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Biomedical subjects

Hiroyuki Watanabe

Publications and source records attributed to Hiroyuki Watanabe.

At least 73 records · Page 4Linked to original sources

Long-term prognosis of duct-narrowing chronic pancreatitis: strategy for steroid treatment.

OBJECTIVES: The purpose of this study was to assess the long-term prognosis in patients with duct-narrowing chronic pancreatitis (DNCP) and determine the indications for steroid therapy. METHODS: We evaluated clinical and imaging outcomes in patients with DNCP classified into 3 groups (A, B, and C) according to the treatment given. Group A included 6 patients who underwent surgical resection. Groups B and C included 21 and 10 patients treated medically with and without steroid therapy, respectively. RESULTS: In group A, 2 patients relapsed in the remnant pancreas. In group B, pancreatic swelling was resolved in all the patients, and moreover, both the irregular narrowing of the main pancreatic duct (MPD) and the strictures of the common bile duct (CBD) improved after initiation of corticosteroid therapy in all but 1 of the patients, including 5 without immunoserologic abnormality. However, clinical recurrences occurred in 4 patients (19%) during or after the maintenance therapy. In group C, all the patients showed an improvement in swelling of the gland, while only 5 showed improvement of pancreatic duct involvement. Four of these 5 patients did not show any serologic data suggesting autoimmune abnormality or CBD involvement. In all the other 5 patients in whom MPD irregularities did not improve, bile duct strictures or positive immunoserologic test results were noted. CONCLUSIONS: Steroid therapy is effective for improving pancreatic duct and bile duct lesions in patients with DNCP and is indicated particularly in those with CBD strictures or immunoserologic abnormality, although some patients have recurrences.

Adrenal Cortex Hormones↗

Effect of azithromycin therapy on coronary circulation in patients with coronary artery disease.

This study examined the effect of azithromycin therapy on the coronary microcirculation using measurement of coronary flow velocity reserve (CFVR) by transthoracic Doppler echocardiography in 35 patients with coronary artery disease. CFVR increased significantly after azithromycin therapy (3.0 +/- 0.7 vs 3.5 +/- 0.7, p <0.001). The changes in CFVR were negatively correlated with changes in high-sensitivity C-reactive protein levels in patients receiving azithromycin.

Aged↗

A Tyr-W-MIF-1 analog containing D-Pro2 acts as a selective mu2-opioid receptor antagonist in the mouse.

The antagonistic properties of Tyr-d-Pro-Trp-Gly-NH(2) (d-Pro(2)-Tyr-W-MIF-1), a Tyr-Pro-Trp-Gly-NH(2)(Tyr-W-MIF-1) analog, on the antinociception induced by the mu-opioid receptor agonists Tyr-W-MIF-1, [d-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO), Tyr-Pro-Trp-Phe-NH(2) (endomorphin-1), and Tyr-Pro-Phe-Phe-NH(2) (endomorphin-2) were studied in the mouse paw-withdrawal test. d-Pro(2)-Tyr-W-MIF-1 injected intrathecally (i.t.) had no apparent effect on the thermal nociceptive threshold. d-Pro(2)-Tyr-W-MIF-1 (0.1-0.4 nmol) coadministered i.t. showed a dose-dependent attenuation of the antinociception induced by Tyr-W-MIF-1 without affecting endomorphin- or DAMGO-induced antinociception. However, higher doses of d-Pro(2)-Tyr-W-MIF-1 (0.8-1.2 nmol) significantly attenuated endomorphin-1- or DAMGO-induced antinociception, whereas the antinociception induced by endomorphin-2 was still not affected by d-Pro(2)-Tyr-W-MIF-1. Pretreatment i.t. with various doses of naloxonazine, a mu(1)-opioid receptor antagonist, attenuated the antinociception induced by Tyr-W-MIF-1, endomorphin-1, endomorphin-2, or DAMGO. Judging from the ID(50) values for naloxonazine against the antinociception induced by the mu-opioid receptor agonists, the antinociceptive effect of Tyr-W-MIF-1 is extremely less sensitive to naloxonazine than those of endomorphin-1 or DAMGO. In contrast, endomorphin-2-induced antinociception is extremely sensitive to naloxonazine. The present results clearly suggest that d-Pro(2)-Tyr-W-MIF-1 is the selective antagonist to be identified for the mu(2)-opioid receptor in the mouse spinal cord. d-Pro(2)-Tyr-W-MIF-1 may also discriminate between Tyr-W-MIF-1-induced antinociception and the antinociception induced by endomorphin-1 or DAMGO, all of which show a preference for the mu(2)-opioid receptor in the spinal cord.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Genomic organization and functional analysis of murine PKD2L1.

