Biomedical subjects

N Sakai

Publications and source records attributed to N Sakai.

At least 73 records · Page 4Linked to original sources

PubMed2001

Ehlers-Danlos syndrome type IV with a unique point mutation in COL3A1 and familial phenotype of myocardial infarction without organic coronary stenosis.

We report on a 43-year-old male patient with Ehlers-Danlos syndrome (EDS) type IV with acute myocardial infarction (MI) without organic coronary stenosis. The disease was complicated with pneumothorax, subcutaneous and mediastinal emphysema, and splenic artery rupture. Three of the patient's family members suffered sudden cardiac death or MI. A diagnosis of EDS type IV was confirmed by decreased production of type III collagen by 86%. Mutation analysis revealed a point mutation in the COL3A1 gene that substituted glycine for aspartate at amino acid position 877. This mutation had not been reported as pathogenic for EDS type IV. These findings suggest close linkage between the mutation and the phenotype with familial MI.

Adult↗

PubMed2001

Sonographically detected malignant transformation of a simple renal cyst.

The clinical course is reported of a simple renal cyst which developed into a septated renal cyst, and finally to a cystic renal cell carcinoma. A 49-year-old man, who had been diagnosed as having a renal cyst, was found by repeated ultrasonography over 6 years to have solid components developing within the cyst. Radical nephrectomy was performed, and pathological examination confirmed cystic renal cell carcinoma (RCC). This case clearly shows a natural history of malignant transformation from a simple renal cyst, and emphasizes that careful follow-up of renal cysts, especially of complicated renal cysts, is mandatory for successful treatment of RCC.

Adult↗

PubMed2001

Generation of a constitutively active fragment of PKN in microglia/macrophages after middle cerebral artery occlusion in rats.

PKN is a fatty acid- and Rho-activated serine/threonine kinase, which has a catalytic domain highly homologous to that of protein kinase C (PKC). Recent studies have demonstrated that PKN is proteolytically cleaved after apoptotic stimulation and then a constitutively active 55-kDa fragment is generated. However, the role of the 55-kDa fragment are poorly understood. Adult Sprague-Dawley (SD) rats underwent middle cerebral artery occlusion (MCAO), and the temporal and spatial changes in the fragmentation of PKN and of PKC delta were examined by immunoblotting. No proteolytic fragment of PKC delta (about 40 kDa) was detected. The 55-kDa fragment of PKN appeared transiently from 3 days after MCAO at the ipsilateral normal cortex. At the boundary zone of infarction, the 55-kDa fragment was markedly induced from day 5 then peaked on day 21 and persisted until day 28. Analysis of anti-phosphoserine immunoprecipitates with an anti-PKN antibody revealed phosphorylation of the 55-kDa band. Double staining for PKN and Ox42 was used to examine the source of the 55-kDa fragment. PKN immunoreactivity was significantly increased in Ox42-positive cells (microglia/hematogenous macrophages). No DNA laddering and only a few terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells were observed on day 14 in despite of the high level appearance of the 55-kDa band. These results suggest that the constitutively active 55-kDa fragment of PKN does not contribute to apoptosis, but may contribute to a function of microglia/macrophages.

Animals↗

PubMed2001

Involvement of p38 mitogen-activated protein kinase followed by chemokine expression in crescentic glomerulonephritis.

p38 Mitogen-activated protein kinase (MAPK) is involved in the production and signal transduction of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, and chemokines in vitro. However, the crucial role of p38 MAPK in the inflammatory processes of crescentic glomerulonephritis in vivo remains to be investigated. We showed a dramatic decrease in IL-1beta-induced phosphorylation of p38 MAPK, not extracellular signal-regulated kinases 1/2 or jun NH2-terminal kinase, in rat cultured mesangial cells by FR167653. We explored the effects of FR167653 as a specific inhibitor of p38 MAPK on renal injury and subsequent renal expression of chemokines in a progressive experimental crescentic glomerulonephritis model in Wistar-Kyoto rats. Rats developed crescentic glomerulonephritis leading to glomerulosclerosis and interstitial fibrosis by 56 days after the administration of nephrotoxic sera. The number of phosphorylated p38 MAPK-positive cells, detected mainly in crescents, correlated well with the percentage of crescents and number of ED-1-positive cells. Phosphorylated p38 MAPK-positive cells were downregulated in glomeruli in rats with the daily subcutaneous administration of FR167653 for 6 days. Concomitantly, renal expression of macrophage inflammatory protein-1alpha and monocyte chemoattractant protein-1/monocyte chemotactic and activating factor was markedly reduced by day 6. The severity of glomerulosclerosis and interstitial fibrosis significantly decreased by day 56, and renal function was preserved. These results suggest that p38 MAPK phosphorylation is pivotal for crescentic glomerulonephritis, followed by the subsequent expression of renal chemokines. This study provides evidence that regulation of p38 MAPK is a novel appealing therapeutic target for crescentic glomerulonephritis.

