bluuebunny/crossref_metadata_2025 huggingface dataset:
Amino Acid Transporters: Roles for Nutrition and Signalling in Embryonic and Induced Pluripotent Stem Cells
Authors: Van Winkle Lon J
Published: September 2013

Amino acids serve both to nourish and signal in cells and, consequently, so do their biomembrane transporters. In fact, some of these transporters may initiate signalling while transporting an amino acid substrate rather than serving simply to transport a signalling molecule. Most amino acid transporters now appear to have been cloned, and virtually all of the cloned transporters are listed in solute carrier tables for easy access online (
http://slc.bioparadigms.org/
). It is more difficult to decide as to which transporters are expressed in a given tissue, and their transport and signalling functions will likely continue to emerge long after all of the transporters have been identified. These ongoing investigations of transporter identification and function for embryonic and induced pluripotent stem cells are illustrated. Surprisingly, characterisation of amino acid transport in these cells is in its infancy. Thus, they serve as an experimental model for investigating the expression of known and novel transporters.

Key Concepts:

At least 55 genes encode amino acid transporters in a minimum of 10 gene families (see tables at
http://slc.bioparadigms.org/
).

An amino acid may be listed as a substrate for a cloned transporter in these tables even though its transport has not been studied in detail.

The characteristics of cloned amino acid transporters may not correspond to the ways they function in cellular physiology.

Stem cells serve as an experimental model for investigating the expression of known and novel transporters.

Threonine uptake and glutamate exodus from stem cells via transporters each fosters cellular proliferation.

Glutamate exodus from stem cells is needed to stimulate glutamate receptors.

Proline uptake by stem cells promotes their differentiation.

mTOR signalling in stem cells is necessary for both proline‐induced differentiation and threonine‐induced proliferation.

Both threonine and glutamate promote stem cell proliferation by enhancing the expression of cMyc.

Threonine and glutamate likely foster proliferation in human as well as mouse stem cells.
Integrin Superfamily
Authors: Danen Erik HJ
Published: September 2013

Integrins are cell‐surface adhesion molecules formed from eight different β chains and 18 different α chains that assemble as heterodimeric transmembrane receptors to mediate cell–cell and cell–matrix interactions. The integrin superfamily first emerged in the metazoa and has expanded with evolution creating 24 different integrins in humans, each recognising a distinct subset of extracellular ligands. Ligands include extracellular matrix proteins found in basement membranes such as laminins or in fibrilar matrices such as collagen or fibronectin meshworks, as well as counter receptors on neighbouring cells. The adhesive potential of integrins can be regulated and their cytoplasmic tails connect through a dynamic protein interaction network to the cytoskeleton. Thus, integrins provide cells with the capacity to sense and respond to their microenvironment and they control vital cellular functions for embryonic development, tissue homoeostasis, blood clotting and immunity.

Key Concepts:

Integrins are heterodimeric transmembrane receptors that mediate cell adhesion to the microenvironment.

More than 600 Mya integrins emerged and the integrin superfamily has expanded throughout evolution.

In humans, 24 different integrins are formed from 18 α and 8 β subunits.

Integrins recognise a wide range of ligands, including extracellular matrix proteins, counter receptors on neighbouring cells, plasma proteins, and microbes and viruses.

Integrins couple the extracellular microenvironment to the cytoskeleton through a protein interaction network associated with their cytoplasmic tails.
Immunological Tolerance: Therapeutic Induction
Authors: Mair Iris , Reynolds Ben C , Anderton Stephen M
Published: September 2013

When the natural mechanisms of immune tolerance break down, autoimmune or allergic disease can result. There is considerable experimental evidence that the ultimate response to antigen, full immunity or tolerance, is dependent on the activation status of the antigen‐presenting dendritic cells, with those in steady state inducing tolerance. Current therapeutic options either deplete immune cell populations, interfere with immune cell trafficking to the tissues or inhibit inflammatory cytokine function or lymphocyte signalling. Although these treatments can be effective for certain diseases, they carry with them significant adverse effects and it is unlikely that they induce true, long‐lived immune tolerance. Cellular therapies using either tolerogenic dendritic cells or regulatory T cells may be able to achieve this. Alternatively, administration of antigen in tolerogenic form can provide the most specific therapy, with the least risk of adversely affecting normal immune function against infection or neoplasia.

Key Concepts:

Peripheral tolerance mechanisms consist of lymphocyte apoptosis, anergy and regulation.

Current therapeutic options for the clinic can be effective, but in general are nonspecific and may not provide long‐term tolerance.

Dendritic cell (DC) activation status determines the type of immune response. Activated DC provokes immunity whereas steady‐state DC promotes tolerance.

‘Tolerogenic’ DC can be administered to give protection from autoimmune disease, allergy and graft rejection as shown in animal models, and are being tested for clinical application.

Administration of antigen in tolerogenic form (without adjuvant) also provides protection from disease in animal models; however, clinical translation is proving challenging.

Transfer of antigen‐specific regulatory T cells (Treg) can also protect against disease, and can be curative in some models.

