Low prevalence of the 'gang of seven' and absence of the O80:H2 serotypes among Shigatoxigenic and enteropathogenic Escherichia coli (STEC and EPEC) in intestinal contents of healthy cattle at two slaughterhouses in Belgium in 2014.

AIMS: The purpose of this survey was to estimate the respective prevalence of the 'gang of seven' and 'non-gang of seven' serotypes of Shigatoxigenic and enteropathogenic Escherichia coli and to identify the O80:H2 serotype in 245 intestinal contents collected at two slaughterhouses in Belgium in 2014. METHODS AND RESULTS: After overnight enrichment growth, the 69 intestinal contents testing positive with PCR targeting the eae, stx1 and stx2 genes were inoculated onto four agar media. Of the 2542 colonies picked up, 677 from 59 samples were PCR confirmed. The most frequent virulotypes were eae+ in 47 (80%) samples, stx2+ in 20 (34%) samples and eae+ stx1+ in 16 (27%) samples. PCR-positive colonies belonged to different virulotypes in 36 samples. No colony was O80-positive, whereas two eae+ colonies from two samples were O26:H11, 50 eae+ stx1+ and eae+ from eight samples were O103:H2 and two eae+ stx1+ stx2+ colonies from one sample were O157:H7. CONCLUSIONS: The 'non-gang of seven' serotypes are more frequent than the 'gang of seven' serotypes and the O80:H2 serotype was not detected among Shigatoxigenic and enteropathogenic Escherichia coli in the intestines of cattle at these two slaughterhouses. SIGNIFICANCE AND IMPACT OF THE STUDY: Although the identification protocols of Shigatoxigenic Escherichia coli focus on the 'gang of seven' serotypes, several other serotypes can be present with possible importance in public health. Innovative selective identification procedures should be designed.

IL28B polymorphism may guide pegylated interferon plus ribavirin therapy even after curative treatment for hepatitis C virus-related hepatocellular carcinoma.

The present study was designed to determine the predictive factors for the viral response to pegylated interferon-alpha plus ribavirin combination therapy (PEGIFN/RBV) administered after curative treatment for hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC). The study group was 78 patients treated between January 2005 and January 2009. The sustained viral response (SVR) rate was 25.8% (15/58) in patients infected with HCV-genotype 1 and 55.0% (11/20) in those with genotype 2. Among the 78 patients, 32 (41.0%) could not complete the treatment protocol, and this was because of HCC recurrence in 17 (53%) of them. Multivariate analysis identified partial early viral response (pEVR) as the only independent determinant of SVR [odds ratio (OR) 14.73, P = 0.013] for patients with genotype 1. Multivariate analysis identified male gender (OR 8.72, P = 0.001) and interleukin-28B (IL-28B) genotype (rs8099917) TT (OR 7.93, P = 0.007) as independent predictors of pEVR. Multivariate analysis also identified IL-28B genotype GG+TG (OR 14.1, P = 0.021) and α-fetoprotein >30 (OR 5.4, P = 0.031) as independent predictors of null response. Patients with SVR showed a better survival rate than those without SVR (P = 0.034). The second HCC recurrence rate tended to be lower in patients with SVR than in those without SVR (P = 0.054). With regard to the prognosis of patients with SVR, it is desirable to achieve SVR with interferon therapy even when administered after HCC treatment. IL-28B genotype is a potentially useful marker for the response to PEGIFN/RBV therapy administered after curative treatment of HCV-related HCC.

Molecular cloning and expression of the human interleukin 5 receptor.

