The 100 Most-Cited Articles Focused on Ultrasound Imaging: A Bibliometric Analysis.

Purpose The number of citations that an article has received reflects its impact on a particular research area. The aim of this study was to identify the 100 most-cited articles focused on ultrasound (US) imaging and to analyze the characteristics of these articles. Methods We determined the 100 most-cited articles on US imaging via the Web of Science database, using the search term. The following parameters were used to analyze the characteristics of the 100 most-cited articles: publication year, journal, journal impact factor, number of citations and annual citations, authors, department, institution, country, type of article, and topic. Results The number of citations for the 100 most-cited articles ranged from 1849 to 341 (median: 442.0) and the number of annual citations ranged from 108.0 to 8.1 (median: 22.1). The majority of articles were published in 1990 - 1999 (39 %), published in radiology journals (20 %), originated in the United States (45 %), were clinical observation studies (67 %), and dealt with the vessels (35 %). The Department of Internal Medicine at the University of California and the Research Institute of Public Health at the University of Kuopio (n = 4 each) were the leading institutions and Salonen JT and Salonen R (n = 4 each) were the most prolific authors. Conclusion Our study presents a detailed list and analysis of the 100 most-cited US articles, which provides a unique insight into the historical development in this field.

Glutathione peroxidase 1 deficiency attenuates concanavalin A-induced hepatic injury by modulation of T-cell activation.

Concanavalin A (Con A)-induced hepatitis model is well-established experimental T cell-mediated liver disease. Reactive oxygen species (ROS) is associated with T-cell activation and proliferation, but continued ROS exposure induces T-cell hyporesponsiveness. Because glutathione peroxidase 1 (Gpx1) is an antioxidant enzyme and is involved in T-cell development, we investigated the role of Gpx1 during Con A-induced liver injury in Gpx1 knockout (KO) mice. Male wild-type (WT) mice and Gpx1 KO mice were intravenously injected with Con A (10 mg/kg), and then killed after 8 h after Con A injection. Serum levels of aspartate transaminase and alanine transaminase were measured to assess hepatic injury. To identify that Gpx1 affects T cell-mediated inflammation, we pretreated Gpx1 inhibitor to Human Jurkat T cells then treated Con A. Con A-induced massive liver damage in WT mice but its damage was attenuated in Gpx1 KO mice. Con A-induced Th1 cytokines such as tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) and interleukin (IL)-2 were also decreased in the liver and spleen of Gpx1 KO mice compared with WT mice. In Jurkat T cells, Con A-induced mRNA levels of IL-2, IFN-γ and TNF-α were downregulated by pretreatment of Gpx inhibitor, mercaptosuccinic acid. We also observed that Gpx1 KO mice showed increasing oxidative stress in the liver and spleen compared with WT mice. These results suggest that Gpx1 deficiency attenuates Con A-induced liver injury by induction of T-cell hyporesponsiveness through chronic ROS exposure.

Mucin 1-mediated chemo-resistance in lung cancer cells.

Paclitaxel (PTX) is a commonly used drug to treat diverse cancer types. However, its treatment can generate resistance and the mechanisms of PTX-resistance in lung cancers are still unclear. We demonstrated that non-small cell lung cancers (NSCLCs) survive PTX treatment. Compared with the progenitor NSCLC A549 cells, the PTX-resistant A549 cells (A549/PTX) displayed enhanced sphere-formation ability. The proportion of the cancer stem cell marker, aldehyde dehydrogenase-positive cells, and epithelial-mesenchymal transition signaling protein levels were also elevated in A549/PTX. Importantly, the levels of oncoproteins phosphoinositide-3 kinase/Akt, mucin 1 cytoplasmic domain (MUC1-C) and ß-catenin were also significantly elevated in A549/PTX. Furthermore, nuclear translocation of MUC1-C and ß-catenin increased in A549/PTX. The c-SRC protein, an activator of MUC1-C, was also overexpressed in A549/PTX. These observations led to the hypothesis that enhanced expression of MUC1-C is associated with stemness and PTX resistance in NSCLCs. To test this, we knocked down or overexpressed MUC1-C in A549/PTX and found that inhibition of MUC1-C expression coupled with PTX treatment was sufficient to reduce the sphere-forming ability and survival of A549/PTX. In summary, our in vitro and in vivo studies have revealed a potential mechanism of MUC1-C-mediated PTX resistance and provided insights into a novel therapeutic measure for lung cancers.

