miR-18a-5p MicroRNA Increases Vascular Smooth Muscle Cell Differentiation by Downregulating Syndecan4

BACKGROUND AND OBJECTIVES: Differentiation and de-differentiation of vascular smooth muscle cells (VSMCs) are important events in atherosclerosis and restenosis after angioplasty. MicroRNAs are considered a key regulator in cellular processes such as differentiation, proliferation, and apoptosis. Here, we report the role of new miR-18a-5p microRNA and its downstream target genes in VSMCs and in a carotid balloon injury model. MATERIALS AND METHODS: Expression of miR-18a-5p and its candidate genes was examined in VSMCs and in a carotid artery injury model by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and microRNA microarray analysis. VSMC differentiation marker genes including smooth muscle (SM) alpha-actin and SM22alpha were determined by Western blot, qRT-PCR, and a SM22alpha promoter study. Gene overexpression or knockdown was performed in VSMCs. RESULTS: miR-18a-5p was upregulated in the rat carotid artery at the early time after balloon injury. Transfection of the miR-18a-5p mimic promoted the VSMC differentiation markers SM alpha-actin and SM22alpha. In addition, miR-18a-5p expression was induced in differentiated VSMCs, whereas it decreased in de-differentiated VSMCs. We identified syndecan4 as a downstream target of miR-18-5p in VSMCs. Overexpression of syndecan4 decreased Smad2 expression, whereas knockdown of syndecan4 increased Smad2 expression in VSMCs. Finally, we showed that Smad2 induced the expression of VSMC differentiation marker genes in VSMCs. CONCLUSION: These results indicate that miR-18a-5p is involved in VSMC differentiation by targeting syndecan4.

Comparison of bare metal stent and paclitaxel-eluting stent using a novel rat aorta stent model

The purpose of our study was to create a novel rat aorta stent implantation model. Stainless steel bare metal stents (BMS) or paclitaxel-eluting stents (PES) were implanted in male Sprague-Dawley rats (BW 400 +/- 20 g). Two and four weeks after stent implantation, the aorta were collected, fixed with 2% glutaraldehyde, and cut into two segments. One segment was used for scanning electron microscopy analysis to evaluate re-endothelialization, and the other segment was used to calculate the neointimal area. At 2 weeks after stenting, the appearance of neointimal hyperplasia was less in the PES group than in the BMS group. At 4 weeks after stenting, no significant difference in neointimal hyperplasia was observed between two groups. On the other hand, the PES group showed more thrombus formation and less re-endothelialization compared to the BMS group. This study demonstrated the ability of a novel rat model of aorta stenting via a common carotid artery to measure the efficacy and safety of commercially available drug-eluting stents.

Perivascular Delivery of Rapamycin in Pluronic Gel Inhibits Neointimal Hyperplasia in a Rat Carotid Artery Injury Model, and the Complementary Role of Carotid Arteriography

BACKGROUND AND OBJECTIVES: Rapamycin has been shown to inhibit the vascular smooth muscle cell migration and proliferation that contributes to neointimal formation. We investigated whether the perivascular delivery of rapamycin in Pluronic gel could inhibit neointimal hyperplasia in a rat carotid artery model, and we tested the usefulness of carotid arteriography. MATERIALS AND METHODS: To assess the kinetics of rapamycin's release from Pluronic gel, a [3H] thymidine incorporation assay was performed with using the media exposed to rapamycin in Pluronic gel for 10, 20, 60 and 120 min. We applied 100 microgram of rapamycin in Pluronic gel to the perivascular space of the carotid artery after the balloon injury (n=9), whereas only gel was applied in a control group (n=9). We performed the carotid arteriography and the morphometric analysis 14 days after injury. RESULTS: The [3H] thymidine incorporation assay showed a reduction of uptake in a time-dependent manner (86%, 48%, 45% and 40% of the control, respectively, at 10, 20, 60 and 120 minutes). The inhibiting effect of rapamycin on neointimal hyperplasia was identified on the carotid arteriography (mean luminal diameter; 0.75+/-0.11 vs. 0.60+/-0.12 arbitrary units, respectively, p< 0.05) and on the morphometric analysis (neointima area: 0.09+/-0.03 vs. 0.17+/-0.06 mm(2), respectively, p< 0.05). CONCLUSION: This study demonstrated that perivascular delivery of rapamycin in Pluronic gel inhibits neointimal hyperplasia in a rat carotid injury model. This animal model combined with arteriography can be used for developing new drugs to treat restenosis. In addition, this technique might be useful for vascular surgery such as coronary artery bypass grafting, arteriovenous fistula formation and peripheral vascular bypass graft insertion.