Translation of cellular therapies (using DC or Treg) or tolerogenic antigen will require a fuller understanding of the critical autoantigens/epitopes that drive autoimmune pathology.
Rapid Evolution of Genes on the Human X Chromosome
Authors: Kvikstad Erika M , Makova Kateryna D
Published: September 2013

There is considerable interest in determining the sequences that are evolving rapidly in our genome, as these may well confer an advantage that has helped to propel the evolution of our species. Owing to sex chromosome‐specific modes of natural selection, genes on the human X chromosome are evolving rapidly in comparison to genes located on autosomes. However, it is not clear to what extent these loci are evolving adaptively or due to other molecular (mutation and recombination) and evolutionary (selection and drift) processes. Biological factors in addition to selection could contribute to elevated rates, such as the evolutionary history and genomic features of the X chromosome. Additionally, genes on the X are distributed in a nonrandom fashion, potentially influencing their evolution. Furthermore, the function and expression profile of each X‐linked gene may play a role in determining its evolutionary rate. Recent technological advances have provided rich datasets for the investigation and unravelling of these confounding factors.

Key Concepts:

The human X chromosome is a compilation of biological contradictions: it is remarkably conserved in gene content between species, while being highly diverged from its Y counterpart; it is present in twice as many copies in females than males, and yet enriched for genes with male‐biased expression.

The theory of fast‐X evolution is based on the observation that genes on the X in XY males will be more easily targeted by natural selection, thus accelerating the rate of adaptive evolutionary change for beneficial mutations.

Many genes on the X tend to evolve more slowly than their Y counterparts, due to the higher mutation rate in the male germline.

Genes on the X are likely to be involved in reproduction, sex biased in their expression profile and tissue‐specific in nature – each of these factors has been linked to accelerated rates of sequence and/or expression divergence independently of the fitness advantage of the associated allele.

Although fast‐X has been observed in different taxa, the relative contribution of the underlying evolutionary forces (selection for advantageous mutations versus drift of slightly deleterious mutations) can be very different between species.
Developmental Models for Wound Healing
Authors: Matsubayashi Yutaka , Millard Tom H
Published: September 2013

The bodies of animals and humans frequently sustain damage as a result of injury or disease, and the ability to repair this damage is essential for life. Tissue repair, or wound healing, is a complex process which is difficult to study experimentally and is, therefore, not fully understood. Over recent years, various studies have identified striking similarities between tissue repair and the process of morphogenesis in which tissues are originally formed during embryonic development. This has raised the possibility of using developmental processes as model systems to help in better understanding of tissue repair. This article describes how comparative studies of embryonic morphogenesis and tissue repair have improved understanding of the mechanisms of repair. The article further discusses the key processes and regulatory mechanisms that are shared between development and repair, including important recent developments in the field.

Key Concepts:

The behaviour of cells during the repair of damaged tissues often parallels that observed when tissues are initially formed during embryogenesis.

Developmental processes such asDrosophiladorsal closure and mouse eyelid closure can be used as models to help in understanding of wound healing.

Common cytoskeletal and signalling machineries regulate cell behaviour during the reepithelialisation episode of wound healing and also during developmental epithelial closure events.

Key regulators of epithelial closure include the Rho GTPases, the JNK cascade and the planar cell polarity pathway.

Coordinated collective migration of many cells is necessary for both wound healing and developmental epithelial remodelling.

Mechanical signalling seems to be important for tissue remodelling, but its molecular mechanisms still largely remain elusive.

Inflammatory cells play instructive roles during tissue remodelling.

Novel techniques such as advanced bioimaging and mathematical modelling will help to uncover the general mechanisms underpinning wound healing and developmental tissue remodelling.
Patch Fluorometry
Authors: Zheng Jie , Yang Fan
Published: September 2013

Patch fluorometry is a biophysical technique that combines the power of patch clamping and optical recording, with the aim of correlating local conformational rearrangements in ion channel protein with the channel gating process. This is achieved through simultaneous recordings of fluorescence and current signals from the same population of ion channels in a membrane patch. The method can be applied to studies of ion channel structure–function relationship as well as membrane protein dynamics. Unlike nuclear magnetic resonance or other biophysical methods for structural study, patch fluorometry provides real‐time dynamic structural information from ion channels in their native membrane environment whereas they carry out their functions. Recent advances greatly expand the scope of this powerful method, allowing researchers to follow structural changes in channel protein with unprecedented spatial and temporal resolutions and accuracy.

Key Concepts:

Ion channels achieve their cell‐sensor functions through changes in conformation in response to physical or chemical stimuli.

Conformational changes in an ion channel protein do not always alter the current, and are thus invisible to patch clamp recording.

Fluorescence emission is highly sensitive to the local environment of fluorophores.

Site‐directed fluorophores serve as sensors for local structural changes.

Patch fluorometry allows direct correlation between channel protein conformational changes and the functional states of the channel.
Forkhead Transcription Factors in Genetic Disease
Authors: Baetens Dorien , Verdin Hannah , Cools Martine , De Baere Elfride
Published: September 2013

Forkhead transcription factors represent an important family of proteins, for which more than 2000 family members have been identified so far, 26 of which can be found in humans.FOXgenes exhibit many important functions in both development and adult life. Therefore, it is not surprising that alterations in these genes can cause of a broad range of developmental diseases and cancer. Today, 13FOXgenes are associated with developmental disorders. Mutations in five of them (FOXC1,FOXC2,FOXD3,FOXE3andFOXL2) lead to an ocular phenotype, while mutations in three genes (FOXG1,FOXP1andFOXP2) are a known cause for neurodevelopmental disorders, mutations in two (FOXL2andFOXO3A) are associated with premature ovarian failure and mutation in other two genes (FOXN1andFOXP3) are involved in immunodeficiency syndromes. Finally,FOXF1mutations cause a lung development disorder. In this article, the different developmental disorders caused by mutations inFOXgenes are reviewed. In addition, the article briefly touches cancers caused by genetic defects inFOXgenes.