Percutaneous radiofrequency ablation for symptomatic uterine leiomyomas: a systematic review and meta-analysis.

PURPOSE: To evaluate the efficacy and safety of percutaneous radiofrequency ablation (RFA) in the treatment of uterine leiomyomas. MATERIALS AND METHODS: Medline, Embase, and Cochrane databases were searched through August 2014 for all relevant studies on RFA for uterine leiomyomas. The efficacy and safety of RFA were assessed using the outcome measures of tumor volume, symptom severity score, health-related quality of life (HRQL) score, procedure-related complications, and reintervention. The authors calculated pooled event rates with 95% confidence intervals using random-effects model to assess the effects of RFA. RESULTS: Eight observational studies were identified as eligible for inclusion in this meta-analysis and included 370 patients. All analyzed outcomes showed statistically significant improvements from baseline to final follow-up. Twenty-seven complications were identified and five of them qualified as major complications. Five patients required reintervention after RFA. CONCLUSIONS: Percutaneous RFA is an effective and safe treatment for patients with uterine leiomyomas.

Neurointerventional research between 2003 and 2012: slow growth, high interdisciplinary collaboration, and a low level of funding.

BACKGROUND AND PURPOSE: Neurointerventional therapy of cerebrovascular disease is a greatly expanding field across many specialty disciplines. The goal of this study was to analyze the characteristics and trends of scientific publications that focused on neurointervention during the past decade. MATERIALS AND METHODS: A bibliometric evaluation of neurointerventional research published between 2003 and 2012 was conducted by using the PubMed data base. Analyzed parameters included the year of publication, type of document, language of the article, topic, declared funding, country of origin, type of collaboration between disciplines, the first author's specialty, and subject category and the Impact Factor of the publishing journal. RESULTS: Between 2003 and 2012, a total of 2123 articles were published, of which 1107 (52.1%) were original articles, 1948 (91.8%) were written in English, 192 (9.0%) received funding, 661 (31.1%) were published by the United States, and 1060 (49.9%) resulted from interdisciplinary collaboration. Neurosurgery departments produced the most articles (n = 910, 42.9%), followed by radiology (n = 747, 35.2%) and neurology (n = 270, 12.7%). The time-trend analysis in the number of publications demonstrated slow growth from 2003 to 2012, with an average annual growth rate of +6.0%. CONCLUSIONS: The fields of neurosurgery, radiology, and neurology have contributed substantially to neurointervention research. Slow growth, high interdisciplinary collaboration, and a low level of funding are peculiar characteristics of research in this field.

Loss of presenilin 2 is associated with increased iPLA2 activity and lung tumor development.

Presenilins are the enzymatic components of γ-secretase complex that cleaves amyloid precursor protein, Notch and ß-catenin, which has critical roles in the development of Alzheimer's disease and cancer cell growth. Therefore, in the present study, we studied the effects and mechanisms of PS2 knockout on lung cancer development and possible mechanisms as a key regulator of lung tumor development. We compared carcinogen-induced tumor growth between PS2 knockout mice and wild-type mice. PS2 knockout mice showed increased urethane (1 mg/g)-induced lung tumor incidence when compared with that of wild-type mice with decreased activity of γ-secretase in the lung tumor tissues. Consequently, iPLA2 activities in lung tumor tissues of PS2 knockout mice were much higher than in tumor tissues of wild-type mice. Furthermore, knockdown of PS2 using PS2 siRNA decreased γ-secretase activity with increased iPLA2 activity in the lung cancer cells (A549 and NCI-H460), leading to increased lung cancer cell growth. PS2 knockout mice and PS2 knockdown lung cancer cells showed increased DNA-binding activities of nuclear factor kappa-beta, signal transducer and activator of transcription 3 (STAT3) and AP-1 which are critical transcriptional factors of iPLA2 than those of PS2 wild-type mice and control lung cancer cells. Taken together, these results suggest that the loss of PS2 could have a critical role in lung tumor development through the upregulation of iPLA2 activity by reducing γ-secretase.

Discrepancy between preoperative MRI evaluation and intraoperative or postoperative pathological findings for the extent of local invasion in maxillary squamous cell carcinoma.