Therapeutic Potential of Umbilical Cord Blood-Derived Mesenchymal Stem Cells in Ischemic Myocardium

BACKGROUND AND OBJECTIVES: We designed this study to determine the therapeutic potentials of umbilical cord blood (UCB)-mesenchymal stem cells (MSCs), as compared with bone marrow (BM)-MSCs. MATERIALS AND METHODS: MSCs were isolated from UCB and BM. For the in vivo study, myocardial infarction was induced by ligation of the left anterior descending coronary artery (LAD) in rats for 30 min, and this was followed by release; the MSCs were then injected into a designated point around the infarcted area. Echocardiographs were performed two weeks after surgery. For the in vitro study, a cDNA microarray and cytokine array were performed to compare the MSCs from UCB and from BM. Cell migration was assessed by a wound scratch assay, and the level of cardiac ankyrin repeat protein (CARP) was determined by reverse transcriptase-polymer chain reaction (RT-PCR) or Western blot analysis. RESULTS: For the echocardiograph findings, the fractional shortening (FS) was 43.9% in the UCB-MSCs group and it was 38.6% in the BM-MSC group. The ejection fraction (EF) was 79.8% in the UCB-MSC group and it was 72.4% in the BM-MSC group (control FS: 26.2% and the control EF: 56.6%). CARP was one of the highly expressed genes in the UCB-MSCs on the cDNA microarray. The mRNA and the expressed level of CARP protein in the UCB-MSCs were higher than those in the BM-MSCs. The cell migration of the CARP small interfering ribonucleic acid (siRNA) transfected UCB-MSCs was delayed compared to that of the normal UCB-MSCs (p<0.05) CONCLUSION: Our study directly compared the two types of MSCs from UCB and BM, and we suggest that the CARP molecule might be responsible for the motility of UCB-MSCs.

A Slight Variation in the Age of Rats Commonly used as a Carotid Artery Injury Model Results in a Large Difference in Neointima Formation

BACKGROUND AND OBJECTIVES: The degree of neointima formation after infliction of a carotid artery balloon injury in rats varies greatly depending on the sex, age, species and operational method. Strong variation is common, even within only a single control. This study attempted to find if there was any significant difference in neointima formation following a carotid artery balloon injury in 6 to 12 week old rats; the age commonly used in these types of experiments. MATERIALS AND METHODS: A balloon injury was inflicted on the carotid arteries of male SpragueDawley rats at 6 (n=9, 250-270 g), 8 (n=8, 280-300 g) and 11 weeks (n=10, 320-340 g) of age. Two weeks postoperation, a histomorphometric analysis was carried out. The vascular smooth muscle cell proliferation was measured in situ via BrdU incorporation 2 days after injury infliction. RESULTS: The neointima areas of the 6 week (0.22+/-0.04 mm2) and 8 week old groups (0.17+/-0.08 mm2) were 3.1 and 2.4 times larger than that of the 11 week old group (0.07+/-0.03 mm2). The mitotic index was significantly reduced in 11 week old group (n=4, 9.22+/-1.51%) compared to those of the 6 (n=4, 25.03+/-3.92%) and 8 week old (n=4, 21.66+/-3.66%) groups. CONCLUSION: Special care should be taken when interpreting neointima formation, as even a slight variation in the age and weight in 6 to 12 week old (250-340 g) rats; the age commonly used in these types of experiments, results in an unexpectedly large difference.

