A feeding trial aimed to determine the effects of dietary lipid level on growth performance, body composition and digestive enzymes activity of juvenile sea cucumber, Apostichopus japonicus. Diets with six crude lipid levels (1.9, 13.8, 29.1, 43.6, 59.6 and 71.6 g kg À1 ) were fed to sea cucumbers (initial weights 0.65 AE 0.01 g) at a density of 30 juveniles, once a day. After 60 days, body weight gain (BWG), specific growth rate (SGR), feed intake (FI) and protein efficiency ratio (PER) decreased with increasing dietary lipid levels. The sea cucumbers fed 1.9 g kg À1 crude lipid showed significantly higher (P < 0.05) BWG than those of the sea cucumbers fed 59.6 and 71.6 g kg À1 crude lipid. Intestinal protease and lipase activities generally increased with increasing dietary lipid levels. Eicosapentaenoic acid (EPA) content of body walls generally increased with increasing dietary lipid levels. Docosahexaenoic acid (DHA) content of body walls reached the maximum value at a dietary lipid level of 13.8 g kg À1 . N-3 highly unsaturated fatty acid content followed the same pattern of DHA. According to the growth performance and body composition of sea cucumbers, it can be indicated that the optimum dietary lipid level for juvenile sea cucumbers is between 1.9 and 13.8 g kg À1 .

Hepatocellular carcinoma (HCC) is the one of most common malignant tumors. The tumor microenvironment has a role in not only supporting growth and survival of tumor cells, but also triggering tumor recurrence and metastasis. Hepatocyte growth factor (HGF), one of the important growth factors in the tumor microenvironment, has an important role in angiogenesis, tumorigenesis and regeneration. However, the exact mechanism by which HGF regulates HCC initiation and development via epigenetic reprogramming has remained elusive. The present study focused on the epigenetic modification and target tumor-suppressive genes of HGF treatment in HCC. Expression profiling and DNA methylation array were performed to investigate the function of HGF and examine global genomic DNA methylation changes, respectively. Integrated analysis of gene expression and DNA methylation revealed potential tumor suppressor genes (TSGs) in HCC. The present study showed the multiple functions of HGF in tumorous and nontumorous pathways and global genomic DNA methylation changes. HGF treatment upregulated the expression of DNA methyltransferase 1 (DNMT1). Overexpression of DNMT1 in HCC patients correlated with the malignant potential and poor prognosis of HCC. Furthermore, integration analysis of gene expression and DNA methylation changes revealed novel potential tumor suppressor genes TSGs including MYOCD, PANX2 and LHX9. The present study has provided mechanistic insight into epigenetic repression of TSGs through HGF-induced DNA hypermethylation.

Abstract.We previously reported the case of a 56-year-old male who underwent surgical treatment for gastric hepatoid adenocarcinoma and splenic metastasis. The present study reports the case of the same patient who underwent successful ex vivo hepatectomy and partial liver autotransplantation. Computed tomography scans demonstrated that the tumor was located in the left and caudate lobes of the liver, with hepatic vein and inferior vena cava involvement, and right portal vein compression. To clarify the association between the vessels and the tumor, a three-dimensional imaging technique was used to reconstruct the liver architecture. During the surgery, the whole liver was removed with the retrohepatic vena cava, which was replaced with a prosthetic graft without a veno-venous bypass; a portacaval shunt for the anhepatic phase was performed simultaneously. The surgery lasted 9 h, and the anhepatic phase lasted 4 h. Blood loss during the surgery was recorded at 1,500 ml. The time taken for recovery was 21 days post-surgery, and at 20 months, the patient was disease-free. To the best of our knowledge, this is the first case of ex vivo liver resection performed for hepatic metastasis of hepatoid adenocarcinoma to be reported.

Correct female meiotic prophase is critical for stable genetic passage. Wang et al. identified a novel E3 ubiquitin ligase, FBXW24, which regulated female meiotic prophase progression from pachytene to metaphase II by promoting SYCP3 degradation and double-strand break repair

A series of indolyl substituted 1,4,6,7‐tetrahydropyrano[4,3‐c]pyrazole derivatives is synthesized via a domino method based on 1,4:6,7‐dianhydrofructose.