Preoperative radiological evaluation of the extent of local invasion in maxillary squamous cell carcinoma (SCC) is very important in planning curative surgery. The aim of this study was to examine the accuracy of preoperative radiological evaluation with magnetic resonance imaging (MRI) for the extent of local invasion in maxillary SCC. A retrospective study was conducted of 33 patients who underwent a maxillectomy for maxillary SCC. We compared the MRI findings for 18 structures around the maxillary sinus with intraoperative or postoperative pathological findings. Discrepancies were found between preoperative MRI findings and intraoperative or postoperative pathological findings for 22 patients (66.7%). Overall, the specificity, sensitivity, positive predictive value, and negative predictive value of MRI were 83.4%, 83.0%, 64.5%, and 90.4%, respectively. The receiver operating characteristic curve showed that MRI evaluation of the posterolateral structures including the pterygoid plate, pterygoid muscle, and infratemporal fossa had a lower area under the curve (0.614) and a significantly lower accuracy when compared with the other structures (P = 0.294, 95% confidence interval 0.405-0.822). In conclusion, as the accuracy of preoperative MRI evaluation of the posterolateral structures is low, careful evaluation of local extension to the posterolateral structures is needed when planning curative surgery for maxillary SCC.

Cystatin SN neutralizes the inhibitory effect of cystatin C on cathepsin B activity.

Cystatin SN (CST1) is one of the several salivary cystatins that form tight equimolar complexes with cysteine proteases, such as the cathepsins. High expression of CST1 is correlated with advanced pTNM stage in gastric cancer. However, the functional role of CST1 in tumorigenesis has not been elucidated. In this study, we showed that CST1 was highly expressed in colon tumor tissues, compared with nontumor regions. Increased cell proliferation and invasiveness were observed in HCT116 cell lines stably transfected with CST1 cDNA (HCT116-CST1) but not in CST3-transfected cells. We also demonstrated that CST1-overexpressing cell lines exhibited increased tumor growth as well as metastasis in a xenograft nude mouse model. Interestingly, CST1 interacted with cystatin C (CST3), a potent cathepsin B (CTSB) inhibitor, with a higher affinity than the interaction between CST3 and CTSB in the extracellular space of HCT116 cells. CTSB-mediated cellular invasiveness and proteolytic activities were strongly inhibited by CST3, but in the presence of CST1 CTSB activities recovered significantly. Furthermore, domain mapping of CST1 showed that the disulfide-bonded conformation, or conserved folding, of CST1 is important for its secretion and for the neutralization of CST3 activity. These results suggest that CST1 upregulation might be involved in colorectal tumorigenesis and acts by neutralizing the inhibition of CTSB proteolytic activity by CST3.

Antitumor activity of IL-32ß through the activation of lymphocytes, and the inactivation of NF-κB and STAT3 signals.

Cytokine and activation of lymphocytes are critical for tumor growth. We investigated whether interleukin (IL)-32ß overexpression changes other cytokine levels and activates cytotoxic lymphocyte, and thus modify tumor growth. Herein, IL-32ß inhibited B16 melanoma growth in IL-32ß-overexpressing transgenic mice (IL-32ß mice), and downregulated the expressions of anti-apoptotic proteins (bcl-2, IAP, and XIAP) and cell growth regulatory proteins (Ki-67 antigen (Ki-67) and proliferating cell nuclear antigen (PCNA)), but upregulated the expressions of pro-apoptotic proteins (bax, cleaved caspase-3, and cleaved caspase-9). IL-32ß also inhibited colon and prostate tumor growth in athymic nude mice inoculated with IL-32ß-transfected SW620 colon or PC3 prostate cancer cells. The forced expression of IL-32ß also inhibited cell growth in cultured colon and prostate cancer cells, and these inhibitory effects were abolished by IL-32 small interfering RNA (siRNA). IL-10 levels were elevated, but IL-1ß, IL-6, and tumor necrosis factor-alpha (TNF-α) levels were reduced in the tumor tissues and spleens of IL-32ß mice, and athymic nude mice. The number of cytotoxic T (CD8(+)) and natural killer (NK) cells in tumor tissues, spleen, and blood was significantly elevated in IL-32ß mice and athymic nude mice inoculated with IL-32ß-transfected cancer cells. Constituted activated NF-κB and STAT3 levels were reduced in the tumor tissues of IL-32ß mice and athymic nude mice, as well as in IL-32ß-transfected cultured cancer cells. These findings suggest that IL-32ß inhibits tumor growth by increasing cytotoxic lymphocyte numbers, and by inactivating the NF-κB and STAT3 pathways through changing of cytokine levels in tumor tissues.

4-O-methylhonokiol, a PPARγ agonist, inhibits prostate tumour growth: p21-mediated suppression of NF-κB activity.