Protection of Cardiomyocytes from Acute Ischemic Injury by Protein Kinase Cepsilon Expression

BACKGROUND AND OBJECTIVES: Ischemic injury is the most common and important cause of myocardial damage. Over past decades, a number of studies have identified a protective mechanism known as ischemic preconditioning, which can block or delay cell death from ischemic injury. Protein kinase C (PKC), especially theepsilonisoform has been proposed as a key factor in the signaling pathway of ischemic preconditioning. However, whether PKCepsilon expression in cardiomyocytes can offer such protection from acute ischemia has not been explored. MATERIALS AND METHODS: To demonstrate a direct effect of PKCepsilon expression, a lentiviral vector system was established. Using the lentiviral vector, PKCepsilon was introduced to neonatal rat ventricular myocytes (NRVM) cultured under ischemic conditions, and also to adult rat myocardium subject to left coronary artery ligation. RESULTS: Compared to control, PKCepsilon expression in cultured NRVM under ischemia resulted in preserved cell density and morphology, and a reduction in cell death (77.6+/-12.8% vs 58.1+/-7.2%, p<0.05). In adult rats, the infarcted area after coronary artery ligation was markedly reduced in myocardium injected with PKCepsilon vector compared to control (11.4+/-5.3% vs 20.5+/-11.3%, p<0.01). CONCLUSION: These results provide direct evidence that PKCepsilon is a central player in protection against cell death from acute ischemia.

Role of Angiotensin II Type 1A Receptor-Mediated Signaling in the Development of Pressure Overload-Induced Left Ventricular Hypertrophy and Fibrosis

BACKGROUND AND OBJECTIVES: The roles of angiotensin II (Ang II) in the regulation of heart function under normal and pathological conditions have been well documented, with its biological actions mainly mediated via the Ang II type 1A receptor (AT(1A)R). Since the inhibition of the renin-angiotensin system can prevent or regress left ventricular hypertrophy (LVH) with hypertension, AT(1A)R-mediated signaling is considered one of the important transcriptional pathways in the development of cardiac hypertrophy. SUBJECTS AND METHODS: To address whether AT(1A)R-mediated signaling plays an important role in the development of pressure overload-induced LVH and fibrosis, the physiological, biochemical, hemodynamic and histopathological parameters were evaluated before and after transverse aortic constriction (TAC) in wild-type (WT) and AT(1A)R knockout (KO) mice. RESULTS: Although the LV systolic pressure (83.2+/-10.0 mmHg, n=5) of the KO mice was lower than that (90.0+/-5.0 mmHg, n=7) of the WT mice, there was no difference in the increase in the LV systolic pressure between the WT and KO mice (WT, 42.0 mmHg; KO, 41.8 mmHg). Also, there was no difference between the baseline LV-to-body weight (LVW/BW) ratio between the two groups (WT, 3.10+/-0.21 mg/g; KO 3.04+/-0.21 mg/g). Two weeks after TAC, the degree of increase in the LVW/BW ratio was markedly increased in both the WT (4.17+/-0.28 mg/g, n=9) and KO mice (4.16+/-0.43 mg/g, n=8), which were almost identical (WT, 34.5%; KO, 36.8%). There were no significant differences in the LV end-diastolic pressure, LV+dP/dt(max), and heart rate between the two groups. The ERK44/42 and p38-MAPK activities in the LV were markedly increased by TAC in both groups, but that of JNK was not. Interstitial and perivascular fibrosis developed in both groups following TAC. However, the degree of increased fibrosis was significantly attenuated in the KO mice. CONCLUSION: These results suggest AT(1A)R-mediated signaling is not indispensable for the development of pressure overload-induced LVH, and provides new insights into the development of novel therapeutic strategies for cardiac hypertrophy.

