bluuebunny/crossref_metadata_2025 huggingface dataset:
Constraining deep‐ocean circulation during glacial times
Authors: Kumar Mohi
Published: July 2011

Scientists have known for 30 years that atmospheric carbon dioxide (CO2) levels varied substantially during the ice ages, yet the cause remains uncertain. Given that the deep ocean contains 50 times more carbon than the atmosphere, variable air‐sea exchange may have played a primary role in regulating atmospheric CO2. One of the primary goals of paleoceanography is to determine whether the deep ocean sequestered more carbon during glacial times. Today the deep Atlantic is filled by water masses that form in the North Atlantic near Greenland and in the Southern Ocean near Antarctica. In the South Atlantic the boundary between these water masses sits approximately 4 kilometers below the ocean's surface. Analyses of microfossils from deep‐sea sediments show the pattern was very different during the Last Glacial Maximum (LGM, ∼20,000 years ago). The carbon isotopic ratio of these fossils, which reflects the chemistry of the water in which they were formed, indicates there was a stronger isotopic gradient with water depth during the LGM. Water from the Southern Ocean also occupied a much larger proportion of the deep Atlantic, filling it from the bottom to an approximately 2‐kilometer water depth. (Paleoceanography, doi:10.1029/2010PA001938, 2011)
Overview of BioSharing
Authors: Sansone Susanna-Assunta
Published: July 2011

Research communities, funding agencies, and journals participate in the development of reporting standards for the bioscience domain to ensure that shared experiments are reported with enough information to be comprehensible and (in principle) reproducible, compared or integrated (Field, Sansone et al., Science, 2009). Similar trends in both the regulatory arena and commercial science.Proliferation of standards is a positive sign of stakeholders’ engagement, but how much do we know about these standards? Which ones are mature and stable enough to use or recommend? Which tools and databases implement which standard? Etc...The BioSharing catalogue (www.biosharing.org) aims to1. centralize community-developed bioscience standards, linking to policies, other portals, open access resources and lists of tools and databases implementing the standards;2. develop and maintain a set of criteria for assessing the usability and popularity of the standards, also the interoperability and relations among them;3. foster interoperability, addressing overlaps and duplication of efforts that hamper their wider uptake and interfere with the creation of standards-compliant systems.
1. MIRIAM Identifiers and Resources / 2. Existing Identifier Schemes
Authors: Juty Nick , Laibe Camille , Le Novere Nicolas
Published: July 2011

(1) An overview of the MIRIAM identifier scheme is presented, together with a description of the supporting tools and resources which allow its use as a robust cross-referencing framework.(2) An overview of existing identifier schemes within the life sciences is presented, describing the status of each scheme, the prerequisites that a user must meet to use them, and their limitations.
CASIMIR & ENFIN
Authors: Hancock John
Published: July 2011

I review the development of draft database registries in the CASIMIR and ENFIN projects and the development of the CASIMIR Database Description Framework.
Intraneuronal Aβ as a trigger for neuron loss: can this be translated into human pathology?
Authors: Bayer Thomas A. , Wirths Oliver
Published: July 2011

In the present review, we summarize the current achievements of modelling early intraneuronal Aβ (amyloid β-peptide) accumulation in transgenic mice with the resulting pathological consequences. Of special importance will be to discuss recent developments and the translation of the results to AD (Alzheimer's disease). N-terminally truncated AβpE3 (Aβ starting with pyroglutamate at position 3) represents a major fraction of all Aβ peptides in the brain of AD patients. Recently, we generated a novel mAb (monoclonal antibody), 9D5, that selectively recognizes oligomeric assemblies of AβpE3 and demonstrated the potential involvement of oligomeric AβpE3in vivo using transgenic mouse models as well as human brains from sporadic and familial AD cases. 9D5 showed an unusual staining pattern with almost non-detectable plaques in sporadic AD patients and non-demented controls. Interestingly, in sporadic and familial AD cases prominent intraneuronal staining was observed. Moreover, passive immunization of 5XFAD mice with 9D5 significantly reduced overall Aβ levels and stabilized behavioural deficits. In summary, we have demonstrated that intraneuronal Aβ is a valid risk factor in model systems and AD patients. This feature of AD pathology was successful in identifying novel low-molecular-mass oligomeric Aβ-specific antibodies for diagnosis and therapy.
A BACwards glance at neurodegeneration: molecular insights into disease from LRRK2, SNCA and MAPT BAC-transgenic mice
Authors: Johnson Sara J. , Wade-Martins Richard
Published: July 2011

BAC (bacterial artificial chromosome)-transgenic mice expressing a transgene from an entire genomic locus under the control of the native promoter offer the opportunity to generate more accurate genetic models of human disease. The present review discusses results of recent studies investigating PD (Parkinson's disease) and tauopathies using BAC-transgenic mice carrying either the LRRK2 (leucine-rich repeat kinase 2), α-synuclein (SNCA) or MAPT (microtubule-associated protein tau) genes. In all lines, expression of the WT (wild-type) gene resulted in physiologically relevant protein expression. The effect of expressing the mutant form of a gene varied depending on the mouse strain or the particular disease mutation used, although it was common to see either neurochemical or behavioural differences in these animals. Overall, BAC technology offers an exciting opportunity to generate a wide range of new animal models of human-disease states.
Mitochondrial β-amyloid in Alzheimer's disease
Authors: Borger Eva , Aitken Laura , Muirhead Kirsty E.A. , Allen Zoe E. , Ainge James A. , Conway Stuart J. , Gunn-Moore Frank J.
Published: July 2011

