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Biomedical subjects

M Hori

Publications and source records attributed to M Hori.

At least 361 records · Page 20Linked to original sources
PubMed1998

Safety evaluation of Nostoc flagelliforme (nostocales, Cyanophyceae) as a potential food.

The safety of the alga genus Nostoc flagelliforme Born. etFlah. as a human food source was evaluated in an oral acute toxicity study and in a 28-day oral subacute toxicity study using rats. In the acute toxicity study, the dried powder of N. flagelliforme was orally administered to male and female rats at a dose of 1250 mg/kg and 2500 mg/kg. Neither mortality nor changes in general condition were observed in either the study groups or the control group over a 14-day observation period. In the subacute toxicity study, N. flagelliforme powder was administered orally to male and female rats at a dose of 500 mg/kg and 1000 mg/kg for a period of 28 days. Neither mortality nor changes in general condition were observed in either the treatment group or the control group throughout the 28-day administration period. No reduction in food consumption or body weight gain was observed in the experimental animals. Ophthalmological tests performed at the end of the administration period revealed no abnormalities within the ophthalmological parameters. In the haematological tests and serum biochemical tests performed at the time of completion of the administration period, no adverse effects of N. flagelliforme were observed. At autopsy, organ weight at the end of the experimental period and histopathological tests of specimens obtained from the autopsied animals revealed no significant influences of N. flagelliforme. In conclusion, considering the absence of adverse effects of N. flagelliforme in this study, findings in the oral acute toxicity study and the 28-day oral subacute toxicity study may indicate the safety of N. flagelliforme for human consumption. This study is in agreement with the novel nutraceutical idea "Phycophagism".

Animals↗
PubMed1998

Impact of coronary risk factors on contribution of nitric oxide and adenosine to metabolic coronary vasodilation in humans.

OBJECTIVES: The contribution of nitric oxide (NO) and adenosine to the increase in coronary blood flow (CBF) induced by cardiac pacing was investigated in 28 subjects with angiographically normal coronary arteries with and without one or more risk factors for atherosclerosis. BACKGROUND: NO and adenosine are important in the regulation of coronary circulation, and the inhibition of NO synthesis increases adenosine production during cardiac pacing in experimental models. METHODS: Coronary artery diameters and CBF were assessed by quantitative coronary arteriography and Doppler flow velocity measurement. Plasma levels of nitrites and nitrates (NOx) (stable end products of NO), adenosine and lactate were measured, and blood gas analysis was performed. RESULTS: The extent of CBF response to cardiac pacing did not differ between the 14 subjects with and the 8 subjects without risk factors for atherosclerosis. NOx (12.0+/-0.9 vs. 14.9+/-1.1 ,amol/liter [mean+/-SD], p < 0.05), but not adenosine (50.8+/-7.2 vs. 50.8+/-6.5 nmol/liter), levels in coronary sinus blood increased in the subjects without risk factors. In contrast, adenosine (58.9+/-7.5 vs. 77.4+/-9.8 nmol/liter, p < 0.05), but not NOx (11.1+/-1.1 vs. 12.2+/-1.1 micromol/liter), levels increased in subjects with risk factors. Aminophylline, an antagonist of adenosine receptors, blunted CBF response to cardiac pacing in six subjects with risk factors. The number of risk factors showed a negative correlation (p < 0.05) with NOx production and a positive correlation (p < 0.05) with adenosine production during cardiac pacing, respectively. CONCLUSIONS: NO and adenosine are increased during metabolic coronary vasodilation induced by cardiac pacing. Adenosine production may be a compensatory mechanism when NO production is reduced.

Adenosine↗
PubMed1998

Increased release of nitric oxide in ischemic hearts after exercise in patients with effort angina.

OBJECTIVES: The aim of this study was to determine whether the release of nitric oxide (NO) from the ischemic heart increases during exercise in patients with effort angina. BACKGROUND: Myocardial ischemia increases NO production in the canine heart, but no such increase has been demonstrated in the ischemic human heart. METHODS: Fifteen patients with effort angina underwent supine ergometer exercise tests. All patients had severe proximal stenosis (>90%) in the left anterior descending coronary artery. The control group consisted of 17 subjects without coronary artery disease or systemic hemodynamic abnormalities. RESULTS: Neither the lactate extraction ratio (LER) nor the difference in NO concentration between coronary venous and arterial blood (deltaVA[NO]) was affected by exercise in the control subjects. In patients with effort angina, neither variable differed from that in the control group at rest; however, exercise markedly decreased LER and significantly increased deltaVA(NO) (from 4.7 +/- 0.3 to 16.5 +/- 1.6 micromol/liter, p < 0.001) in the patient group. The extent of decrease in LER was significantly correlated with the extent of increase in deltaVA(NO) in the patients with effort angina (r2 = -0.837, p < 0.001). CONCLUSIONS: Provocation of myocardial ischemia by exercise stress increases NO production in the hearts of patients with effort angina.