Perivascular Delivery of Paclitaxel with F-127 Pluronic Gel Inhibits Neointimal Hyperplasia in a Rat Carotid Artery Injury Model

BACKGROUND AND OBJECTIVES: The local delivery of drugs to the arterial wall represents a strategy for the treatment of fibroproliferative vascular disease. Paclitaxel has been shown to inhibit vascular smooth muscle cell proliferation and migration, which contribute to neointimal formation. This study tested whether the perivascular delivery of paclitaxel can prevent neointimal formation in a rat carotid artery injury model. MATERIALS AND METHODS: The ability of locally-administered paclitaxel to prevent the neointimal hyperplastic response was tested by incorporating 10 microgram paclitaxel into 40% F-127 pluronic gel, which was then applied to the adventitial surface of the rat carotid artery immediately following balloon injury. Fourteen days after angioplasty, the neointimal growth was compared between paclitaxel- (n=12) and pluronic gel only treated (control group, n=11) rats. RESULTS: The paclitaxel-treated group showed significant neointimal formation reductions compared to the control group (0.10+/-0.05 versus 0.21+/-0.05 mm2, p<0.05). The perivascular application of paclitaxel produced a highly localized pattern of neointimal growth inhibition in the arterial cross-section. Although 10 microgram paclitaxel showed no significant cytotoxicity, 20 microgram paclitaxel (n=3) demonstrated cytotoxicity, with medial cell drop out in the region of application. CONCLUSION: We have demonstrated that the local extravascular application of 40% F-127 pluronic gel containing paclitaxel provides an effective mechanism for inhibiting the proliferative response to vascular injury in the rat. The cellular response to paclitaxel is highly focal. Locally sustained delivery of paclitaxel, as little as 10 microgram, was effective in preventing neointimal growth, without destroying medial wall smooth muscle cells.

Cellular Cardiomyoplasty Using Bone Marrow Derived Mesenchymal Stem Cells Transplantation in Post Myocardial Infarction Heart Failure

BACKGROUND AND OBJECTIVES: Cellular cardiomyoplasty (CCM) is considered to be a novel therapeutic approach for post-myocardial infarction (MI) heart failure. In this study, the functional effects of cultured mesenchymal stem cells (MSCs) transplantation and the associated histopathologic changes were evaluated in a rat model of MI. MATERIALS AND METHODS: Rats were subjected to 5 hours of coronary ligation followed by reperfusion, and 10 days after MI, animals were randomized into either the MSCs transplantation (MI-MSC, n=8) group or the control (n=8) group. Allogeneic MSCs (3x10(6) cells) or media were epicardially injected into the center and the border area of the infarct scar. RESULTS: Four weeks after the MSCs transplantation, the echocardiogram showed preserved anterior regional wall motion and increases in fractional shortening in the MI-MSC heart relative to the control heart. Left ventricular (LV) end diastolic pressure was smaller in the MI-MSC than in the control group. Implanted MSCs formed islands of cell clusters on the border of the infarct scar, and the cells were positively immunostained by sarcomeric alpha-actinin and cardiac troponin T. In addition, the number of microvessels on the border area of the infarct scar was greater in the MI-MSC than in the control group. CONCLUSION: Allogeneic MSCs transplanted into the MI scar formed clusters of cell grafts on the border of the infarct, expressed cardiac muscle proteins, increased microvessel formation, and improved regional and global LV function. Our data indicate that CCM using MSCs may have a significant role in the treatment of post-MI heart failure.