Key Concepts:

Forkhead transcription factor genes represent an important gene family, consisting out of more than 2000 members. In human, 26 family members have been identified and there are 8FOXgene clusters.

The forkhead domain is built up by three α‐helices, two β‐sheets and two loops. These loops resemble wings of a butterfly, giving the family its nickname: winged helix transcription factors.

Forkhead transcription factors play important roles in a wide range of signalling pathways.

Mutations inFOXgenes are known to cause hereditary developmental disorders. Five mutatedFOXgenes are associated with an ocular phenotype.

Forkhead transcription factors are also involved in cancer and ageing.
Genetics of Phosphate Regulation Disorders
Authors: Gattineni Jyothsna
Published: September 2013

Phosphate is an abundant anion in humans and plays an important role in many metabolic processes. Maintenance of phosphate homoeostasis is critical, and kidney plays an important role in the regulation of phosphate homoeostasis. Phosphate reabsorption by the kidney is the final determinant of serum phosphate levels. Fibroblast growth factor 23 (FGF23), parathyroid hormone and Klotho are important hormones that regulate phosphate homoeostasis. Dysregulation of FGF23 is the most common inherited cause of hypophosphatemic and hyperphosphatemic disorders. Mutations of sodium phosphate cotransporters, responsible for phosphate reabsorption, also result in inherited disorders of phosphate homoeostasis. Recent discoveries in the field of FGF23 have led to better understanding of the pathophysiology of many of the inherited hypophosphatemic and hyperphosphatemic disorders.

Key Concepts:

Maintenance of normal phosphate homoeostasis is integral for many bodily functions.

Both hyperphosphatemia and hypophosphatemia have detrimental effects.

Fibroblast growth factor 23 (FGF23), parathyroid hormone and Klotho are well‐known phosphaturic hormones.

Sodium phosphate cotransporters (NaPi‐2a and NaPi‐2c) that are present in the proximal tubule of the kidney are the final regulators of phosphate reabsorption. Mutations of sodium phosphate cotransporters result in hypophosphatemia.

Disturbances in hormones such as FGF23, parathyroid hormone and Klotho result in many inherited hypophosphatemic and hyperphosphatemic disorders.

X‐linked hypophosphatemic rickets is the most common form of inherited rickets in children and is due to excess FGF23.

Autosomal dominant hypophosphatemic rickets, autosomal recessive hypophosphatemic rickets, fibrous dysplasia and osteoglophonic dysplasia are also inherited hypophosphatemic disorders resulting from excessive FGF23.

Tumoural calcinosis is an inherited hyperphosphatemic disorder resulting from decreased FGF23 activity.
Genomic Studies of Adaptation in Natural Populations
Authors: Martin Simon H , Jiggins Chris D
Published: September 2013

Understanding the genetic basis of adaptive evolution is a problem almost as old as evolutionary biology itself. Recent advances in genome sequencing and the ability to generate genomic samples from natural populations promises to provide answers to many long‐standing questions. The recent surge in genomic studies of adaptation has been accompanied by the development of numerous powerful techniques to analyse these enormous data sets. The state of the field is reviewed in this article, with an emphasis on the various approaches used. This article covers both ‘top‐down’, used to identify the genetic basis of a known trait, and ‘bottom‐up’ approaches, used to identify the footprints of selection on the genome. It shows how recent studies highlight the benefits of combining multiple methods and also discusses important goals for the future of the field.

Key Concepts:

Association mapping is used to identify genomic loci that control a trait of interest, by identifying molecular markers that display genotype‐by‐phenotype associations.

Either offspring from controlled crosses or population samples can be used as the recombinant ‘mapping population’.

Numerous loci underlying important adaptive traits have been identified using association mapping; however, this approach is biased towards loci of large effect and may not accurately capture the true genetic architecture of a trait.

Genome‐wide scans for the footprints of selection are less sensitive to effect‐size biases but are naive with regard to the trait(s) under selection.

Selective sweeps can be identified by the presence of reduced variation, enhanced linkage disequilibrium and a shift in the ‘site frequency spectrum’.

Loci under divergent selection between populations can be identified as outliers displaying greater differentiation between populations than expected under neutral evolution.

