Three-dimensional binary superlattices of magnetic nanocrystals and semiconductor quantum dots

Recent advances in strategies for synthesizing nanoparticles--such as semiconductor quantum dots, magnets and noble-metal clusters--have enabled the precise control of composition, size, shape, crystal structure, and surface chemistry. The distinct properties of the resulting nanometre-scale building blocks can be harnessed in assemblies with new collective properties, which can be further engineered by controlling interparticle spacing and by material processing. Our study is motivated by the emerging concept of metamaterials-materials with properties arising from the controlled interaction of the different nanocrystals in an assembly. Previous multi-component nanocrystal assemblies have usually resulted in amorphous or short-range-ordered materials because of non-directional forces or insufficient mobility during assembly. Here we report the self-assembly of PbSe semiconductor quantum dots and Fe2O3 magnetic nanocrystals into precisely ordered three-dimensional superlattices. The use of specific size ratios directs the assembly of the magnetic and semiconducting nanoparticles into AB13 or AB2 superlattices with potentially tunable optical and magnetic properties. This synthesis concept could ultimately enable the fine-tuning of material responses to magnetic, electrical, optical and mechanical stimuli.     

Structure of the extracellular region of HER2 alone and in complex with the Herceptin Fab

HER2 (also known as Neu, ErbB2) is a member of the epidermal growth factor receptor (EGFR; also known as ErbB) family of receptor tyrosine kinases, which in humans includes HER1 (EGFR, ERBB1), HER2, HER3 (ERBB3) and HER4 (ERBB4). ErbB receptors are essential mediators of cell proliferation and differentiation in the developing embryo and in adult tissues, and their inappropriate activation is associated with the development and severity of many cancers. Overexpression of HER2 is found in 20-30% of human breast cancers, and correlates with more aggressive tumours and a poorer prognosis. Anticancer therapies targeting ErbB receptors have shown promise, and a monoclonal antibody against HER2, Herceptin (also known as trastuzumab), is currently in use as a treatment for breast cancer. Here we report crystal structures of the entire extracellular regions of rat HER2 at 2.4 A and human HER2 complexed with the Herceptin antigen-binding fragment (Fab) at 2.5 A. These structures reveal a fixed conformation for HER2 that resembles a ligand-activated state, and show HER2 poised to interact with other ErbB receptors in the absence of direct ligand binding. Herceptin binds to the juxtamembrane region of HER2, identifying this site as a target for anticancer therapies.     

CTCF-binding sites flank CTG/CAG repeats and form a methylation-sensitive insulator at the DM1 locus

An expansion of a CTG repeat at the DM1 locus causes myotonic dystrophy (DM) by altering the expression of the two adjacent genes, DMPK and SIX5, and through a toxic effect of the repeat-containing RNA. Here we identify two CTCF-binding sites that flank the CTG repeat and form an insulator element between DMPK and SIX5. Methylation of these sites prevents binding of CTCF, indicating that the DM1 locus methylation in congenital DM would disrupt insulator function. Furthermore, CTCF-binding sites are associated with CTG/CAG repeats at several other loci. We suggest a general role for CTG/CAG repeats as components of insulator elements at multiple sites in the human genome.     

Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death

Programmed cell death is a fundamental requirement for embryogenesis, organ metamorphosis and tissue homeostasis. In mammals, release of mitochondrial cytochrome c leads to the cytosolic assembly of the apoptosome-a caspase activation complex involving Apaf1 and caspase-9 that induces hallmarks of apoptosis. There are, however, mitochondrially regulated cell death pathways that are independent of Apaf1/caspase-9. We have previously cloned a molecule associated with programmed cell death called apoptosis-inducing factor (AIF). Like cytochrome c, AIF is localized to mitochondria and released in response to death stimuli. Here we show that genetic inactivation of AIF renders embryonic stem cells resistant to cell death after serum deprivation. Moreover, AIF is essential for programmed cell death during cavitation of embryoid bodies-the very first wave of cell death indispensable for mouse morphogenesis. AIF-dependent cell death displays structural features of apoptosis, and can be genetically uncoupled from Apaf1 and caspase-9 expression. Our data provide genetic evidence for a caspase-independent pathway of programmed cell death that controls early morphogenesis.     

N-ethylmaleimide antagonizes stress-induced gastric ulcers in rats

Summary N-ethylmaleimide (NEM) 10 or 25 mg/kg b.wt, given s.c. 20 min beforehand, dose-dependently and significantly antagonizes the severity of gastric glandular ulcers produced by restraint at 4°C (stress) for 2 h. These findings suggest that reduced activity of endogenous nonprotein sulfhydryl substances in gastric tissue does not worsen stress-induced ulceration in rat stomachs, unlike the deleterious effect its depletion is claimed to have on ethanol-evoked gastric mucosal damage. Thus, decreased SH activity appears not to play a role in the aetiology of mucosal ulcers due to stress.     

Variance intervention

Variance intervention is a simple state-space approach to handling sharp discontinuities of level or slope in the states or parameters of models for non-stationary time-series. It derives from earlier procedures used in the 1960s for the design of self-adaptive, state variable feedback control systems. In the alternative state-space forecasting context considered in the present paper, it is particularly useful when applied to structural time series models. The paper compares the variance intervention procedure with the related ‘subjective intervention’ approach proposed by West and Harrison in a recent issue of the Journal of Forecasting, and demonstrates it efficacy by application to various time-series data, including those used by West and Harrison.     

Enhancement of Au-Ag-Te contents in tellurium-bearing ore minerals via bioleaching

The purpose of this study was to enhance the content of valuable metals, such as Au, Ag, and Te, in tellurium-bearing minerals via bioleaching. The ore samples composed of invisible Au and Au paragenesis minerals (such as pyrite, chalcopyrite, sphalerite and galena) in combination with tellurium-bearing minerals (hessite, sylvanite and Tellurobismuthite) were studied. Indigenous microbes from mine drainage were isolated and identified as Acidithiobacillus ferrooxidans, which were used in bioleaching after adaption to copper. The effect of the microbial adaption on the bioleaching performance was then compared with the results produced by the non-adaptive process. The microbial adaption enhanced the Au-Ag-Te contents in biological leaching of tellurium-bearing ore minerals. This suggests that bioleaching with adapted microbes can be used both as a pretreatment and in the main recovery processes of valuable metals.