Human interleukin 5 (IL-5) plays an important role in proliferation and differentiation of human eosinophils. We report the isolation of cDNA clones from cDNA libraries of human eosinophils by using murine IL-5 receptor alpha chain cDNA as a probe. Analysis of the predicted amino acid sequence indicated that the human IL-5 receptor has approximately 70% amino acid sequence homology with the murine IL-5 receptor and retains features common to the cytokine receptor superfamily. One cDNA clone encodes a glycoprotein of 420 amino acids (Mr 47,670) with an NH2-terminal hydrophobic region (20 amino acids), a glycosylated extracellular domain (324 amino acids), a transmembrane domain (21 amino acids), and a cytoplasmic domain (55 amino acids). Another cDNA encodes only the extracellular domain of this receptor molecule. Other cDNA clones encode molecules having diversified cytoplasmic domains. COS7 cells transfected with the cDNA expressed a approximately 60-kD protein and bound IL-5 with a single class of affinity (Kd = 250-590 pM). The Kd values were similar to that observed in normal human eosinophils. In contrast to the murine 60-kD alpha chain, which binds IL-5 with low affinity (Kd = approximately 10 nM), the human alpha chain homologue can bind IL-5 with much higher affinity by itself. RNA blot analysis of human cells demonstrated two transcripts (approximately 5.3 and 1.4 kb). Both of them were expressed in normal human eosinophils and in erythroleukemic cell line TF-1, which responds to IL-5. The human IL-5 receptor characterized in this paper is essential for signal transduction, because expression of this molecule in murine IL-3-dependent cell line FDC-P1 allowed these cells to proliferate in response to IL-5.

Reconstitution of the functional receptors for murine and human interleukin 5.

The murine interleukin 5 receptor (mIL-5R) is composed of two distinct subunits, alpha and beta. The alpha subunit (mIL-5R alpha) specifically binds IL-5 with low affinity. The beta subunit (mIL-5R beta) does not bind IL-5 by itself, but forms the high-affinity receptor with mIL-5R alpha. mIL-5R beta has been revealed to be the mIL-3R-like protein, AIC2B which is shared with receptors for IL-3 and granulocyte/macrophage colony-stimulating factor. We demonstrated here the reconstitution of the functional receptors for murine and human IL-5 on the mouse IL-2-dependent cell line, CTLL-2. CTLL-2 was transfected with the cDNAs for mIL-5R alpha and/or AIC2B. Only CTLL-2 transfectant expressing both mIL-5R alpha and AIC2B expressed the high-affinity receptor and proliferated in response to murine IL-5. Then CTLL-2 was transfected with the cDNAs for hIL-5R alpha and/or KH97 (beta c), the human homologue of AIC2B. Though beta c did not contribute much to binding affinity of hIL-5R, only CTLL-2 transfectant expressing both hIL-5R alpha and beta c proliferated in response to human IL-5. These results showed that the beta subunit is indispensable in IL-5 signal transduction. We further investigated the function of IL-5-specific alpha subunit in transmitting IL-5 signals. Mutant mIL-5R alpha, which lacks its whole cytoplasmic domain, was transfected into mouse IL-3-dependent cell line, FDC-P1 expressing AIC2B intrinsically. The resulting transfectant did not respond to IL-5, though the transfectant expressed the high-affinity IL-5R, indicating that the cytoplasmic portion of the alpha subunit also has some important role in IL-5-mediated signal transduction.

Transgenic mice expressing a B cell growth and differentiation factor gene (interleukin 5) develop eosinophilia and autoantibody production.

Interleukin 5 (IL-5) has been suggested to be involved in the growth and differentiation of B cells and eosinophils. Especially, Ly-1+ B cells, which have been considered to produce autoantibodies, are selectively developed by this lymphokine in long-term bone marrow culture. To envisage the possible engagement of IL-5 in the development of these cells in vivo, transgenic mice carrying the mouse IL-5 gene ligated with a metallothionein promoter were generated. Transgenic mice carrying the IL-5 gene exhibited elevated levels of IL-5 in the serum and an increase in the levels of serum IgM and IgA. A massive eosinophilia in peripheral blood, bone marrow, and spleen, and an infiltration of muscle and liver with eosinophils, were observed. When cadmium-containing saline was injected intraperitoneally into transgenic mice, IL-5 production was augmented about five times within 24 h, and a distinctive Ly-1+ B cell population became apparent in the spleen after 5 d. IL-5 receptors were detected on those cells by monoclonal antibodies against IL-5 receptors. Another interesting finding in these transgenic mice was an increase in polyreactive anti-DNA antibodies of IgM class. It is suggested, therefore, that aberrant expression of the IL-5 gene may induce accumulation of Ly-1+ B cells and eosinophils. Furthermore, this IL-5 transgenic mouse can be a model mouse for eosinophilia, and we can determine the role of IL-5 in the differentiation of Ly-1+ B cells and eosinophils by using this mouse.