By comparing between‐species divergence with within‐species polymorphism at synonymous and nonsynonymous sites, it has been estimated that a large proportion of the genome is involved in adaptive evolution.
Molecular Evolution of Genes Involved in Vertebrate Sex Determination
Authors: Ito Michihiko , Mawaribuchi Shuuji
Published: September 2013

Four sex‐determining genes (SDGs) had been reported in vertebrates until 2011: Y‐linked
Sry
in eutherian mammals, Z‐linked
Dmrt1
in the chicken, W‐linked
Dm‐W
in the African clawed frog

Xenopus laevis

and Y‐linked
Dmy
(also called as
dmrt1bY
) in the teleost fish medaka. These genes encode
deoxyribonucleic acid (DNA)
‐binding proteins. Both
Dm‐W
and
Dmy
emerged through duplication of
Dmrt1
, whereas
Sry
evolved from allelic
Sox3
. Interestingly, in 2012, four different types of SDGs, which might not encode DNA‐binding proteins, were reported in teleost fish: Patagonian pejerrey
amhy
,

Oryzias luzonensis

GsdfY
,

Takifugu rubripes

Amhr2
, and rainbow trout
sdY
. Although these SDGs are all sex chromosome‐linked, a variety of them may be involved in the evolution of sex chromosomes. A coevolution model of SDGs and sex chromosomes has been proposed: undifferentiated or specialised sex chromosomes could allow diversity of SDGs or tend to fix a certain SDG, respectively, during species diversity in vertebrates.

Key Concepts:

There are a variety of SDGs including transcription factor genes and TGF‐β signal‐related genes.

SDGs could be classified into two types: insertion and mutations after duplication, and mutations of an allelic gene.

SDGs
Dmy
/
Dm‐W
and
Sry
, which evolved through duplication of
Dmrt1
and an allelic mutation of
Sox3
, respectively, have a higher substitution rate than their prototype genes.

Cis
‐regulatory elements in most of the SDGs should have evolved for their mRNA expressions at a sex‐determining stage, but only an amino acid change by SNP between
Amhr2
alleles could determine the sex in fugu fish.

SDGs and sex chromosomes would have coevolved during vertebrate evolution: undifferentiated or specialised sex chromosomes could allow diversity of SDGs or tend to fix a certain sex‐determining gene, respectively.
Causes and Consequences of Structural Genomic Alterations in the Human Genome
Authors: Hart Lesley , O'Driscoll Mark
Published: September 2013

The revolutionary development and application of microarray‐based comparative genomic hybridisation (aCGH) technology within the past decade or so represents a profound and continuing fundamental contribution to the molecular dissection and characterisation of complex human disorders: disorders ranging from developmental pathologies including intellectual disability, schizophrenia and autism spectrum disorders to more common conditions such as cancer. A unifying underlying feature here is that these disorders are associated with complex structural rearrangements in chromosomes. aCGH technology application has also enabled the refinement of ‘old’ and identification of ‘new’ mechanisms to explain the origin of these complex chromosomal alterations. Interestingly, these structural variations can also incorporate genes whose products play fundamental roles in aspects of
deoxyribonucleic acid
repair, replication and recombination, thereby having an impact on genome‐wide stability and integrity. In this article, the mechanisms underlying complex structural chromosomal rearrangements are reviewed and their implications with respect to genome‐wide stability are discussed.

Key Concepts:

The locus‐specific frequency of CNVs are orders of magnitude higher than SNPs.

CNVs are a significant contributor to human disease.

CNVs can be recurrent or nonrecurrent.

Nonallelic homologous recombination between low copy number repeats is a common mechanism of recurrent CNV.

Nonhomologous end joining can underlie nonrecurrent CNVs.

Complex Chromosomal Rearrangements (CCRs) are complex CNVs involving multiple contiguous changes in copy number.

DNA replication based‐mechanisms have been invoked to explain CCRs.

CNVs are fundamental contributors to cancer development and progression.

CNVs incorporating genome instability pathway components can adversely impact on genome‐wide stability.

Certain genomic disorders are characterised by impaired genome stability.
Concepts in Fetal Gene Therapy
Authors: Mattar Citra N , Biswas Arijit , Choolani Mahesh , Chan Jerry KY
Published: September 2013

Many congenital anomalies have a genetic basis. With the evolution of fetal therapy over the past half‐century since the first intrauterine transfusion was performed, novel treatments including genetic correction of such diseases may be possible. Using a variety of therapeutic vector constructs, proof of concept for fetal gene therapy (FGT) has been achieved in several single‐gene disorders including thalassaemia and haemophilia B. The current challenge is to determine the long‐term safety and efficacy of FGT, as well as important maternal bystander effects, in clinically relevant large‐animal models, and to individualise FGT strategies according to the disease of interest, with respect to target organ and vector construct.

Key Concepts:

Fetal gene therapy research has been directed towards monogenic diseases, but there is scope for this target to be expanded to include chromosomal and structural anomalies in the near future.

The fetus, weighing several log‐fold less than an infant or child, allows gene therapy to be economised, facilitating a widespread effect with a smaller amount of vector, and an easier task in adjusting vector dose to achieve the desired outcome.

The goal of fetal gene therapy is to achieve phenotypic rescue of a lethal or severely morbid monogenic disease. If cure is not achievable, correction of the disorder to the point of downgrading its severity is the other worthy goal.

In addition to genetic correction, treatment initiated in early gestation may encourage tolerance to the gene therapy vector and transgenic protein, events critical to facilitating sustained transgene expression.

Gene therapy may be achievedin vivo, through the direct introduction of the transgene enveloped in a vector, orex vivowith the use of genetically manipulated stem cells to achieve the desired effect.