Animals↗

PubMed2001

SPARC expression in primary human renal cell carcinoma: upregulation of SPARC in sarcomatoid renal carcinoma.

SPARC (secreted protein acidic and rich in cysteine, also called osteonectin, BM-40, and 43K protein) is a matricellular protein and is associated with cell-matrix interactions during cell proliferation and extracellular remodeling. It is also implicated in the neovascularization, invasion, and metastasis of human malignancies. To investigate a potential role of the SPARC in renal tumorigenesis, we examined primary renal cell carcinomas (RCCs) for SPARC expression by Northern blot analysis and for protein distribution by immunohistochemistry. We found that 6 (100%) of 6 sarcomatoid and 25 (70%) of 36 clear-cell carcinomas had enhanced SPARC transcription compared with that of the corresponding normal kidney tissue. In contrast, papillary and chromophobe RCCs characterized by a hypovascular or avascular tumor phenotype had undetectable SPARC expression. Immunohistochemical analysis showed that SPARC was strongly stained in the cytoplasm of the sarcomatoid neoplastic cells in sarcomatoid RCCs, whereas it was expressed only in the vascular endothelial cells and fibroblasts in clear-cell RCCs. SPARC staining intensity in the stromal cells was increased in the invading portion in some clear-cell RCCs. These findings suggest that tumor development, including neovascularization and invasion in clear-cell RCCs, might be regulated by SPARC from stromal endothelial cells and fibroblasts and that sarcomatoid transformation from common-type RCCs is associated with upregulation of SPARC expression; SPARC may contribute to its aggressive tumor phenotype.

Blotting, Northern↗

PubMed2001

Treatment of the unstable distal radius fracture with external fixation and a hydroxyapatite spacer.

A prospective study was performed on 25 patients (15 women, 10 men) with unstable fractures of the distal radius selectively treated with a dynamic type of external fixation combined with a hydroxyapatite spacer. The fractures ranged from type VI to type VIII according to Frykman's classification. The patients' mean age at surgery was 49 years (range, 19-75 years). The mean follow-up period was 2.5 years, and overall outcome was assessed using Gartland and Werley's demerit point system as modified by Sarmiento. Radial inclination was 26 degrees +/- 4 degrees at the time of reduction and 26 degrees +/- 5 degrees at follow-up, palmar tilt was 9 degrees +/- 2 degrees at reduction and 8 degrees +/- 3 degrees at follow-up, and ulnar variance was 1.4 +/- 0.6 mm at reduction and 2.1 +/- 0.9 mm at follow-up. The mean range of motion at follow-up was 80 degrees +/- 10 degrees in flexion, 80 degrees +/- 10 degrees in extension, 85 degrees +/- 10 degrees in supination, and 80 degrees +/- 5 degrees in pronation. The outcome in 24 of 25 patients was evaluated as excellent. In the surgical treatment of unstable fractures of the distal radius using external fixator, the fracture reduction should be supported with bone graft or a bone substitute, and a hydroxyapatite spacer was considered to be a useful substitute for a bone graft.

Adult↗

PubMed2001

Distal plantar area reconstruction using a flexor digitorum brevis muscle flap with reverse-flow lateral plantar artery.

It is difficult to resurface skin defects of the sole because of its unique anatomy, which is resistant to mechanical stimuli. Though various methods have been reported, few are functionally satisfactory, and it is especially difficult to repair the distal plantar area. We report a reconstruction of the distal plantar area using a flexor digitorum brevis muscle flap based on a reverse-flow lateral plantar artery pedicle in a patient with a malignant melanoma on the right lateral metatarsal head of the fifth toe. The muscle flap was sufficient to cover the exposed fifth metatarsal and was covered with a full-thickness skin graft. The result was favourable and the patient has a normal gait and no pressure sores.

Aged↗

PubMed2001

Sequence analysis of fibroblast growth factor receptor 2 ( FGFR2 ) in Japanese patients with craniosynostosis.