It is well established that the intracellular accumulation of Aβ (amyloid β-peptide) is associated with AD (Alzheimer's disease) and that this accumulation is toxic to neurons. The precise mechanism by which this toxicity occurs is not well understood; however, identifying the causes of this toxicity is an essential step towards developing treatments for AD. One intracellular location where the accumulation of Aβ can have a major effect is within mitochondria, where mitochondrial proteins have been identified that act as binding sites for Aβ, and when binding occurs, a toxic response results. At one of these identified sites, an enzyme known as ABAD (amyloid-binding alcohol dehydrogenase), we have identified changes in gene expression in the brain cortex, following Aβ accumulation within mitochondria. Specifically, we have identified two proteins that are up-regulated not only in the brains of transgenic animal models of AD but also in those of human sufferers. The increased expression of these proteins demonstrates the complex and counteracting pathways that are activated in AD. Previous studies have identified approximate contact sites between ABAD and Aβ; on basis of these observations, we have shown that by using a modified peptide approach it is possible to reverse the expression of these two proteins in living transgenic animals and also to recover mitochondrial and behavioural deficits. This indicates that the ABAD–Aβ interaction is potentially an interesting target for therapeutic intervention. To explore this further we used a fluorescing substrate mimic to measure the activity of ABAD within living cells, and in addition we have identified chemical fragments that bind to ABAD, using a thermal shift assay.
FDG–PET imaging, EEG and sleep phenotypes as translational biomarkers for research in Alzheimer's disease
Authors: Platt Bettina , Welch Andy , Riedel Gernot
Published: July 2011

The lack of reliable translational procedures applicable to both patients and experimental models are a major obstacle for the advancement of basic research as well as for the development of therapeutics. This is particularly relevant to neurodegenerative disorders such as AD (Alzheimer's disease), where the predictive validity of animal models and procedures applied preclinically have met with little success. Two approaches available for human diagnostics are currently experiencing major advancements in preclinical research: in vivo imaging using MRI (magnetic resonance imaging) or PET (positron-emission tomography) and recordings of brain electrical activity via surface EEG (electroencephalogram). The present paper reviews the results obtained so far in rodent AD models, and summarizes advantages and disadvantages of such procedures.
Axon–glial disruption: the link between vascular disease and Alzheimer's disease?
Authors: Horsburgh Karen , Reimer Michell M. , Holland Philip , Chen Guiquan , Scullion Gillian , Fowler Jill H.
Published: July 2011

Vascular risk factors play a critical role in the development of cognitive decline and AD (Alzheimer's disease), during aging, and often result in chronic cerebral hypoperfusion. The neurobiological link between hypoperfusion and cognitive decline is not yet defined, but is proposed to involve damage to the brain's white matter. In a newly developed mouse model, hypoperfusion, in isolation, produces a slowly developing and diffuse damage to myelinated axons, which is widespread in the brain, and is associated with a selective impairment in working memory. Cerebral hypoperfusion, an early event in AD, has also been shown to be associated with white matter damage and notably an accumulation of amyloid. The present review highlights some of the published data linking white matter disruption to aging and AD as a result of vascular dysfunction. A model is proposed by which chronic cerebral hypoperfusion, as a result of vascular factors, results in both the generation and accumulation of amyloid and injury to white matter integrity, resulting in cognitive impairment. The generation of amyloid and accumulation in the vasculature may act to perpetuate further vascular dysfunction and accelerate white matter pathology, and as a consequence grey matter pathology and cognitive decline.
Alzheimer's disease genetics: lessons to improve disease modelling
Authors: Guerreiro Rita J. , Hardy John
Published: July 2011

In the present review, we look back at the recent history of GWAS (genome-wide association studies) in AD (Alzheimer's disease) and integrate the major findings with current knowledge of biological processes and pathways. These topics are essential for the development of animal models, which will be fundamental to our complete understanding of AD.
Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimer's disease: lessons from ApoE mouse models
Authors: Huang Yadong
Published: July 2011

ApoE4 (apolipoprotein E4) is the major known genetic risk factor for AD (Alzheimer's disease). In most clinical studies, apoE4 carriers account for 65–80% of all AD cases, highlighting the importance of apoE4 in AD pathogenesis. Emerging data suggest that apoE4, with its multiple cellular origins and multiple structural and biophysical properties, contributes to AD in multiple ways either independently or in combination with other factors, such as Aβ (amyloid β-peptide) and tau. Many apoE mouse models have been established to study the mechanisms underlying the pathogenic actions of apoE4. These include transgenic mice expressing different apoE isoforms in neurons or astrocytes, those expressing neurotoxic apoE4 fragments in neurons and human apoE isoform knock-in mice. Since apoE is expressed in different types of cells, including astrocytes and neurons, and in brains under diverse physiological and/or pathophysiological conditions, these apoE mouse models provide unique tools to study the cellular source-dependent roles of apoE isoforms in neurobiology and in the pathogenesis of AD. They also provide useful tools for discovery and development of drugs targeting apoE4's detrimental effects.
Systemic inflammation and delirium: important co-factors in the progression of dementia
Authors: Cunningham Colm
Published: July 2011

