrin homology domain and a phosphotyrosine binding domain (PTB) implicated in protein-protein and protein-lipid interactions. In a yeast two-hybrid screening using Xenopus IRS-1 (xIRS-1) pleckstrin homology-PTB domains as bait, we identified a Xenopus homolog of Rho-associated kinase alpha (xROKalpha) as a potential xIRS-1-binding protein. The original clone contained the carboxyl terminus of xROKalpha (xROK-C) including the putative Rho binding domain but lacking the amino-terminal kinase domain. Further analyses in yeast indicated that xROK-C bound to the putative PTB domain of xIRS-1. Binding of xROK-C to xIRS-1 was confirmed in Xenopus oocytes after microinjection of mRNA corresponding to xROK-C. Furthermore, microinjection of xROK-C mRNA inhibited insulin-induced mitogen-activated protein kinase activation with a concomitant inhibition of oocyte maturation. In contrast, microinjection of xROK-C mRNA did not inhibit mitogen-activated protein kinase activation or oocyte maturation induced by progesterone or by microinjection of viral Ras (v-Ras) mRNA. These results suggest that xROKalpha may play a role in insulin signaling via a direct interaction with xIRS-1.

Amino Acid Sequence↗

PubMed1998

Displacement of insulin-like growth factors from their binding proteins as a potential treatment for stroke.

Insulin-like growth factors I and II (IGF-I and IGF-II) play an important role in normal growth and brain development and protect brain cells from several forms of injury. The effects of IGFs are mediated by type-I and type-II receptors and modulated by potentially six specific binding proteins that form high-affinity complexes with IGFs in blood and cerebrospinal fluid (CSF) and under most circumstances inactivate them. Because brain injury is commonly associated with increases in IGFs and their associated binding proteins, we hypothesized that displacement of this large "pool" of endogenous IGF from the binding proteins would elevate "free" IGF levels to elicit neuroprotective effects comparable to those produced by administration of exogenous IGF. A human IGF-I analog [(Leu24, 59, 60, Ala31)hIGF-I] with high affinity to IGF-binding proteins (Ki = 0.3-3.9 nM) and no biological activity at the IGF receptors (Ki = >10,000 nM) increased the levels of "free, bioavailable" IGF-I in the CSF. Intracerebroventricular administration of this analog up to 1h after an ischemic insult to the rat brain had a potent neuroprotective action comparable to IGF-I. This novel strategy for increasing "free" IGF levels in the brain may be useful for the treatment of stroke and other neurodegenerative diseases.

Animals↗

PubMed1998

Posterior gut development in Drosophila: a model system for identifying genes controlling epithelial morphogenesis.

The posterior gut of the Drosophila embryo, consisting of hindgut and Malpighian tubules, provides a simple, well-defined system where it is possible to use a genetic approach to define components essential for epithelial morphogenesis. We review here the advantages of Drosophila as a model genetic organism, the morphogenesis of the epithelial structures of the posterior gut, and what is known about the genetic requirements to form these structures. In overview, primordia are patterned by expression of hierarchies of transcription factors; this leads to localized expression of cell signaling molecules, and finally, to the least understood step: modulation of cell adhesion and cell shape. We describe approaches to identify additional genes that are required for morphogenesis of these simple epithelia, particularly those that might play a structural role by affecting cell adhesion and cell shape.

Animals↗

PubMed1998

Molecular cloning and characterization of Xenopus insulin-like growth factor-1 receptor: its role in mediating insulin-induced Xenopus oocyte maturation and expression during embryogenesis.