Aged↗
PubMed1998

Helicobacter pylori infection induces cyclooxygenase-2 expression in human gastric mucosa.

Recent studies indicate that expression of mitogen-inducible cyclooxygenase-2 (COX-2) occurs in gastrointestinal tumors. We investigated the effects of Helicobacter pylori (H. pylori) infection, a class I carcinogen for the human stomach, on gastric COX-2 expression using immunohistochemistry. Human subjects without macroscopic lesions, as determined by endoscopic screening, were biopsied for H. pylori infection. The biopsy samples were immunohistochemically examined for COX-2 expression. COX-2 was expressed in gastric epithelia and subepithelial inflammatory cells in all H. pylori-infected subjects. There was no expression of COX-2 in the gastric mucosa of H. pylori-negative subjects. COX-2 expression has been reported in gastrointestinal carcinomas, gastrointestinal cancer cell-lines, and in the gut after carcinogenic treatment. The present study demonstrates that H. pylori infection leads to gastric mucosal expression of COX-2, indicating that the enzyme is involved in H. pylori-related gastric pathology in humans.

Adult↗
PubMed1998

Increased contractility of rat uterine smooth muscle at the end of pregnancy.

Upon stimulation with high K+, oxytocin, prostaglandin E2, prostaglandin F2 alpha or carbachol, myometrium isolated from pregnant rats (21 days after pregnancy) developed 2-3 times greater isometric force than that from non-pregnant rats (estrus). High K+ increased the level of myosin light chain (MLC) phosphorylation to a similar extent in these tissues, and therefore pregnant myometrium developed greater contraction than non-pregnant myometrium at a given MLC phosphorylation. In the permeabilized muscle with alpha-toxin, Ca2+ (0.1-10 microM) induced greater contraction in pregnant myometrium than in non-pregnant myometrium. Ca2+ sensitivity was not altered after pregnancy. MLC kinase and phosphatase activities did not differ significantly between pregnant and non-pregnant myometria. Stimulation with 10 microM Ca2+ and 1 microM calyculin-A elicited similar magnitudes of contractions in the permeabilized muscles isolated from non-pregnant and pregnant rats. SDS-PAGE showed that the percentage of the content of MLC was not altered between these preparations, although actin content increased after pregnancy. These results suggest that the stress generating capacity of myometrium is increased after pregnancy without changing the MLC phosphorylation step. The equal capacity of force generation after the maximum phosphorylation by Ca2+ and phosphatase inhibitor suggests that a MLC phosphorylation-independent mechanism is responsible for the development of greater force in the pregnant myometrium.

Actins↗
PubMed1998

Effects of a weekly injection of human parathyroid hormone (1-34) and withdrawal on bone mass, strength, and turnover in mature ovariectomized rats.

One hundred fifteen Wistar rats, 7 months of age, were ovariectomized (ovx) or sham-operated to evaluate the effects of a weekly injection of human parathyroid hormone (hPTH) and withdrawal on the bone mass, strength, and turnover in mature ovariectomized rats. At 3 months, ovx rats were given a weekly injection of hPTH(1-34) at the respective doses of 0 (vehicle), 10, and 90 microg/kg body weight (BW) for 3 months. Then, hPTH-treated rats were divided into two groups each: continuously treated groups, and the groups treated with vehicle only for another 3 months. Weekly hPTH injections at doses of 10 or 90 microg/kg BW maintained the lumbar BMD values and increased the values of the femoral cortical bone, increasing the bone formation rates in the trabecular, endocortical, and periosteal envelopes. Trabecular osteoclasts were increased in the 90 microg/kg dose group. Trabecular bone surface relative to the volume was decreased by hPTH. The compressive load of the lumbar bone and the bending moment of the midfemur were increased. The lumbar compressive load values, corrected for BMD and volume, and the moment of inertia of the midfemur were also increased. The intracortical porosity values were not increased by the treatment. After withdrawal of hPTH treatment, the BMD values in both the lumbar and the midfemur were reduced to ovx control levels. The bone mass stimulated by the 90 microg/kg dose was reduced faster than that by the 10 microg/kg dose. However, the parameters of bone strength were still larger than those of the ovx controls after cessation of the hPTH treatment. Thus, a weekly hPTH injection effectively stimulated the bone formation in both the trabecular and cortical bone, leading to positive effects on mass and structure of the bone. These data suggest the possibility of benefits of both a lower frequency of hPTH injections as well as high-frequency injections for human osteoporotics.