It is widely accepted that inflammation plays some role in the progression of chronic neurodegenerative diseases such as AD (Alzheimer's disease), but its precise role remains elusive. It has been known for many years that systemic inflammatory insults can signal to the brain to induce changes in CNS (central nervous system) function, typically grouped under the syndrome of sickness behaviour. These changes are mediated via systemic and CNS cytokine and prostaglandin synthesis. When patients with dementia suffer similar systemic inflammatory insults, delirium is a frequent consequence. This profound and acute exacerbation of cognitive dysfunction is associated with poor prognosis: accelerating cognitive decline and shortening time to permanent institutionalization and death. Therefore a better understanding of how delirium occurs during dementia and how these episodes impact on existing neurodegeneration are now important priorities. The current review summarizes the relationship between dementia, systemic inflammation and episodes of delirium and addresses the basic scientific approaches currently being pursued with respect to understanding acute cognitive dysfunction during aging and dementia. In addition, despite there being limited studies on this subject, it is becoming increasingly clear that infections and other systemic inflammatory conditions do increase the risk of AD and accelerate the progression of established dementia. These data suggest that systemic inflammation is a major contributor to the progression of dementia and constitutes an important clinical target.
Distant cousins: genomic and sequence diversity within the BPI fold-containing (BPIF)/PLUNC protein family
Authors: Bingle Colin D. , Bingle Lynne , Craven C. Jeremy
Published: July 2011

PLUNC (palate, lung and nasal epithelium clone) proteins make up the largest branch of the BPI (bactericidal/permeability-increasing protein)/LBP (lipopolysaccharide-binding protein) family of lipid-transfer proteins. PLUNCs make up one of the most rapidly evolving mammalian protein families and exhibit low levels of sequence similarity coupled with multiple examples of species-specific gene acquisition and gene loss. Vertebrate genomes contain multiple examples of genes that do not meet our original definition of what is required to be a member of the PLUNC family, namely conservation of exon numbers/sizes, overall protein size, genomic location and the presence of a conserved disulfide bond. This suggests that evolutionary forces have continued to act on the structure of this conserved domain in what are likely to be functionally important ways.
The BPI-like/PLUNC family proteins in cattle
Authors: Wheeler Thomas T. , Haigh Brendan J. , Broadhurst Marita K. , Hood Kylie A. , Maqbool Nauman J.
Published: July 2011

Members of the protein family having similarity to BPI (bactericidal/permeability increasing protein) (the BPI-like proteins), also known as the PLUNC (palate, lung and nasal epithelium clone) family, have been found in a range of mammals; however, those in species other than human or mouse have been relatively little characterized. Analysis of the BPI-like proteins in cattle presents unique opportunities to investigate the function of these proteins, as well as address their evolution and contribution to the distinct physiology of ruminants. The present review summarizes the current understanding of the nature of the BPI-like locus in cattle, including the duplications giving rise to the multiple BSP30 (bovine salivary protein 30 kDa) genes from an ancestral gene in common with the single PSP (parotid secretory protein) gene found in monogastric species. Current knowledge of the expression of the BPI-like proteins in cattle is also presented, including their pattern of expression among tissues, which illustrate their independent regulation at sites of high pathogen exposure, and the abundance of the BSP30 proteins in saliva and salivary tissues. Finally, investigations of the function of the BSP30 proteins are presented, including their antimicrobial, lipopolysaccharide-binding and bacterial aggregation activities. These results are discussed in relation to hypotheses regarding the physiological role of the BPI-like proteins in cattle, including the role they may play in host defence and the unique aspects of digestion in ruminants.
Distribution of human PLUNC/BPI fold-containing (BPIF) proteins
Authors: Bingle Lynne , Bingle Colin D.
Published: July 2011

Although gene expression studies have shown that human PLUNC (palate, lung and nasal epithelium clone) proteins are predominantly expressed in the upper airways, nose and mouth, and proteomic studies have indicated they are secreted into airway and nasal lining fluids and saliva, there is currently little information concerning the localization of human PLUNC proteins. Our studies have focused on the localization of three members of this protein family, namely SPLUNC1 (short PLUNC1), SPLUNC2 and LPLUNC1 (long PLUNC1). Western blotting has indicated that PLUNC proteins are highly glycosylated, whereas immunohistochemical analysis demonstrated distinct patterns of expression. For example, SPLUNC2 is expressed in serous cells of the major salivary glands and in minor mucosal glands, whereas SPLUNC1 is expressed in the mucous cells of these glands. LPLUNC1 is a product of a population of goblet cells in the airway epithelium and nasal passages and expressed in airway submucosal glands and minor glands of the oral and nasal cavities. SPLUNC1 is also found in the epithelium of the upper airways and nasal passages and in airway submucosal glands, but is not co-expressed with LPLUNC1. We suggest that this differential expression may be reflected in the function of individual PLUNC proteins.
Functional roles of SPLUNC1 in the innate immune response against Gram-negative bacteria
Authors: Di Y. Peter
Published: July 2011

