Li3PO4 Matrix Enables a Long Cycle Life and High Energy Efficiency Bismuth-Based Battery.

Bismuth is a lithium-ion battery anode material that can operate at an equilibrium potential higher than graphite and provide a capacity twice as high as that of Li4Ti5O12, making it intrinsically free from lithium plating that may cause catastrophic battery failure. However, the potential of bismuth is hampered by its inferior cyclability (limited to tens of cycles). Here, we propose an "ion conductive solid-state matrix" approach to address this issue. By homogeneously confining bismuth nanoparticles in a solid-state γ-Li3PO4 matrix that is electrochemically formed in situ, the resulting composite anode exhibits a reversible capacity of 280 mA hours per gram (mA h/g) at a rate of 100 mA/g and a record cyclability among bismuth-based anodes up to 500 cycles with a capacity decay rate of merely 0.071% per cycle. We further show that full-cell batteries fabricated from this composite anode and commercial LiFePO4 cathode deliver a stable cell voltage of ∼2.5 V and remarkable energy efficiency up to 86.3%, on par with practical batteries (80-90%). This work paves a way for harnessing bismuth-based battery chemistry for the design of high capacity, safer lithium-ion batteries to meet demanding applications such as electric vehicles.

Src kinase inhibition decreases thrombin-induced injury and cell cycle re-entry in striatal neurons.

Since Src kinase inhibitors decrease brain injury produced by intracerebral hemorrhage (ICH) and thrombin is activated following ICH, this study determined whether Src kinase inhibitors decrease thrombin-induced brain injury. Thrombin injections into adult rat striatum produced focal infarction and motor deficits. The Src kinase inhibitor PP2 decreased thrombin-induced Src activation, infarction in striatum and motor deficits in vivo. Thrombin applied to cultured post-mitotic striatal neurons caused: injury to axons and dendrites; many TUNEL positive neuronal nuclei; and re-entry into the cell cycle as manifested by cyclin D1 expression, induction of several other cell cycle genes and cyclin-dependent kinase 4 activation. PP2 dose-dependently attenuated thrombin-induced injury to the cultured neurons; and attenuated thrombin-induced neuronal cell cycle re-entry. These results are consistent with the hypotheses that Src kinase inhibitors decrease injury produced by ICH by decreasing thrombin activation of Src kinases and, at least in part, by decreasing Src induced cell cycle re-entry.

Blocking Oxidation Failures of Carbon Nanotubes through Selective Protection of Defects.

The selective growth of Al2 O3 islands over defect sites on the surface of carbon nanotubes significantly increases the oxidation breakdown threshold to 6.8 W cm(-2) , more than double than that of unprotected films. The elevated input power enables thermoacoustic emissions at loud audible sound pressure levels of 90.1 dB, which are inaccessible with the unprotected films.

[Expression and purification of telomerase resever transcriptase motifs in E.coli].

Our project is designed to clone a 1.3kb gene fragment of telomerase catalytic subunit gene which contains seven reverse transcriptase motifs and specific region with conserved sequence termed "T motif". The gene fragment was amplified by PCR and was inserted into expression vector pET28-b. The recombinant plasmid was induced by IPTG for 4h and a 52KD recombinant protein was produced. Amount of hTRT recombinant protein expression was 20% of total bacterial protein in the form of inclusion. Inclusion was dissolved in 8 mol/L urea and 10 mmol/L DTT and carried out affinity purification under denaturing condition. The purified hTRT recombinant protein was conformed by Western-blot successfully.

Antisense Sp1 oligodeoxynucleotide decreases telomerase activity by inhibiting hTERT mRNA expression in Jurkat T cells.

AIM: To study the effects of transcriptional factor Sp1 antisense oligodeoxynucleotide (ODN) on telomerase activity and human telomerase reverse transcriptase (hTERT) expression. METHODS: Antisense oligodeoxynucleotide (ODN) was designed to inhibit Sp1 expression and transferred to Jurkat T cells by lipofectamin. Telomerase PCR-ELISA was used to detect telomerase activity. RT-PCR analysis was used to assess the mRNA expression of Sp1 and hTERT, and Western blot was used to analyze the levels of Sp1 protein. RESULTS: Treatment of Jurkat T cells with Sp1 antisense ODN (1 micromol/L) dramatically reduced Sp1 mRNA and protein levels. The inhibition rate was 44.8 % (P <0.05) and 57 % (P <0.01), respectively. Following the transcriptional factor Sp1 functionally altering, hTERT mRNA expression were suppressed with a 43.7 % inhibition rate (P <0.01). A dose-dependent inhibition of telomerase activity by antisense Sp1 ODN was also discovered. From 0.25 to 2.0 micromol/L, telomerase activity was reduced from 27.1 % to 64.6 %. CONCLUSION: Antisense Sp1 ODN decreases telomerase activity by inhibiting hTERT mRNA expression in Jurkat T cells.