Mutations in genes that encode polycystins 1 or 2 cause polycystic kidney disease (PKD). Here, we report the genomic organization and functional expression of murine orthologue of human polycystin-2L1 (PKD2L1). The murine PKD2L1 gene comprises 15 exons in chromosome 19C3. Coexpression of PKD2L1 together with polycystin-1 (PKD1) resulted in the expression of PKD2L1 channels on the cell surface, whereas PKD2L1 expressed alone was retained within the endoplasmic reticulum (ER). This suggested that interaction between PKD1 and PKD2L1 is essential for PKD2L1 trafficking and channel formation. Deletion analysis at the cytoplasmic tail of PKD2L1 revealed that the coiled-coil domain was important for trafficking by PKD1. Mutagenesis within two newly identified ER retention signal-like amino acid sequences caused PKD2L1 to be expressed at the cell surface. This indicated that the coiled-coil domain was responsible for retaining PKD2L1 within the ER. Functional analysis of murine PKD2L1 expressed in HEK 293 cells was undertaken using calcium imaging. Coexpression of PKD1 and PKD2L1 resulted in the formation of functional cation channels that were opened by hypo-osmotic stimulation, whereas neither molecule formed functional channels when expressed alone. We conclude that PKD2L1 forms functional cation channels on the plasma membrane by interacting with PKD1. These findings raise the possibility that PKD2L1 represents the third genetic locus that is responsible for PKD.

Amino Acid Sequence↗

Reduced cerebrospinal fluid production and intracranial pressure in mice lacking choroid plexus water channel Aquaporin-1.

Aquaporin-1 (AQP1) is a water channel expressed strongly at the ventricular-facing surface of choroid plexus epithelium. We developed novel methods to compare water permeability in isolated choroid plexus of wild-type vs. AQP1 null mice, as well as intracranial pressure (ICP) and cerebrospinal fluid (CSF) production and absorption. Osmotically induced water transport was rapid in choroid plexus from wild-type mice and reduced by fivefold by AQP1 deletion. AQP1 deletion did not affect choroid plexus size or structure. By stereotaxic puncture of the lateral ventricle with a microneedle, ICP was 9.5 +/- 1.4 cm H2O in wild-type mice and 4.2 +/- 0.4 cm H2O in AQP1 null mice. CSF production, an isosmolar fluid secretion process, was measured by a dye dilution method involving fluid collections using a second microneedle introduced into the cisterna magna. CSF production in wild-type mice was (in microl min(-1)) 0.37 +/- 0.04 (control), 0.16 +/- 0.03 (acetazolamide-treated), and 1.14 +/- 0.15 (forskolin-treated), and reduced by approximately 25% in AQP1 null mice. Pressure-dependent CSF outflow, measured from steady-state ICP at different ventricular infusion rates, was not affected by AQP1 deletion. In a model of focal brain injury, AQP1 null mice had remarkably reduced ICP and improved survival compared with wild-type mice. The reduced ICP and CSF production in AQP1 null mice provides direct functional evidence for the involvement of AQP1 in CSF dynamics, suggesting AQP1 inhibition as a novel option for therapy of elevated ICP.

Animals↗

Overexpression of human acyl-CoA thioesterase upregulates peroxisome biogenesis.

The biological functions of human acyl-CoA thioesterase III (ACTEIII/PTE-1), initially identified as an HIV-1 Nef binding protein, have remained unclear. We report herein that the stable overexpression of ACTEIII/PTE-1 in human and murine T-cell lines resulted in an increase in both peroxisome number and lipid droplet formation in a manner dependent on the amount of the protein. Peroxisome proliferation was evidenced by immunofluorescence staining for catalase, a peroxisome marker protein, as well as by direct peroxisome enumeration on electron micrographs. Consistently, the amount of catalase was elevated as the amount of ACTEIII/PTE-1 was increased. ACTEIII/PTE-1 mutants with reduced enzymatic activity or with the defect in peroxisome localization did not induce peroxisome proliferation, indicating that peroxisome proliferation was mediated by metabolites generated by ACTEIII/PTE-1 within peroxisomes. Finally, thymocytes isolated from a T-cell-specific ACTEIII/PTE-1 transgenic mouse as well as human and murine cell lines of lymphoid and non-lymphoid origins exhibited a similar proliferation of peroxisomes. Thus, ACTEIII/PTE-1 may be involved in the metabolic regulation of peroxisome proliferation.