Recently, mutations of the fibroblast growth factor receptor ( FGFR ) genes have been detected in syndromic craniosynostosis. We examined nucleotide sequences of FGFR2 in Japanese craniosynostosis patients (Crouzon syndrome: 9 cases; Apert syndrome: 6 cases; scaphocephaly: 3 cases as non-syndromic patients) by polymerase chain reaction (PCR) followed by direct sequencing methods. The results demonstrated FGFR2 heterozygous mutations at codons 252, 290 of exon 7, and at codon 342, 354 of exon 9 in Crouzon syndromes. In Apert syndrome patients, Ser252Trp and Pro253Arg were detected in five and one patients, respectively. No mutation was detected in one case of Crouzon, all cases of scaphocephaly and healthy individuals. Thus far sequence analysis of FGFR2 in syndromic craniosynostosis has been reported in many white patients, whereas in Japanese only several cases have been studied. The current study with 18 patients confirmed that a similar series of mutations occur in Japanese patients as in white patients regardless of ethnicity and environment. The frequency of the mutation was 82% (9/11 cases) in Japanese Crouzon patients. The ratio of S252W:P253R was 5 : 1 in Japanese Apert patients. Moreover, in Japanese Apert patients, complication rate of cleft palate was 60% for mutation of Ser252Trp and 0 of 2 patients for Pro253Arg, with their syndactyly score being 4.90 and 5.50, respectively.

Acrocephalosyndactylia↗

PubMed2001

Hip adductor muscle strength in patients with varus deformed knee.

The isometric muscle strength of the muscles around 49 medial compartmental osteoarthritic knees of 32 women was measured quantitatively using a Musculater GT-50 (osteoarthritis group). The patients pushed up a pad containing an electrical sensor and values were compared with those obtained from the nonaffected knees of subjects (control group). The mean age of the patients in the osteoarthritis group was 62.3 years (range, 43-78 years). The control group consisted of 13 women (13 knees) with a mean age of 60.5 years (range, 49-73 years). In the osteoarthritis group, the medial joint space was preserved in 17 knees (Grade A), 23 knees had narrowing of the joint space (Grade 2), and nine knees showed joint space obliteration (Grade 3). Quadriceps strength was significantly weaker in Grade 2 knees than in Grade 0 knees; however, there was no significant difference in quadriceps to hamstrings ratio between each grade. The hip adductors to hamstrings ratio was significantly greater in Grade 2 knees than in Grade 0 knees, and was greater in Grade 3 knees than in Grade 0, Grade 1, and Grade 2 knees. The findings suggested that in patients with medial compartmental osteoarthritis of the knee, the hip adductor muscles may become strengthened to decrease varus decrease varus deformity of the limb.

Adult↗

PubMed2001

Spinal injuries in snowboarders: risk of jumping as an integral part of snowboarding.

BACKGROUND: The purpose of this study was to clarify the occurrence rate and characteristics of spinal injuries caused by snowboarding that were sustained at the Okumino skiing area in Gifu Prefecture, Japan, from 1988 to 2000. METHODS: This study was a retrospective review of 13,490 cases of snowboard- or ski-related injury treated at Sumi Memorial Hospital over this period. RESULTS: A total of 7,188 patients sustained snowboard-related injuries, and 238 of these had spinal injuries caused by snowboarding (3.3%), whereas 6,302 patients sustained ski-related injuries, and 86 of these had spinal injuries caused by skiing (1.4%). Although there were no significant differences in the difficulty of slope, location of vertebral fracture, or spinal cord injury between snowboarders and skiers, the incidence of transverse process fractures was significantly higher in snowboard-related than in skiing-related injury (p < 0.05). In addition, there was a significantly higher incidence of spinal injury among beginner snowboarders than among beginner skiers (p = 0.04). Furthermore, intermediate or expert snowboarders were more likely to be injured because of jumping than beginners (p < 0.001), whereas about 70% of spinal injuries caused by skiing resulted from a simple fall. CONCLUSION: Spinal injuries sustained while snowboarding are increasing considerably in incidence and are characterized as complex injuries. We must educate young snowboarders of the risk of this sport, to prevent these serious injuries.

Adolescent↗

PubMed2001

Effectiveness of manual cleaning and disinfection of gastroendoscopes with 3% glutaraldehyde for decreasing risk of transmission of hepatitis C virus.