BACKGROUND AND PURPOSE: The effects of 4-O-methylhonokiol (MH), a constituent of Magnolia officinalis, were investigated on human prostate cancer cells and its mechanism of action elucidated. EXPERIMENTAL APPROACH: The anti-cancer effects of MH were examined in prostate cancer and normal cells. The effects were validated in vivo using a mouse xenograft model. KEY RESULTS: MH increased the expression of PPARγ in prostate PC-3 and LNCap cells. The pull-down assay and molecular docking study indicated that MH directly binds to PPARγ. MH also increased transcriptional activity of PPARγ but decreased NF-κB activity. MH inhibited the growth of human prostate cancer cells, an effect attenuated by the PPARγ antagonist GW9662. MH induced apoptotic cell death and this was related to G(0) -G(1) phase cell cycle arrest. MH increased the expression of the cell cycle regulator p21, and apoptotic proteins, whereas it decreased phosphorylation of Rb and anti-apoptotic proteins. Transfection of PC3 cells with p21 siRNA or a p21 mutant plasmid on the cyclin D1/ cycline-dependent kinase 4 binding site abolished the effects of MH on cell growth, cell viability and related protein expression. In the animal studies, MH inhibited tumour growth, NF-κB activity and expression of anti-apoptotic proteins, whereas it increased the transcriptional activity and expression of PPARγ, and the expression of apoptotic proteins and p21 in tumour tissues. CONCLUSIONS AND IMPLICATION: MH inhibits growth of human prostate cancer cells through activation of PPARγ, suppression of NF-κB and arrest of the cell cycle. Thus, MH might be a useful tool for treatment of prostate cancer.

Extraskeletal myxoid chondrosarcoma of the neck.

Extraskeletal myxoid chondrosarcoma is a rare malignant soft-tissue tumour that is typically in the deep soft tissues of the lower extremity. The tumour is usually a well-defined, multinodular soft-tissue mass without calcifications. A 62-year-old woman with a history of nasopharyngeal cancer presented with a palpable mass in the anterior neck. Radiologically, the lesion was a well-defined soft-tissue mass with the extensive calcifications on various imaging examinations. Although this lesion was histopathologically diagnosed as extraskeletal myxoid chondrosarcoma, the unusual imaging findings were challenging and very intriguing.

Imaging features of intradural spinal paragonimiasis: a case report.

Spinal paragonimiasis is a rare form of ectopic infestation caused by Paragonimus westermani. We report a case of pathologically proven intradural paragonimiasis associated with concurrent intracranial involvement. MRI revealed multiple well-defined intradural masses that were markedly hypointense on T(2) weighted images and hypointense with a peripheral hyperintense rim on T(1) weighted images. Contrast-enhanced T(1) weighted images showed slight peripheral rim enhancement.

IL-32γ inhibits cancer cell growth through inactivation of NF-κB and STAT3 signals.

Several studies have shown physiological functions of interleukin (IL)-32, a novel cytokine. However, the role of IL-32 in cancer development has not been reported. In this study, we showed that IL-32γ inhibited tumor growth in IL-32γ-overexpressing transgenic mice inoculated with melanoma as well as colon tumor growth in xenograft nude mice inoculated with IL-32γ-transfected colon cancer cells (SW620). The inhibitory effect of IL-32γ on tumor growth was associated with the inhibition of constitutive activated nuclear transcription factor-κB (NF-κB) and of signal transducer and activator of transcription 3 (STAT3). The expression of antiapoptotic, cell proliferation and tumor-promoting genes (bcl-2, X-chromosome inhibitor of apoptosis protein (IAP), cellular IAP and cellular FADD-like IL-1ß-converting enzyme-inhibitory protein, cyclin D), cyclin-dependent kinase 4, cycolooxygenase-2 and inducible nitric oxide synthase was decreased, whereas the expression of apoptotic target genes (caspase-3 and -9, bax) increased. In tumor, spleen and blood, the number of cytotoxic CD8(+) T cells and CD57(+) natural killer cells and the levels of IL-10 increased, but that of tumor necrosis factor-α (TNF-α), IL-1ß and IL-6 decreased. We also found that forced overexpression of IL-32γ inhibited colon cancer cell (SW620 and HCT116) growth accompanied with the inhibition of activated NF-κB and STAT3 in vitro. In addition, when IL-32γ was knocked down by small interfering RNA (siRNA) or neutralized with an anti-IL-32γ antibody, IL-32γ-induced colon cancer cell growth inhibition, the IL-32γ-induced decrease of TNF-α, IL-1 and IL-6 production, and the increase of IL-10 production were abolished. However, siRNA of NF-κB and STAT3 augmented IL-32γ-induced colon cancer cell growth inhibition. These findings indicate significant pathophysiological roles of IL-32γ in cancer development.