Absorptiometry, Photon↗
PubMed1998

Nisoldipine selectively induces coronary vasodilation and improves mild myocardial ischemia in dogs: a potential role of cellular acidosis.

We examined whether nisoldipine, a calcium (Ca) channel blocker, increases coronary blood flow (CBF) without decreasing aortic blood pressure (AoP) with ischemic and nonischemic hearts, and whether the presence of cellular acidosis in ischemic myocardium contributes to the augmentation of coronary vasodilation due to nisoldipine. In 42 dogs, coronary perfusion pressure (CPP) was reduced so that CBF decreased to 60% of the baseline, and CPP was maintained constant thereafter. First, we administered nisoldipine into a systemic vein in the ischemic and nonischemic hearts. Second, nisoldipine was administered into the canine coronary artery of the ischemic myocardium, with and without administration of either sodium bicarbonate (NaHCO3), sodium hydroxide (NaOH), or amiloride. Nisoldipine (0.25-4.0 mg/kg, i.v.) increased CBF by 59% in the ischemic myocardium more than the nonischemic myocardium (by 34%) without reducing AoP. The infusion of nisoldipine (40 ng/kg/min, IC) increased CBF markedly by about 55% in the ischemic myocardium with increases in fractional shortening (FS; 11 +/- 2% to 21 +/- 2%) and lactate extraction ratio (LER; -19 +/- 4% to 15 +/- 2%). Increases in CBF, FS, and LER were markedly attenuated during administration of nisoldipine with concomitant administration of either NaHCO3 or NaOH. Furthermore, the extent of increases in CBF (54 +/- 2 mL/100 g/min), FS (13 +/- 2%), and LER (-17 +/- 4%) were also markedly attenuated due to the concomitant treatment with amiloride. We conclude that myocardial cellular acidosis plays an important role in mediating coronary vasodilation affected by nisoldipine in the ischemic myocardium. H+ may modulate the property of voltage-dependent Ca channels via Na(+)-H+ exchange.

Acidosis↗
PubMed1998

Elevation of plasma adenosine levels may attenuate the severity of chronic heart failure.

Adenosine is known to be an endogenous cardioprotective substance. Since we have reported that adenosine levels increase in patients with chronic heart failure, we tested whether further elevation of the adenosine levels due to dipyridamole or dilazep for 6 months modulates the pathophysiology of chronic heart failure. In patients with chronic heart failure, either dipyridamole (300 mg/d n = 17) or dilazep (300 mg/d n = 5) were administered for 6 months. Twenty-two patients (mean +/- SE age 58 +/- 4 years old) attending a specialized chronic heart failure (CHF) clinic over 6 months and judged as in New York Heart Association (NYHA) function class II or III were examined. The other drugs used for the treatment of CHF were not altered during the study. There were 5 patients with CHF caused by ischemic heart diseases, and 17 patients with either valvular heart diseases or dilated cardiomyopathy. We found that increases in the plasma adenosine levels (202 +/- 34 and 372 +/- 74) nmol/L before and after dipyridamole administration, P < 0.005 ameliorate the severity of CHF (NYHA: 2.1 +/- 0.5 to 1.7 +/- 0.2). Both ejection fraction and maximal oxygen consumption increased. These improvements in the severity of chronic heart failure returned to baseline levels 6 months after discontinuation of dipyridamole. Comparable results were obtained in the dilazep protocol. We suggest that the elevation of plasma adenosine levels improves the pathophysiology of CHF.

Adenosine↗
PubMed1998

Serum thrombopoietin level is mainly regulated by megakaryocyte mass rather than platelet mass in human subjects.