IL-5 receptor-mediated tyrosine phosphorylation of SH2/SH3-containing proteins and activation of Bruton's tyrosine and Janus 2 kinases.

Interleukin 5 (IL-5) induces proliferation and differentiation of B cells and eosinophils by interacting with its receptor (IL-5R) which consists of two distinct polypeptide chains, alpha and beta (beta c). Although both IL-5R alpha and beta c lack a kinase catalytic domain, IL-5 is capable of inducing tyrosine phosphorylation of cellular proteins. We investigated the role of IL-5R alpha in tyrosine phosphorylation of molecules involved in IL-5 signal transduction, using an IL-5-dependent early B cell line, Y16 and transfectants expressing intact or mutant IL-5R alpha together with intact beta c. The results revealed that the transfectants expressing truncated IL-5R alpha, which entirely lacks a cytoplasmic domain, together with beta c, showed neither protein-tyrosine phosphorylation nor proliferation in response to IL-5. This confirms that IL-5R alpha plays a critical role in protein-tyrosine phosphorylation which triggers cell growth. IL-5 stimulation results in rapid tyrosine phosphorylation of beta c and proteins containing Src homology 2 (SH2) and/or SH3 domains such as phosphatidyl-inositol-3 kinase, Shc, Vav, and HS1, suggesting their involvement in IL-5-mediated signal transduction. IL-5 stimulation significantly enhanced activities of Janus 2 and B cell-specific Bruton's tyrosine kinases (JAK2 and Btk) and increased the tyrosine phosphorylation of JAK2 kinase. These results and recent data on signaling of growth factors taken together, multiple biochemical pathways driven by tyrosine kinases such as JAK2 and Btk are involved in IL-5 signal transduction.

A critical cytoplasmic domain of the interleukin-5 (IL-5) receptor alpha chain and its function in IL-5-mediated growth signal transduction.

Interleukin-5 (IL-5) regulates the production and function of B cells, eosinophils, and basophils. The IL-5 receptor (IL-5R) consists of two distinct membrane proteins, alpha and beta. The alpha chain (IL-5R alpha) is specific to IL-5. The beta chain is the common beta chain (beta c) of receptors for IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF). The cytoplasmic domains of both alpha and beta chains are essential for signal transduction. In this study, we generated cDNAs of IL-5R alpha having various mutations in their cytoplasmic domains and examined the function of these mutants by expressing them in IL-3-dependent FDC-P1 cells. The membrane-proximal proline-rich sequence of the cytoplasmic domain of IL-5R alpha, which is conserved among the alpha chains of IL-5R, IL-3R, and GM-CSF receptor (GM-CSFR), was found to be essential for the IL-5-induced proliferative response, expression of nuclear proto-oncogenes such as c-jun, c-fos, and c-myc, and tyrosine phosphorylation of cellular proteins including JAK2 protein-tyrosine kinase. In addition, analysis using chimeric receptors which consist of the extracellular domain of IL-5R alpha and the cytoplasmic domain of beta c suggested that dimerization of the cytoplasmic domain of beta c may be an important step in activating the IL-5R complex and transducing intracellular growth signals.

Neurotoxicity and pharmacokinetics of intrathecal perfusion of ACNU in dogs.

To test the feasibility of intrathecal perfusion of ACNU (3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitro sou rea hydrochloride) in the treatment of subarachnoid dissemination of malignant glioma, the neurotoxicity and pharmacokinetics of ACNU were studied in dogs. ACNU [1-2 mg dissolved in 10-20 ml of lactated Ringer's solution or artificial cerebrospinal fluid (CSF)] was administered via the right lateral ventricle by constant drip infusion and CSF was drained by lumbar puncture. The infusion time was from 15 to 71 min. For the control, a bolus injection was given. No neurological and systemic symptoms were noted after perfusion. Histological examination of the brain and spinal cord revealed only mild denudation of ependyma in the wall of the ventricles in a dog treated three times with 2 mg ACNU (perfusion twice, bolus injection once) and in 2 dogs perfused with 1 mg ACNU once a week for 10 weeks. ACNU was not detected in lumbar CSF after bolus injection into the lateral ventricle. When 1 mg of ACNU, dissolved in 10 ml of artificial CSF, was perfused for a duration of 22 to 31 min, it started to appear in the lumbar CSF 10 to 15 min after the start of perfusion, reaching a maximum concentration of 13.88 to 22.31 micrograms/ml. The area under the drug concentration-time curve was 344 to 706 micrograms x min/ml; the half-time was 15.5 to 19.5 min. The distribution volume was 30.6 to 54.1 ml. These findings suggest the feasibility of intrathecal perfusion of ACNU in the treatment of patients with subarachnoid dissemination of glioma.