PLUNC (palate, lung and nasal epithelium clone)-associated gene originally referred to one gene, but now has been extended to represent a gene family that consists of a number of genes with peptide sequence homologies and predicted structural similarities. PLUNC-like proteins display sequence homology with BPI (bactericidal/permeability-increasing protein), a 456-residue cationic protein produced by precursors of polymorphonuclear leucocytes that have been shown to possess both bactericidal and LPS (lipopolysaccharide)-binding activities. The human PLUNC is also known as LUNX (lung-specific X protein), NASG (nasopharyngeal carcinoma-related protein) and SPURT (secretory protein in upper respiratory tract). The gene originally named PLUNC is now recognized as SPLUNC1. Its gene product SPLUNC1 is a secretory protein that is abundantly expressed in cells of the surface epithelium in the upper respiratory tracts and secretory glands in lung, and in the head and the neck region. The functional role of SPLUNC1 in innate immunity has been suggested but not clearly defined. The present review describes recent findings that support antimicrobial and anti-inflammatory functions of SPLUNC1 in Gram-negative bacteria-induced respiratory infection.
Bacteria in the pathogenesis of inflammatory bowel disease
Authors: Flanagan Paul , Campbell Barry J. , Rhodes Jonathan M.
Published: July 2011

Twin studies have demonstrated the importance of environmental factors in the pathogenesis of inflammatory bowel disease, but progress has been relatively slow in identifying these, with the exception of smoking, which is positively associated with Crohn's disease and negatively associated with ulcerative colitis. Genetic studies have identified risk alleles which are involved in host–bacterial interactions and the mucosal barrier, and evidence is building for a likely pathogenic role for changes in the gut microbiome, with respect to both faecal and mucosa-associated microbiota. Some of these changes may be secondary to inflammation, nevertheless promising new therapeutic targets are beginning to emerge.
Genetic relationships betweenA20/TNFAIP3, chronic inflammation and autoimmune disease
Authors: Vereecke Lars , Beyaert Rudi , van Loo Geert
Published: July 2011

A20 [also known as TNFAIP3 (tumour necrosis factor α-induced protein 3)] restricts and terminates inflammatory responses through modulation of the ubiquitination status of central components in NF-κB (nuclear factor κB), IRF3 (interferon regulatory factor 3) and apoptosis signalling cascades. The phenotype of mice with full or conditional A20 deletion illustrates that A20 expression is essential to prevent chronic inflammation and autoimmune pathology. In addition, polymorphisms within the A20 genomic locus have been associated with multiple inflammatory and autoimmune disorders, including SLE (systemic lupus erythaematosis), RA (rheumatoid arthritis), Crohn's disease and psoriasis. A20 has also been implicated as a tumour suppressor in several subsets of B-cell lymphomas. The present review outlines recent findings that illustrate the effect of A20 defects in disease pathogenesis and summarizes the identified A20 polymorphisms associated with different immunopathologies.
Histone deacetylase inhibitors and their potential role in inflammatory bowel diseases
Authors: Edwards Alexander J.P. , Pender Sylvia L.F.
Published: July 2011

IBDs (inflammatory bowel diseases) are lifelong manifestations that significantly impair the quality of life of those who suffer from them. Although many therapies are now available, including immunomodulatory drugs such as Infliximab which have efficacy in IBD, not all patients respond and some patients generate autoantibodies against these drugs. Hence the search for novel treatments is ongoing. HDACs (histone deacetylases) are responsible for condensation of chromatin in the nucleus of cells and inhibition of gene transcription and are often dysregulated during cancer. HDAC inhibitors allow normal gene transcription to be restored and provide attractive therapeutic options, as they have been shown to be anti-inflammatory and anti-proliferative in cancer. Indeed, two HDAC inhibitors have been recently approved for the treatment of cutaneous T-cell lymphoma in the U.S.A. Recent research using animal models has shown that HDAC inhibitors may have a beneficial effect in colitis by boosting levels of Foxp3+ (forkhead box P3+) T-regulatory cells that dampen inflammation. In the present paper, we outline the background to IBD, HDACs and their inhibitors as well as discussing their current use in models of IBD.
Dilution effect of Ar/H2 on the microstructures and photovoltaic properties of nc-Si:H deposited in low frequency inductively coupled plasma
Authors: Zhou H. P. , Wei D. Y. , Xu S. , Xiao S. Q. , Xu L. X. , Huang S. Y. , Guo Y. N. , Yan W. S. , Xu M.
Published: July 2011

This work reports upon the dilution effect of Ar + H2 on the microstructures, optical, and photovoltaic properties of the hydrogenated nanocrystalline silicon (nc-Si:H) thin films. High crystallinity (up to 82.6%) nc-Si:H thin films were fabricated from silane diluted by Ar + H2 in a low-frequency inductively coupled plasma (LFICP) facility at a low temperature of 300 °C. The substitution of H2 by Ar in the diluent gas leads to an increase of the deposition rate, grain size, and crystallinity, and a decrease of the optical bandgap. Varying the Ar content caused a fluctuation of the H concentration and a change of the preferential orientation from (111) to (220) in the synthesized thin films. These effects physically originated from changes of the Ar + H2 + SiH4 plasma environment in the LFICP system. The enhancement of the dissociation of SiH4/H2 molecules by ion Ar+ and the metastable state Ar* were discussed in terms of related chemical reactions between the diluent gases and silane. Furthermore, it was found that a heterojunction solar cell prototype based on the as-deposited nc-Si:H thin films exhibits an excellent photovoltaic response.
Non-invasive nano-imaging of ion implanted and activated copper in silicon
Authors: Ballout Fouad , Samson Jean-Sébastien , Schmidt Diedrich A. , Bründermann Erik , Mathis Yves-Laurent , Gasharova Biliana , Dirk Wieck Andreas , Havenith Martina
Published: July 2011

