Surface-immobilized cross-linked cationic polyelectrolyte enables CO2 reduction with metal cation-free acidic electrolyte.

Electrochemical CO2 reduction in acidic electrolytes is a promising strategy to achieve high utilization efficiency of CO2. Although alkali cations in acidic electrolytes play a vital role in suppressing hydrogen evolution and promoting CO2 reduction, they also cause precipitation of bicarbonate on the gas diffusion electrode (GDE), flooding of electrolyte through the GDE, and drift of the electrolyte pH. In this work, we realize the electroreduction of CO2 in a metal cation-free acidic electrolyte by covering the catalyst with cross-linked poly-diallyldimethylammonium chloride. This polyelectrolyte provides a high density of cationic sites immobilized on the surface of the catalyst, which suppresses the mass transport of H+ and modulates the interfacial field strength. By adopting this strategy, the Faradaic efficiency (FE) of CO reaches 95 ± 3% with the Ag catalyst and the FE of formic acid reaches 76 ± 3% with the In catalyst in a 1.0 pH electrolyte in a flow cell. More importantly, with the metal cation-free acidic electrolyte the amount of electrolyte flooding through the GDE is decreased to 2.5 ± 0.6% of that with alkali cation-containing acidic electrolyte, and the FE of CO maintains above 80% over 36 h of operation at -200 mA·cm-2.

Clinicopathological and prognostic significance of pretreatment thrombocytosis in patients with endometrial cancer: a meta-analysis.

Background: The prognostic and clinicopathological role of pretreatment thrombocytosis in cancer has been widely studied, but conclusions in endometrial cancer (EnCa) remain controversial. Therefore, we conducted a meta-analysis to assess the pathologic and prognostic impacts of pretreatment thrombocytosis in patients with EnCa. Methods: We searched PubMed, Embase, SpringerLink, ScienceDirect and China National Knowledge Infrastructure databases. Pooled HR or OR with their 95% CIs were applied to assess the association of pretreatment thrombocytosis with survival outcomes and clinical parameters of EnCa patients. Results: In total, 10 studies containing 2,995 cases of EnCa met the criteria. The results suggested that pretreatment thrombocytosis was significantly associated with high International Federation of Gynecology and Obstetrics (FIGO) stage (pooled OR 3.45, 95% CI 1.68-7.08, P=0.001), poor tumor differentiation (pooled OR 2.00, 95% CI 1.22-3.29, P=0.006), lymph-vascular space invasion (pooled OR 2.04, 95% CI 1.35-3.07, P=0.001); myometrial invasion (pooled OR 2.14, 95% CI 1.39-3.32, P=0.001); cervical involvement (pooled OR 2.54, 95% CI 1.56-4.15, P=0.000) and lymph node metastasis (OR 3.15, 95% CI 1.71-5.80, P=0.001). No significant difference existed between pretreatment thrombocytosis and overall survival (P=0.012), cancer/disease-specific survival (P=0.07) or disease-free survival (P=0.25). Conclusion: pretreatment thrombocytosis was associated with advanced clinicopathological features in patients with EnCa, which may serve as a potential therapeutic target for EnCa.

Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway.

Resistance to cisplatin-based therapy is a major challenge in the control of lung cancer progression. However, the underlying mechanisms remain largely unclear. Autophagy is closely associated with resistance to lung cancer therapy, but the function of autophagy in cisplatin treatment is still controversial. Here, we investigated whether autophagy was involved in lung adenocarcinoma resistance to cisplatin and further elucidated the underlying molecular mechanisms. Cisplatin-refractory lung adenocarcinoma cells increased autophagic vacuole formation detected by monodansylcadaverine staining. When exposed to cisplatin, lung adeno-carcinoma cells demonstrated increased levels of autophagy detected by MAP1A/1B LC3B and mammalian homologue of yeast Atg6 (Beclin-1) expression using Western blot analysis. Activation of cisplatin-induced autophagic flux was increased by using chloroquine (CQ), which can accumulate LC3B-II protein and increase punctate distribution of LC3B localization. The combination of cisplatin with CQ was more potent than cisplatin alone in inhibiting lung adenocarcinoma cell growth, which also increased cisplatin-induced apoptosis. Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. These findings demonstrate that activation of autophagy is a hallmark of cisplatin exposure in human lung adenocarcinoma cells, and that there is a cisplatin-induced autophagic response via activation of the AMPK/mTOR signaling pathway. We speculate that autophagy can be used as a novel therapeutic target to overcome cisplatin-resistant lung adenocarcinoma.

Prognostic value of Notch-1 expression in hepatocellular carcinoma: a meta-analysis.

Association of Notch-1 expression with prognosis of patients with hepatocellular carcinoma (HCC) remains controversial. We conducted a meta-analysis to reevaluate the association of Notch-1 expression with clinicopathological characteristics and prognosis of HCC. PubMed, Embase, Web of Science, and China National Knowledge Infrastructure were searched to look for relevant studies. The association between Notch-1 expression and clinicopathological parameters and overall survival (OS) was then reassessed using the meta-analysis for odds ratio (OR) or hazard ratio (HR) and 95% confidence interval (CI). A total of seven studies, including 810 HCC patients, were eligible for the meta-analysis. Our data showed that high Notch-1 expression was able to predict poor OS (HR 1.50, 95% CI 1.17-1.83, P=0.0001). The pooled OR showed that high Notch-1 expression was significantly associated with tumor metastasis (OR 0.37, 95% CI 0.16-0.86, P=0.02) and tumor size >5 cm (OR 0.48, 95% CI 0.26-0.88, P=0.02). In contrast, there was no association between high Notch-1 expression and tumor differentiation, late TNM stage, tumor number, and portal vein invasion of HCC. In conclusion, Notch-1 overexpression might predict poorer survival and more aggressive behavior in patients with HCC.