Proof of this concept has been demonstrated using viral vectors in small genetic knockout models of diseases, including haemophilia B and inborn errors of metabolism disease.

Evidence of safety and efficacy has been demonstrated in sheep and nonhuman primates which, being physiologically more representative of human pregnancies, are considered robust preclinical models.

The success of this intervention depends on the efficacy of cellular transduction, accessibility of the target organ, the type of vector used, immune maturity and route of vector administration.

Fetal gene therapy must be optimised to each condition of interest, in terms of appropriate gestation at intervention, efficacy of vector and principal objectives of therapy (gestation at which peak transgene expression is desired, importance of immune maturity and desired duration of transgene expression).

Several ethical issues raised by fetal gene therapy have to be considered in anticipation of eventual clinical translation. These include reliance on data from preclinical large animal models that are not genetic knockouts, the consequences of partial correction, the possibility of germ‐line transmission and the long‐term risk of oncogenesis.
Inorganic Spintronic Materials
Authors: Bao Ningzhong , Gupta Arunava
Published: September 2013

Utilization of the spin degree of freedom in metallic, semiconducting, and insulating materials is an active pursuit for spin‐based devices. Besides some existing devices, many new ones have been proposed on the basis of spin‐dependent transport. For these devices to become reality, new materials and methods for efficient injection, manipulation, and detection of electron spins are required. In this article, we present an overview of the research progress in inorganic spintronic materials, with emphasis on their structural and magnetic properties. The materials discussed include perovskite‐type oxides, spinel ferrites, transition metal monoxides, iron oxides, nickel oxides, chromium oxides, layered ruthenates, and chromium‐based chalcogenides. Recent advancements related to single‐phase multiferroic materials are also presented.
B. Electron Motion in Highly Excited States and Radiationless Transitions. General Dynamical Theory and Experiment. Intramolecular Dynamics and Charge Separation in Large Systems
Authors: Jortner Joshua , Bixon M.
Published: September 2013

We adopt the theory of intramolecular dynamics to explore charge separation and recombination in two classes of ‘isolated’ solvent‐free molecular systems: (A) Supermolecules containing bridged electron donor and electron acceptor, where electron transfer occurs on a spatial scale of ≈︁ 10 Å. (B) Ultrahigh molecular Rydberg excitations with a principle quantum number n ≃ 50−300 and spatial dimensions of ≈︁ 104 Å, where relaxation processes, e.g., electron‐core recombination via internal conversion or predissociation, and charge separation by autoionization, are manifested. The molecular limit for photoinduced long‐range ET in isolated supermolecules [class (A)] is treated on the basis of the statistical limit for interstate radiationless transitions, which involve either a direct or a mode‐selective mediated coupling. The level structure, optical excitation modes and dynamics of high molecular Rydbergs [class (B)] interrogated by time‐resolved ZEKE (zero‐electron kinetic energy) spectroscopy, are treated by the effective Hamiltonian formalism. We pursue the formal analogy between the coupling, accessibility and decay of ultrahigh Rydbergs in an external weak (F = 0.01−1.0 V/cm) electric field and intramolecular (interstate and intrastate) relaxation in a bound level structure. Model calculations for the field‐induced (l) mixing reveal that the Rydberg dynamics is characterized by two distinct (≈︁ ns and ≈︁μs) time scales. Up to date, long time‐resolved (10 μs − 100 ns time scales) nonexponential decay of ZEKE Rydbergs was experimentally documented, in accord with our analysis. The predicted existence of the short decay times (1 − 10 ns) was not yet subjected to an experimental test.
F. Laser Control and Femtosecond Dynamics. Femtosecond Dynamics of Reactions: Elementary Processes of Controlled Solvation
Authors: Zewail Ahmed H.
Published: September 2013

The summary presented here attempts to describe recent studies in our laboratory of the effect of microscopic solvation, controlled in a cluster cage or fluid environment, on the elementary dynamics of reactions. We selected reactions of two atoms (dissociation) and many atoms, proton transfer in acid‐base reactions and double‐bond twisting in isomerization reactions.
Quantum Calculations of Femtosecond Pump‐Probe Spectroscopy in K2 for Low Laser Field Intensities
Authors: De Vivie‐Riedle Regina , Reischl Birgit
Published: September 2013

Quantum dynamical simulations of pump‐probe femtosecond experiments of the potassium dimer are presented for low laser field excitation. The results show that a (1 + 2)‐photon pump‐probe process takes place. The 21 Π g state determines as an optimal resonant state the transition process. Its properties open the pathway for the 2‐photon ionization in the outer turning point region. The oscillations in the total ion yield of K2+ correspond to the motion of the vibrational wavepacket prepared by the pump laser in the A1Σu+ state of the neutral K2 molecule. Contributions of wavepackets in other electronic states are not detected in the ionization signal.
The Rotational and Rotation‐Bending Spectrum of HC15NO: An Extended Analysis of the Spectral Regions 18‐40 GHz, 90‐440 GHz and 170‐1300 cm−1
Authors: Islami Kastriot , Jabs Wolfgang , Preusser Jürgen , Winnewisser Manfred , Winnewisser Brenda P.
Published: September 2013