We have cloned a complementary DNA encoding the putative Xenopus insulin-like growth factor-1 (xIGF-1) receptor. Injection of messenger RNA derived from the cloned complementary DNA into Xenopus oocytes resulted in the expression and correct processing of the receptor's alpha- and beta-subunits. Using antibodies generated against protein expressed against the cloned sequence, we demonstrated that the endogenous xIGF-1 receptor in Xenopus oocytes was activated by nanomolar concentrations of mammalian IGF-1 and by insulin approximately 100-fold higher in concentration. This receptor activation profile correlated with hormone-induced Xenopus oocyte maturation. Furthermore, injection of a neutralizing antiinsulin receptor antibody into Xenopus oocytes inhibited hormone-induced xIGF-1 receptor activation. These results provide molecular and biochemical evidence supporting a role for xIGF-1 receptor in mediating insulin/IGF-1-induced Xenopus oocyte maturation. We also report here that embryonic transcription of xIGF-1 receptor is activated during the formation of the central nervous system in early Xenopus embryos.

Amino Acid Sequence↗

PubMed1998

A novel insulin receptor substrate protein, xIRS-u, potentiates insulin signaling: functional importance of its pleckstrin homology domain.

A novel Xenopus insulin receptor substrate cDNA was isolated by hybridization screening using the rat insulin receptor substrate-1 (IRS-1) cDNA as a probe. The xIRS-u cDNA encodes an open reading frame of 1003 amino acids including a putative amino-terminal pleckstrin homology (PH) domain and phosphotyrosine-binding (PTB) domain. The carboxy terminus of xIRS-u contains several potential Src homology 2 (SH2)-binding sites, five of which are in the context of YM/LXM (presumptive binding sites for phosphatidylinositol 3-kinase). It also contains a putative binding site for Grb2 (YINID). Pair-wise amino acid sequence comparisons with the previously identified xIRS-1 and the four members of the mammalian IRS family (1 through 4) indicated that xIRS-u has similar overall sequence homology (33-45% identity) to all mammalian IRS proteins. In contrast, the previously isolated xIRS-1 is particularly similar (67% identical) to IRS-1 and considerably less similar (31-46%) to the other IRS family members (2 through 4). xIRS-u is also distinct from xIRS-1, having an overall sequence identity of 47%. These sequence analyses suggest that xIRS-u is a novel member of the IRS family rather than a Xenopus homolog of an existing member. Microinjection of mRNA encoding a Myc-tagged xIRS-u into Xenopus oocytes resulted in the expression of a 120-kDa protein (including 5 copies of the 13-amino acid Myc tag). The injection of xIRS-u mRNA accelerated insulin-induced MAP kinase activation with a concomitant acceleration of insulin-induced oocyte maturation. An aminoterminal deletion of the PH domain (xIRS-u deltaPH) significantly reduced the ability of xIRS-u to potentiate insulin signaling. In contrast to the full-length protein, injection of xIRS-u (1-299), which encoded the PH and PTB domain, or xIRS-u (1-170), which encoded only the PH domain, blocked insulin signaling in Xenopus oocytes. Finally, xIRS-u (119-299), which had a truncated PH domain and an intact PTB domain, had no effect on insulin signaling. This is the first report that the PH domain of an IRS protein can function in a dominant negative manner to inhibit insulin signaling.

Adaptor Proteins, Signal Transducing↗

PubMed1998

[Regulatory effect of hepatic stimulator substance on the proliferation of human hepatoma cells].

The hepatic stimulator substance (HSS) was prepared from weanling rat livers by ultracentrifugation and Sephadex G-75 chromatography. The stimulatory effects of HSS on cell proliferation, EGF receptor expression and receptor tyrosine phosphorylation were investigated in serum-free cultured human hepatoma cell line SMMC-7721. The results showed: (1) The relative percentage of S-phase cells was increased in HSS-treated cells. (2) EGF receptor protein level was increased after the cells were treated with HSS for 12-24 h and this effect was dose- and time-dependent. (3) Treatment of the cells with HSS for 0.5-15 min resulted in the autophosphorylation of EGF receptor tyrosine residue dramatically. The above results suggest that the proliferative action of HSS on hepatocytes might be due to its modulation of EGF receptor expression and the signaling pathway.

Animals↗

PubMed1997

Immunosuppressive phenotype of corticotropin-releasing factor transgenic mice is reversed by adrenalectomy.