OBJECTIVES: The effectiveness of manual cleaning and disinfection of gastroendoscopes with 3% glutaraldehyde in decreasing the risk of transmission of hepatitis C virus (HCV) was examined. METHODS: Gastroendoscopes used for treatment of endoscopic esophageal variceal ligation in patients with HCV infection were manually cleaned and disinfected with 3% glutaraldehyde (n = 25), 2% glutaraldehyde (n = 17), or 0.1% benzethonium chloride (n = 25). Samples were obtained by pouring 20 ml of 0.9% NaCl solution into the biopsy-suction channel of the scope before and after cleaning and disinfection. HCV was detected with the polymerase chain reaction. RESULTS: Of the 25 scopes in 3% glutaraldehyde group, nine (36%) were positive for HCV before cleaning and disinfection, but all became negative after cleaning and disinfection; the difference was statistically significant (p < 0.01). In contrast, in 2% glutaraldehyde group and in the routine cleaning group, there were no significant differences in the number of positive samples between before and after cleaning and disinfection. CONCLUSION: Manual cleaning and disinfection of gastroscopes with 3% glutaraldehyde is useful for decreasing the risk of transmission of HCV among patients.

Benzethonium↗

PubMed2001

Subtype-specific translocation of the delta subtype of protein kinase C and its activation by tyrosine phosphorylation induced by ceramide in HeLa cells.

We investigated the functional roles of ceramide, an intracellular lipid mediator, in cell signaling pathways by monitoring the intracellular movement of protein kinase C (PKC) subtypes fused to green fluorescent protein (GFP) in HeLa living cells. C(2)-ceramide but not C(2)-dihydroceramide induced translocation of delta PKC-GFP to the Golgi complex, while alpha PKC- and zeta PKC-GFP did not respond to ceramide. The Golgi-associated delta PKC-GFP induced by ceramide was further translocated to the plasma membrane by phorbol ester treatment. Ceramide itself accumulated to the Golgi complex where delta PKC was translocated by ceramide. Gamma interferon also induced the delta PKC-specific translocation from the cytoplasm to the Golgi complex via the activation of Janus kinase and Mg(2+)-dependent neutral sphingomyelinase. Photobleaching studies showed that ceramide does not evoke tight binding of delta PKC-GFP to the Golgi complex but induces the continuous association and dissociation of delta PKC with the Golgi complex. Ceramide inhibited the kinase activity of delta PKC-GFP in the presence of phosphatidylserine and diolein in vitro, while the kinase activity of delta PKC-GFP immunoprecipitated from ceramide-treated cells was increased. The immunoprecipitated delta PKC-GFP was tyrosine phosphorylated after ceramide treatment. Tyrosine kinase inhibitor abolished the ceramide-induced activation and tyrosine phosphorylation of delta PKC-GFP. These results suggested that gamma interferon stimulation followed by ceramide generation through Mg(2+)-dependent sphingomyelinase induced delta PKC-specific translocation to the Golgi complex and that translocation results in delta PKC activation through tyrosine phosphorylation of the enzyme.

Adenoviridae↗

PubMed2001

Upregulation of fractalkine in human crescentic glomerulonephritis.

BACKGROUND/AIM: To evaluate the importance of fractalkine, a novel member of the CX3C chemokine, and natural killer (NK) cells in human crescentic glomerulonephritis, we determined the presence of fractalkine in the diseased kidneys immunohistochemically, and the correlation among fractalkine, NK cells and the degree of renal damage. METHODS: Twenty-three patients (13 males and 10 females) with primary or secondary crescentic glomerular disease were evaluated in this study. Fractalkine and CD16-positive cells including NK cells were detected immunohistochemically. RESULTS: Fractalkine-positive cells were detected in the interstitium of 23 patients with crescentic glomerulonephritis, while they were not detected in the glomeruli. In addition, CD16-positive cells were detected in both the glomeruli (1.3 +/- 0.2/glomerulus) and interstitium (1.3 +/- 0.2/visual field). The number of fractalkine-positive cells in the interstitium correlated with the number of CD16-positive cells before glucocorticoid therapy (r = 0.43, p = 0.047, n = 23). The number of fractalkine-positive cells in the interstitium before glucocorticoid therapy (0.2 +/- 0.1/visual field) decreased after therapy (0.1 +/- 0.1/visual field, p = 0.050) in 11 cases tested. The number of CD16-positive cells in the diseased kidneys did not change after glucocorticoid therapy. CONCLUSION: These results suggest that the local production of fractalkine may explain the presence of CD16-positive cells including NK cells, which may participate in the interstitial lesions of human crescentic glomerulonephritis before corticoid therapy.

