The incidence of detection of accessory hepatic vein (AHV) using MRI or CT has been reported. However, previous studies had a small sample size or only reported on the incidence of hepatic vein variants. To the best of our knowledge, there has been no previous report evaluating the factors predictive of the presence of an AHV. To evaluate the incidence and morphology of the accessory hepatic vein (AHV) using multidetector row computed tomography (MDCT) and to investigate the factors which may be helpful in predicting the presence of an AHV. We enrolled 360 patients who underwent abdominal MDCT. We investigated whether the AHV was present and evaluated the frequency of AHVs greater than 5 mm in diameter. We classified the morphology of the AHV entering the inferior vena cava (IVC). We also examined the factors that predicted the presence of an AHV by comparing the diameter of the middle hepatic vein (MHV) and the right hepatic vein (RHV). We identified an AHV in 164 of the 360 patients (45.6 %). Among the 164 AHVs, 56.7 % were larger than 5 mm in diameter. The most common morphologies of the inferior RHV were a single main trunk (58.5 %), followed by two main trunks with a V-shape (19.5 %) and two trunks entering the IVC separately (17.0 %). The possibility that an AHV will be present was significantly higher when the diameter of the RHV was smaller than that of the MHV. MDCT can provide important information regarding AHV incidence and morphology. The possibility of an AHV being present was significantly higher when the diameter of the RHV was smaller than that of the MHV.

Se ha informado de la incidencia de la detección de la vena hepática accesoria (VHA) mediante RM o TC. Sin embargo, estudios previos tenían un tamaño muestral pequeño o solo informaban sobre la incidencia de variantes de las venas hepáticas. Hasta donde sabemos, no ha habido ningún informe previo que evalúe los factores predictivos de la presencia de una VHA. El objetivo del estudio fue evaluar la incidencia y morfología de la vena hepática accesoria (VHA) mediante tomografía computarizada multidetector (TCMD) e investigar los factores que pueden ser útiles para predecir la presencia de un VHA. Se evaluaron 360 pacientes que se sometieron a TCMD abdominal. Se investigó si la VHA estaba presente y se evaluó la frecuencia de VHA mayores de 5 mm de diámetro. Se clasificó la morfología del VHA que drenaba en la vena cava inferior (VCI). Además, se examinaron los factores que predijeron la presencia de una VHA mediante la comparación del diámetro de la vena hepática media (VHM) y la vena hepática derecha (VHD). Se identificó un VHA en 164 de los 360 pacientes (45,6%). Entre las 164 VHA, el 56,7% tenía más de 5 mm de diámetro. Las morfologías más frecuentes del VHD inferior fueron un tronco principal único (58,5%), seguido por dos troncos principales con forma de V (19,5%) y dos troncos que drenaban en la VCI por separado (17,0%). La posibilidad de que una VHA esté presente fue significativamente mayor cuando el diámetro de la VHD era menor que la de la VHM. La MDCT puede proporcionar información importante sobre la incidencia de la VHA y su morfología. La posibilidad de que un VHA estuviera presente era significativamente mayor cuando el diámetro del VHD era menor que la VHM.

Abstract Background Pathologic vascular smooth muscle cell (VSMC) proliferation and migration after vascular injury promotes the development of occlusive vascular disease. Therefore, an effective chemical agent to suppress aberrant proliferation and migration of VSMCs can be a potential therapeutic modality for occlusive vascular disease such as atherosclerosis and restenosis. To find an anti-proliferative chemical agent for VSMCs, we screened an in-house small molecule library, and the selected small molecule was further validated for its anti-proliferative effect on VSMCs using multiple approaches, such as cell proliferation assays, wound healing assays, transwell migration assays, and ex vivo aortic ring assay. Results Among 43 initially screened small molecule inhibitors of kinases that have no known anti-proliferative effect on VSMCs, a spleen tyrosine kinase (Syk) inhibitor (BAY61-3606) showed significant anti-proliferative effect on VSMCs. Further experiments indicated that BAY61 attenuated the VSMC proliferation in both concentration- and time-dependent manner, and it also significantly suppressed the migration of VSMCs as assessed by both wound healing assays and transwell assays. Additionally, BAY61 suppressed the sprouting of VSMCs from endothelium-removed aortic rings. Conclusion The present study identified a Syk kinase inhibitor as a potent VSMC proliferation and migration inhibitor and warrants further studies to elucidate its underlying molecular mechanisms, such as its primary target, and to validate its in vivo efficacy as a therapeutic agent for restenosis and atherosclerosis.

