Fast Lithium-Ion Transportation in Crystalline Polymer Electrolytes.

Fast lithium-ion transportation is found in the crystalline polymer electrolytes, α-CD-PEOn /Li+ (n=12, 40), prepared by self-assembly of α-cyclodextrin (CD), polyethylene oxide (PEO) and Li+ salts. A detailed solid-state NMR study combined with the X-ray diffraction technique reveals the unique structural features of the samples, that is, a) the tunnel structure formed by the assembled CDs, providing the ordered long-range pathway for Li+ ion transportation; b) the all-trans conformational sequence of the PEO chains in the tunnels, attenuating significantly the coordination between Li+ and the EO segments. The origin of the fast lithium-ion transportation has been attributed to these unique structural features. This work demonstrates the first example in solid polymer electrolytes (SPEs) for "creating" fast ion transportation through material design and will find potential applications in the design of new ionconducting SPE materials.

Mannose inhibits proliferation and promotes apoptosis to enhance sensitivity of glioma cells to temozolomide through Wnt/ß-catenin signaling pathway.

BACKGROUND: Temozolomide (TMZ) is generally applied for glioma treatment, while drug resistance of TMZ limits its therapeutic efficacy. Mannose exerts evident anti-tumor effect. We intended to investigate whether mannose enhanced TMZ sensitivity to glioma and examined the underlying mechanism. METHODS: MTT and clone formation assays were performed to detect cell viability and proliferation. Cell apoptosis was measured by flow cytometry. The protein and gene expression levels were detected by Western blot and qRT-PCR assays. Xenograft glioma model was established to explore the influence of mannose in vivo. RESULTS: Mannose inhibited glioma cell growth, which was facilitated by knockdown of phosphomannose isomerase (PMI) while reversed by overexpression of PMI. Mannose enhanced the sensitivity of glioma cells to TMZ, indicated by the further inhibited cell viability and colony formation and the aggravated cell apoptosis, which was reversed by overexpression of O6-methylguanine DNA methyltransferase (MGMT). Furthermore, mannose and TMZ inhibited MGMT expression and Wnt/ß-catenin activation. Moreover, activating Wnt/ß-catenin pathway blocked anti-proliferative effect induced by mannose and TMZ, which was further suppressed by overexpressed MGMT. Mannose inhibited glioma growth, suppressed Ki67 and downregulated MGMT and ß-catenin in vivo. CONCLUSION: Mannose inhibited MGMT to enhance sensitivity of glioma cells to TMZ, with Wnt/ß-catenin pathway involvement. Our data suggested that mannose could be an innovative agent to improve glioma treatment, particularly in TMZ-resistant glioma with high MGMT.

Association of HLA-DRB1, HLA-DQB1 Polymorphisms with HPV 16 E6 Variants among Young Cervical Cancer Patients in China.

Potential correlation of human papillomavirus (HPV) 16 E6 variants and human leukocyte antigen (HLA) class II polymorphisms has been suggested in patients with cervical cancer, so far little information is available about the possible interaction between E6 variants and HLA class II variability during the obviously accelerated progression to cervical cancer in young women. In this study, we aimed to explore the association between the HPV16 E6 variants and HLA-DRB1, DQB1 alleles in a Chinese young cervical cancer population. The HLA-DRB1, HLA-DQB1 polymophisms were genotyped by low-resolution polymerase chain reaction (PCR) with sequence-specific primer. HPV16 E6 DNA was tested by Sanger fluorescent dye dideoxy-termination technique. The difference of DRB1, DQB1 polymorphisms between young cervical cancer patients (≤35ys, n=61) and older ones (>35ys, n=85) and the association with E6 variants were analyzed. Results showed that the distribution pattern of HLA-DRB1, DQB1 alleles was different between young cervical cancer patients and older ones. The allele frequency of DQB1*0501 in young patients was significantly lower than older ones (6.6% vs. 23.5%, p<0.05). The HPV16 E6 A4 lineage was the exclusive type observed in young patients, and its prevalence was significantly higher than that of older cases (82.86% vs.41.94%, p<0.05). DRB1*03 was not found in young patients positive for the HPV16 E6 A4 lineage, whereas it was observed in 19.2 % older patients with A4 positive(Pc<0.05). In conclusion, specific association between certain HPV16 E6 variant and genetic polymorphisms of HLA may play a role during the progression of early onset cervical cancer in young patients. Certain HLA-DRB1 and HLA-DQB1 alleles may be related to the A4 lineage among young cervical cancer patients, which was the unique HPV16 E6 variant found in Chinese young patients. Our finding may provide an insight into the pathogenic factors that associated with cervical cancer in young women.

[Protective effect of ligustrazine and propofol on peri-operational liver ischemia-reperfusion injury].

OBJECTIVE: To explore the protective effect and mechanism of ligustrazine (LGT) and propofol (PRO) on peri-operational liver ischemia-reperfusion injury (HIRI). METHODS: Thirty-six patients scheduled for hepatic surgery were randomly divided into the control group, the LGT group, the PRO group and the LGT + PRO group, 9 patients in each group. Changes of superoxide dismutase (SOD), lipid peroxide (LPO), ratio of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha), alanine aminotransferase (ALT) activity, and the ultrastructure of liver tissue were dynamically observed. RESULTS: Compared with the control group, SOD activity was significantly higher, LPO concentration, TXB2/6-keto-PGF1alpha ratio and ALT value were significantly lower (P < 0.05 and P < 0.01) in the LGT group, the PRO group and the LGT + PRO group during HIRI, with the abnormal changes of hepatic ultrastructure 25 min after reperfusion significantly alleviated in the three treated group. CONCLUSION: Combination of ligustrazine and propofol shows protective effect on liver by decreasing oxygen free radical level, reducing lipid peroxidation and adjusting TXA2/PGI2 imbalance after hepatic ischemia-reperfusion in patients undergoing hepatic cancer surgery.

[Protective effect of propofol on liver during ischemia-reperfusion injury in patients undergoing liver surgery].

OBJECTIVE: To explore the protective effect of propofol on liver during hepatic ischemia/reperfusion injury (HIRI) and its mechanisms in patients undergoing liver surgery. METHODS: Eighteen patients who were scheduled for selective hepatic surgery were randomly divided into control group (n=9) and propofol treatment group (n=9). Changes of several parameters in plasma and effects of propofol on them were observed before liver ischemia, at end of ischemia and at reperfusion for 25 minutes, parameters of which included superoxide dismutase (SOD), xanthine oxidase (XO), lipid peroxide (LPO) and alanine aminotransferase (ALT) activity, and the ultrastructure changes in liver tissue were observed under electron microscope at 25 minutes after reperfusion. RESULTS: SOD activity decreased remarkably (P<0.01); XO activity, LPO concentration and ALT value increased significantly (P<0.01) during HIRI, and there were abnormal changes of the hepatic ultrastructure at 25 minutes after reperfusion. Afer treatment with propofol, the variation of all parameters were alleviated markedly (P<0.05 and P<0.01). CONCLUSION: Propofol has protective effects on HIRI by reducing oxygen free radical level and inhibiting lipid peroxidation after hepatic ischemia/reperfusion in patients undergoing liver cancer surgery.