Expression vector system based on the chicken beta-actin promoter directs efficient production of interleukin-5.

We examined the promoter activity of the 1.3-kb chicken beta-actin gene sequence located between the 5' flanking region and the proximal region of the second exon. This promoter region showed higher promoter activity than the simian virus 40 (SV40) early promoter or the Rous sarcoma virus (RSV) long terminal repeat (LTR) as assayed by transient lacZ gene expression in mouse L cells. Furthermore, replacement of the 3' splice sequence in this promoter by that derived from the rabbit beta-globin gene resulted in a approximately 2.5-fold enhancement in the synthesis of beta-galactosidase (beta Gal). Introduction of the SV40 origin of DNA replication (ori) into the vector carrying this hybrid promoter, which we designate the AG promoter, markedly enhanced the production of beta Gal in an SV40 T antigen-producing cell, BMT10. We have constructed a useful vector containing the strong AG promoter, several unique restriction sites, a SV40 polyadenylation signal and the SV40 ori for transient expression of cDNA in BMT10 or COS cells. We demonstrate the use of this vector for efficient production of interleukin-5 in BMT10 cells.

Biochemical and functional characterization of soluble form of IL-5 receptor alpha (sIL-5R alpha). Development of ELISA system for detection of sIL-5R alpha.

Interleukin-5 (IL-5) mediates pleiotropic functions in various types of cells through its specific receptor (IL-5R) which is composed of two distinct subunits, alpha and beta. In mice, the alpha subunit (IL-5R alpha) specifically binds IL-5 with low affinity. The beta subunit (IL-5R beta) does not bind IL-5 by itself, but constructs the high affinity receptor with IL-5R alpha. We have isolated cDNA encoding the soluble form of IL-5R alpha (sIL-5R alpha). To elucidate the biochemical and functional properties of sIL-5R alpha, we developed an expression system for sIL-5R alpha cDNA in insect cell line Sf21 using baculovirus expression vector and obtained conditioned medium containing large quantities of mouse sIL-5R alpha. Mouse sIL-5R alpha was purified from the conditioned medium by using anti-IL-5R alpha mAb-coupled beads. Immunoaffinity-purified sIL-5R alpha with an approximate molecular mass of 42 kDa inhibited the binding of 125I-labeled IL-5 to IL-5R. By using purified sIL-5R alpha, we prepared rabbit anti-sIL-5R alpha antibody and developed a sandwich ELISA for detection of sIL-5R alpha. Significant amounts of sIL-5R alpha were detected in sera and ascitic fluids of mice bearing tumors (BCL1 and MOPC104E) that responded to IL-5 for DNA synthesis, but not in sera of normal mice. Interestingly, elevated levels of serum sIL-5R alpha were observed in NZB and NZW mice. The sIL-5R alpha may, therefore, have an immunoregulatory role in vivo.

Differentiation of glioma-cells by a pdgf-antagonist.

We previously reported that trapidil, a Platelet-derived Growth Factor (PDGF) antagonist, can inhibit the proliferation of PDGF-dependent glioma cells. In the current study, we explored the effect of trapidil on the differentiation of glioma cells by observing the morphological changes in glioma cells in control and trapidil-treated cultures under a phase contrast microscope. Most cells in the control cultures were flat, large, and irregularly shaped. On the other hand, most cells treated with trapidil formed several long cytoplasmic processes and exhibited fibrous morphology. Western blots and immunocytochemical analysis of glial fibrillary acidic protein (GFAP)-stained, trapidil-treated cultures revealed an increase in GFAP content over the control cultures. From these results we propose that trapidil induces the differentiation of glioma cells.

The murine interleukin-5 receptor alpha-subunit gene: characterization of the gene structure and chromosome mapping.