A patient with idiopathic thrombocytopenic purpura (ITP) developed T-cell lymphoma while undergoing steroid therapy. We examined the relationship between the patient's serum thrombopoietin (Tpo) level, platelet count, megakaryocyte number and CFU-Meg number during the second 5 d course of chemotherapy for lymphoma in which megakaryopoiesis switched from ITP phase to amegakaryocytic phase. The patient's platelet count was temporarily elevated but CFU-Meg numbers were markedly suppressed, and megakaryocyte numbers were decreased in this period, whereas serum Tpo level was not suppressed despite an increased platelet count, indicating that serum Tpo level is mainly regulated by megakaryocyte mass.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

Cross-linking of Fc(gamma)-receptor on monocytes inhibits hepatitis C virus-specific cytotoxic T-lymphocyte induction in vitro.

In hepatitis C virus (HCV) infection, immune complex (IC)-type virus particles are frequently observed in circulation. The IC leads to cross-linking of Fcgamma receptors (FcgammaR) on monocytes and exerts immunoinhibitory function. To test the roles of IC in HCV-specific cytotoxic T lymphocyte (CTL) induction, we generated HCV CTL from peripheral blood mononuclear cells of chronic hepatitis C patients with or without HCV-IC- or immunoglobulin G (IgG)-coated culture plates and compared their lytic activities. HCV-IC or adherent IgG, which induces FcgammaR cross-linking, significantly reduced CTL activity. Expression of B7-1 on monocytes decreased on adherent IgG. In addition, tumour necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) production increased from cells on adherent IgG and their mRNA expression in monocytes was enhanced. Anti-TNF-alpha antibody during induction on adherent IgG inhibited lysis; however, anti-TGF-beta completely reversed its inhibitory effect. These results demonstrated that HCV-IC or adherent IgG impaired HCV-CTL induction in vitro. The FcgammaR-mediated CTL suppression occurred via decreased expression of monocyte B7-1 and/or enhanced production of TGF-beta1.

Adult↗
PubMed1998

Mental health of visually and hearing impaired students from the viewpoint of the University Personality Inventory.

Tsukuba College of Technology is the first national university established as an institute of higher education for the visually and hearing impaired. We have been systematically conducting a University Personality Inventory (UPI) survey on our students since 1989 to understand their mental health. In this study, we compared the UPI scores of the new students of Tsukuba College of Technology in 1993 and 1994 with unimpaired students from the University of Tsukuba (control group), but found no significant difference in the UPI scores of the visually impaired and the control group. However, we noticed a significant difference in the average UPI scores between the hearing impaired and the control group. The visually impaired group were divided into four subgroups, UPI scores descended in order from degree 1 (total blindness), to degrees 2 and 3 (amblyopia), to degree 4 (visual acuity > or = 0.3). The UPI scores of the degree 4 subgroup were significantly lower than those of the control group. An investigation of the items for which the check rate was at least 50% showed that the visually impaired students had a variety of psychological problems, most of which seemed to concern depression or anxiety as did the normal control group. The number of affirmative responses increased with low visual acuity. The only one belonging to the 'lie' scale item was observed in the group of hearing impaired students. Thus, comparing these three groups from the viewpoint of mental health, we noticed the hearing impaired group was slightly different from the other two groups, but the visually impaired group was similar to the normal control group.

Adolescent↗
PubMed1998

Inhibition of myo-inositol transport causes acute renal failure with selective medullary injury in the rat.

Myo-inositol is a major compatible osmolyte in the renal medulla that is accumulated under hypertonic conditions via the Na+/myo-inositol cotransporter (SMIT). We have recently reported that SMIT is predominantly present in the thick ascending limb of Henle (TAL) and is strongly induced by acute NaCl loading, suggesting an important role of myo-inositol in this nephron segment. In the present study, we sought to examine in vivo effects of inhibition of myo-inositol transport using a transport inhibitor, 2-O, C-methylene-myo-inositol (MMI). Intraperitoneal injection of MMI caused acute renal failure in the rats. Serum creatinine and urea nitrogen were significantly increased 12 hours after MMI injection. Morphologic study revealed that the tubular cells were extensively injured in the outer medulla. A considerable number of the tubular cells were injured in the cortex as well. Immunohistochemical study for Tamm-Horsfall protein (THP), which was used for identification of the TAL cells, showed that THP-positive cells were predominantly injured. The tubular injury apparently appeared to worsen when high concentration of NaCl was injected with MMI. Administration of myo-inositol prevented acute renal failure and improved the tubular injury after MMI injection. Furthermore, supplementation of betaine, another osmolyte in the TAL cells, partially prevented the toxic effects of MMI. These results suggest that myo-inositol play a crucial role in the TAL regarding osmoregulation of the cells.

Acute Kidney Injury↗
PubMed1998

Isolation of genes identified in mouse renal proximal tubule by comparing different gene expression profiles.