Effects of Pressure Overload and its Recovery on Vascular Reactivity and Remodeling of the Rat Carotid Artery

BACKGROUND AND OBJECTIVES: The Vascular system exhibits altered morphological and functional properties during hypertension and after anti-hypertensive therapy. To characterize such changes, the contractile, histological and molecular responses in the common carotid arteries (CCA) were compared in 35 rats. MATERIALS AND METHODS: By partial transverse aortic constriction (TAC), the right CCAs were made to lie under a high pressure environment, while the left CCAs remained under normotension, the latter being used as control vessels. The ligations were removed after two weeks, to enable the recovery process to begin. RESULTS: The vessel contractility, two weeks after the TAC, was nearly abolished. The recovery process from high pressure showed an initial hypercontractile period of around 1-2 week after recovery, prior to the subsequent decline to a normal contractility after 2 weeks. The relaxation response due to acetylcholine was minimal at the end of the hypertensive period, recovered slowly, and reached a normal magnitude after 4 weeks. A high pressure increases the medial thickness & area, and enhances the adventitial tissue formation. These changes persist during the first 4 weeks of recovery, after which normotension returns. Apoptosis at the endothelial layer was significantly increased two weeks after the TAC, but normalized two weeks after recovery. The expression of ecNOS was not detect 2 weeks after the TAC, but gradually returned to a basal level at 2 weeks after the untying. CONCLUSION: A high blood pressure causes decreases in the contractility and endothelium-dependent relaxation. It also increases endothelial apoptosis, the medial thickness & area, and enhances the adventitial tissue formation. The recovery processes from high blood pressure are not uniform, but show different normalizations among the structural, contractile and apoptotic parameters.

Expression of Nitric Oxide Synthase Isoforms after Endothelial Denudation of the Rat Carotid Artery

BACKGROUND AND OBJECTIVES: The nitric oxide synthase (NOS) system may be involved in the healing process following arterial injury. The expressions of eNOS or iNOS have been observed separately following endothelial denudation of rat carotid arteries. However, the expressions of nitric oxide synthase isoforms (eNOS, iNOS and nNOS) have not been observed simultaneously. MATERIALS AND METHODS: Using balloon catheter denudation of the rat carotid artery, as a model for arterial injury and restenosis, we have evaluated the time course of the expressions of eNOS, iNOS and nNOS simultaneously using immunohistochemistry and RT-PCR. RESULTS: From the immunohistochemistry, the iNOS protein was shown to be rapidly induced following injury (day 1) and was later seen to be relocalized to the neointima (day 5). Two weeks following injury the iNOS expression had declined. After 4 weeks the iNOS expression had disappeared completely. The eNOS protein was not detected until three days post injury. Two weeks following injury the eNOS expression was observed at the "pseudoendothelial" surface forming intimal smooth muscle cells. By week 4 the eNOS expression was detected on the morphological endothelium. The nNOS expression was detected at the media one day following injury and for the subsequent two weeks, but it was not detected at the neointima at all. RT-PCR demonstrated that iNOS mRNA was faintly expressed 1 day following endothelial denudation. The expression level of the iNOS mRNA was highest at 5 days, but gradually decreased until 2 weeks following injury. CONCLUSION: These results suggest that endothelial disruption may induce the expressions of iNOS and nNOS, and the re-expression of eNOS may reduce these expressions. The expressions of iNOS and nNOS could be a homeostatic mechanism that compensates for the loss of endothelium.

Establishment and Magnetocardiographic Changes of Pressure Overload Left Ventricular Hypertrophy and Its Regression in Rats

