A facile imine-linked covalent organic framework doped with a carbon dot composite for the detection and removal of Hg2+ in surface water.

Hg2+ is one of the most toxic chemical species in the water environment, and thus developing a new fluorescent covalent organic framework for both the detection and removal of Hg2+ is highly desirable. Herein, a fluorescent composite, termed TpPa-1 COF@CDs, was synthesized by inverse emulsion polymerization method using an imine covalent organic framework as the supporting material and carbon dots as the fluorescent sensor element. The crystallinity, porosity, rich functional receptors (hydroxyl and amino groups), thermal stability and fluorescent properties of TpPa-1 COF@CDs were characterized. The results showed that TpPa-1 COF@CDs exhibited a good detection and removal performance for Hg2+, which was evidenced by its high sensitivity (LOD = 0.75 µg L-1), superior selectivity, large adsorption capacity (235 mg g-1), fast adsorption rate (30 min equilibrium time) and good regeneration (at least five cycles). More importantly, the simple functional monomer, short reaction time and metal-free raw material made TpPa-1 COF@CDs reliable, cost effective and eco-friendly. This research demonstrated the facile construction of a functional covalent organic framework composite for water environmental remediation technologies of metal pollution.

The value of radical radiotherapy in the primary tumor of newly diagnosed oligo-metastatic nasopharyngeal carcinoma patients.

BACKGROUND: To explore the efficacy and patterns of treatment failure of radical radiotherapy in newly diagnosed oligo-metastatic nasopharyngeal carcinoma patients. METHODS: We included 39 newly diagnosed oligo-metastatic nasopharyngeal carcinoma patients who received radical radiotherapy and chemotherapy in Zhejiang Cancer Hospital. Treatment and prognosis information were collected. The Kaplan-Meier methods and Cox proportional hazards models were used to calculate survival rates and analyze prognostic factors. RESULTS: After a median follow-up time of 38 months, the 1-, 3-, and 5-year overall survival rates were 97, 70, and 57.9%, while the 1-, 3-, and 5-year progression-free survival rates were 87, 59, and 50.9%, respectively. Age, numbers of metastases lesions, cycles, and schemes of chemotherapy were independent prognostic factors of the overall survival. Patients with no more than three metastasis lesions had a higher survival rate than those with ≥ 3 metastatic lesions (P = 0.023). More than four cycles chemotherapy provide a higher survival rate than less than four cycles. Chemotherapy including docetaxel had a significantly survival advantages (P = 0.041). CONCLUSION: Radical radiotherapy is important for newly diagnosed oligo-metastatic nasopharyngeal carcinoma patients, which can still achieve long-term survival after chemo-radiotherapy.

PKG inhibits TCF signaling in colon cancer cells by blocking beta-catenin expression and activating FOXO4.

Activation of cGMP-dependent protein kinase (PKG) has anti-tumor effects in colon cancer cells but the mechanisms are not fully understood. This study has examined the regulation of beta-catenin/TCF signaling, as this pathway has been highlighted as central to the anti-tumor effects of PKG. We show that PKG activation in SW620 cells results in reduced beta-catenin expression and a dramatic inhibition of TCF-dependent transcription. PKG did not affect protein stability, nor did it increase phosphorylation of the amino-terminal Ser33/37/Thr41 residues that are known to target beta-catenin for degradation. However, we found that PKG potently inhibited transcription from a luciferase reporter driven by the human CTNNB1 promoter, and this corresponded to reduced beta-catenin mRNA levels. Although PKG was able to inhibit transcription from both the CTNNB1 and TCF reporters, the effect on protein levels was less consistent. Ectopic PKG had a marginal effect on beta-catenin protein levels in SW480 and HCT116 but was able to inhibit TCF-reporter activity by over 80%. Investigation of alternative mechanisms revealed that cJun-N-terminal kinase (JNK) activation was required for the PKG-dependent regulation of TCF activity. PKG activation caused beta-catenin to bind to FOXO4 in colon cancer cells, and this required JNK. Activation of PKG was also found to increase the nuclear content of FOXO4 and increase the expression of the FOXO target genes MnSOD and catalase. FOXO4 activation was required for the inhibition of TCF activity as FOXO4-specific short-interfering RNA completely blocked the inhibitory effect of PKG. These data illustrate a dual-inhibitory effect of PKG on TCF activity in colon cancer cells that involves reduced expression of beta-catenin at the transcriptional level, and also beta-catenin sequestration by FOXO4 activation.