An expression profile is a list based on a large scale sequencing of 1000 cDNA clones, showing the expressed genes and the abundance of their transcripts in a given cell or tissue (Okubo K et al: Nature Genet 2:173, 1992). We constructed an expression profile of mouse renal proximal tubules (PT) carefully isolated by microdissection in order to characterize its gene expression. Altogether 1000 clones were analyzed; there were 646 types of transcripts in PT, among which 196 were identical or homologous to the previously reported genes. The most abundant transcript was kidney-androgen regulated protein. By comparing the expression profile of PT with those obtained from other sources, several genes were identified only in PT. They included known transcripts and transcripts that were not homologous to the known genes. Three (GS4001, 3991, and 4059) of the non-homologous genes were analyzed by Northern blotting and in situ hybridization, and GS4001 and 4059 were predominantly expressed in the kidney, whereas GS3991 was detected in the liver as well as in the kidney. The sequence analysis of the full-size cDNAs demonstrated that GS4001 was a new member of aspartic proteinases and GS4059 was a novel gene. It also revealed that GS3991 was a mouse homologue of SA gene known to be expressed in PT. The expression profile of mouse PT and its comparison with those of other tissues and cells provide an alternate way of isolating genes predominantly expressed in PT, and also provides probes to study the molecular mechanisms of gene expression in the kidney.

3T3 Cells↗
PubMed1998

Effects of hypertonic stress on transforming growth factor-beta activity in normal rat kidney cells.

Hypertonicity is known to modulate the expression of some genes and the action of several cytokines. We evaluated whether hypertonicity would increase the expression and/or activity of transforming growth factor-beta (TGF-beta) in normal rat kidney (NRK) cells. The bioassay for TGF-beta showed that mature TGF-beta activity was significantly increased when the cells were cultured in a hypertonic medium (500 mOsm/kg). Comparing to the isotonic medium, hypertonicity accelerated the increase in TGF-beta activity during the initial 24 hours after changing the medium. The activity was increased as the medium osmolality increased from 300 to 500 mOsm/kg. Raffinose was found to be the most effective in increasing TGF-beta activity. NaCl, glucose, and mannitol also increased TGF-beta activity. In contrast, total TGF-beta (mature and latent) activity and TGF-beta mRNA abundance did not change significantly, suggesting that hypertonicity activated TGF-beta without affecting the synthesis of TGF-beta. To determine whether collagen synthesis was increased by hypertonicity, we examined [3H] proline incorporation into NRK cells cultured in hypertonic medium. Proline incorporation increased in an osmolality-dependent manner. Raffinose was also the most effective solute at increasing the proline incorporation. Furthermore, anti-TGF-beta antibody prevented the increase in proline incorporation induced by hypertonicity. These results suggest that hypertonicity promotes the processing of latent TGF-beta to the biologically active form, resulting in the stimulation of collagen synthesis in NRK cells.

Animals↗
PubMed1998

Up-regulation of HSP47 in the mouse kidneys with unilateral ureteral obstruction.

BACKGROUND: Unilateral ureteral obstruction (UUO) is a well established experimental model of renal injury leading to interstitial fibrosis. The molecular and cellular mechanism(s) of interstitial fibrosis in UUO are beginning to be elucidated. In the progression of interstitial fibrosis in UUO, up-regulation of collagen synthesis is commonly observed. HSP47 is a collagen-binding stress protein and is thought to be a collagen-specific molecular chaperone, which plays a pivotal role during the biosynthesis and secretion of collagen molecules in the endoplasmic reticulum. The synthesis of HSP47 has been demonstrated to always parallel that of collagen in physiological and pathophysiological conditions. It is well recognized that renin-angiotensin system (RAS) is enhanced in the setting of UUO and that enhanced RAS has been implicated in the pathogenesis of interstitial fibrosis in the obstructed kidneys. METHODS: To investigate the role of HSP47 in the progression of interstitial fibrosis in mouse UUO, the expression of HSP47 was examined by Northern blotting, immunohistochemistry and in situ hybridization in the obstructed kidneys. To test the possible involvement of enhanced RAS on the HSP47 expression, we examined the effects of lisinopril, an angiotensin converting enzyme inhibitor, on interstitial fibrosis. HSP47 and type I collagen mRNA expression. RESULTS: By Northern blot analysis, HSP47 mRNA was significantly up-regulated at 12 hours (about twice that of sham operated kidneys) after the onset of ureteral obstruction, further increased and stayed at the increased level until seven days (about 8 times that of sham operated kidneys). HSP47 mRNA and protein expression were observed in the periglomerular and peritubular interstitial regions of the obstructed kidneys. Distribution of smooth muscle alpha actin and type I collagen immunoreactivity were similar to the HSP47 distribution pattern, suggesting that HSP47 was up-regulated in the myofibroblasts. Lisinopril ameliorated the expansion of cortical interstitium in the obstructed kidneys at four and seven days after ureteral obstruction. HSP47 mRNA expression was suppressed at four and seven days, whereas type I collagen mRNA was suppressed only at seven days after the onset of ureteral obstruction. CONCLUSIONS: These results demonstrate the early and persistent up-regulation of HSP47 during the progression of interstitial fibrosis in mouse UUO kidneys, and further suggest the potential role of HSP47 in the pathogenesis of interstitial fibrosis in the obstructed kidneys. Partial suppression of HSP47 mRNA expression by lisinopril at day 4 and day 7 after ureteral obstruction suggests that there are other immediate trigger(s) that induce the HSP47 mRNA expression. Identification of the molecular mechanism of HSP47 induction during UUO may give an insight into the novel aspects of the molecular pathophysiology of interstitial fibrosis in obstructive nephropathy.

