Annealing-induced interfacial toughening using a molecular nanolayer

Self-assembled molecular nanolayers (MNLs) composed of short organic chains and terminated with desired functional groups are attractive for modifying surface properties for a variety of applications. For example, organosilane MNLs are used as lubricants, in nanolithography, for corrosion protection and in the crystallization of biominerals. Recent work has explored uses of MNLs at thin-film interfaces, both as active components in molecular devices, and as passive layers, inhibiting interfacial diffusion, promoting adhesion and toughening brittle nanoporous structures. The relatively low stability of MNLs on surfaces at temperatures above 350-400 degrees C (refs 12, 13), as a result of desorption or degradation, limits the use of surface MNLs in high-temperature applications. Here we harness MNLs at thin-film interfaces at temperatures higher than the MNL desorption temperature to fortify copper-dielectric interfaces relevant to wiring in micro- and nano-electronic devices. Annealing Cu/MNL/SiO2 structures at 400-700 degrees C results in interfaces that are five times tougher than pristine Cu/SiO2 structures, yielding values exceeding approximately 20 J m(-2). Previously, similarly high toughness values have only been obtained using micrometre-thick interfacial layers. Electron spectroscopy of fracture surfaces and density functional theory modelling of molecular stretching and fracture show that toughening arises from thermally activated interfacial siloxane bridging that enables the MNL to be strongly linked to both the adjacent layers at the interface, and suppresses MNL desorption. We anticipate that our findings will open up opportunities for molecular-level tailoring of a variety of interfacial properties, at processing temperatures higher than previously envisaged, for applications where microlayers are not a viable option-such as in nanodevices or in thermally resistant molecular-inorganic hybrid devices.     

Experimental implementation of heat-bath algorithmic cooling using solid-state nuclear magnetic resonance

The counter-intuitive properties of quantum mechanics have the potential to revolutionize information processing by enabling the development of efficient algorithms with no known classical counterparts. Harnessing this power requires the development of a set of building blocks, one of which is a method to initialize the set of quantum bits (qubits) to a known state. Additionally, fresh ancillary qubits must be available during the course of computation to achieve fault tolerance. In any physical system used to implement quantum computation, one must therefore be able to selectively and dynamically remove entropy from the part of the system that is to be mapped to qubits. One such method is an 'open-system' cooling protocol in which a subset of qubits can be brought into contact with an external system of large heat capacity. Theoretical efforts have led to an implementation-independent cooling procedure, namely heat-bath algorithmic cooling. These efforts have culminated with the proposal of an optimal algorithm, the partner-pairing algorithm, which was used to compute the physical limits of heat-bath algorithmic cooling. Here we report the experimental realization of multi-step cooling of a quantum system via heat-bath algorithmic cooling. The experiment was carried out using nuclear magnetic resonance of a solid-state ensemble three-qubit system. We demonstrate the repeated repolarization of a particular qubit to an effective spin-bath temperature, and alternating logical operations within the three-qubit subspace to ultimately cool a second qubit below this temperature. Demonstration of the control necessary for these operations represents an important step forward in the manipulation of solid-state nuclear magnetic resonance qubits.     

Analysis of the human protein interactome and comparison with yeast, worm and fly interaction datasets

We present the first analysis of the human proteome with regard to interactions between proteins. We also compare the human interactome with the available interaction datasets from yeast (Saccharomyces cerevisiae), worm (Caenorhabditis elegans) and fly (Drosophila melanogaster). Of >70,000 binary interactions, only 42 were common to human, worm and fly, and only 16 were common to all four datasets. An additional 36 interactions were common to fly and worm but were not observed in humans, although a coimmunoprecipitation assay showed that 9 of the interactions do occur in humans. A re-examination of the connectivity of essential genes in yeast and humans indicated that the available data do not support the presumption that the number of interaction partners can accurately predict whether a gene is essential. Finally, we found that proteins encoded by genes mutated in inherited genetic disorders are likely to interact with proteins known to cause similar disorders, suggesting the existence of disease subnetworks. The human interaction map constructed from our analysis should facilitate an integrative systems biology approach to elucidating the cellular networks that contribute to health and disease states.     

LaConf:A Localized Address Autoconfiguration Scheme for Wireless Ad Hoc Networks

We propose a localized address autoconfiguration (LaConf) scheme for wireless ad hoc networks.Address allocation information is maintained on the network border nodes,called addressing agents (AAs),which are locally identified by a geographic routing protocol GFG (Greedy-FACE-Greedy).When a node joins the network,it acquires an address from a neighboring AA (if any exists) by local communication or from the head AA (a geographic extreme AA) by GFG-based multi-hop communication.A Geographic Hash Table (GHT) ...     

Role of a novel photopigment,melanopsin, in behavioral adaptation to light

Adaptation to changes in the ambient light is of critical importance to life. In mammals, three principal photoadaptation mechanisms depend on ocular photoreception and exhibit spectral sensitivity suggestive of the opsin class of photopigment(s). These include rapid adaptation of the visual system to the ambient light by pupil constriction, direct modulation of neuroendocrine function and entrainment of the circadian clock to the day:night cycle. Surprisingly, these processes can largely function independent of classical rod/cone photoreceptors, suggesting a novel opsin-based signaling mechanism. They appear to involve a recently discovered network of intrinsically photosensitive retinal ganglion cells that make direct or indirect axonal connections to brain centers regulating photoadaptive behaviors. The discovery of a novel opsin, melanopsin, in these cells has offered an exciting entry point to explore, at the molecular level, how mammals adapt to their light environment. There is now genetic proof of a principal role for melanopsin in all three major photoadaptation processes.     

FAN1 mutations cause karyomegalic interstitial nephritis, linking chronic kidney failure to defective DNA damage repair

Chronic kidney disease (CKD) represents a major health burden. Its central feature of renal fibrosis is not well understood. By exome sequencing, we identified mutations in FAN1 as a cause of karyomegalic interstitial nephritis (KIN), a disorder that serves as a model for renal fibrosis. Renal histology in KIN is indistinguishable from that of nephronophthisis, except for the presence of karyomegaly. The FAN1 protein has nuclease activity and acts in DNA interstrand cross-link (ICL) repair within the Fanconi anemia DNA damage response (DDR) pathway. We show that cells from individuals with FAN1 mutations have sensitivity to the ICL-inducing agent mitomycin C but do not exhibit chromosome breakage or cell cycle arrest after diepoxybutane treatment, unlike cells from individuals with Fanconi anemia. We complemented ICL sensitivity with wild-type FAN1 but not with cDNA having mutations found in individuals with KIN. Depletion of fan1 in zebrafish caused increased DDR, apoptosis and kidney cysts. Our findings implicate susceptibility to environmental genotoxins and inadequate DNA repair as novel mechanisms contributing to renal fibrosis and CKD.