Asarone inhibits adipogenesis and stimulates lipolysis in 3T3-L1 adipocytes.

Asarone is a molecule found in certain plants such as Acorus calamus, the root of which is used in traditional medicine to treat diabetes. We determined the molecular mechanism underlying the anti-diabetic activity of asarone. Treatment of asarone significantly inhibited the differentiation of 3T3-L1 preadipocytes through suppression of expression of the transcription factors, CCAAT/enhancer binding protein-alpha and peroxisome proliferator activated receptor-gamma, which activate adipogenesis. Intracellular triglyceride levels were reduced by asarone in a dose-dependent manner and asarone treatment stimulated the phosphorylation of hormone-sensitive lipase. Together, the present findings indicate that asarone inhibits adipogenesis by down-regulation of PPARgamma and C/EBPalpha and reduces lipid accumulation by stimulation of lipolysis through an increase in hormone-sensitive lipase activity.

Aryl hydrocarbon nuclear translocator (hypoxia inducible factor 1beta) activity is required more during early than late tumor growth.

c4 is a derivative of the mouse hepatoma cell line, Hepa-1, that harbors a mutation in the aryl hydrocarbon receptor nuclear translocator gene (Arnt, or hypoxia inducible factor 1beta [HIF-1beta]) leading to loss of activity. Clone 3 cells were generated by introducing a doxycycline-repressible Arnt expression vector into c4 cells. Clone 3 cells were injected subcutaneously into immunosuppressed mice, which were treated with doxycyline (a) throughout the growth of the subsequent tumor xenografts, or (b) from day 7 through to the end of the experiment (day 30), or not treated (c). Tumors in all groups grew exponentially between days 14 and 30, and at rates that were indistinguishable from each other. However, tumors in group a were smaller than those of the other two groups throughout the measurable growth period, while tumor volumes in groups b and c were not significantly different from each other. The degrees of vascularity and apoptosis did not correlate with the differences in degrees of growth between the different groups. Thus, Arnt is required during the early stages of growth of the tumors but less in later stages. Since Arnt does not detectably effect the growth kinetics of Hepa-1 cells either during hypoxia or normoxia, this requirement is unlikely to reflect a direct effect of Arnt on cell proliferation, and is therefore probably a consequence of altered interaction(s) between the tumor cells and the host. These studies suggest that Arnt (and HIF-1alpha/HIF-2alpha) inhibitors will be particularly effective against smaller tumors, including micrometastases.

Multidetector row CT angiography in spontaneous lobar intracerebral hemorrhage: a prospective comparison with conventional angiography.

BACKGROUND AND PURPOSE: The aim of our study was to assess the accuracy of multidetector row CT angiography (MDCTA) in the detection of the underlying vascular abnormalities causing spontaneous lobar intracerebral hemorrhage (ICH) compared with conventional digital subtraction angiography (DSA). MATERIALS AND METHODS: Seventy-eight patients who underwent MDCTA with use of a 16-detector row scanner and DSA were prospectively included in this study. Each study was assessed by 2 independent blinded neuroradiologists; decisions were made in consensus. Findings on CT angiograms, including the original axial data, multiplanar reformations, and volume-rendered images with and without automated bone segmentation, were used to identify the underlying causes of ICH. RESULTS: Twenty-two of the 78 patients (28.2%) exhibited angiographic abnormalities, including aneurysms of the proximal arteries (n = 9), arteriovenous malformations (n = 7), Moyamoya disease (n = 4), and aneurysms of the distal arteries (n = 2). MDCTA detected the underlying vascular abnormalities in 21 patients except 1 case of small arteriovenous malformation. Overall sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of MDCTA for detection of underlying vascular abnormalities were 95.5%, 100%, 100%, 98.2%, and 98.7%, respectively. CONCLUSIONS: MDCTA is a highly accurate imaging technique in the diagnosis of underlying vascular abnormalities in patients with spontaneous lobar ICH.

Caspase-3 activation as a key factor for HBx-transformed cell death.