Stress elicits a wide range of physiological changes involving the nervous, endocrine, and immune systems. Corticotropin-releasing factor (CRF) plays a key role in orchestrating this response, activating both the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, resulting in release of corticosteroids. The present study examines the immunological phenotype and responsiveness of CRF-transgenic (CRF-Tg) mice. The immune system of the CRF-Tg animals has profound changes compared to littermate controls, including a marked reduction in both cell number and immune responsiveness. There were also phenotypic changes in the lymphocytic composition of the various lymphoid organs, most notably in the spleen, where CRF-Tg mice had a greater percentage of T lymphocytes compared to littermate controls. Adrenalectomy of CRF-Tg reversed the immunological phenotype observed and restored immune responsiveness. These results demonstrate that CRF overexpression leads to profound impairment on lymphocyte development and function mediated via corticosteroids.

Adrenalectomy↗

PubMed1997

Maternal dietary glucose modifies phosphoenolpyruvate carboxykinase (PEPCK) gene expression in the kidney of newborn rats.

The consequence of low maternal dietary glucose on perinatal phosphoenolpyruvate carboxykinase (PEPCK EC 4.1.32) gene expression was investigated. Pregnant rats were fed isoenergetic diets containing graded levels of glucose (0, 12, 24, and 60%) from gestation day 2 to lactation day 15. The postnatal developmental profile of PEPCK mRNA in the neonatal kidney was analysed by Northern blot and presented as PEPCK/GAPDH mRNA ratios. In comparison with the 24 and 60% dietary groups, maternal dietary glucose restriction (0 or 12%) during pregnancy resulted in a significant delay in postnatal renal PEPCK gene expression. In these glucose restricted pups, renal PEPCK mRNA was barely detected at birth and was fully visualized only at 4-6 hr; it peaked 24 hr after birth, which was 12 hr later than pups born to dams fed 24 or 60% glucose diets. These results demonstrate for the first time that maternal dietary glucose can modify postnatal renal PEPCK gene expression during perinatal development when glucose homeostasis via gluconeogenesis is critical for neonatal survival.

Animals↗

PubMed1997

A comparison of 99mTc-MIBI myocardial SPET with electron beam computed tomography in the assessment of coronary artery disease.

UNLABELLED: We compared technetium-99m methoxyisobutylisonitrile (MIBI) myocardial perfusion single-photon emission tomography (SPET) (MPS) and electron beam computed tomography (EBCT) in order to assess their respective value in the detection of coronary artery disease (CAD). 99mTc-MIBI SPET (stress-resting) and EBCT studies were performed in 51 patients with suspected CAD who underwent coronary angiography (CAG). CAG showed that of the 51 patients, 36 had coronary stenosis >/=50% while 15 had normal results. A moderate positive rank correlation was found between coronary calcification detected by EBCT and MPS score (rs=0.5283, P<0.01). The concordance between EBCT and MPS for the evaluation of CAD was 72.5% (37/51). The sensitivity of EBCT in detecting CAD in 51 patients was comparable to that of MPS (81% vs 94%, NS). However, the accuracy of EBCT was lower than that of MPS (78% vs 94%, P<0.025). As regards the detection of individual coronary artery disease, there was no significant difference in sensitivity between EBCT and MPS (65% vs 75%, NS); however, the specificity and accuracy of EBCT were lower than those of MPS (specificity: 77% vs 95%, P<0.005; accuracy 71% vs 85%, P<0.005). The sensitivity, specificity and accuracy of MPS in detecting single-vessel disease were higher than those of EBCT (sensitivity: 86% vs 42%, P<0.025; specificity: 96% vs 70%, P<0.025; accuracy: 93% vs 61%, P<0.005). However, no significant differences in the sensitivity, specificity and accuracy of MPS and EBCT were found in respect of multivessel disease. IN CONCLUSION: 99mTc-MIBI myocardial perfusion SPET and EBCT provide different information in the assessment of CAD. The sensitivity of EBCT for the detection of CAD is comparable with that of MPS; however, the specificity and accuracy of EBCT are lower than those of MPS. More reliable results will be obtained if both myocardial perfusion SPET and EBCT are performed.

Adult↗