Superconductor-insulator transition in La2 - xSrxCuO4 at the pair quantum resistance

High-temperature superconductivity in copper oxides arises when a parent insulator compound is doped beyond some critical concentration; what exactly happens at this superconductor-insulator transition is a key open question. The cleanest approach is to tune the carrier density using the electric field effect; for example, it was learned in this way that weak electron localization transforms superconducting SrTiO(3) into a Fermi-glass insulator. But in the copper oxides this has been a long-standing technical challenge, because perfect ultrathin films and huge local fields (>10(9)?V?m(-1)) are needed. Recently, such fields have been obtained using electrolytes or ionic liquids in the electric double-layer transistor configuration. Here we report synthesis of epitaxial films of La(2-?x)Sr(x)CuO(4) that are one unit cell thick, and fabrication of double-layer transistors. Very large fields and induced changes in surface carrier density enable shifts in the critical temperature by up to 30?K. Hundreds of resistance versus temperature and carrier density curves were recorded and shown to collapse onto a single function, as predicted for a two-dimensional superconductor-insulator transition. The observed critical resistance is precisely the quantum resistance for pairs, R(Q) = h/(2e) = 6.45?kΩ, suggestive of a phase transition driven by quantum phase fluctuations, and Cooper pair (de)localization.     

Structural basis for a [4Fe-3S] cluster in the oxygen-tolerant membrane-bound [NiFe]-hydrogenase

Membrane-bound respiratory [NiFe]-hydrogenase (MBH), a H(2)-uptake enzyme found in the periplasmic space of bacteria, catalyses the oxidation of dihydrogen: H(2)?→?2H(+)?+?2e(-) (ref. 1). In contrast to the well-studied O(2)-sensitive [NiFe]-hydrogenases (referred to as the standard enzymes), MBH has an O(2)-tolerant H(2) oxidation activity; however, the mechanism of O(2) tolerance is unclear. Here we report the crystal structures of Hydrogenovibrio marinus MBH in three different redox conditions at resolutions between 1.18 and 1.32??. We find that the proximal iron-sulphur (Fe-S) cluster of MBH has a [4Fe-3S] structure coordinated by six cysteine residues--in contrast to the [4Fe-4S] cubane structure coordinated by four cysteine residues found in the proximal Fe-S cluster of the standard enzymes--and that an amide nitrogen of the polypeptide backbone is deprotonated and additionally coordinates the cluster when chemically oxidized, thus stabilizing the superoxidized state of the cluster. The structure of MBH is very similar to that of the O(2)-sensitive standard enzymes except for the proximal Fe-S cluster. Our results give a reasonable explanation why the O(2) tolerance of MBH is attributable to the unique proximal Fe-S cluster; we propose that the cluster is not only a component of the electron transfer for the catalytic cycle, but that it also donates two electrons and one proton crucial for the appropriate reduction of O(2) in preventing the formation of an unready, inactive state of the enzyme.     

MECHANISM OF CHLORATE FORMATION IN CHLORINE DIOIXDE DELIGNIFICATION

The effect of pH on chlorate formation during chlorine dioxide delignification of oxygen delignified kraft pulp was studied. Chlorate formation was found to increase slightly when pH was increased from 1.8 to 2.5, further increase of pH decreased chlorate formation.The above phenomenon is explained by the combination of two mechanisms, one by the reaction between hypochlorous acid and chlorite, another by the effect of chlorine on the regeneration of chlorine dioxide. The first mechanism suggests that chlorate formation is highly dependent on HCIO concentration which decreases with increasing pH and causes chlorate formation to behave in the same trend. The second mechanism suggests that chlorine favors the regeneration of chlorine dioxide while HCIO favors chlorate formation, thus lowering the pH from about 4 to the acidic end should decreases chlorate formation. The two opposite effects lead to the maximum formation of chlorate at around pH 2.5.     

A technique for improving salivary chromosome preparations

Zusammenfassung Es wird eine verbesserte Methode zur Herstellung von Quetschpräparaten von Speicheldrüsenchromosomen beschrieben. Die Methode gibt scharfe Bilder der feinsten Chromosomenbänder auf klarem Hintergrund.

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Research supported by U.S. Public Health Service Research Grants No. GM-11609 and GM-19616 from the National Institute of General Medical Sciences.     