Using vibrational imaging techniques including Fourier-transform infrared (FTIR) synchrotron microscopy, Raman microscopy, and scattering scanning near-field infrared microcscopy (s-SNIM), we mapped a sample of phosphor and copper ions implanted in a high-purity silicon wafer. While Raman microscopy monitors the structural disorder within the implantation fields, the aforementionedinfrared techniques provide a detailed picture of the distribution of the free carriers. On a large scale (tens of micrometers), we visualized the channeling effects of phosphor dopants in silicon using FTIR microscopy. In comparison, using s-SNIM we were able to image, on a nanometer scale, local variations of the dielectric properties of the silicon substrate due to the activation of copper dopants.
The different initial oxidation kinetics of Zr(0001) and Zr(101−0) surfaces
Authors: Bakradze Georgijs , Jeurgens Lars P. H. , Mittemeijer Eric J.
Published: July 2011

The growth kinetics of thin (thickness <10 nm) oxide films on Zr(0001) and Zr(101−0) single-crystal surfaces were investigated by real-time in situ spectroscopic ellipsometry (RISE) and angle-resolved x-ray photoemission spectroscopy (AR-XPS). To this end, clean crystalline Zr(0001) and Zr(101−0) surfaces were prepared under UHV conditions by a cyclic treatment of alternating ion-sputtering and in vacuo annealing steps. The thus-obtained bare Zr surfaces were then exposed to dry O2(g) in the temperature range of 300 − 450 K (at a partial oxygen pressure of 10−4 Pa), while monitoring the growth kinetics by RISE. It was found that the less-densely packed Zr(101−0) surface oxidizes more readily than the densely packed Zr(0001) surface. A near-limiting thickness of the oxide film on both surfaces is attained only at oxidation temperatures T < 375 K. At T ≥ 375 K, the oxidation rate becomes controlled by the thermally activated dissolution and diffusion of oxygen in the α-Zr substrate. The higher oxidation rate of the Zr(101−0) surface for T ≥ 375 K is attributed mainly to the higher oxygen diffusivity in α-Zr along the Zr(101−0) direction than along the Zr(0001) direction.
Near infrared image sensor with integrated germanium photodiodes.
Authors: Kaufmann R. , Isella G. , Sanchez-Amores A. , Neukom S. , Neels A. , Neumann L. , Brenzikofer A. , Dommann A. , Urban C. , von Känel H.
Published: July 2011

A near-infrared image sensor with monolithically integrated Ge photodiodes is demonstrated. The technology for the integration of the Ge photodiodes into the CMOS process is outlined, and the measurement results of test-diodes and the full imager are discussed in detail. The heterojunction-photodiodes show a quantum efficiency of about 30% up to a wavelength of 1500 nm. A tensile strain of 0.17% was measured in the epitaxial Ge layer, which is in good agreement with the optically measured direct bandgap absorption edge of 1580 nm. The image sensor can be operated at room temperature or with moderate cooling.
C6H and C6D: Electronic spectra and Renner-Teller analysis
Authors: Zhao Dongfeng , Haddad Mohammad Ali , Linnartz Harold , Ubachs Wim
Published: July 2011

Rotationally resolved spectra of the B2Π - X2Π 000 electronic origin bands and 1111 μ2Σ - μ2Σ vibronic hot band transitions of both C6H and C6D have been recorded in direct absorption by cavity ring-down spectroscopy through a supersonically expanding planar plasma. For both origin and hot bands accurate spectroscopic parameters are derived from a precise rotational analysis. The origin band measurements extend earlier work and the 1111 μ2Σ - μ2Σ vibronic hot bands are discussed here for the first time. The Renner-Teller effect for the lowest bending mode ν11 is analyzed, yielding the Renner parameters ε11, vibrational frequencies ω11, and the true spin-orbit coupling constants ASO for both 2Π electronic states. From the Renner-Teller analysis and spectral intensity measurements as a function of plasma jet temperature, the excitation energy of the lowest-lying 111 μ2Σ vibronic state of C6H is determined to be (11.0 ± 0.8) cm−1.
Alignment of dust particles by ion drag forces in subsonic flows
Authors: Piel Alexander
Published: July 2011

The role of ion drag forces for the alignment of dust particles is studied for subsonic flows. While alignment by wake-field attraction is a well known mechanism for supersonic flows, it is argued here that ion-scattering forces become more important in subsonic ion flows. A model of non-overlapping collisions is introduced and numerical results are discussed. For typical conditions of dusty plasma experiments, alignment by drag forces is found strong enough to overcome the destabilizing force from Coulomb repulsion between dust particles. It turns out that the major contribution to the horizontal restoring force originates from the transverse momentum transfer, which is usually neglected in ion drag force calculations because of an assumed rotational symmetry of the flow.
Design and realization of a two-dimensional spatial magnetic field mapping apparatus to measure magnetic fields of metamaterials
Authors: Jiang Quan , Zhou Xiao Yang , Chin Jessie Yao , Cui Tie Jun
Published: July 2011