BACKGROUND AND OBJECTIVES: Regression of left ventricular hypertrophy (LVH) is important because development of myocardial ischemia, heart failure or arrhythmias may be reduced. However, an animal model for LVH regression is not well established and there are no useful parameters to predict LVH regression. Magnetocardiogram (MCG), magnetic signal generated from the heart, has recently been investigated for the detection of electrical current changes of the heart. This study was undertaken to establish rat models of LVH-regression and to assess MCG changes during LVH induction and regression. MATERIALS AND METHODS: Rat models of pressure overload LVH were established by transverse aortic constriction (TAC) and LVH regression was generated by untying 2 weeks after TAC. Hemodynamic, echocardiographic and biochemical evaluation were performed in order to confirm this model. Magnetic fields were recorded with a SQUID gradiometer before and after TAC, and also recorded at 1, 3, 7, and 14 days after untying, respectively. RESULTS: Rat models of LVH-regression were established successfully by TAC and untying. The pressure gradient across TAC disappeared within 10 minutes after untying. LV weight, LV weight/body weight ratio, LV mass and expression level of atrial natriuretic factor were significantly increased following TAC and decreased to baseline value after pressure unloading. Deeper S waves and strain patterns were observed after LVH induction and gradually returned to basal levels over the 2 weeks after untying. CONCLUSION: MCG changes in the rat models of LVH-regression indicate that MCG can be a helpful modality for the diagnosis and evaluation of LVH as well as follow-up after treatment of LVH.

Role of Calcineurin-Dependent Signaling Pathway on the Left Ventricular Hypertrophy Induced by Pressure Overload

BACKGROUND AND OBJECTIVES: Calcineurin-dependent transcriptional pathway has recently been implicated in cardiac hypertrophy. Whether calcineurin inhibition can prevent the development of pressure-overload left ventricular hypertrophy (LVH) is still controversial. To elucidate this issue, the effects of calcineurin inhibitors on the prevention of pressure-overload LVH were examined in mice. MATERIALS AND METHODS: Pressure overload was induced by transverse aortic contriction (TAC) in 57 ICR mice. Three different doses of CsA (TAC/CsA group, n=21) and FK506 (TAC/FK group, n=20) were administered subcutaneously from -2 to 14 days after surgery and 16 mice were treated with vehicle (TAC group). Another 60 mice were sham-operated and treated with CsA (CsA group, n=19), FK506 (FK group, n=18) or vehicle (Control group, n=23). RESULTS: Two weeks after TAC, the LV weight-to-body weight (LVW/BW) ratio was not significantly different among the Control, CsA and FK groups although it was greater in the TAC group (4.55+/-0.69 mg/g) than in the Control(2.78+/-0.70 mg/g) and other sham-operated groups (p<0.00005). Low-dose CsA (5 mg/kg/day) or FK506 (0.6 mg/kg/day) injection following TAC did not decrease the LVW/BW ratio. However, intermediate-dose and high-dose CsA (25 and 50 mg/kg/day) or FK506 (2 and 6 mg/kg/day) treatment prevented pressure-overload induced LVH and the degree of LVH inhibition was dose-dependent. Interstitial and/or perivascular fibrosis was remarkably decreased by the administration of intermediate and high doses of calcineurin inhibitors for 2 weeks following TAC. CONCLUSION: Taken together, calcineurin inhibitors, CsA and FK506, attenuated pressure-overload LVH response in a dose-dependent fashion. This data indicates that a calcineurin-dependent signaling pathway is crucial in the development of pressure-overload LVH.

Reaction Difference of Glue-Lipiodol Mixture According to the Different Lot Number

PURPOSE: We noted that in a catheter, glue-lipiodol mixtures (GLM) prematurely turned into a cast duringembolization of brain arteriovenous maliformation, and to avoid this problem, added tungsten to GLM. The reactiontime and hardness of GLM were then evaluated in vitro. MATERIALS AND METHODS: Six lots of Lipiodol (Nos.97LU009A, 96LU018A, 96LU017A, 96LUollA and 95Lu020A)(Laboratoire Guerbet, Cedex, France) and three lots HistoacrylBlue (2/7121, Ex. Date 03/99 (993);2/6263, 06/98 (986);2/6132 03/98 (983))(B. Brown, Melsungen, Germany) weremixed in a 5cc bottle at concentrations of 25-50%(glue:lipiodol=1:1 to 1:3) and observed for two weeks. Thehardness of polymerized GLM was classified as liquid, gel, semi-solid or solid. After the addition of tungsten ortantalum powder (0.2gm) and a drop of blood to GLM, different series of experiments were performed. pH wasmeasured in distilled water mixed with tungsten of tantalum(0.1 to 0.5 gm). RESULTS: At a concentration of 50%,most GLM turned into solid casts within 48 hours;at one of 25%, most GLM gelled within 24hrs. At concentrations of28 and 33%, hardness was between that of a solid and that of a gel. After the addition of tungsten to 50% and 25%GLM, this remained in a liquid state until two weeks later, regardless of lipiodol products. In 5cc distilledwater with 0.1 to 0.5 gm tungsten, pH changed from 3.5 to 2.6, and on the addition of tantalum from 6.4 to 5.7.The addition of blood to the mixture immediately turned the cast solid at a GLM concentration of 50%, andsemi-solid at one of 25%. CONCLUSION: The reaction time of GLM differed according to the lot number of lipiodol.The addition of tungsten seemed to prevent premature cast formation by decreasing pH;the mechanism was similar tothat observed when acetic acid was added.

