Prophylactic uterine artery embolization during cesarean delivery for placenta previa complicated by placenta accreta.

OBJECTIVE: To evaluate the efficacy and safety of prophylactic uterine artery embolization (UAE) during cesarean delivery for women with placenta previa complicated by placenta accreta. METHODS: A retrospective analysis of women with placenta previa admitted to The Second Affiliated Hospital of Soochow University, Suzhou, China, for elective cesarean between February 2003 and July 2016. Postpartum estimated blood loss, blood transfusion, hysterectomy, disseminated intravascular coagulation (DIC) incidence, intensive care unit (ICU) duration, and postoperative stay were compared between control women who underwent cesarean delivery only and women who underwent prophylactic intraoperative UAE during cesarean. RESULTS: There were 28 and 26 women in the UAE and control group, respectively. There were no differences in hysterectomy incidence (P=0.291), or duration of ICU stay (P=0.085), or postoperative hospitalization (P=0.668) between the groups; however, the incidence of DIC was lower in the UAE group (P=0.035). Mean estimated blood loss (P=0.018) and blood transfusion (P=0.011) were also lower in the UAE group. No serious complications were associated with the endovascular procedures. CONCLUSION: Prophylactic intraoperative UAE seemed to effectively reduce blood loss, need for blood transfusion, and incidence of DIC among women with placenta previa complicated by placenta accreta.

Totally implantable venous access devices: The supraclavicular percutaneous approach and early complications.

BACKGROUND: The background of this study was to explore the success rate and early complications concerning the implantation of totally implantable venous access devices (TIVADs) by percutaneous venipuncture and management strategies for early complications. MATERIALS AND METHODS: This was a retrospective study of 1923 patients who received TIVAD implantation by percutaneous venipuncture (mostly via the supraclavicular route). The percutaneous access sites were internal jugular vein (810 patients; right/left: 158/652) or proximal right internal jugular vein, brachiocephalic vein, and proximal subclavian vein (1113 patients). Success rates and early complications related to TIVAD placement techniques were summarized, and strategies for managing complications were also analyzed. RESULTS: In 627 patients, TIVAD implantation was first performed by interventional radiologists using a "blind" approach relying on anatomical landmarks, having a 91.9% success rate. In contrast, there was a 100% success rate among the remaining 1296 patients who received ultrasound-guided implantation, a difference which was statistically significant (P < 0.05). Ultrasound-guided implantation was also successful for the 51 patients for whom the first attempt failed using the blind technique. Further, we found that the incidence of early complications was 5.41% (104/1923) and that the occurrence of immediate complications was significantly higher in the blind technique group compared to the ultrasound-guided group (37 vs. 12; P < 0.05). CONCLUSIONS: It is safe and feasible to implant TIVADs by supraclavicular venipuncture. Ultrasound guidance combined with X-ray monitoring during operation significantly improves the surgery success rate and reduces the risk of early complications. Unclear anatomical landmarks and vascular variation are the main factors affecting success using a blind (nonguided) technique.

Identification of DNA-PKcs as a primary resistance factor of TIC10 in hepatocellular carcinoma cells.

The current study tested the anti-hepatocellular carcinoma (HCC) cell activity of TIC10, a first-in-class small-molecule tumor necrosis (TNF)-related apoptosis-inducing ligand (TRAIL) inducer. TIC10 exerted potent anti-proliferative and pro-apoptotic actions in primary and established human HCC cells. TIC10 blocked Akt-Erk activation, leading to Foxo3a nuclear translocation, as well as TRAIL and death receptor-5 (DR5) transcription in HCC cells. We propose that DNA-PKcs is a major resistance factor of TIC10 possibly via inhibiting Foxo3a nuclear translocation. DNA-PKcs inhibition, knockdown or mutation facilitated TIC10-induced Foxo3a nuclear translocation, TRAIL/DR5 expression and cell apoptosis. Reversely, exogenous DNA-PKcs over-expression inhibited above actions by TIC10. In vivo, oral administration of TIC10 significantly inhibited HepG2 tumor growth in nude mice, which was further potentiated with Nu7026 co-administration. Thus, TIC10 shows promising anti-HCC activity, alone or together with DNA-PKcs inhibitors.

Prediction of cancer progression in a group of 73 gastric cancer patients by circulating cell-free DNA.