The rotational spectrum of the 15N‐substituted quasilinear molecule fulminic acid, HCNO, has been measured in the frequency range from 90 to 440 GHz covering rotational transitions up to J = 19←18. Rotational transitions arising from HC15NO molecules in 52 vibrational levels were detected and assigned. Additional information was obtained by measuring the direct l‐type transitions for v5 = 1 and 3 and for v4 = 1 in the frequency range from 18 to 40 GHz. With the information from the rotational spectrum the analysis of the far and mid‐infrared spectra (170‐1300cm−1), which was started by Wagner et al. [J. Mol. Spectrosc. 162, 82 (1993)], could be extended so that the vibrational term values of HC15NO were determined for almost every state below 2500cm−1. The assignment of the 114 subbands involved allowed in turn the assignment of 25 subbands in the mid‐infrared from the data of Quapp et al. [J. Mol. Spectrosc. 160, 540 (1993)]. The infrared spectra were recorded with a Bruker IFS 120 HR interferometer at resolutions between 0.0019 and 0.0034 cm−1. For the vibrational states (v1 v2v3v4v5) = (00000), (00001), (00002), (00003), (00004), (00010), (00011) an (00100) the spectroscopic constants of an effective Hamiltonian for linear molecules could be improved by combining the already published infrared data with the millimeter wave, microwave and newly assigned infrared data presented in this work. For the states (00013) and (00101) these constants were also calculated. A calibration problem with the infrared data became obvious and important. The effects of a Fermi‐type resonance between the vibrational levels (00004)oe and (00100)oe and a Coriolis resonance between the states (00002) and (00010) on the rotational and rovibrational spectra were observed and analysed. The difficulties encountered in determining the Coriolis resonance parameters are discussed.
Association of Modic changes with health-related quality of life among patients referred to spine surgery
Authors: Määttä Juhani , Kautiainen Hannu , Leinonen Ville , Niinimäki Jaakko , Järvenpää Salme , Koskelainen Tatu , Mäkelä Pirkka , Pesälä Juha , Nyyssönen Timo , Savolainen Sakari , Airaksinen Olavi , Kyllönen Eero , Cheung Kenneth M.C. , Karppinen Jaro
Published: September 2013

Background and purpose

Modic changes (MC) are bone marrow and vertebral endplate lesions seen in magnetic resonance imaging (MRI) which have been found to be associated with low back pain (LBP), but the association between MC and health-related quality of life (HRQoL) is poorly understood. The aim of this study was to assess the relationship between MC and HRQoL among patients referred to spine surgery.

Methods

The study population consisted of 181 patients referred to lumbar spine surgery in Northern and Eastern Finland between June 2007 and January 2011. HRQoL was assessed using RAND-36 health survey. Lumbar MC were evaluated and classified into ‘No MC’, ‘Type I’ (Type I or I/II), and ‘Type II’ (Type II, II/III or III).

Results

In total, 84 patients (46%) had MC. Of these, 37% had ‘Type I’ and 63% ‘Type II’. Patients with MC were older, more likely females, had longer duration of LBP and a higher degree of disc degeneration than patients without MC. The total physical component or physical dimensions did not differ significantly between the groups. The total mental component of RAND-36 (P = 0.010), and dimensions of energy (P = 0.023), emotional well-being (P = 0.012) and emotional role functioning (P = 0.016) differed significantly between the groups after adjustments for age and gender. In the mental dimension scores, a statistically significant difference was found between ‘No MC’ and ‘Type II’.

Conclusions

Among patients referred to spine surgery, MC were not associated with physical dimensions of HRQoL including dimension of pain. However, ‘Type II’ MC were associated with lower mental status of HRQoL.

Implications

Our study would suggest that Type II MC were associated with a worse mental status. This may affect the outcome of surgery as it is well recognized that patients with depression, for instance, have smaller improvements in HRQoL and disability. Thus the value of operative treatment for these patients should be recognized and taken into consideration in treatment. Our study shows that MC may affect outcome and thus clinicians and researchers should be cognizant of this and take this into account when comparing outcomes of surgical treatment in the future. A longitudinal study would be needed to properly address the relationship of MC with surgical outcome.
Hall and Chambers: Oakham Castle Reconsidered
Authors: Hill Nick
Published: September 2013

The late twelfth-century aisled hall at Oakham Castle, Rutland, is well known as the earliest and most complete building of its type in England. This study, based on detailed fabric analysis and little-known excavations of the 1950s, puts forward a new theory for the building's development. It is proposed that the original hall had attached lean-to buildings at both gable ends, probably built of timber, housing services and other lesser rooms. Like other early halls, the principal chamber at Oakham took the form of a free-standing chamber block, some of whose features have been later incorporated in the surviving hall, including its great east window. Tree-ring dating has shown that, although the roof was rebuilt around 1737, many original timbers survive from the 1180s. A comparative study of other early halls is made, to set Oakham into its wider Anglo-Norman context.
The effects of precipitation regime on soil carbon pools on the Yucatan Peninsula
Authors: Roa-Fuentes Lilia L. , Hidalgo Claudia , Etchevers Jorge D. , Campo Julio
Published: September 2013

