Elevated MTSS1 expression associated with metastasis and poor prognosis of residual hepatitis B-related hepatocellular carcinoma.

BACKGROUND: Hepatectomy generally offers the best chance of long-term survival for patients with hepatocellular carcinoma (HCC). Many studies have shown that hepatectomy accelerates tumor metastasis, but the mechanism remains unclear. METHODS: An orthotopic nude mice model with palliative HCC hepatectomy was performed in this study. Metastasis-related genes in tumor following resection were screened; HCC invasion, metastasis, and some molecular alterations were examined in vivo and in vitro. Clinical significance of key gene mRNA expression was also analyzed. RESULTS: Metastasis suppressor 1 (MTSS1) located in the central position of gene function net of residual HCC. MTSS1 was up-regulated in residual tumor after palliative resection. In hepatitis B-related HCC patients undergone palliative hepatectomy, those with higher MTSS1 mRNA expression accompanied by activation of matrix metalloproteinase 2 (MMP2) in residual HCC, had earlier residual HCC detection after hepatectomy and poorer survival when compared to those with lower MTSS1. In different cell lines, the levels of MTSS1 mRNA increased in parallel with metastatic potential. MTSS1 down regulation via siRNA decreased MMP2 activity, reduced invasive potentials of HCC by 28.9 % in vitro, and averted the deteriorated lung metastatic extent in vivo. CONCLUSIONS: The poor prognosis of hepatitis B-related HCC patients following palliative hepatectomy associates with elevated MTSS1 mRNA expression; therefore, MTSS1 may provide a new research field for HCC diagnosis and treatment.

Autoimmune pancreatitis and non-necrotizing acute pancreatitis: computed tomography pattern.

OBJECTIVES: To retrospectively differentiate diffuse autoimmune pancreatitis from non-necrotizing acute pancreatitis at clinical onset with multi detector row computed tomography. METHODS: 36 Patients suffering from diffuse autoimmune pancreatitis (14) or non-necrotizing acute pancreatitis (22) were enrolled. Qualitative analysis included stranding, retroperitoneal fluid film, capsule-like rim enhancement and pleural effusion. In quantitative analysis pancreatic density was measured in all phases. The vascularization behaviour was assessed using the relative enhancement rate across all phases. RESULTS: Pancreatic density resulted lower in non-necrotizing acute pancreatitis compared to diffuse autoimmune pancreatitis patients in pre-contrast phase and higher in pancreatic phase. Relative enhancement rate evaluation confirmed different vascularization behaviours of the two diseases. Only non-necrotizing acute pancreatitis Patients presented peripancreatic stranding and fluid in the retromesenteric interfascial plane. CONCLUSIONS: Multi detector row computed tomography is a useful technique for differentiating diffuse autoimmune pancreatitis from non-necrotizing acute pancreatitis at clinical onset. Peripancreatic stranding and retroperitoneal fluid film, characteristic of non-necrotizing acute pancreatitis, and late-phase peripheral rim enhancement, characteristic of diffuse autoimmune pancreatitis, provide qualitative clues to the differentiation. A quantitative study of contrast enhancement patterns, considering the relative enhancement rate, can assist in the differential diagnoses of two diseases.

Early formative stage of human focal cortical gyration anomalies: fetal MRI.

OBJECTIVE: Limited information is available about the development of focal cortical gyration anomalies in the human brain. Using prenatal MRI, we characterized focal cortical gyration anomalies at an early formative stage and sought clues about the mechanisms of their development. MATERIALS AND METHODS: From a large prenatal MRI database, 30 cases (gestational age, ≤ 24 weeks) with reported focal distortion of the cortical rim profile were selected. Eight cases were matched with histologic examinations; another seven had prenatal MRI, MRI autopsy, or postnatal MRI follow-up; and 15 had no follow-up but did present analogous abnormal cortical features. Focal cortical gyration anomalies were detectable when the brain was still smooth (i.e., physiological lissencephaly). RESULTS: Four patterns of cortical plate anomaly were identified: wartlike (11 cases), abnormal invaginating sulcus (11 cases), sawtooth (six cases), and single or multiple bumps (two cases). A thinned or blurred subplate and intermediate zone in the focal cortical gyration anomaly site was detected in 80% of cases. All but two cases had other intracranial anomalies. Seven cases were classified as hypoxic-ischemic, five as genetic, and three as infective. In 15 cases, the cause could not be established. In five fetuses with further intrauterine or postnatal MRI, focal cortical gyration anomalies increased in complexity, fulfilling postnatal imaging criteria of polymicrogyria. CONCLUSION: Focal cortical gyration anomalies can be detected at the early sulcation process stage. The process leading to abnormal gyration may evolve faster than physiologic ones and seems to be related to alterations of parenchymal layering occurring before 24 weeks' gestation. Most focal cortical gyration anomalies evolve toward what is currently considered polymicrogyria.

Fetal MRI features related to the Chiari malformations.

Fetal magnetic resonance (MR) imaging may add to ultrasonography some valuable information in the assessment of Chiari malformations during their developmental stage. In Chiari type I, MR imaging role seems mainly related to research on pathophysiology issues rather than to real clinical applications. Some Chiari type II features may be better characterized in utero by MR imaging: such as the degree of downward displacement of cerebellum, possible abnormal signal changes within brain parenchyma and the type of meningocele (covered or uncovered).