To understand better the regulation of interleukin-5 receptor alpha-subunit (IL-5R alpha) expression, we have isolated the genomic clones of mouse IL-5R alpha (mIL-5R alpha) and analyzed the structure of the gene. The gene spans more than 35 kb and is composed of 11 exons. We found that two mRNAs encoding secreted forms of mIL-5R alpha result from differential splicing events. We identified the transcriptional start site by primer extension analysis of mIL-5R alpha mRNA. Nucleotide sequence of the 5'-flanking region contains potential binding sites for transcription factor Ap1, AP-1, GATA-1, and PU.1. About 260 bp sequence of the 5'-flanking region exhibited promoter activity when it was linked to a promoterless bacterial chloramphenicol acetyltransferase (CAT) gene. The promoter activity was seen not only in the IL-5-dependent pre-B-cell line Y16, but also in fibroblast cell line NIH-3T3. Comparison of the exon-intron boundaries of mIL-5R alpha genes with those of other members of the cytokine receptor family reveals a conserved evolutionary structure. By fluorescence in situ hybridization analysis, the mIL-5R alpha gene has been assigned to chromosome 6.

Lymphoproliferative lesion of the hypoglossal nerve: case report.

A rare case of a lymphoproliferative lesion in the hypoglossal nerve is reported. The patient, a 52-year-old woman, had symptoms identical with those of hypoglossal neurinoma. Computed tomography and magnetic resonance imaging revealed a lesion at the left cerebellomedullary angle. The tumor was removed, and histopathological studies revealed that the tumor consisted predominantly of lymphocytes.

Significance of elevated thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex in the acute stage of nontraumatic subarachnoid hemorrhage.

Thrombin-antithrombin III complex (TAT) and plasmin-alpha 2-plasmin inhibitor complex (PIC) were examined in the acute stage in 51 patients with nontraumatic subarachnoid hemorrhage. TAT and PIC values were correlated with severity at the time of onset and with outcome. In the patients whose TAT levels were 25 ng/ml or more and PIC levels were 3.0 micrograms/ml or more (n = 16), only 25% had a good or fair outcome. In the patients with TAT levels less than 25 ng/ml or PIC levels less than 3.0 micrograms/ml (n = 35), on the other hand, 82.9% had a good or fair outcome. There were no significant differences in TAT and PIC levels between patients who experienced arterial spasm and those who did not. These results indicate that TAT and PIC values may reflect the severity of the brain damage induced by subarachnoid hemorrhage. It is speculated that marked coagulation and fibrinolytic disorders occur in the acute stage of subarachnoid hemorrhage.

Ventriculolumbar perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitrosou rea hydrochloride.

We report on the toxicity, intrathecal pharmacokinetics, and therapeutic effect of the ventriculolumbar perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitros our ea hydrochloride (ACNU) against the subarachnoid dissemination of primary central nervous system tumors. Fifteen patients received ventriculolumbar perfusion of ACNU. One was treated with ventriculolumbar perfusion of ACNU alone, and the others underwent concomitant systemic chemotherapy; three of these patients received irradiation as well. ACNU was administered at an initial dose of 0.5 and was increased to 1.5 to 10.0 mg in six patients. Because of a lack of Level 2 or greater toxicity, the subsequent seven patients received 8.7 to 10.0 mg of ACNU dissolved in artificial cerebrospinal fluid (CSF) at a concentration of 0.1 mg/ml, from the start of the treatment. During ACNU administration, the lumbar CSF was drained at approximately the same rate as that of the infusion. Twelve patients received from 3 to 42 courses (average, 14 courses). The cumulative dose of ACNU ranged from 5 to 330.4 mg (average, 82.9 mg). One patient had a convulsion; two patients experienced transient headache, nausea, and vomiting; two others reported transient headache, nausea, vomiting, and fecal incontinence; and one experienced transient nausea, vomiting, and fecal incontinence. No side effects were noted in the other nine patients. When 9.0 to 9.5 mg of ACNU, dissolved in 90 to 95 ml of artificial CSF, was administered for 37 to 52 min, the maximum concentration of ACNU in the lumbar CSF was 9.86 to 12.79 micrograms/ml and the area under the drug concentration-time curve was 260.8 to 502.5 micrograms.min/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Endothelial cell chemotactic factor derived from human glioma cell lines.