Animals↗

Black tea increases coronary flow velocity reserve in healthy male subjects.

Epidemiologic studies suggest that tea consumption decreases the risk for cardiovascular events. However, there has been no clinical report examining the effects of tea consumption on coronary circulation. The purpose of this study was to evaluate the effects of black tea on coronary flow velocity reserve (CFVR) using transthoracic Doppler echocardiography (TTDE). This was a double-blind crossover study of 10 healthy male volunteers conducted to compare the effects of black tea and caffeine on coronary circulation. The coronary flow velocity of the left anterior descending coronary artery was measured at baseline and at hyperemia during adenosine triphosphate infusion by TTDE to determine CFVR. The CFVR ratio was defined as the ratio of CFVR after beverage consumption to CFVR before beverage consumption. All data were divided into 2 groups according to beverage type: group T (black tea) and group C (caffeine). Two-way analysis of variance showed a significant group effect and interaction in CFVR before and after beverage consumption (p = 0.001). CFVR significantly increased after tea consumption in group T (4.5 +/- 0.9 vs 5.2 +/- 0.9, p <0.0001). The CFVR ratio of group T was larger than that of group C (1.18 +/- 0.07 vs 1.04 +/- 0.08, p = 0.002). Acute black tea consumption improves coronary vessel function, as determined by CFVR.

Adult↗

Differential involvement of mu 1-opioid receptors in dermorphin tetrapeptide analogues-induced antinociception.

The involvement of putative mu(1)-opioid receptors in the antinociception induced by the dermorphin tetrapeptide analogues Try-D-Arg-Phe-beta-Ala (TAPA) and Tyr-D-Arg-Phe-beta-Ala-NH(2) (TAPA-NH(2)) was determined in mice, using a tail-pressure test and a formalin test. TAPA and TAPA-NH(2) injected i.c.v. and i.t. produced dose-dependent antinociception in both assays. In the tail-pressure test, the antinociception induced by i.c.v. or i.t. injected TAPA, but not TAPA-NH(2), was significantly attenuated by pretreatment with naloxonazine, a selective antagonist for putative mu(1)-opioid receptors. Moreover, naloxonazine also significantly attenuated the antinociception induced by i.c.v. injected TAPA, but not TAPA-NH(2), in the formalin test. In contrast, the antinociception induced by both TAPA and TAPA-NH(2) given i.t. was significantly attenuated by pretreatment with naloxonazine in the formalin test. The present results suggest that TAPA and TAPA-NH(2) should be considered selective agonists for putative mu(1)- and mu(2)-opioid receptors, respectively. The C-terminal amidation of TAPA-NH(2) may be critical for distinguishing between putative mu(1)- and mu(2)-opioid receptors.

Analgesics↗

Decoupling of automatic control systems in a continuous-wave electron paramagnetic resonance spectrometer for biomedical applications.

This article describes a systematic approach to decoupling automatic tuning control (ATC) and automatic matching control (AMC) systems in continuous-wave (CW) electron paramagnetic resonance (EPR) spectroscopy for animal experiments. This technique enables us to improve the stability of CW-EPR spectroscopy even if the animal is moving during the data acquisition of EPR spectra. The control systems are formulated to allow the behavior of interference between them to be investigated, since they are generally coupled due to the characteristics of the microwave resonator. The stability of the entire control system in a 1.1 GHz CW-EPR spectrometer is evaluated with the generalized Nyquist stability criterion. We compare the EPR spectra of a triarylmethyl (TAM) radical that is dosed in anesthetized mice in terms of the signal-to-noise ratio (SNR) to test the precompensator for decoupling the ATC and AMC systems. The experimental findings suggest that the present technique is useful for improving the SNR of EPR spectra in animal experiments. The SNR of the measured EPR spectra was improved by about 50% with the precompensator.

Algorithms↗

The anticancer natural product pironetin selectively targets Lys352 of alpha-tubulin.