The effects of precipitation regime on the size of soil carbon (C) pools were compared in mature tropical dry forests of the Yucatan Peninsula. Our study included three forest stands in each, a dry site (potential evapotranspiration ratio = 3.2 mm mm−1; mean annual precipitation = 537 mm), a wetter site (2.0 mm mm−1; 993 mm) and a site in which water was comparatively less limiting (1.3 mm mm−1; 1086 mm). At each site, soil C pools in dead fallen phytomass (includes leaves, flowers, fruits, small twigs and deadwood debris) deposited on the litter layer and in roots and organic matter of the mineral soil (from the upper 10 cm) were measured in samples collected during the dry season. A high proportion of the total C pool (93–95%) was in the top 10 cm of soil in all forest sites. The smallest C pool was in roots (1.8–2.4% of the total C), meanwhile the C in the litter layer represented 3–5% of the total pool. These patterns were observed irrespective of study site. However, distribution of C (i.e. wood debris vs. fine litter) varied across sites; the proportion of the forest-floor C pool in wood debris decreased from 80% in the driest site, to 51% and 42% in 993-mm and 1086-mm sites, respectively. Overall, we observed that three pools (wood debris, roots and soil organic C) provide evidence for the significant decrease in soil C storage with increase in mean annual precipitation in Yucatan Peninsula. A potential explanation for this unexpected pattern includes an increasing C turnover time with decreasing mean annual precipitation, resulting in higher C accumulation per unit of C input in the driest site.
Testing pathogen host specificity: a reciprocal field experiment in two types of tropical forest on Hainan, China
Authors: Zheng Wen , He He , Xiao Lin , Yu Shixiao
Published: September 2013

The Janzen–Connell hypothesis suggests that highly specific pathogens decrease seedling survival close to the parent plant; however, the underlying mechanism remains unclear. Here, we tested the host specificity of soil pathogens to germinating seeds of Cyclobalanopsis fleuryi and Cryptocarya chinensis in tropical montane rain forest and cloud forest on Hainan, south China. Rhizospheric soils surrounding eight adult trees per species were collected in each forest type and divided into five soil treatments: parent, fungicide-sterilized, autoclave-sterilized, Fusarium-added and Pythium-added soils. Surface-sterilized seeds were sown in each of the five soil treatments and grown in two forest types. The seed germination percentages were significantly higher in sterilized soils (C. fleuryi, 41.5%; C. chinensis, 29.4%) than in non-sterilized soils (C. fleuryi, 28.3%; C. chinensis, 17.1%) in montane rain forest. The seed germination percentages in rhizospheric soil of conspecific parent trees were significantly lower in montane rain forest (C. fleuryi, 17.3%; C. chinensis, 10.5%) than in cloud forest (C. fleuryi, 37.1%; C. chinensis, 21.1%). Our results also suggest that the level of pathogen activity in each tree species varies depending on the environment. Our results support the hypothesis that host-specific pathogens shape tree species composition by differentially affecting seed germination under different environmental conditions.
Groups of p-deficiency one
Authors: THILLAISUNDARAM ANITHA
Published: September 2013

In a previous paper, Button and Thillaisundaram proved that all finitely presented groups of p-deficiency greater than one are p-large. Here we prove that groups with a finite presentation of p-deficiency one possess a finite index subgroup that surjects onto the integers. This implies that these groups do not have Kazhdan's property (T). Additionally, we show that the aforementioned result of Button and Thillaisundaram implies a result of Lackenby.
Economics and Ethics under the Same Umbrella: Edgeworth's ‘Exact Utilitarianism’, 1877–1881
Authors: KAMINITZ SHIRI COHEN
Published: September 2013

Edgeworth's original mathematical formalization of utilitarianism as presented in his works of 1877–81 illustrates an intriguing phase in the mutually intertwined history of economics and utilitarianism. In this article I analyse Edgeworth's motivations and point to its interesting implications. In particular, it is pointed out that the starting point of Edgeworth's project had little to do with the field of economics, but formed part of an attempt to present utilitarianism in the most scientific way possible; an attempt made in the context of intensive dispute between the three opposing camps in the field of ethics at the time. Nevertheless, the project concluded with the monographMathematical Psychics(1881) that embodied an original relationship between economics and utilitarianism.
SET SIZE AND THE PART–WHOLE PRINCIPLE
Authors: PARKER MATTHEW W.
Published: September 2013

Gödel argued that Cantor’s notion of cardinal number was uniquely correct. More recent work has defended alternative “Euclidean”' theories of set size, in which Cantor’s Principle (two sets have the same size if and only if there is a one-to-one correspondence between them) is abandoned in favor of the Part–Whole Principle (if A is a proper subset of B then A is smaller than B). Here we see from simple examples, not that Euclidean theories of set size are wrong, nor merely that they are counterintuitive, but that they must be either very weak or in large part arbitrary and misleading. This limits their epistemic usefulness.
Interplay between polymorphisms and methylation in the H19/IGF2 gene region may contribute to obesity in Mexican-American children
Authors: Hernández-Valero M. A. , Rother J. , Gorlov I. , Frazier M. , Gorlova O.
Published: September 2013