OBJETIVO: Descrever os achados de imagem de RM no hemangioma hepático com realce perilesional. MATERIAIS E MÉTODOS: Realizou-se uma pesquisa no banco de dados da unidade de RM para identificar todos os casos de hemangioma hepático com realce perilesional entre março de 2008 e julho de 2009. Todos os pacientes foram submetidos a RM pré-contraste em imagens ponderadas em T1 e T2 e em imagens dinâmicas após injeção de gadolínio. Características do hemangioma e do realce perilesional foram avaliadas nas imagens de RM. RESULTADOS: Sete hemangiomas em sete pacientes (cinco homens, duas mulheres; faixa etária entre 41-69 anos; média de 57 anos) foram incluídos no presente estudo. O tamanho das lesões variou de 7 a 20 mm (média de 12,4 mm). Na fase dominante arterial hepática, todos os sete hemangiomas mostraram realce perilesional cuneiforme que se atenuou nas imagens dois minutos após injeção de gadolínio. Quatro dessas lesões demonstraram realce capsular adjacente. CONCLUSÃO: Todos os hemangiomas hepáticos com realce perilesional eram lesões capsulares medindo menos que 2 cm. Tal localização sugere que esses hemangiomas podem recrutar vasos capsulares responsáveis pelo realce perilesional

OBJECTIVE: To describe the MR imaging features of hepatic hemangioma with perilesional enhancement. MATERIALS AND METHODS: A search was performed of the MRI section database to identify all cases of hepatic hemangioma with perilesional enhancement between March 2008 and July 2009. All patients underwent MR examinations including precontrast T1- and T2-weighted images and postgadolinium dynamic images. On MR images, characteristics of the hemangioma and perilesional enhancement were evaluated. RESULTS: Seven hemangiomas in seven patients (five men, two women; age range, 41-69 years; mean, 57 years) were included in this study. Lesion size ranged from 7 to 20 mm (mean, 12.4 mm). On hepatic arterial dominant phase, all seven hemangiomas exhibited wedge-shaped perilesional enhancement which faded on two minutes postgadolinium images. Four of these lesions demonstrated adjacent capsular enhancement. CONCLUSION: All hepatic hemangiomas with perilesional enhancement were < 2 cm capsule-based lesions. This location suggests that these hemangiomas may conscript capsular vessels to account for the perilesional enhancement

Tumor cells are often found under hypoxic conditions due to the rapid outgrowth of their vascular supply, and, in order to survive hypoxia, these cells induce numerous signaling factors. Akt is an important kinase in cell survival, and its activity is regulated by the upstream phosphoinositide 3-kinase (PI3K) and receptor tyrosine kinases (RTKs). In this study, we examined Akt activation and RTKs/PI3K/Akt signaling using the hypoxia-mimetic cobalt chloride in oral squamous carcinoma cells. Cobalt chloride increases Akt phosphorylation in both a dose- and time-dependent manner. Blocking the activation of the PI3K/Akt pathway using LY294002 abolished Akt activation in response to cobalt chloride, suggesting that Akt phosphorylation by cobalt chloride is dependent on PI3K. In addition, activation of the PI3K/Akt pathway seems to rely on the epidermal growth factor receptor (EGFR), since the inhibition of EGFR attenuated cobalt chloride-induced Akt activation. The results in this study also demonstrate that cobalt chloride increases EGFR protein levels and induces oral squamous cell carcinoma cells to enter S phase.