Perfusion contributes to the ADCs of abdominal organs and hepatic lesions. The D and f values are useful for the characterization of hepatic lesions.

Objective: The clinical significance of microRNA-21 (miR-21) and miR-155 in colorectal cancer (CRC) patients remains elusive. In this study, we established the prognostic value of miR-21 and miR-155 using clinical samples from CRC patients. Furthermore, relationships between these microRNAs and target genes (PDCD4 and TP53INP1 mRNAs) were examined. Methods: miR-21 and miR-155 expression was assessed in tumor tissue and in adjacent normal tissue of 156 CRC patients by TaqMan MicroRNA assays, and PDCD4 and TP53INP1 mRNA levels were measured by quantitative real-time reverse transcriptase PCR (RT-PCR). Results: High miR-21 expression was significantly associated with venous invasion, liver metastasis and tumor stage, and high miR-155 expression was significantly correlated with lymph node metastases. The overall (OS) and disease-free survival (DFS) rates of patients with high miR-21 expression were significantly worse than those of patients with low miR-21 expression. The OS and DFS of patients with high miR-155 expression were also significantly worse than those in patients with low miR-155 expression. miR-21 and miR-155 expression levels in CRC tissue were independent prognostic factors for OS and DFS. Significant inverse correlations were demonstrated between miR-21 and PDCD4 mRNA, and miR-155 and TP53INP1 mRNA. Conclusion: Increases in miR-21 and miR-155 expression may represent effective biomarkers for the prediction of a poor prognosis.

Objective. MicroRNA, a class of noncoding RNA, play a role in human diseases. MicroRNA-146a (miR146a) is a negative regulator of immune and inflammatory responses, and is strongly expressed in rheumatoid arthritis (RA) synovium and peripheral blood mononuclear cells (PBMCs). This study was undertaken to examine whether miR-146a expression inhibits osteoclastogenesis, and whether administration of miR-146a prevents joint destruction in mice with collagen-induced arthritis (CIA).Methods. PBMCs from healthy volunteers were isolated and seeded in culture plates. The following day, double-stranded miR-146a was transfected and cultured in the presence of macrophage colony-stimulating factor and either tumor necrosis factor ␣ or RANKL. After 3 weeks, tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells were counted. Three days after miR-146a culture, the expression of c-Jun, nuclear factor of activated T cells c1 (NF-ATc1), PU.1, and TRAP was evaluated by quantitative reverse transcriptase-polymerase chain reaction. After the onset of distinct arthritis in mice with CIA, doublestranded miR-146a or nonspecific double-stranded RNA was administered twice by intravenous injection. Radiographic and histologic examinations were performed at 4 weeks.

Purpose:To evaluate the use of apparent diffusion coefficient (ADC) measurements based on diffusion-weighted MRI (DWI) to assess stage of liver disease. Materials and Methods:A total of 31 patients who underwent both a liver biopsy and DWI and 132 patients who only underwent DWI were enrolled. Biopsy specimens were scored for fibrosis and necroinflammation according to the Knodell histology activity index (HAI). The 31 patients consisted of 21 patients with chronic hepatitis and 10 with cirrhosis (ChildPugh stage A in nine and stage B in one), and the 132 patients consisted of 56 patients with cirrhosis (Child-Pugh stage A in 41, stage B in 10, and stage C in five), 42 with chronic hepatitis, and 34 with normal liver function. The ADCs in the liver parenchyma were measured using DWI with relatively low b factors (b ϭ 0.01 and 128.01 seconds/mm 2 ) and were compared among the HAI scores and among patients with cirrhosis, chronic hepatitis, and normal liver function. Results:The ADCs decreased as the fibrosis score in the HAI increased, and the correlation was statistically significant (P Ͻ 0.0001). No relationship between the ADCs and the necroinflammation scores in the HAI was found. The ADCs decreased as the stage of liver disease progressed or as the Child-Pugh stage progressed, and these relationships were statistically significant (P Ͻ 0.0001).Conclusion: ADC measurements are potentially useful for the evaluation of fibrosis staging in the liver.

MicroRNA (miRNA)s are a class of non-coding RNAs that regulate gene expression post-transcriptionally. Muscle-specific miRNA, miRNA (miR)-1, miR-133 and miR-206 play a crucial role in the regulation of muscle development and homeostasis. Muscle injuries are a common muscloskeletal disorder, and the most effective treatment has not been established yet. The purpose of this study was to demonstrate that a local injection of double-stranded (ds) miR-1, miR-133 and 206 can accelerate muscle regeneration in a rat skeletal muscle injury model. After the laceration of the rat tibialis anterior muscle, ds miR-1, 133 and 206 mixture mediated atelocollagen was injected into the injured site. The control group was injected with control siRNA. At 1 week after injury, an injection of miRNAs could enhance muscle regeneration morphologically and physiologically, and prevent fibrosis effectively compared to the control siRNA. Administration of exogenous miR-1, 133 and 206 can induce expression of myogenic markers, MyoD1, myogenin and Pax7 in mRNA and expression in the protein level at 3 and 7 days after injury. The combination of miR-1, 133 and 206 can promote myotube differentiation, and the expression of MyoD1, myogenin and Pax7 were up-regulated in C2C12 cells in vitro. Local injection of miR-1, 133 and 206 could be a novel therapeutic strategy in the treatment of skeletal muscle injury.

Silencing of miR-34a by LNA-modified anti-sense could effectively reduce rat chondrocyte apoptosis induced by IL-1β. This present study revealed that silencing of miR-34a might develop a novel intervention for OA treatment through the prevention of cartilage degradation.

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Low-attenuation hemangiomas and those that changed from homogeneous high to isoattenuation are atypical and difficult to differentiate from other neoplasms. Most early parenchymal enhancement is caused by associated arterioportal shunts.