Imprinted genes often affect body size-related traits such as weight. However, the association of imprinting with obesity, especially childhood obesity, has not been well studied. Mexican-American children have a high prevalence, approaching 50%, of obesity and/or overweight. In a pilot study of 75 Mexican-American children, we analyzed the relationships among obese/overweight status, methylation status and single-nucleotide polymorphism (SNP) status at a CpG site in a differentially methylated region (DMR) of the imprinted H19/IGF2 locus. We observed a significant difference in SNP rs10732516 frequency between boys and girls among the overweight and obese children but not among the lean children. We also found that children with lower methylation of the polymorphic CpG site (CpG4) in the H19 DMR had higher birth weights than did children with higher methylation (P= 0.04). Our results suggest that CpG4 methylation status may be associated with childhood obesity in Mexican-American children in a sex-specific manner.
Screening for Posttraumatic Stress Disorder
Authors: Kröger Christoph , Kliem Sören
Published: September 2013

Symptom-based self-rating measures were established to detect individuals with posttraumatic stress disorder (PTSD) after specific traumatic events. The aim of the present study was to compare the diagnostic efficiency of the German version of the Trauma Screening Questionnaire (TSQ), the Posttraumatic Diagnostic Scale (PDS), and an 8-item subset of the PDS. Receiver-operating-characteristic analyses are determined in a treatment-seeking outpatient sample (N = 208) with mixed trauma type. The areas under the curve (AUC) for all measures were found to be moderate (AUC = 0.77–0.81); hence, measures did not differ in terms of their discriminatory abilities. Using the favored cutoff points, sensitivity (53–81%) and specificity (71–84%) values were at a level that was only moderate. Considering the high economic burden due to PTSD and the moderate specificity values, a two-stage screening approach might result in only moderate cost-efficiency for treatment-seeking outpatients. In addition, our results support the notion that discriminatory abilities and operating characteristics based on samples with a specific trauma type have to be cross-validated.
Spotlighting motors and controls of single FoF1-ATP synthase
Authors: Börsch Michael , Duncan Thomas M.
Published: September 2013

Subunit rotation is the mechanochemical intermediate for the catalytic activity of the membrane enzyme FoF1-ATP synthase. smFRET (single-molecule FRET) studies have provided insights into the step sizes of the F1 and Fo motors, internal transient elastic energy storage and controls of the motors. To develop and interpret smFRET experiments, atomic structural information is required. The recent F1 structure of the Escherichia coli enzyme with the ϵ-subunit in an inhibitory conformation initiated a study for real-time monitoring of the conformational changes of ϵ. The present mini-review summarizes smFRET rotation experiments and previews new smFRET data on the conformational changes of the CTD (C-terminal domain) of ϵ in the E. coli enzyme.
Mitochondrial genome function and maternal inheritance
Authors: Allen John F. , de Paula Wilson B.M.
Published: September 2013

The persistence of mtDNA to encode a small subset of mitochondrial proteins reflects the selective advantage of co-location of key respiratory chain subunit genes with their gene products. The disadvantage of this co-location is exposure of mtDNA to mutagenic ROS (reactive oxygen species), which are by-products of aerobic respiration. The resulting ‘vicious circle’ of mitochondrial mutation has been proposed to underlie aging and its associated degenerative diseases. Recent evidence is consistent with the hypothesis that oocyte mitochondria escape the aging process by acting as quiescent genetic templates, transcriptionally and bioenergetically repressed. Transmission of unexpressed mtDNA in the female germline is considered as a reason for the existence of separate sexes, i.e. male and female. Maternal inheritance then circumvents incremental accumulation of age-related disease in each new generation.
Rewiring cell signalling through chimaeric regulatory protein engineering
Authors: Wang Baojun , Barahona Mauricio , Buck Martin , Schumacher Jörg
Published: September 2013

Bacterial cells continuously sense and respond to their environment using their inherent signalling and gene regulatory networks. Cells are equipped with parallel signalling pathways, which can specifically cope with individual input signals, while interconnectivities between pathways lead to an enhanced complexity of regulatory responses that enable sophisticated adaptation. In principle, any cell signalling pathway may be rewired to respond to non-cognate signals by exchanging and recombining their underlying cognate signalling components. In the present article, we review the engineering strategies and use of chimaeric regulatory proteins in cell signalling pathways, especially the TCS (two-component signalling) system in bacteria, to achieve novel customized signalling or regulatory functions. We envisage that engineered chimaeric regulatory proteins can play an important role to aid both forward and reverse engineering of biological systems for many desired applications.
Influence of ionization on reflection of solitary waves in a magnetized plasma
Authors: Jyoti  , Kumar Ravinder , Malik Hitendra K. , Dahiya Raj P.
Published: September 2013

The reflection of nonlinear solitary waves is studied in a nonuniform, magnetized plasma diffusing from an ionization source along the magnetic field lines. Contribution of the ionization term is included in the continuity equation. The behavior of solitary waves is governed by modified form of Korteweg–de Vries equation (called mKdV equation). In order to investigate the reflection of solitary waves, the mKdV equations for the right and left going waves are derived, and solved by finding new transformations coupled at the point of reflection, for obtaining the expression of reflection coefficient. Contrary to the case of usual inhomogeneous plasma, the present analysis shows that a combination of usual sech2 structure and tanh structure (called the tail of soliton) arises due to the influence of ionization term. Interestingly, this tailing structure disappears after the reflection of the soliton and hence, the soliton is downshifted prominently.