Adult↗

PubMed2001

Point mutation (-69 G-->A) in the promoter region of cholesteryl ester transfer protein gene in Japanese hyperalphalipoproteinemic subjects.

Cholesteryl ester transfer protein (CETP) transfers cholesteryl ester (CE) from HDL to apolipoprotein (apo) B-containing lipoproteins and plays a crucial role in reverse cholesterol transport, which is a major protective system against atherosclerosis. Genetic CETP deficiency is the most common cause of a marked hyperalphalipoproteinemia (HALP) in the Japanese, and various mutations have been identified in the coding region as well as in the exon/intron boundaries in the CETP gene. In the present study, we identified a novel mutation in the promoter region of the CETP gene. This mutation was a G-to-A substitution at the -69 nucleotide of the promoter region (-69 G-->A), corresponding to the second nucleotide of the PEA3/ETS binding site (CGGAA) located upstream of the putative TATA box. Four (2.0%) of 196 unrelated subjects with a marked HALP (HDL cholesterol >/=2.59 mmol/L=100 mg/dL) were revealed to be heterozygous for the -69 G-->A mutation, and the allelic frequency of the mutant was 0.0102 in the subjects with a marked HALP. The subjects with the -69 G-->A mutation had low plasma CETP levels. Reporter gene assay showed that this mutation markedly reduced the transcriptional activities in HepG2 cells (8% of wild type). These results suggested that this mutation would be dominant negative. In conclusion, a novel -69 G-->A mutation in the CETP gene causes the decreased transcriptional activity leading to HALP.

Carrier Proteins↗

PubMed2001

Prolonged mild hypothermia therapy protects the brain against permanent focal ischemia.

BACKGROUND AND PURPOSE: The efficacy of hypothermic intervention for permanent focal ischemia has yet to be clarified. This study investigated the effect of a prolonged moderate or mild hypothermia on permanent focal ischemia in rats. METHODS: Two permanent focal ischemia models in male Sprague-Dawley rats were used. Moderate (30 degrees C, in experiment 1) or mild (33 degrees C, in experiment 2) hypothermia was achieved at the time of the induction of focal ischemia and was maintained for 2 hours under general anesthesia. Thereafter, the hypothermic condition was maintained by means of a cold room for a total of 24 hours. The infarct volume and neurological function were analyzed for a maximum of 21 days and compared with that of the normothermia group. Regional cerebral blood flow was monitored for 6 hours in the ischemic core and penumbra region. RESULTS: In experiment 1, the total infarct volume in the normothermic group was 368+/-59 mm(3); in contrast, it was significantly smaller in the hypothermia group: 169+/-33 mm(3) at 48 hours (mean+/-SEM, P:<0.05). In experiment 2, the infarct volume was 211+/-19 mm(3) in the normothermia group and 88+/-15 mm(3) in the hypothermia group at 21 days (P:<0.05). There were significant differences in neurological function from days 2 through 21 between the two groups. Mean regional cerebral blood flow in the penumbra region increased to a level >50% of baseline. CONCLUSIONS: Prolonged mild hypothermia suppressed the development of cerebral infarct and neurological deficit chronically after the induction of permanent focal ischemia.

Animals↗

PubMed2001

Broad-spectrum and selective serine protease inhibitors prevent expression of platelet-derived growth factor-BB and cerebral vasospasm after subarachnoid hemorrhage: vasospasm caused by cisternal injection of recombinant platelet-derived growth factor-BB.

