In the short term, the incidence of dysphagia was significantly lower after Toupet fundoplication, but the difference decreased significantly with extension of the postoperative recovery period. For patients with moderate to severe GERD, the laparoscopic Nissen fundoplication may be optimal; for elderly patients or for patients with significantly reduced esophageal peristalsis detected in preoperative examinations, the laparoscopic Toupet fundoplication should be considered.

In order to investigate the prognostic value of circulating tumor cells (CTCs) in patients with metastatic breast cancer (MBC), the blood cells from 98 MBC patients and 60 controls were evaluated by RT-PCR to detect the presence of markers EpCAM, CK19, and hMAM. Peripheral blood was obtained from all patients with MBC before any systemic therapy. Immunofluorescence staining experiment was conducted on CTCs samples from 10 patients to investigate the coexpression of EpCAM, CK19, and hMAM. In addition, analyses were carried out for their correlation with patients' clinicopathologic features. EpCAM+, CK19+, and hMAM+ cells were detected in 50 (51.0 %), 43 (43.9 %), and 68 (69.4 %) of the 98 patients, respectively. Triple-marker-positive CTCs were detected in 86 of 98 (87.8 %) patients with a significantly higher rate than the control group. Among the 98 patients, 12 (12.2 %) patients were negative for three genes, 34 (34.7 %) positive for one gene, 29 (29.6 %) positive for any two genes, and 23 (23.5 %) positive for all three genes. Compared to single-marker detection, the triple combined marker detection exhibited significantly higher rate. Furthermore, the specificity of triple combined markers of serial test was 100 %. The expression of three genes was significantly correlated with lymph node metastasis, high histological grade, and high levels of serum CA153 and CEA. Double-immunofluorescence labeling confirmed the presence of following CTCs phenotypes: CK19+/hMAM+, CK19+/hMAM-, CK19-/hMAM+, CK19+/EpCAM+, CK19-/EpCAM+, CK19+/EpCAM-, hMAM+/EpCAM+, and hMAM+/EpCAM-. After 2 years of follow-up, the presence of CTCs with triple-marker positive in peripheral blood was an independent risk factor for reduced progression-free survival (PFS) and overall survival (OS), and the presence of CTCs before any chemotherapy predicts poor OS and PFS in patients with MBC.

Bladder cancer is the most common neoplasm in the urinary system. This study assesses arctigenin anti-tumor activity in human bladder cancer T24 cells in vitro and the underlying molecular events. The flow cytometry analysis was used to detect cell-cycle distribution and apoptosis. Western blotting was used to detect changes in protein expression. The data showed that arctigenin treatment reduced viability of bladder cancer T24 cells in a dose-and time-dependent manner after treatment with arctigenin (10, 20, 40, 80, and 100 lmol/L) for 24 hr and 48 hr. Arctigenin treatment clearly arrested tumor cells in the G1 phase of the cell cycle. Apoptosis was detected by hoechst stain and flow cytometry after Annexin-V-FITC/PI double staining. Early and late apoptotic cells were accounted for 2.32-7.01% and 3.07-7.35%, respectively. At the molecular level, arctigenin treatment decreased cyclin D1 expression, whereas CDK4 and CDK6 expression levels were unaffected. Moreover, arctigenin selectively altered the phosphorylation of members of the MAPK superfamily, decreasing phosphorylation of ERK1/2 and activated phosphorylation of p38 significantly in a dose-dependent manner. These results suggest that arctigenin may inhibit cell viability and induce apoptosis by direct activation of the mitochondrial pathway, and the mitogen-activated protein kinase pathway may play an important role in the anti-tumor effect of arctigenin. The data from the current study demonstrate the usefulness of arctigenin in bladder cancer T24 cells, which should further be evaluated in vivo before translation into clinical trials for the chemoprevention of bladder cancer. Anat

The mechanisms underlying the effects of COX-2 on tumor lymphangiogenesis remain largely undefined. Here, the human lung cancer cell lines A549, 95D, Anip973, and AGZY83-a with different metastatic capacities were investigated by immunostaining, western blotting, and real-time RT-PCR. We observed increased expressions of COX-2 and VEGF-C in the three highly metastatic cell lines compared with the less metastatic AGZY83-a cell line. The COX-2-specific inhibitor Celecoxib suppressed VEGF-C expression whereas the main COX-2 metabolite PGE 2 elevated VEGF-C expression in Anip973 and AGZY83-a cells in positive and negative experiments. To determine the functional link to COX-2 more specifically and elucidate the mechanistic pathway, we used a siRNA to knock down the high COX-2 expression in Anip973 cells and transfected a COX-2 cDNA to enhance the low COX-2 expression in AGZY83-a cells, and then treated the cells with EP1/EP4 agonists or antagonists, respectively. The results revealed that the EP1/EP4 agonists significantly increased VEGF-C production in the COX-2-knockdown Anip973 cells. In contrast, the EP1/ EP4 antagonists diminished VEGF-C production in the COX-2-overexpressing AGZY83-a cells. Furthermore, animal models provided evidence that Celecoxib decreased VEGF-C expression, lymphangiogenesis, and lymph node metastases in Anip973 cells, whereas PGE 2 treatment increased the same factors in the parental AGZY83-a cells. A positive correlation between COX-2 and VEGF-C was also confirmed in vivo. The present data suggest that COX-2 regulates VEGF-C expression via the PGE 2 pathway, and that EP1/EP4 receptors are involved in PGE 2 -mediated VEGF-C production. Thus, COX-2 may represent a candidate gene for blocking tumor lymphangiogenesis and lymph node metastasis. Anat Rec, 293:1838Rec, 293: -1846

Background Hiatal hernias negatively damage patients’ health and life quality. Laparoscopic hiatal hernia repair is currently the gold standard for the treatment of hiatal hernia (LHHR). Numerous clinical trials on laparoscopic hiatal hernia repair have been done, but the published findings are highly variable due to the lack of unique outcome sets. Basic outcome sets have ever been established over the previous decade for a few procedures, but not for hiatal hernia repair yet. This protocol outlines the procedure to develop a core outcome set for laparoscopic hiatal hernia repair COS-LHHR). COS-LHHR will provide a unique criteria for clinical investigations. Methods This study will be conducted in four phases: (1) scoping reviews of existing qualitative studies and outcome reporting in randomized controlled trials to develop a list of potential outcome domains; (2) qualitative interviews with patients to explore the impact of laparoscopic hiatal hernia repair and the outcomes that they care most; (3) a multi-round e-Delphi study to achieve preliminary consensus on the core outcome set; and (4) an evidence-based consensus on a core outcome set will be achieved through a structured group consensus meeting, recommending best assessment outcome sets. Discussion The development the COS-LHHR will guide clinical research of laparoscopic hiatal hernia repair with unique outcome assessment. This would improve comparative analyses among studies.