The two-dimensional (2D) spatial electric-field mapping apparatus [Opt. Express 14, 8694 (2006)] plays an important role in experiments involving metamaterials, such as the verification of free-space and ground-plane invisibility cloaks. However, such an apparatus is valid only for the transverse-electric (TE) mode and is invalid for the transverse-magnetic (TM) mode, as it requires perfectly magnetic conducting (PMC) planes, which do not exist in nature. In this paper, we propose a 2D spatial magnetic-field mapping apparatus based on artificial magnetic conductor (AMC) plates. The AMC structure is designed using periodically perfectly electrical conducting patches with a sub-wavelength size on a dielectric substrate backed with the ground plane, which can simulate a PMC plane. Using two parallel PMC plates to form a TM-wave planar waveguide, we realize the 2D spatial magnetic-field mapping apparatus in order to measure the external and internal magnetic fields of metamaterials. Two types of excitations, a plane-wave source and a magnetic dipole, are used to feed the system. In order to validate the performance of the magnetic-field mapper, two gradient-index metamaterial lenses are measured, and the experimental results are in good agreement with the full-wave simulations.
Sensitive spin-polarization effects in an Aharonov-Bohm double quantum dot ring
Authors: Hedin Eric R. , Joe Yong S.
Published: July 2011

We study spin-dependent transport and spin polarization through two asymmetric quantum dots (QD’s) embedded in the arms of an Aharonov-Bohm (AB) ring, in which spin splitting produced by external magnetic fields is incorporated into a tight-binding model Hamiltonian. This device shows a sensitive spin-polarization effect by manipulating either in-plane or perpendicular magnetic fields. In particular, an extremely small Zeeman splitting leads to a reversal of the polarization polarity in the differential weighted spin-polarization function. Finally, we demonstrate that the degree of spin polarization is affected by the additional AB effects in the ring. In comparison, the polarization is substantially lower through a single QD in a one-dimensional system.
H+ versus D+ transfer from HOD+ to N2: Mode- and bond-selective effects
Authors: Bell David M. , Boyle Jason M. , Anderson Scott L.
Published: July 2011

Reactions of HOD+ with N2 have been studied for HOD+ in its ground state and with one quantum of excitation in each of its vibrational modes: (001)—predominately OH stretch, 0.396 eV, (010)—bend, 0.153 eV, and (100)—predominately OD stretch, 0.293 eV. Integral cross sections and product recoil velocities were recorded for collision energies from threshold to 4 eV. The cross sections for both H+ and D+ transfer rise slowly from threshold with increasing collision energy; however, all three vibrational modes enhance reaction much more strongly than equivalent amounts of collision energy and the enhancements remain large even at high collision energy, where the vibration contributes less than 10% of the total energy. Excitation of the OH stretch enhances H+ transfer by a factor of ∼5, but the effect on D+ transfer is only slightly larger than that from an equivalent increase in collision energy, and smaller than the effect from the much lower energy bend excitation. Similarly, OD stretch excitation strongly enhances D+ transfer, but has essentially no effect beyond that of the additional energy on H+ transfer. The effects of the two stretch vibrations are consistent with the expectation that stretching the bond that is broken in the reaction puts momentum in the correct coordinate to drive the system into the exit channel. From this perspective it is quite surprising that bend excitation also results in large (factor of 2) enhancements of both H+ and D+ transfer channels, such that its effect on the total cross section at collision energies below ∼2 eV is comparable to those from the two stretch modes, even though the bend excitation energy is much smaller. For collision energies above ∼2 eV, the vibrational effects become approximately proportional to the vibrational energy, though still much larger than the effects of equivalent addition of collision energy. Measurements of the product recoil velocity distributions show that reaction is direct at all collision energies, with roughly half the products in a sharp peak corresponding to stripping dynamics and half with a broad and approximately isotropic recoil velocity distribution. Despite the large effects of vibrational excitation on reactivity, the effects on recoil dynamics are small, indicating that vibrational excitation does not cause qualitative changes in the reaction mechanism or in the distribution of reactive impact parameters.
In-situ characterization of Ga2O passivation of In0.53Ga0.47As prior to high-k dielectric atomic layer deposition
Authors: Milojevic M. , Contreras-Guerrero R. , O’Connor E. , Brennan B. , Hurley P. K. , Kim J. , Hinkle C. L. , Wallace R. M.
Published: July 2011

Ga2O interfacial passivation layers (IPLs) on In0.53Ga0.47As are investigated using in-situ monochromatic x-ray photoelectron spectroscopy. The oxide is entirely composed of Ga2O when deposited with an effusion cell temperature of 1500 °C and substrate temperature of 425 °C. The growth on In0.53Ga0.47As reveals slight chemical modification of the surface. The Ga2O behavior and ability to protect the III-V surface are observed following Al2O3 deposition by atomic layer deposition following each precursor pulse. Al2O3 growth by trimethyl-Al (TMA) and water reveals that the IPL undergoes the “clean-up” effect following TMA exposures causing As-As bonding formation resulting in a high interface state density.
Effect of thermal stresses on the dielectric properties of strontium titanate thin films
Authors: Zhang J. , Weiss C. V. , Alpay S. P.
Published: July 2011