OBJECTIVES: Nuclear factor-kappa B (NF-kappaB) activation has been associated with the tumorigenic growth of hepatitis B virus X protein (HBx)-transformed cells. This study was aimed to find a key target for treatment of HBx-mediated cancers. MATERIALS AND METHODS: NF-kappaB activation, endoplasmic reticulum-stress (ER-stress), caspase-3 activation, and cell proliferation were evaluated after Chang/HBx cells permanently expressing HBx viral protein were treated with inhibitors of NF-kappaB, proteasome and DNA topoisomerase. RESULTS: Inhibition of NF-kappaB transcriptional activity by transient transfection with mutant plasmids encoding Akt1 and glycogen synthase kinase-3beta (GSK-3beta), or by treatment with chemical inhibitors, wortmannin and LY294002, showed little effect on the survival of Chang/HBx cells. Furthermore, IkappaBalpha (S32/36A) mutant plasmid or other NF-kappaB inhibitors, 1-pyrrolidinecarbonidithioic acid and sulphasalazine, were also shown to have little effect on the cell proliferation. By contrast, proteasome inhibitor-1 (Pro1) and MG132 enhanced the HBx-induced ER-stress response and the subsequent activation of caspase-12, -9 and -3 and reduced cell proliferation. Camptothecin (CPT), however, triggered activation of caspase-3 without induction of caspase-12, and reduced cell proliferation. In addition, CPT-induced cell death was reversed by pre-treatment with z-DEVD, a caspase-3-specific inhibitor. CONCLUSIONS: Detailed exploitation of the regulators of caspase-3 activation could open the gate for finding an efficient target for development of anticancer therapeutics against HBx-transformed hepatocellular carcinoma.

Protective effect of oxidative stress in HaCaT keratinocytes expressing E7 oncogene.

In a previous study, we established a stable cell line which constitutively expresses E7 in HaCaT human keratinocyte cell line and identified various relevant factors including oxygen modulators affected by the E7 oncogene. E7-expressing HaCaT cells (HaCaT/E7) appeared to be more resistant to H2O2-induced cell death. Here, we demonstrate how E7 oncogene would modulate oxidative stress-induced cell death. In addition, we verified the increased expression of catalase in the HaCaT/E7 by Western blot analysis. The results suggest that the E7 oncogene would induce higher resistance to ROS-induced cell injury in the E7-infected cells via the upregulation of catalase. To investigate these paradoxical effects of high concentrations of H2O2 (500 microM-1 mM), we examined their effects on receptor mediated apoptosis, cell death via the mitochondrial pathway and modulation of apoptosis related factors. Our results revealed that HaCaT keratinocytes infected with HPV 16 E7 oncogene modulated expressions of catalase, Bcl-xL, IL-18, Fas, Bad, and cytochrome c as well as NF-kappaB, resulting in the resistance to oxidative stress-induced cell death.

Detection and characterization of intracranial aneurysms with 16-channel multidetector row CT angiography: a prospective comparison of volume-rendered images and digital subtraction angiography.

BACKGROUND AND PURPOSE: The aim of our study was to compare multidetector row CT angiography (MDCTA) with digital subtraction angiography (DSA) in the detection and characterization of intracranial aneurysms. MATERIALS AND METHODS: In our blinded prospective study, 85 patients with suspected intracranial aneurysm (47 women, 38 men; age range, 19-83 years) underwent both 16-channel MDCTA and DSA. The MDCT angiograms were interpreted for the presence, location, size, ratio of the neck to the dome (N/D ratio), and lobularity of the aneurysms and relationship of the aneurysm with the adjacent arterial branches, by using volume-rendering techniques. MDCTA and DSA images (reference standard) were interpreted by 2 independent readers, and the results were compared. RESULTS: A total of 93 aneurysms were detected at DSA in 71 patients, whereas no aneurysms were detected in 14 patients. Compared with DSA, the overall sensitivity, specificity, and accuracy of MDCTA on a per-aneurysm basis were 92.5%, 93.3%, and 92.6%, respectively, for both independent readers. For aneurysms of <3 mm, however, MDCTA had a sensitivity of 74.1% for reader 1 and 77.8% for reader 2. There was excellent agreement between readers in the detection of aneurysms (kappa = 0.822). In addition, MDCTA was also accurate in determining N/D ratio of aneurysms, aneurysm lobularity, and adjacent arterial branches. CONCLUSION: MDCTA is accurate in the detection and characterization of intracranial aneurysms and can be used as a reliable alternative imaging technique to DSA in selected cases.