The authors report a study of the human umbilical vein endothelial cell chemotactic factor derived from human malignant glioma cell lines. The endothelial cell chemotactic activity of serum-free conditioned medium from cultures of U-373MG, U-251MG, or U-105MG cell lines was measured using a 48-well microchemotaxis chamber. The best response was from U-373MG, which was selected for further study. Chemotactic activity was contained in materials unadsorbed and adsorbed to the heparin-affinity column. Because the higher activity was seen in the unadsorbed material, it was used for characterization and partial isolation. The chemotactic activity was decreased under the condition of tumor protein synthesis inhibition. Heating, exposure to acid, and trypsin digestion also decreased the activity. The factor was found to be a protein with a relative molecular weight of greater than 200 kD; it has no mitogenic activity for endothelial cells in vitro and, partially purified, it was not identical to any other known endothelial cell chemotactic or mitogenic factor. Fibronectin was not detected, and anti-fibronectin antibody failed to inhibit the activity of the factor. These results suggest that malignant glioma cells produce a yet unknown endothelial cell chemotactic factor.

Satiety function of neurons containing a CCK-like substance in the dorsal parabrachial nucleus.

Glutaryl-CCK-8 (Glt-CCK-8, 16-160 pmol) suppressed food intake dose dependently when injected into the ventromedial hypothalamus (VMH) bilaterally, but not when injected unilaterally. In contrast, CCK-8 (160 and 320 pmol) did not suppress food intake when injected into the VMH bilaterally. When injected intraperitoneally, Glt-CCK-8 significantly decreased food intake at a dose of 320 pmol, though not at a dose of 160 pmol, whereas CCK-8 significantly reduced food intake even at a dose of 160 pmol. Pretreatment with proglumide, an antagonist of CCK-8, counteracted the effect on food intake of CCK-8 injected intraperitoneally, but did not influence that of Glt-CCK-8 injected either into the VMH or intraperitoneally. However, CCK-8 (800 pmol) prevented the satiety action of Glt-CCK-8 when injected into the VMH before the latter. Since a large dose of CCK-8 injected into the VMH was reported to suppress food intake, these findings suggest that, among the receptors for the satiety action of CCK, intracranial receptor has lower affinity for CCK-8 than for Glt-CCK-8 and peripheral receptor has higher affinity for CCK-8 than for Glt-CCK-8. Furthermore, bilateral lesions of the lateral part of the dorsal parabrachial nucleus (LPBD), from which the neurons containing a CCK-8-like substance extend fibers to the VMH, enhanced the satiety action of Glt-CCK-8 injected into the VMH. These results support the idea that these neurons which project to the VMH are involved in the satiety action.

Antiproliferative effect of YM881 (SMANCS) on glioma cells in vitro.

Growth inhibitory activity of YM881 (SMANCS) against 3 human cultured cell lines and one rat cultured cell line derived from glioma cells was assessed quantitatively. YM881 showed potent cytotoxicity against all glioma cell lines tested; the IC50 of this drug was 1.9-8.4 micrograms/ml. YM881 may be classified as a concentration-dependent drug but it has also a time-dependent effect. Flow cytometric studies of the DNA histogram showed accumulation in the G2-M phase with YM881. These findings suggest that YM881 may be useful in the treatment of glioma.

Occlusion of internal carotid artery and formation of anterior communicating artery aneurysm in cervicocephalic fibromuscular dysplasia--follow-up case report.

A 44-year-old female with cervicocephalic-fibromuscular dysplasia (FMD) suffered a subarachnoid hemorrhage 10 years after presenting with left impaired extraocular movement. Carotid and vertebral angiography had shown string-of-beads sign in the left external carotid artery and fusiform aneurysms in the left carotid cavernous portion and in the left vertebral artery. On admission, the left carotid angiogram showed complete occlusion of the left internal carotid artery and the right carotid angiogram showed a new anterior communicating artery aneurysm. The territory of the left middle cerebral artery was supplied from the right internal carotid artery via the anterior communicating artery and from the basilar artery via the posterior communicating artery. Occlusion of the main arteries is rare in the clinical course of FMD. We suggest that hemodynamic stress due to occlusion of the internal carotid artery contributed to formation of the anterior communicating artery aneurysm, possibly associated with intrinsic changes of the arterial wall induced by FMD.