BACKGROUND AND PURPOSE: Plasma serine protease cascade, including the complement system and thrombin, is activated in the subarachnoid space during the acute phase after subarachnoid hemorrhage (SAH). To examine the effect of protease cascade-based inflammation and subsequent vascular repair in the development of cerebral vasospasm, we examined the effect of 2 synthetic serine protease inhibitors-FUT-175, an inhibitor of thrombin and the complement system, and argatroban, a selective inhibitor of thrombin-on the development of cerebral vasospasm in a rabbit SAH model. METHODS: One hundred Japanese White male rabbits were used in the study. The SAH was simulated by a single injection of autologous arterial blood into the cisterna magna. To evaluate the development of cerebral vasospasm, the caliber of the basilar artery was measured on x-ray film before and at 2 days after SAH. Nine groups of rabbits (n=6 each) were treated with continuous intravenous injection of FUT-175 (2.5, 5, 10, or 20 mg/d), argatroban (1.25, 2.5, or 5 mg/d), or the same amount of saline (vehicle) for 48 hours, starting 40 minutes after SAH. Two days after SAH, the expression of homodimer of platelet-derived growth factor-BB (PDGF-BB) in the basilar artery was examined with immunohistochemical techniques. In 20 normal rabbits, 5 microg of recombinant PDGF-BB or vehicle was injected into the cisterna magna, and the basilar arteries were examined on angiograms for 48 hours. RESULTS: Significant differences were observed in the caliber of the basilar arteries between the vehicle group and the groups with the 3 larger doses of FUT-175 (vehicle, 52+/-5.0%; 5 mg, 79+/-5.7%; 10 mg, 80+/-2.5%; 20 mg, 80+/-3.7%) and between the vehicle group and the groups with the 2 larger doses of argatroban (vehicle, 52+/-6.4%; 2.5 mg, 81+/-9.0%; 5 mg, 85+/-4.1%) (P<0.05). In the histological examination, administration of effective doses of FUT-175 or argatroban suppressed the expression of PDGF-BB in the endothelial and medial smooth muscle cell layers. Exogenous PDGF-BB caused delayed and prolonged vasoconstriction on normal basilar arteries. CONCLUSIONS: Activation of the serine protease cascade and/or thrombin after SAH was demonstrated to play an essential role in the development of cerebral vasospasm. The expression of PDGF-BB-like protein in the arterial walls correlated with the development of cerebral vasospasm. Elevated PDGF-BB level in the subarachnoid space was found to induce delayed and chronic vasoconstriction.

Animals↗

PubMed2001

Crucial role of calpain in hypoxic PC12 cell death: calpain, but not caspases, mediates degradation of cytoskeletal proteins and protein kinase C-alpha and -delta.

Ca2+ influx is one of the main causative events in hypoxic PC12 cell death, because an extracellular Ca2+ chelator, ethylene glycol bis (2-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) inhibited and Ca2+ ionophore A23187 mimicked the hypoxic cell death. The hypoxic cell death was markedly prevented by a broad spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-FMK) as well as a calpain inhibitor, calpeptin, as assessed by nuclear staining with Hoechst 33258 and lactate dehydrogenase release. The processing of procaspase-3 was inhibited by z-VAD-FMK, but not by calpeptin. In contrast, z-VAD-FMK failed to block the proteolytic cleavage of fodrin-alpha, a preferential substrate for calpain. On the other hand, degradation of actin and fodrin-alpha was prevented by calpeptin but not by z-VAD-FMK. In addition, not only protein kinase C (PKC)-alpha but also PKC-delta were cleaved to generate approximately 46 kDa fragments. The PKC fragmentation was inhibited by calpeptin but not by z-VAD-FMK. These findings suggest that the extracellular Ca2+ influx induced by hypoxic stress activates calpain, resulting in the degradation of cytoskeletal proteins and generation of PKC fragments almost independently of caspase activation. Therefore, calpain may play an important role in hypoxic PC12 cell death.

Animals↗

PubMed2001

The clinical utility of contrast-enhanced 3D MR angiography for cerebrovascular disease.

The purpose of this study was to evaluate the usefulness of contrast-enhanced 3D MR angiography (CE-MRA) with an automated bolus-detection algorithm (SmartPrep technique) and the specialized phased-array coils for the patients suspected cerebrovascular disease. Forty-three patients with brain attack were examined with CE-MRA. A tracker volume of SmartPrep technique was placed along the ascending aorta in the coronal image. After the bolus injection of gadolinium, an increase in signal that corresponded to the arrival of gadolinium was used to trigger centric re-ordered spoiled gradient echo arterial selective MRA with imaging time of 20-40 sec. We were able to achieve a 100% successful triggering rate of SmartPrep technique and selectively arterial-phase carotid and vertebral arteries with almost no venous contamination could be delineated. These techniques enabled high resolution imaging of entire craniocervical arteries from aortic arch to the circle of Willis. This CE-MRA was useful to evaluate both occlusion of arteries and the collateral pathways and to measure stenosis and residual flow of dissection accurately. CE-MRA was a reliable less-invasive alternative to investigate the patients of cerebrovascular disease.

Brain↗