We develop a quantitative thermodynamic model to understand the role of thermal stresses on the dielectric permittivity and tunability of (001)-textured polycrystalline monodomain strontium titanate (SrTiO3) films. This methodology is used to compute the dielectric constant and tunability of SrTiO3 films on Si, c-sapphire, LaAlO3, and MgO substrates. Results show that dielectric properties of SrTiO3 depend strongly on the growth/processing temperature TG. For substrates such as MgO that induce compressive in-plane thermal stresses, the dielectric response of SrTiO3 is enhanced. However, for SrTiO3 films on IC-compatible substrates (Si and c-sapphire), thermal stresses can significantly degrade the dielectric permittivity and tunability.
Ultra-deep sequencing of foraminiferal microbarcodes unveils hidden richness of early monothalamous lineages in deep-sea sediments
Authors: Lecroq Béatrice , Lejzerowicz Franck , Bachar Dipankar , Christen Richard , Esling Philippe , Baerlocher Loïc , Østerås Magne , Farinelli Laurent , Pawlowski Jan
Published: July 2011

Deep-sea floors represent one of the largest and most complex ecosystems on Earth but remain essentially unexplored. The vastness and remoteness of this ecosystem make deep-sea sampling difficult, hampering traditional taxonomic observations and diversity assessment. This problem is particularly true in the case of the deep-sea meiofauna, which largely comprises small-sized, fragile, and difficult-to-identify metazoans and protists. Here, we introduce an ultra-deep sequencing-based metagenetic approach to examine the richness of benthic foraminifera, a principal component of deep-sea meiofauna. We used Illumina sequencing technology to assess foraminiferal richness in 31 unsieved deep-sea sediment samples from five distinct oceanic regions. We sequenced an extremely short fragment (36 bases) of the small subunit ribosomal DNA hypervariable region 37f, which has been shown to accurately distinguish foraminiferal species. In total, we obtained 495,978 unique sequences that were grouped into 1,643 operational taxonomic units, of which about half (841) could be reliably assigned to foraminifera. The vast majority of the operational taxonomic units (nearly 90%) were either assigned to early (ancient) lineages of soft-walled, single-chambered (monothalamous) foraminifera or remained undetermined and yet possibly belong to unknown early lineages. Contrasting with the classical view of multichambered taxa dominating foraminiferal assemblages, our work reflects an unexpected diversity of monothalamous lineages that are as yet unknown using conventional micropaleontological observations. Although we can only speculate about their morphology, the immense richness of deep-sea phylotypes revealed by this study suggests that ultra-deep sequencing can improve understanding of deep-sea benthic diversity considered until now as unknowable based on a traditional taxonomic approach.
Craniofacial divergence and ongoing adaptation via the hedgehog pathway
Authors: Roberts Reade B. , Hu Yinan , Albertson R. Craig , Kocher Thomas D.
Published: July 2011

Adaptive variation in craniofacial structure contributes to resource specialization and speciation, but the genetic loci that underlie craniofacial adaptation remain unknown. Here we show that alleles of the hedgehog pathway receptor
Patched1
(
Ptch1
) gene are responsible for adaptive variation in the shape of the lower jaw both within and among genera of Lake Malawi cichlid fish. The evolutionarily derived allele of
Ptch1
reduces the length of the retroarticular (RA) process of the lower jaw, a change predicted to increase speed of jaw rotation for improved suction-feeding. The alternate allele is associated with a longer RA and a more robustly mineralized jaw, typical of species that use a biting mode of feeding. Genera with the most divergent feeding morphologies are nearly fixed for different
Ptch1
alleles, whereas species with intermediate morphologies still segregate variation at
Ptch1
. Thus, the same alleles that help to define macroevolutionary divergence among genera also contribute to microevolutionary fine-tuning of adaptive traits within some species. Variability of craniofacial morphology mediated by
Ptch1
polymorphism has likely contributed to niche partitioning and ecological speciation of these fishes.
RETRACTED: Bacterial persistence by RNA endonucleases
Authors: Maisonneuve Etienne , Shakespeare Lana J. , Jørgensen Mikkel Girke , Gerdes Kenn
Published: July 2011

Bacteria form persisters, individual cells that are highly tolerant to different types of antibiotics. Persister cells are genetically identical to nontolerant kin but have entered a dormant state in which they are recalcitrant to the killing activity of the antibiotics. The molecular mechanisms underlying bacterial persistence are unknown. Here, we show that the ubiquitous Lon (Long Form Filament) protease and mRNA endonucleases (mRNases) encoded by toxin-antitoxin (TA) loci are required for persistence in
Escherichia coli
. Successive deletion of the 10 mRNase-encoding TA loci of
E
.
coli
progressively reduced the level of persisters, showing that persistence is a phenotype common to TA loci. In all cases tested, the antitoxins, which control the activities of the mRNases, are Lon substrates. Consistently, cells lacking
lon
generated a highly reduced level of persisters. Moreover, Lon overproduction dramatically increased the levels of persisters in wild-type cells but not in cells lacking the 10 mRNases. These results support a simple model according to which mRNases encoded by TA loci are activated in a small fraction of growing cells by Lon-mediated degradation of the antitoxins. Activation of the mRNases, in turn, inhibits global cellular translation, and thereby induces dormancy and persistence. Many pathogenic bacteria known to enter dormant states have a plethora of TA genes. Therefore, in the future, the discoveries described here may lead to a mechanistic understanding of the persistence phenomenon in pathogenic bacteria.
Ryanodine receptor leak mediated by caspase-8 activation leads to left ventricular injury after myocardial ischemia-reperfusion
Authors: Fauconnier Jérémy , Meli Albano C. , Thireau Jérôme , Roberge Stephanie , Shan Jian , Sassi Yassine , Reiken Steven R. , Rauzier Jean-Michel , Marchand Alexandre , Chauvier David , Cassan Cécile , Crozier Christine , Bideaux Patrice , Lompré Anne-Marie , Jacotot Etienne , Marks Andrew R. , Lacampagne Alain
Published: July 2011

