Red persistent luminescence excited by visible light in CaS:Eu2+,Tm3+

Excitation wavelength dependence of red persistent luminescence in CaS:Eu2+,Tm3+ phosphor is reported. Persistent luminescence appears under visible light excitation in the wavelength region of 400–600nm. Photon energy from white light-emitting diode lamps is possibly stored in this material. This sulfide phosphor is synthesized using iodine vapor. Under iodine vapor, Eu2+ and Tm3+ are found to be efficiently included in CaS. The concentration dependence of Eu2+ is studied, and the optimum concentration is 0.05%. Trap depth of 0.27–0.33eV contributing to persistent luminescence is evaluated by using thermoluminescence

Red afterglow and luminescence arising from defects in CaS:Eu2+, Tm3+

CaS:Eu^2+, Tm^3+ is a phosphor known to emit a long afterglow of red emission (650 nm) when excited by blue light (450 nm). It shows a long afterglow time of 700 s for Eu = 0.05% and Tm = 2%. The mechanism of this afterglow is investigated using time-resolved fluorescence (TR-F) spectroscopy from the nanosecond to millisecond region. At room temperature, it is not possible to investigate shallow levels because of the effects of thermal vibrations. The mechanism of the emission characteristics at room temperature would be affected by these levels that can be observed only at low temperatures. Therefore, the samples are cooled to 15 K for the TR-F measurements. The host material CaS emits blue light (420 nm) arising from sulfur defects, and the typical decay time is measured to be 6 ms. This blue emission becomes stronger when Tm^3+ is doped. Furthermore, the doped Eu ions emit a broad red spectrum at 650 nm originating from the Eu^2+ -specific 4f^6 5d^1 –4f^7 transition. When the excitation is ceased, the red emission decays with a fast time constant of 0.6 μs. This value is a typical decay time for Eu^2+. This red emission has multiple decay time constants, and a component with a decay time of 6 ms appears. This 6 ms decay time is the same as that of the blue emission from the sulfur defects, which have an important role on the red afterglow

Impact of postoperative complications after primary tumor resection on survival in patients with incurable stage IV colorectal cancer: A multicenter retrospective cohort study

[Aims] Primary tumor resection for patients with incurable stage IV colorectal cancer can prevent tumor-related complications but may cause postoperative complications. Postoperative complications delay the administration of chemotherapy and can lead to the spread of malignancy. However, the impact of postoperative complications after primary tumor resection on survival in patients with incurable stage IV colorectal cancer remains unclear. Therefore, this study aimed to investigate how postoperative complications after primary tumor resection affect survival in this patient group. [Methods] We reviewed data on 966 patients with stage IV colorectal cancer who underwent palliative primary tumor resection between January 2006 and December 2007. We examined the association between major complications (National Cancer Institute Common Terminology Criteria for Adverse Events v3.0 grade 3 or more) and overall survival using Cox proportional hazard model and explored risk factors associated with major complications using multivariable logistic regression analysis. [Results] Ninety-three patients (9.6%) had major complications. The 2-year overall survival rate was 32.7% in the group with major complications and 50.3% in the group with no major complications. Patients with major complications had a significantly poorer prognosis than those without major complications (hazard ratio: 1.62; 95% confidence interval: 1.21-2.18; P < .01). Male, rectal tumor, and open surgery were identified to be risk factors for major complications. [Conclusions] Postoperative complications after primary tumor resection was associated with decreased long-term survival in patients with incurable stage IV colorectal cancer

Dynamic localization of a yeast development–specific PP1 complex during prospore membrane formation is dependent on multiple localization signals and complex formation

During the developmental process of sporulation in Saccharomyces cerevisiae, membrane structures called prospore membranes are formed de novo, expand, extend, acquire a round shape, and finally become plasma membranes of the spores. GIP1 encodes a regulatory/targeting subunit of protein phosphatase type 1 that is required for sporulation. Gip1 recruits the catalytic subunit Glc7 to septin structures that form along the prospore membrane; however, the molecular basis of its localization and function is not fully understood. Here we show that Gip1 changes its localization dynamically and is required for prospore membrane extension. Gip1 first associates with the spindle pole body as the prospore membrane forms, moves onto the prospore membrane and then to the septins as the membrane extends, distributes around the prospore membrane after closure, and finally translocates into the nucleus in the maturing spore. Deletion and mutation analyses reveal distinct sequences in Gip1 that are required for different localizations and for association with Glc7. Binding to Glc7 is also required for proper localization. Strikingly, localization to the prospore membrane, but not association with septins, is important for Gip1 function. Further, our genetic analysis suggests that a Gip1–Glc7 phosphatase complex regulates prospore membrane extension in parallel to the previously reported Vps13, Spo71, Spo73 pathway