A tumour suppressor network relying on the polyamine-hypusine axis

Tumour suppressor genes encode a broad class of molecules whose mutational attenuation contributes to malignant progression. In the canonical situation, the tumour suppressor is completely inactivated through a two-hit process involving a point mutation in one allele and chromosomal deletion of the other. Here, to identify tumour suppressor genes in lymphoma, we screen a short hairpin RNA library targeting genes deleted in human lymphomas. We functionally identify those genes whose suppression promotes tumorigenesis in a mouse lymphoma model. Of the nine tumour suppressors we identified, eight correspond to genes occurring in three physically linked 'clusters', suggesting that the common occurrence of large chromosomal deletions in human tumours reflects selective pressure to attenuate multiple genes. Among the new tumour suppressors are adenosylmethionine decarboxylase 1 (AMD1) and eukaryotic translation initiation factor 5A (eIF5A), two genes associated with hypusine, a unique amino acid produced as a product of polyamine metabolism through a highly conserved pathway. Through a secondary screen surveying the impact of all polyamine enzymes on tumorigenesis, we establish the polyamine-hypusine axis as a new tumour suppressor network regulating apoptosis. Unexpectedly, heterozygous deletions encompassing AMD1 and eIF5A often occur together in human lymphomas and co-suppression of both genes promotes lymphomagenesis in mice. Thus, some tumour suppressor functions can be disabled through a two-step process targeting different genes acting in the same pathway.     

A comparative analysis of the cell biology of senescence and aging

Various intracellular organelles, such as lysosomes, mitochondria, nuclei, and cytoskeletons, change during replicative senescence, but the utility of these changes as general markers of senescence and their significance with respect to functional alterations have not been comprehensively reviewed. Furthermore, the relevance of these alterations to cellular and functional changes in aging animals is poorly understood. In this paper, we review the studies that report these senescence-associated changes in various aging cells and their underlying mechanisms. Changes associated with lysosomes and mitochondria are found not only in cells undergoing replicative or induced senescence but also in postmitotic cells isolated from aged organisms. In contrast, other changes occur mainly in cells undergoing in vitro senescence. Comparison of age-related changes and their underlying mechanisms in in vitro senescent cells and aged postmitotic cells would reveal the relevance of replicative senescence to the physiological processes occurring in postmitotic cells as individuals age.     

Inverting generating functions with increased numerical precision �� A computational experience

In this paper, we consider the numerical inversion of a variety of generating functions (GFs) that arise in the area of engineering and non-engineering fields. Three classes of GFs are taken into account in a comprehensive manner: classes of probability generating functions (PGFs) that are given in rational and non-rational forms, and a class of GFs that are not PGFs. Among others, those PGFs that are not explicitly given but contain a number of unknowns are largely considered as they are often encountered in many interesting applied problems. For the numerical inversion of GFs, we use the methods of the discrete (fast) Fourier transform and the Taylor series expansion. Through these methods, we show that it is remarkably easy to obtain the desired sequence to any given accuracy, so long as enough numerical precision is used in computations. Since high precision is readily available in current software packages and programming languages, one can now lift, with little effort, the so-called Laplacian curtain that veils the sequence of interest. To demonstrate, we take a series of representative examples: the PGF of the number of customers in the discrete-time GeoX/Geo/c queue, the same in the continuous-time MX/D/c queue, and the GFs arising in the discrete-time renewal process.     

A three-parameter fault-detection software reliability model with the uncertainty of operating environments

As requirements for system quality have increased, the need for high system reliability is also increasing. Software systems are extremely important, in terms of enhanced reliability and stability, for providing high quality services to customers. However, because of the complexity of software systems, software development can be time-consuming and expensive. Many statistical models have been developed in the past years to estimate software reliability. In this paper, we propose a new three-parameter fault-detection software reliability model with the uncertainty of operating environments. The explicit mean value function solution for the proposed model is presented. Examples are presented to illustrate the goodness-of-fit of the proposed model and several existing non-homogeneous Poisson process (NHPP) models based on three sets of failure data collected from software applications. The results show that the proposed model fits significantly better than other existing NHPP models based on three criteria such as mean squared error (MSE), predictive ratio risk (PRR), and predictive power (PP).