BACKGROUND: Circulating cell-free DNA (ccf-DNA) in plasma may contain both specific and non-specific of tumor markers. The concentration and integrity of ccf-DNA may be clinical useful for detecting and predicting cancer progression. METHODS: Plasma samples from 40 healthy controls and 73 patients with gastric cancers (two stage 0, 17 stage I, 11 stage II, 33 stage III, and 10 stage IV according to American Joint Committee on Cancer stage) were assessed respectively. qPCR targeting the Alu repeats was performed using two different sets of primers amplifying the long and short segments. DNA integrity was calculated as a ratio of the long to the short fragments of Alu repeats. RESULTS: Plasma DNA concentration was significantly higher in patients with stage III and IV gastric cancers than in healthy controls (p = 0.028 and 0.029 respectively). The receiver operating characteristic (ROC) curve for discriminating patients with stage III and IV gastric cancers from healthy controls had an area under the curve (AUC) of 0.744 (95% CI, 0.64 to 0.85). Circulating cell-free DNA concentration increased within 21 days following surgery and dropped by 3 months after surgery. CONCLUSIONS: Concentration of ccf-DNA is a promising molecular marker for assessing gastric cancer progression. TRIAL REGISTRATION: Current Controlled Trials ChiCTR-DDT-12002848 , 8 October 2012.

New species of Cystolepiota from China.

In this paper, a new species, Cystolepiota pseudofumosifolia, is introduced. C. pseudofumosifolia is characterized by granulose or powdery pileus with an anatomic structure that is loosely globose, as well as ellipsoid cells in chains in the pileus covering the cheilocystidia. This new species is compared to the related and similar Cystolepiota species in morphology and molecular phylogeny based on Internal transcribed spacer sequences. Both types of data support our specimens as a new species in the genus Cystolepiota.

Ceramide production mediates cinobufotalin-induced growth inhibition and apoptosis in cultured hepatocellular carcinoma cells.

Hepatocellular carcinoma (HCC) is a highly aggressive and lethal neoplasm with poor prognosis. The aim of this study is to investigate the anticancer activity of cinobufotalin, a bufadienolide isolated from toad venom, in cultured HCC cells, and to study the underlying mechanisms. We found that cinobufotalin (at nmol/L) significantly inhibited HCC cell growth and survival while inducing considerable cell apoptosis. Further, cinobufotalin inhibited sphingosine kinase 1 (SphK1) activity and induced pro-apoptotic ceramide production. Ceramide synthase-1 small hairpin RNA (shRNA)-depletion inhibited cinobufotalin-induced ceramide production and HCC cell apoptosis. On the other hand, the glucosylceramide synthase (GCS) inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) facilitated cinobufotalin-induced ceramide production and cell apoptosis. SphK1 inhibitor II (SKI-II), similar to cinobufotalin, increased cellular ceramide level and promoted HCC cell apoptosis. Finally, we observed that cinobufotalin inactivated Akt-S6K1 signaling in HepG2 cells, which was again inhibited by ceramide synthase-1 shRNA-depletion. In conclusion, the results of this study suggest that cinobufotalin induces growth inhibition and apoptosis in cultured HCC cells through ceramide production. Cinobufotalin may be investigated as a novel anti-HCC agent.

Copy number variation at 6q13 is associated with lung cancer risk in a Han Chinese population.

Copy number variations (CNVs), a major source of human genetic polymorphism, have been suggested to have an important role in genetic susceptibility to common diseases such as cancer, immune diseases, and neurological disorders. Lung cancer is a multifactorial tumor closely associated with genetic background. Previous genome-wide association studies have identified single nucleotide polymorphisms (SNPs) that are associated with lung cancer susceptibility. This study examined the CNVR2966.1 at 6q13 and its association with lung cancer susceptibility. The CNVR2966.1 was found to be a 10,379 bp nucleotides deletion/insertion within the uniform boundaries chromosome 6: 74,648,791-74,659,169. The risk of lung cancer observed in 503 cases and 623 controls was significantly associated with copy number of CNVR2966.1, with the odds ratio (OR) being 1.38 [95% confidence interval (CI) = 1.05-1.79; P = .007] for one copy genotype compared with two copies genotype. These results suggest that CNVR2966.1 is associated with lung cancer risk.