Computational characterization and identification of human polycystic ovary syndrome genes.

Human polycystic ovary syndrome (PCOS) is a highly heritable disease regulated by genetic and environmental factors. Identifying PCOS genes is time consuming and costly in wet-lab. Developing an algorithm to predict PCOS candidates will be helpful. In this study, for the first time, we systematically analyzed properties of human PCOS genes. Compared with genes not yet known to be involved in PCOS regulation, known PCOS genes display distinguishing characteristics: (i) they tend to be located at network center; (ii) they tend to interact with each other; (iii) they tend to enrich in certain biological processes. Based on these features, we developed a machine-learning algorithm to predict new PCOS genes. 233 PCOS candidates were predicted with a posterior probability >0.9. Evidence supporting 7 of the top 10 predictions has been found.

[Identification and expression of cytochrome C in tumor-bearing mice model with neuroblastoma].

OBJECTIVE: To screen, identify and verify the serum specific protein of neuroblastoma in a tumor-bearing murine model and speculate about the source of cytochrome C. METHODS: NB cells (KP-N-NS) were inoculated subcutaneously into nude mice. And the sera samples of tumor-bearing mice (observation group, n = 14) and controls (control group, n = 25) were collected at 4 weeks to screen for and identify differentially expressed proteins. The method of surface-enhanced laser desorption-ionization time-of-flight mass spectrometry (SELDI-TOF-MS) was employed to screen the serum specific protein of neuroblastoma between two groups. Then serum protein targets were purified by high-performance liquid chromatography (HPLC) and identified by LC-MS/MS (LTQ). RESULTS: By comparing protein peaks among two sera groups, we identified the peak (11 609) showing significant differential expression between two groups. The expression of peak (11 609) was 3338.4 ± 1410.9 in observation group and 59.8 ± 40.7 in control group. This peak was identified as murine cytochrome C. CONCLUSION: Cytochrome C is a serum specific protein for neuroblastoma tumor and it comes from the apoptosis of non-tumor cells.

Surgical management of intrahepatic vessels in children with stage III/IV hepatoblastoma.

BACKGROUND: Hepatoblastoma (HB) is a rare childhood tumor. We investigated the effect of intraoperative management of the intrahepatic major vessels in children with HB. METHODS: Between April 2005 and August 2012, surgical resection was performed on 50 children with hepatoblastoma. These children were divided into a vessel-ligation group (n = 20) and a vessel-repair group (n = 30). In the vessel-ligation group, the intrahepatic major vessels were ligated and removed together with the tumor and the affected liver lobe/liver parenchyma. In the vessel-repair group, the affected intrahepatic major vessels were dissected and preserved as much as possible and the normal liver lobe/liver parenchyma and blood supply from these vessels were also preserved. The outcomes were analyzed by postoperative follow-up. RESULTS: In the vessel-ligation group, two patients gave up surgery, six patients underwent palliative resection, and 12 patients underwent en bloc resection; four patients died of liver failure and eight patients fully recovered and were discharged. In the vessel-repair group, all 30 patients underwent en bloc resection and were discharged after satisfactory healing. After a follow-up time of 5 - 36 months (median: 20 months), two patient in the vessel-ligation group survived and 22 patients in the vessel-repair group survived. CONCLUSIONS: Patients with HB can be successfully treated by tumor resection with vascular repair. This method prevents postoperative liver failure, ensures patient safety during the perioperative period, and allows for early chemotherapy.

The immunosuppressive tumor microenvironment in hepatocellular carcinoma.

Increasing evidence indicates the immunosuppressive nature of the local environment in tumor. The present study was focused on analyzing the immune status within hepatocellular carcinoma. In contrast to the increasing number of CD4(+) T cells, CD8(+), CD3(-)CD56(+), CD3(+)CD56(+), and gammadeltaT cells were all found to be under-represented in tumor infiltrating lymphocytes. Notably, the relative abundance of CD3(+)CD56(+) cells appeared to be correlated with patient survival. Functional analysis demonstrated that CD4(+) cells in the tumor tended to produce more IL-10 but less IFN-gamma, whereas CD8(+) cells showed impaired capacity for the production of both IFN-gamma and perforin. Consistent with previous reports, we observed a significant increase of Foxp3(+) cells in the tumor tissue. Intriguingly, although over 90% of CD4(+)CD25(high) cells were found to be Foxp3(+), the majority of Foxp3(+) cells were identified in the CD4(+)CD25(medium) and CD4(+)CD25(-) subsets. In support of its role as a negative regulator, CD4(+)CD25(high) cells suppressed the proliferation of CD4(+)CD25(-) cells isolated from the same tissues in an APC dependent manner. In conclusion, the tumor microenvironment of hepatocellular carcinoma is featured by the presence of multiple immunosuppressive factors.