Serum cytokine profiles predict survival benefits in patients with advanced hepatocellular carcinoma treated with sorafenib: A retrospective cohort study

金沢大学先進予防医学研究科Background: Sorafenib is a multiple receptor tyrosine kinase inhibitor known to prolong overall survival in patients with advanced hepatocellular carcinoma (HCC). Predicting this drug\u27s survival benefits is challenging because clinical responses are rarely measurable during treatment. In this study, we hypothesized that serum cytokines levels could predict the survival of advanced HCC patients, as sorafenib targets signaling pathways activated in the tumor stromal microenvironment and potentially affects serum cytokine profiles. Methods: Of 143 patients with advanced-stage HCC, 104 who were recruited between 2003 and 2007 received hepatic arterial infusion chemotherapy (HAIC) that mainly targets tumor epithelial cells at S-phase (cohort 1); additionally, 39 recruited between 2010 and 2012 received sorafenib, which primarily targets the stromal vascular endothelial cells. Serum samples were collected and aliquoted prior to the treatment. Serum EGF, bFGF, HGF, IFN-γ, IL-10, IL-12, IL-2, IL-4, IL-5, IL-6, IL-8, IP-10, MIG, PDGF-BB, SCF, SDF1, TGF-β, TGF-α, TNF-α, and VEGF-A were measured via enzyme-linked immunosorbent assays. The Modified Response Evaluation Criteria in Solid Tumors were used to assess tumor responses. Results: The median survival time of HCC patients in cohorts 1 (HAIC-treated) and 2 (sorafenib-treated) were 12.0 and 12.4 months, respectively. Kaplan-Meier analysis revealed no significant survival differences between the 2 groups. Patients who survived more than 2 years after sorafenib treatment exhibited higher serum levels of IL-10, IL-12, TNF-a, IL-8, SDF-1, EGF, PDGF-BB, SCF, and TGF-α. Furthermore, cohort 2 patients with higher serum IL-5 (>12 pg/mL), IL-8 (>10 pg/mL), PDGF-BB (>300 pg/mL), and VEGF-A (>50 pg/mL) levels achieved longer survival; cohort 1 patients did not. Hierarchical cluster analysis of 6 cytokines robustly enriched for comparison analysis between cohorts 1 and 2 (IL-5, IL-8, TGF-α, PDGF-BB, CXCL9, and VEGF-A) revealed that elevation of these cytokines correlated with better survival when treated with sorafenib but not with HAIC. Conclusions: Patients who exhibited survival benefits owing to sorafenib treatment tended to present higher serum cytokines levels, potentially reflecting the activation of stromal signaling in the tumor microenvironment. Our study thus introduces novel biomarkers that may identify advanced HCC patients who may experience survival benefits with sorafenib treatment. © 2017 The Author(s)

Dickkopf-1 Promotes Angiogenesis and is a Biomarker for Hepatic Stem Cell-like Hepatocellular Carcinoma

Cancer stemness evinces interest owing to the resulting malignancy and poor prognosis. We previously demonstrated that hepatic stem cell-like hepatocellular carcinoma (HpSC-HCC) is associated with high vascular invasion and poor prognosis. Dickkopf-1 (DKK-1), a Wnt signaling regulator, is highly expressed in HpSC-HCC. Here, we assessed the diagnostic and prognostic potential of serum DKK-1. Its levels were significantly higher in 391 patients with HCC compared with 205 patients with chronic liver disease. Receiver operating characteristic curve analysis revealed the optimal cutoff value of DKK-1 to diagnose HCC and predict the 3-year survival as 262.2 and 365.9 pg/mL, respectively. HCC patients with high-serum DKK-1 levels showed poor prognosis. We evaluated the effects of anti-DKK-1 antibody treatment on tumor growth in vivo and of recombinant DKK-1 on cell proliferation, invasion, and angiogenesis in vitro. DKK-1 knockdown decreased cancer cell proliferation, migration, and invasion. DKK-1 supplementation promoted angiogenesis in vitro; this effect was abolished by an anti-DKK-1 antibody. Co-injection of the anti-DKK-1 antibody with Huh7 cells inhibited their growth in NOD/SCID mice. Thus, DKK-1 promotes proliferation, migration, and invasion of HCC cells and activates angiogenesis in vascular endothelial cells. DKK-1 is a prognostic biomarker for HCC and a functional molecule for targeted therapy