Actins↗
PubMed1998

Expression of the Na+/myo-inositol cotransporter in the juxtaglomerular region.

Myo-inositol is a major compatible osmolyte in the renal medulla and is accumulated in cells under hypertonic conditions by uptake via a Na+/myo-inositol cotransporter (SMIT). SMIT is regulated by extracellular osmolarity at the transcription level. We investigated localization of SMIT in rat kidney by immunohistochemical staining using an anti-SMIT-antibody raised against a synthetic peptide corresponding to part of SMIT and by in situ hybridization. SMIT protein localized predominantly to the basolateral membranes of cells of the thick ascending limb of Henle (TAL) and inner medullary collecting duct (IMCD). Macula densa (MD) cells, identified as the Tamm-Horsfall-protein (THP)-unreactive cells surrounded by THP-reactive TAL cells, also stained for anti-SMIT. In situ hybridization yielded the intense SMIT signals in the TAL and IMCD and also in the juxtaglomerular (JG) region. Prior loading of the animal with a high concentration of NaCl rapidly induced SMIT mRNA; furosemide down-regulated it. The high level of SMIT expression suggests that MD cells are exposed to hypertonicity at the basolateral surface. Because SMIT expression seemed to be proportional to the magnitude of NaCl reabsorption, it may be a good marker for examination of the tubuloglomerular feedback mechanism in vivo.

Amino Acid Sequence↗
PubMed1998

Sensitivity in detection of hypervascular hepatocellular carcinoma by helical CT with intra-arterial injection of contrast medium, and by helical CT and MR imaging with intravenous injection of contrast medium.

PURPOSE: To determine the effectiveness of i.a. contrast-enhanced helical CT and of i.v. contrast-enhanced helical CT and MR imaging, in detecting hypervascular hepatocellular carcinoma (HCC). MATERIAL AND METHODS: Fifty patients with 125 hypervascular HCC nodules underwent helical CT both during arterial portography (CTAP) and during hepatic arteriography (CTHA). Helical CT and MR imaging of the entire liver with i.v. administration of contrast medium were also performed. Helical CT images were obtained at 30-33 s (arterial-phase CT) and at 5 min (equilibrium-phase CT) after the initiation of an i.v. bolus injection of contrast medium. After T1- and T2-weighted spin-echo MR imaging, gradient-echo images during breath-holding were obtained prior to and 20 s, 1 min, and 2 min after the bolus administration of 0.1 mmol/kg of gadopentetate dimeglumine (dynamic MR). The sensitivity and positive predictive value of the various techniques were evaluated and compared. RESULTS: In terms of sensitivity for hypervascular HCC nodules of less than 1 cm in diameter, CTAP (90%) and CTHA (88%) were significantly superior to dynamic MR imaging (44%), arterial-phase CT (39%), spin-echo MR imaging (20%), and equilibrium-phase CT (7%) (p < 0.001). However, there was no significant difference in the techniques with regard to the detection of lesions equal to or more than 2 cm in diameter. CONCLUSION: For detecting small hypervascular HCCs, helical CT with i.a. contrast enhancement is superior to helical CT and MR imaging with i.v. enhancement.

Adult↗