Leigh Syndrome: Serial MRI Findings

PURPOSE: The purpose of this study was to evaluate the effect of the temporal changes in brain lesions onserial MR images during the course of Leigh syndrome. MATERIALS AND METHODS: We retrospectively reviewed 11 MRimages in four patients diagnosed as suffering from Leigh syndrome on the basis of clinical features, MRIfindings, and biochemical data. Follow-up and earlier, MR images were compared and temporal changes in lesionswere analyzed, with particular attention to location, size, signal intensity, and contrast enhancement. RESULTS: Initial MRI showed that in order of frequency, the following were involved : bilateral putamina (4/4), caudatenuclei (2/4), the brain stem (2/4), medial thalamic nuclei (1/4), and the cerebral cortex (1/4). In two patients,the size of acute putaminal lesions, as seen on follow-up MRI, decreased in the short term (within two weeks); inone patient, strong contrast enhancement of the lesions was observed twelve days after initial MRI. Long termfollow-up MRI, over 7 - 19 months, showed newly developed lesions (2/4) and atrophy (2/4) or obliteration ofprevious lesions (3/4) in the basal ganglia, thalami, and brain stem. CONCLUSION: Serial MRI demonstratedtemporal changes in brain lesions during the course of Leigh syndrome. On follow-up MRI, the appearance ofbilateral lesions in basal ganglia and the brain stem, not present on initial MRI, may be helpful corroborativeevidence to support a diagnosis of this syndrome.

Metastatic Breast Carcinoma from Gastric Cancer: A Case Report

We encountered a patient with a breast mass which had metastasized from gastric carcinoma representing as aninflammatory carcinoma on ultrasonography. We described the radiologic and clinical features, and review theliterature. The patient had advanced gastric carcinoma and breast ultrasonography demonstrated the presence ofvery ill-defined, infiltrating, and mixed echoic lesions indistinguishable from findings of primary inflammatorybreast carcinoma. Metastatic gastric adenocarcinoma was confirmed pathologically.

Analysis of Angiographic Findings in Cerebral Arteriovenous Malformation with Hemorrhage: Comparison between Intracerebral and Intraventricular Hemorrhage

PURPOSE: The purpose of this study was to analyze the angioarchitectures of cerebral arteriovenousmalformation(AVM) and to determine whether there was correlation between angioarchitectures and patterns ofintracranial hemorrhage(intracerebral, intraventricular, and both) in cerebral AVM. MATERIALS AND METHODS: Onehundred and twenty-eight patients who between November 1989 and December 1994 suffered supratentorial AVM withintracranial hemorrhage were studied retrospectively. Among 128 patients, intracerebral and intraventricularhemorrhage were seen in 68 (53%) and 24 patients (19%), respectively, while both types were seen in the remaining36 (28%). We analyzed the angioarchitectual characteristics of AVM. namely nidi, feeding arteries and drainingveins, in three hemorrhagic groups of patients with intracerebral hemorrhage, intraventricular hemorrhage andboth. The kappa2 test or Fisher's exact test was used for statistical analysis. RESULTS: A cortically located niduswas most common in patients with intracerebral hemorrhage, while a periventricular location was most common inthose with intraventricular hemorrhage (p<0.001). Location in the corpus callosum, choroid plexus, orintraventricular area was more frequent in the intraventricular than the intracerebral hemorrhagic group (p<0.05). Superficial venous drainage was most common in patients with intracerebral hemorrhage (p<0.001), and deep venousdrainage in those with intraventricular hemorrhage (p=0.001). CONCLUSION: The angioarchitectual characteristicsof cerebral arteriovenous malformation correlate significantly with patterns of intracranial hemorrhage, andawareness of the type of hemorrhage could help to manage patients and determine prognosis.