Pironetin is a potent inhibitor of tubulin assembly and arrests cell cycle progression in M phase. Analyses of its structure-activity relationships suggested that pironetin covalently binds tubulin. To determine the binding site of pironetin, we synthesized biotinylated pironetin, which inhibited tubulin assembly both in vitro and in situ. The biotinylated pironetin selectively and covalently bound with tubulin. Partial digestion of biotinylated pironetin-treated tubulin by several proteases revealed that the binding site is the C-terminal portion of alpha-tubulin. By systematic alanine scanning, the pironetin binding site was determined to be Lys352 of alpha-tubulin. Lys352 is located at the entrance of a small pocket of alpha-tubulin, and this pocket faces the beta-tubulin of the next dimer. This is the first compound that covalently binds to the alpha subunit of tubulin and Lys352 of alpha-tubulin and inhibits the interaction of tubulin heterodimers.

Amino Acid Sequence↗

Simple detection of occluded coronary artery using retrograde flow in septal branch and left anterior descending coronary artery by transthoracic Doppler echocardiography at rest.

BACKGROUND: We hypothesized that coronary flow assessment by transthoracic Doppler echocardiography (TTDE) for both intramyocardial collateral channel and epicardial channels would be useful for identifying occluded left anterior descending coronary artery (LAD). METHODS: We assessed flow direction in the LAD and the septal branch (SEP) by TTDE in 302 consecutive patients who were suggested to have ischemic heart disease. We defined antegrade LAD flow as a direction from the base to the apex of the left ventricle in the anterior groove area, and antegrade SEP flow as a direction from anterior to inferior in the anterior interventricular septum. By contrast, we defined retrograde LAD and SEP flow as an inverse direction. We performed angiography on all patients. RESULTS: Retrograde flow was detected in 22 (LAD, 16 patients; SEP, 6 patients) of 23 patients with occluded LAD, and antegrade flow was detected in all patients without occluded LAD. The sensitivity and specificity for identification of occluded LAD by TTDE were 96% and 100%, respectively. CONCLUSIONS: Assessment of flow direction in both LAD and SEP by TTDE is a useful method in identification of occluded LAD.

Aged↗

Postprandial plasma fructose level is associated with retinopathy in patients with type 2 diabetes.

The aim of the present study was to investigate the association of fructose on microangiopathy in patients with diabetes. Postprandial plasma fructose concentrations and postprandial plasma glucose concentrations were simultaneously measured 3 times within a 24-hour period (2 hours after each meal) in 38 patients with type 2 diabetes that had been admitted to the hospital. The mean postprandial plasma fructose concentrations (MPPF) and the mean postprandial plasma glucose concentrations (MPPG) were calculated. Fructose was measured by gas chromatography-mass spectrometry (GCMS). Based solely on MPPF, we were able to divide the patients into three groups: the high MPPF (31.9 +/- 6.5 micromol/L) group (n = 12), the middle MPPF (21.2 +/- 1.8 micromol/L) group (n = 13), and the low MPPF (15.2 +/- 2.4 micromol/L) group (n = 13). Prevalence and degree of retinopathy and nephropathy were then evaluated in the 3 different groups. A significant correlation was observed in the prevalence of proliferative diabetic retinopathy (PDR) among the 3 MPPF groups (P =.024). The prevalence of PDR was higher in the high MPPF group (75.0%) than in the middle and low MPPF groups (23.1% and 38.5%, respectively). Although not significantly different statistically, the prevalence of all degrees of retinopathy showed a tendency to be higher in the high MPPF group (83.3%) than in the middle and low MPPF groups (46.2% and 46.2%, respectively) (P =.081). Nephropathy prevalence also showed a tendency to be higher in the high MPPF group (66.7%) than in the middle and low MPPF groups (38.5% and 30.8%, respectively), although the differences were not significant. The prevalence of clinical albuminuria was not significantly different among the 3 groups, but there was a tendency for it to be higher in the low MPPF group (30.8%) than in the high and middle MPPF groups (16.7% and 0%, respectively). No significant differences in glycemic indicators and mean duration of diabetes were observed among the 3 groups. The increased prevalence of retinopathy in the high MPPF group suggests that fructose is associated with retinopathy in patients with type 2 diabetes.

Aged↗

Involvement of the histaminergic system in the nociceptin-induced pain-related behaviors in the mouse spinal cord.

