New-onset glucose disorders in peritoneal dialysis patients: a meta-analysis and systematic review.

Background: Peritoneal dialysis (PD) patients are at high risk of developing glucose metabolism disturbance (GMD). The incidence and prevalence of new-onset GMD, including diabetes mellitus (DM), impaired glucose tolerance (IGT) and impaired fast glucose (IFG), after initiation of PD, as well as their correlated influence factors, varies among studies in different areas and of different sample sizes. Also, the difference compared with hemodialysis (HD) remained unclear.

Laparoscopic hepatectomy for the treatment of Caroli's disease: a case report.

Caroli disease is a rare congenital disorder characterized by nonobstructive dilatation of intrahepatic ducts. In cases with symptomatic intrahepatic manifestations, treatment should correspond to the type with hepatic resection for localized disease and transplantation for diffuse forms. If possible, complete resection of the cysts can cure the symptoms and avoid the risk of malignancy.

Vascular invasion in hepatitis B virus-related hepatocellular carcinoma with underlying cirrhosis: possible associations with ascites and hepatitis B viral factors?

Vascular invasion is one of the most important prognostic factors for patients with hepatocellular carcinoma (HCC). The objective of the current, retrospective study was to determine the associations of ascites and hepatitis B viral factors (HBeAg and anti-HBe status and HBV DNA levels), as well as tumor-related factors (size, tumor number, grade, and location) with micro- or macroscopic vascular invasion in patients with HCC that developed as a result of hepatitis B virus (HBV)-related cirrhosis. A total of 336 consecutive patients were included.

[Effect of glucocorticoid on dendritic cells in children with chronic immune thrombocytopenia].

Objective: To investigate the change in dendritic cells (DCs) in children with chronic immune thrombocytopenia (cITP) and the effect of glucocorticoid on DCs in children with cITP.

Methods: Fifteen children with cITP and 20 healthy controls were included in the study. Flow cytometry was used to measure the DC subsets count in the 15 children with cITP before and after glucocorticoid treatment as well as the corresponding values in the 20 healthy controls.

p14ARF interacts with E2F factors to form p14ARF-E2F/partner-DNA complexes repressing E2F-dependent transcription.

Primarily, E2F factors such as E2F1, -2, and -3 stimulate cell-cycle progression, while ARF tumor suppressor mediates growth suppression. The ARF gene can be induced by oncogenic signal through activating E2F-dependent transcription. In turn, ARF may target E2F for its degradation via a p53-dependent mechanism.

Antitumor activity of novel fluoro-substituted (-)-epigallocatechin-3-gallate analogs.

Epidemiological studies support the cancer-preventive effects of green tea and its main constituent (-)-epigallocatechin gallate [(-)-EGCG], however, (-)-EGCG is unstable under physiological conditions. Here we report that two novel fluoro-substituted (-)-EGCG analogs inhibited tumor growth with similar potency to that of Pro-EGCG (1) which has improved potency over parental compound (-)-EGCG in human breast cancer MDA-MB-231 xenografts. MDA-MB-231 tumors treated with each fluoro-substituted (-)-EGCG analog showed proteasome inhibition and apoptotic cell death, suggesting that the proteasome might be one of the cellular targets of fluoro-(-)-EGCGs and that proteasome inhibition is partially responsible for the observed antitumor activity.

[Activation ability of CpG ODNs 2216 on PBMNCs from leukemia patients in remission and killing effect of activated PBMNCs on K562 cells].

The aim of this study was to investigate the activation ability of CpG oligodeoxynucleotide (CpG ODN) 2216 on the peripheral blood mononuclear cells (PBMNCs) from leukemia patients in remission and the killing effect of activated PBMNCs on K562 cells. PBMNCs obtained from leukemia patients in remission were incubated with CpG ODN 2216. In control group, PBMNCs were incubated with normal saline (NS).

Induction of p14ARF by E2F1 contributes to 8-chloro-adenosine-induced apoptosis in human lung cancer H1299 cells.

Background: 8-Chloro-adenosine (8-Cl-Ado) inhibits tumor cell proliferation by inducing cell-cycle arrest and apoptosis. We speculate that upregulation of p14ARF by E2F1 might contribute to 8-Cl-Ado-induced late apoptosis.

Methods: Hoechst staining, cell proliferation and TUNEL assays, real-time quantitative PCR, Western blotting, chromatin immunoprecipitation and RNA interference were employed in investigating the role of induction of p14ARF by E2F1 in 8-Cl-Ado-induced apoptosis in human lung cancer H1299 cells.

Prodrugs of fluoro-substituted benzoates of EGC as tumor cellular proteasome inhibitors and apoptosis inducers.

The most potent catechin in green tea is (-)-epigallocatechin-3-gallate [(-)-EGCG], which, however, is unstable under physiological conditions. To discover more stable and more potent polyphenol proteasome inhibitors, we synthesized several novel fluoro-substituted (-)-EGCG analogs, named F-EGCG analogs, as well as their prodrug forms with all of -OH groups protected by acetate. We report that the prodrug form of one F-EGCG analog exhibited greater potency than the previously reported peracetate of (-)-EGCG to inhibit proteasomal activity, suppress cell proliferation, and induce apoptosis in human leukemia Jurkat T cells, demonstrating the potential of these compounds to be developed into novel anti-cancer and cancer-preventive agents.

[Effects of flavonoids with different structures on proliferation of leukemia cell line HL-60].

Background & Objective: Flavonoids, with some beneficial biological activities, exist extensively in foods and herbal products. This study was to evaluate the effects of 23 flavonoids on the proliferation of leukemia cell line HL-60, and elucidate the structure-activity relationship (SAR).

Methods: HL-60 cells were treated with 23 flavonoids with high purity and definite structure.

8-Chloro-adenosine inhibits growth at least partly by interfering with actin polymerization in cultured human lung cancer cells.

A key feature of actin is its ability to bind and hydrolyze ATP. 8-Chloro-adenosine (8-Cl-Ado), which can be phosphorylated to the moiety of 8-Cl-ATP in living cells, inhibits tumor cell proliferation. Therefore we tested the hypothesis that 8-Cl-Ado can interfere with the dynamic state of actin polymerization.

Exposure of human lung cancer cells to 8-chloro-adenosine induces G2/M arrest and mitotic catastrophe.

8-Chloro-adenosine (8-Cl-Ado) is a potent chemotherapeutic agent whose cytotoxicity in a variety of tumor cell lines has been widely investigated. However, the molecular mechanisms are uncertain. In this study, we found that exposure of human lung cancer cell lines A549 (p53-wt) and H1299 (p53-depleted) to 8-Cl-Ado induced cell arrest in the G2/M phase, which was accompanied by accumulation of binucleated and polymorphonucleated cells resulting from aberrant mitosis and failed cytokinesis.