Analysis of Angiographic Findings in Arteriovenous Malformations (AVM) of Brain According to PresentingClinical Manifestations

PURPOSE: To evaluate the different angio-architectures of brain arteriovenour malformatigns (AVMs) accordingto the presence of non-hemorrhagic symptoms or intracerebral (ICH) and/or intraventricular hemorrhage(IVH). MATERIALS AND METHODS: The results of complete cerebral angiography obtained in 215 patients with AVM between1989 and 1994 were retrospectively reviewed. The M:F ratio was 136:78 and their mean age was 29 (ranged 4 - 66)years. On the based of clincal presentation, CT and/or MR images, they were divided into hemorrhagic andnon-hemorrhagic groups. Angiograms were analyzed by two radiologists for the size and location of nidus; thenumber of feeding arteries and the extent of aneurysm, stenosis, dural supply, and angiomatous change; the numberof draining veins and the extent of deep or superficial drainage, stenosis, ectasia, kinking, and stasis. Thestandard chi-square test was used for statistical analysis. RESULTS: Hemorrhage was noted in 140 patients(65%),and no hemorrhage in 75(35%). Hemorrhage was more common in AVM with deep-seated and callosal locations, a nidusof less than 2cm, single feeder and single venous drainage, and deep venous drainage only (p < 0.05 - 0.001).Non-hemorrhagic presentations were more common in AVM with cortical and subcortical location, a nidus of more than5cm, angiomatous change, dural supply, both superficial and deep venous drainage, kinking, and stasis (p <0.05-0.001). CONCLUSION: The angio-architechture of AVM with hemorrhage correlated with clinical symptomaticpresentation. Analysis of the patterns of angioarchitectureis useful for prognosis and in deeiding the direetionof freatment.

Pulmonary Sarcoidosis: CT Findings and Correlation with sACE Level and PFT

PURPOSE: To assess CT findings of pulmonary sarcoidosis and correlate these with sACE level and PFT. MATERIALS AND METHODS: Between 1989 and 1995, 14 patients (4 men and 10 women, aged between 28 and 55 years) with histologically confirmed pulmonary sarcoidosis were consecutively selected. HRCT scans were performed in 12 patients and conventional CT scans in two. CT findings were reviewed by three radiologists, and were correlated with the index of disease activity based on sACE level and pulmonary function test. RESULTS: Pulmonary parenchymal abnormalities were seen in all patients ; small nodules of less than 3 mm in diameter were seen in eight. Other abnormalities were nodules of more than 3 mm in diameter (n=7), confluent nodules (n=5), ground glass opacity (n=5), patchy areas of consolidation with air bronchogram (n=5), and architectural distortion (n=3). The upper lung zone was more frequently involved than the middle or lower zone. In ten patients, the peripheral interstitum was predominantly involved, while only three patients showed predominant peribronchovascular involvement. Lymphadenopathy was noted in 13. There was no correlation between sACE level, the results of a pulmonary function test and the extent of parenchymal involvement. CONCLUSION: HRCT is valuable for the identification, characterization, and determination of the extent to which parenchymal lung is involved in sarcoidosis. The extent of this involvement does not correlate with sACE level and pulmonary function test results.