Intrathecal (i.t.) injection of nociceptin elicited a behavioral response mainly consisting of biting and licking, which were eliminated by the i.t. co-administration of opioid receptor-like-1 (ORL-1) receptor antagonists. The behavioral response induced by nociceptin was characteristically similar to that by i.t.-administered histamine, and was attenuated by i.t. co-administration of the H1 receptor antagonists, but not by the H2 receptor antagonists, whereas the H3 receptor antagonist promoted the nociceptin-induced behavior. H1 receptor knockout (H1R-KO) mice did not show the nociceptin-induced nociceptive behavior, which was observed in wild-type mice. Pretreatment with a histamine antiserum or a histidine decarboxylase inhibitor resulted in a significant reduction of the response to nociceptin. The previous studies showed that NK1 receptor antagonists and a novel substance P (SP)-specific antagonist given i.t. could reduce the behavioral response to nociceptin and histamine. On the other hand, the nociceptive response induced by nociceptin, but not histamine, was completely attenuated by the i.t. co-administration of agonists for GABAA and GABAB receptors. In contrast, the antagonists for GABAA and GABAB receptors injected i.t. showed same nociceptive response with nociceptin and histamine, and their nociceptive responses were significantly blocked by the i.t. co-administration of the H1 receptor antagonists, but not H2 receptor antagonists or ORL-1 receptor antagonists. The present results suggest that the activation of the ORL-1 receptor by nociceptin may induce the disinhibition of histaminergic neuron and enhance the release of histamine, which subsequently acts on the H1 receptor located on the SP-containing neurons to produce the spinal cord-mediated nociceptive response.

Animals↗

Detection of p53 gene mutations in the supernatant of pancreatic juice and plasma from patients with pancreatic carcinomas.

AIM: The sensitivity of pure pancreatic juice (PPJ) cytology for the diagnosis of pancreatic carcinoma (PCa) is still low. The usefulness of genetic analyses of PPJ seems to be limited because of insufficient sensitivity or false positivity. To improve the molecular diagnosis of PCa, we analyzed mutations of p53 together with K-ras in DNA extracted not only from the sediment but also from the supernatant of PPJ samples. METHOD: Polymerase chain reaction-single-strand conformation polymorphism and direct sequencing were used for analyses of p53 mutations in exons 5-8. K-ras mutations at codon 12 were examined by mutant allele-specific amplification. RESULTS: In PPJ supernatant from patients with PCa, p53 and K-ras mutations were detected in 42.9% (9 of 21) and 81.0% (17 of 21) of cases, respectively. The incidence of p53 and K-ras mutations in the sediment was 28.6% and 71.4%, respectively. By a combination assay with supernatant and sediment, p53 mutations were detected in 52.4% (11 of 21) of PCa cases. Moreover, p53 mutations were detected in 7 of 15 (46.7%) cases of PCa in which the cytologic diagnosis was negative. Among 25 patients with chronic pancreatitis (CP), none harbored mutant p53, although K-ras mutations were detected at an incidence of 28% (7 of 25) in the supernatant and 20% (5 of 25) in the sediment. In addition, mutant bands of p53 in plasma were detected in 2 of 11 patients with PCa in whom p53 mutations were detectable in PPJ. CONCLUSION: These results suggest that the sensitivity of detection for p53 mutations with high cancer specificity could be improved by using the Sup in PPJ samples of PCa. Genetic analysis of p53 could complement PPJ cytology. p53 mutations were detectable in PCa from plasma samples.

Adult↗

Serum tumor markers and molecular biological diagnosis in pancreatic cancer.