Myocardial ischemic disease is the major cause of death worldwide. After myocardial infarction, reperfusion of infracted heart has been an important objective of strategies to improve outcomes. However, cardiac ischemia/reperfusion (I/R) is characterized by inflammation, arrhythmias, cardiomyocyte damage, and, at the cellular level, disturbance in Ca
2+
and redox homeostasis. In this study, we sought to determine how acute inflammatory response contributes to reperfusion injury and Ca
2+
homeostasis disturbance after acute ischemia. Using a rat model of I/R, we show that circulating levels of TNF-α and cardiac caspase-8 activity were increased within 6 h of reperfusion, leading to myocardial nitric oxide and mitochondrial ROS production. At 1 and 15 d after reperfusion, caspase-8 activation resulted in S-nitrosylation of the RyR2 and depletion of calstabin2 from the RyR2 complex, resulting in diastolic sarcoplasmic reticulum (SR) Ca
2+
leak. Pharmacological inhibition of caspase-8 before reperfusion with Q-LETD-OPh or prevention of calstabin2 depletion from the RyR2 complex with the Ca
2+
channel stabilizer S107 (“rycal”) inhibited the SR Ca
2+
leak, reduced ventricular arrhythmias, infarct size, and left ventricular remodeling after 15 d of reperfusion. TNF-α–induced caspase-8 activation leads to leaky RyR2 channels that contribute to myocardial remodeling after I/R. Thus, early prevention of SR Ca
2+
leak trough normalization of RyR2 function is cardioprotective.
Functional CD47/signal regulatory protein alpha (SIRPα) interaction is required for optimal human T- and natural killer- (NK) cell homeostasis in vivo
Authors: Legrand Nicolas , Huntington Nicholas D. , Nagasawa Maho , Bakker Arjen Q. , Schotte Remko , Strick-Marchand Hélène , de Geus Sandra J. , Pouw Stephan M. , Böhne Martino , Voordouw Arie , Weijer Kees , Di Santo James P. , Spits Hergen
Published: July 2011

The homeostatic control mechanisms regulating human leukocyte numbers are poorly understood. Here, we assessed the role of phagocytes in this process using human immune system (HIS) BALB/c Rag2−/−IL-2Rγc−/−mice in which human leukocytes are generated from transplanted hematopoietic progenitor cells. Interactions between signal regulatory protein alpha (SIRPα; expressed on phagocytes) and CD47 (expressed on hematopoietic cells) negatively regulate phagocyte activity of macrophages and other phagocytic cells. We previously showed that B cells develop and survive robustly in HIS mice, whereas T and natural killer (NK) cells survive poorly. Because human CD47 does not interact with BALB/c mouse SIRPα, we introduced functional CD47/SIRPα interactions in HIS mice by transducing mouse CD47 into human progenitor cells. Here, we show that this procedure resulted in a dramatic and selective improvement of progenitor cell engraftment and human T- and NK-cell homeostasis in HIS mouse peripheral lymphoid organs. The amount of engrafted human B cells also increased but much less than that of T and NK cells, and total plasma IgM and IgG concentrations increased 68- and 35-fold, respectively. Whereas T cells exhibit an activated/memory phenotype in the absence of functional CD47/SIRPα interactions, human T cells accumulated as CD4+or CD8+single-positive, naive, resting T cells in the presence of functional CD47/SIRPα interactions. Thus, in addition to signals mediated by T cell receptor (TCR)/MHC and/or IL/IL receptor interactions, sensing of cell surface CD47 expression by phagocyte SIRPα is a critical determinant of T- and NK-cell homeostasis under steady-state conditions in vivo.
Electronic properties of the highly ruffled heme bound to the heme degrading enzyme IsdI
Authors: Takayama Shin-ichi J. , Ukpabi Georgia , Murphy Michael E. P. , Mauk A. Grant
Published: July 2011

IsdI, a heme-degrading protein from
Staphylococcus aureus
, binds heme in a manner that distorts the normally planar heme prosthetic group to an extent greater than that observed so far for any other heme-binding protein. To understand better the relationship between this distinct structural characteristic and the functional properties of IsdI, spectroscopic, electrochemical, and crystallographic results are reported that provide evidence that this heme ruffling is essential to the catalytic activity of the protein and eliminates the need for the water cluster in the distal heme pocket that is essential for the activity of classical heme oxygenases. The lack of heme orientational disorder in
1
H-NMR spectra of the protein argues that the catalytic formation of β- and δ-biliverdin in nearly equal yield results from the ability of the protein to attack opposite sides of the heme ring rather than from binding of the heme substrate in two alternative orientations.