We report the chemical intercalation of Li+ into the interlayer of V2O5·nH2O with enlarged layer spacing and fast Zn2+ diffusion, resulting in high rate capability and excellent long-term cycling performance.

Autosomal-dominant spinocerebellar ataxias constitute a large, heterogeneous group of progressive neurodegenerative diseases with multiple types. To date, classical genetic studies have revealed 31 distinct genetic forms of spinocerebellar ataxias and identified 19 causative genes. Traditional positional cloning strategies, however, have limitations for finding causative genes of rare Mendelian disorders. Here, we used a combined strategy of exome sequencing and linkage analysis to identify a novel spinocerebellar ataxia causative gene, TGM6. We sequenced the whole exome of four patients in a Chinese four-generation spinocerebellar ataxia family and identified a missense mutation, c.1550T-G transition (L517W), in exon 10 of TGM6. This change is at a highly conserved position, is predicted to have a functional impact, and completely cosegregated with the phenotype. The exome results were validated using linkage analysis. The mutation we identified using exome sequencing was located in the same region (20p13-12.2) as that identified by linkage analysis, which cross-validated TGM6 as the causative spinocerebellar ataxia gene in this family. We also showed that the causative gene could be mapped by a combined method of linkage analysis and sequencing of one sample from the family. We further confirmed our finding by identifying another missense mutation c.980A-G transition (D327G) in exon seven of TGM6 in an additional spinocerebellar ataxia family, which also cosegregated with the phenotype. Both mutations were absent in 500 normal unaffected individuals of matched geographical ancestry. The finding of TGM6 as a novel causative gene of spinocerebellar ataxia illustrates whole-exome sequencing of affected individuals from one family as an effective and cost efficient method for mapping genes of rare Mendelian disorders and the use of linkage analysis and exome sequencing for further improving efficiency.

We have confirmed that the PLA2G6 gene allocated PARK14 locus and is associated with AREP.

Abstract. The widespread land degradation in an alpine meadow ecosystem would affect ecosystem carbon (C) balance. Biomass, soil chemical properties and carbon dioxide (CO 2 ) of six levels of degraded lands (D1-D6, according to the number of rodent holes and coverage) were investigated to examine the effects of rodent-induced land degradation on an alpine meadow ecosystem. Soil organic carbon (SOC), labile soil carbon (LC), total nitrogen (TN) and inorganic nitrogen (N) were obtained by chemical analysis. Soil respiration (R s ), net ecosystem exchange (NEE) and ecosystem respiration (ER) were measured by a Li-Cor 6400XT. Gross ecosystem production (GEP) was the sum of NEE and ER. Aboveground biomass (AGB) was based on a linear regression with coverage and plant height as independent variables. Root biomass (RB) was obtained by using a core method. Soil respiration, ER, GEP and AGB were significantly higher in slightly degraded (D3 and D6, group I) than in severely degraded land (D1, D2, D4 and D5, group II). Positive values of NEE average indicate that the alpine meadow ecosystem is a weak C sink during the growing season. The only significant difference was in ER among different degradation levels. R s , ER and GEP were 38.2, 44.3 and 46.5 % higher in group I than in group II, respectively. Similar difference of ER and GEP between the two groups resulted in an insignificant difference of NEE. Positive correlations of AGB with ER, NEE and GEP, and relatively small AGB and lower CO 2 fluxes in group II, suggest the control of AGB on ecosystem CO 2 fluxes. Correlations of RB with SOC, LC, TN and inorganic N indicate the regulation of RB on soil C and N with increasing number of rodent holes in an alpine meadow ecosystem in the permafrost region of the Qinghai-Tibet Plateau (QTP).

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