Recent studies on genetic abnormalities in pancreatic ductal cancer have led to the investigation of tumor markers and genetic markers in both serum and pancreatic juice (PJ). Serum type 1 chain carbohydrate antigens such as CA19-9 are positive in nearly 80% of patients with pancreatic cancer (PCa), of which most are in advanced stage, whereas false-positive rates are relatively high at 20%-30% in benign hepatobiliary and pancreatic diseases. Although the prevalence of type 2 chain carbohydrate antigens, such as SLX, is relatively low, cancer specificity of these antigens is high. However, serum tumor markers have limited diagnostic value for early detection of PCa. In PJ collected endoscopically from patients with PCa, K-ras mutations (KRM) are detectable in > 80%, whereas KRM are observed in 20%-30% of PJ from patients with chronic pancreatitis (CP), reflecting benign mucous cell hyperplasia harboring KRM. Thus, a qualitative analysis of KRM in PJ is unsuitable for diagnosis of PCa. On the other hand, using an hybridization protection assay that can quantitatively determine KRM, KRM were positive in 66% of PCa but only in 40% of CP cases, indicating that qualitative analysis of KRM in PJ may be useful for differentiating PCa from CP. p53 Mutations are found in 4%-50% in PJ from patients with PCa but are not detectable in PJ from CP, suggesting that the specificity of p53 mutations is very high for PCa. Furthermore, p53 mutations were detected in 7 of 15 (47%) patients with PCa in which the PJ cytologic diagnosis was negative. Telomerase (TE) activity or its catalytic subunit, h-TERT, was reportedly positive >80% in PJ from PCa but was detected in <20% of PJ from CP. TE activity in PJ from CP originates from lymphocytes. The development and application of these new genetic and epigenetic markers with high specificity and sensitivity for PCa in serum and PJ will significantly improve our diagnostic accuracy.

Adult↗

Innate immune response in Th1- and Th2-dominant mouse strains.

C57BL/6 and BALB/c mice are prototypical Th1- and Th2-type mouse strains, respectively. In the present study, we attempted to characterize the innate immune response of macrophages from these mouse strains. Macrophages from C57BL/6 mice produced higher levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-12 than those from BALB/c mice after stimulation with macrophage-activating lipopeptide-2 (MALP-2, a synthetic TLR-2 ligand) or lipopolysaccharide (LPS, a TLR-4 ligand). The augmented IL-12 production by C57BL/6 macrophages increased interferon-gamma and, in contrast, decreased IL-13 production by CD4+ T cells. On stimulation with MALP-2 or LPS, C57BL/6 macrophages produced lysosomal enzyme and nitric oxide, effector molecules for bacterial killing, whereas BALB/c macrophages did not. Bactericidal activity of BALB/c macrophages was impaired relative to C57BL/6 macrophages when cells were infected with live bacteria in vitro. In a murine model of septic peritonitis induced by cecal ligation and puncture (CLP), BALB/c mice failed to facilitate bacterial clearance relative to C57BL/6 mice despite an augmented peritoneal leukocyte infiltration that was associated with increased peritoneal levels of cytokines/chemokines. BALB/c mice exhibited increased plasma and hepatic levels of cytokines/chemokines, resulting in an exaggerated systemic inflammation as determined by acute-phase proteins. Finally, BALB/c mice were vulnerable to CLP-induced lethality relative to C57BL/6 mice. Altogether, innate immune response of macrophages is different between these mouse strains, which may affect the development of Th1 and Th2 adaptive immunity in these strains. Reduced systemic inflammatory response in C57BL/6 mice that may result from an eminent local response appears to be beneficial during sepsis.

Acute-Phase Reaction↗

Quantitative intravenous myocardial contrast echocardiography predicts recovery of left ventricular function after revascularization in chronic coronary artery disease.

BACKGROUND: Quantitative intravenous myocardial contrast echocardiography (MCE) has been shown to measure regional myocardial blood flow velocity noninvasively. PURPOSE: To determine whether quantitative intravenous MCE could be used clinically to predict functional recovery after revascularization in patients with chronic coronary artery disease. METHODS: Twenty-eight patients with chronic stable coronary artery disease and resting regional left ventricular dysfunction were included in this study. The study permits myocardial perfusion analysis by intravenous MCE before revascularization with continuous infusion of Levovist and intermittent ultrasonic exposure. Wall motion assessment by echocardiography at rest was repeated after long-term follow-up period (7 +/- 2 months). In dysfunctional segments, we analyzed myocardial perfusion quantitatively by fitting to an exponential function, Y = A(1 - e-betat) to obtain the rate of rise (beta) of background-subtracted intensity, which represented myocardial blood flow velocity. RESULTS: Of the 101 revascularized dysfunctional segments, MCE was adequately visualized in 91 (90%) segments, and wall motion was recovered in 45 (49%) segments. The value of beta in the recovery segments was significantly higher than that in nonrecovery segments (0.80 +/- 0.50 vs 0.39 +/- 0.24, P < 0.001). The value of beta > 0.5 predicted recovery of segmental function with a sensitivity of 71%, specificity of 78%. CONCLUSION: Quantitative intravenous MCE can predict functional recovery after revascularization in patients with chronic coronary artery disease.

Aged↗