bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of the mbd cluster encoding the anaerobic 3‐methylbenzoyl‐CoA central pathway
Authors: Juárez Javier F. , Zamarro María T. , Eberlein Christian , Boll Matthias , Carmona Manuel , Díaz Eduardo 
Published: June 2012

SummaryThe mbd cluster encoding genes of the 3‐methylbenzoyl‐CoA pathway involved in the anaerobic catabolism of 3‐methylbenzoate and m‐xylene was characterized for the first time in the denitrifying β‐Proteobacterium Azoarcus sp. CIB. The mbdA gene product was identified as a 3‐methylbenzoate‐CoA ligase required for 3‐methylbenzoate activation; its substrate spectrum was unique in activating all three methylbenzoate isomers. An inducible 3‐methylbenzoyl‐CoA reductase (mbdONQP gene products), displaying significant amino acid sequence similarities to known class I benzoyl‐CoA reductases catalysed the ATP‐dependent reduction of 3‐methylbenzoyl‐CoA to a methyldienoyl‐CoA. The mbdW gene encodes a methyldienoyl‐CoA hydratase that hydrated the methyldienoyl‐CoA to a methyl‐6‐hydroxymonoenoyl‐CoA compound. The mbd cluster also contains the genes predicted to be involved in the subsequent steps of the 3‐methylbenzoyl‐CoA pathway as well as the electron donor system for the reductase activity. Whereas the catabolic mbd genes are organized in two divergent inducible operons, the putative mbdR regulatory gene was transcribed separately and showed constitutive expression. The efficient expression of the mbd genes required the oxygen‐dependent AcpR activator, and it was subject of carbon catabolite repression by some organic acids and amino acids. Sequence analyses suggest that the mbd gene cluster was recruited by Azoarcus sp. CIB through horizontal gene transfer.
Determinants of Strategic HR Capabilities in MNC Subsidiaries
Authors: Mäkelä Kristiina , Sumelius Jennie , Höglund Mathias , Ahlvik Catarina 
Published: June 2012

abstractGiven the established association between organizational capabilities and organizational performance, shedding light on the determinants of capabilities remains a priority. We seek to narrow this research gap by providing empirical evidence concerning the influence of individual‐level determinants of strategic HR capabilities in subsidiaries of multinational corporations (MNCs). More specifically, we focus on two different conditions of individual action that function as microfoundations for organizational level strategic HR capabilities: the experience of subsidiary HR managers; and the social capital between managers working with HR issues in the subsidiary and those in the corporate HR function. Analysis of quantitative data gathered from 123 subsidiaries of 12 Nordic MNCs finds significant relationships between several microfoundations and the development of strategic HR capabilities in MNC subsidiaries.
Entropy by design: Gilles Clément, Parc Henri Matisse and the Limits to Avant‐garde Urbanism
Authors: GANDY MATTHEW 
Published: June 2012

AbstractDerborence Island, an inaccessible concrete structure set in the middle of Lille's Parc Henri Matisse, is an intriguing example of recent landscape design. The park, which was completed in 1995 as part of the vast Euralille development, was designed by the French landscape architect Gilles Clément. The idea for the park is derived from several sources, including the aesthetic characteristics of uncultivated ground, the symbolic reconstruction of a fragment of primary forest and the enhancement of urban biodiversity. It is suggested that Clément's novel synthesis of nature and culture is significantly different from prevailing discourses of landscape design and is best interpreted as a form of site‐specific art. Clément's project reveals tensions between the aesthetic and scientific significance of so‐called ‘waste spaces’ in contemporary cities and the widening scope of utilitarian approaches to landscape design.RésuméL'île Derborence, structure de béton inaccessible au cæur du Parc Henri Matisse de Lille, est un exemple fascinant de conception paysagère récente. Le parc, réalisé en 1995 dans le cadre du vaste aménagement d'Euralille, a été créé par l'architecte paysagiste français Gilles Clément. Le projet a eu plusieurs sources d'inspiration, dont les caractéristiques esthétiques d'un terrain non cultivé, la reconstitution symbolique d'un fragment de forêt primaire et l'enrichissement de la biodiversité urbaine. La synthèse novatrice entre nature et culture qu'effectue Clément est très différente des courants dominants de la création paysagère et trouve sa meilleure interprétation comme forme artistique propre à un lieu. Le projet de Clément met en évidence des tensions entre l'importance esthétique et scientifique des espaces dits ‘à l'abandon’ dans les villes contemporaines, et la dimension accrue des approches utilitaristes dans l'aménagement des paysages.
Diversity of intervertebral disc cells: phenotype and function
Authors: Pattappa Girish , Li Zhen , Peroglio Marianna , Wismer Nadine , Alini Mauro , Grad Sibylle 
Published: June 2012

AbstractThe intervertebral disc (IVD) is a moderately moving joint that is located between the bony vertebrae and provides flexibility and load transmission throughout the spinal column. The disc is composed of different but interrelated tissues, including the central highly hydrated nucleus pulposus (NP), the surrounding elastic and fibrous annulus fibrosus (AF), and the cartilaginous endplate (CEP), which provides the connection to the vertebral bodies. Each of these tissues has a different function and consists of a specific matrix structure that is maintained by a cell population with distinct phenotype. Although the healthy IVD is able to balance the slow matrix turnover of synthesis and degradation, this balance is often disturbed, leading to degenerative disorders. Successful therapeutic management of IVD degeneration requires a profound understanding of the cellular and molecular characteristics of the functional IVD. Hence, the phenotype of IVD cells has been of significant interest from multiple perspectives, including development, growth, remodelling, degeneration and repair. One major challenge that complicates our understanding of the disc cells is that both the cellular phenotype and the extracellular matrix strongly depend on disc maturity and health and as a consequence are continuously evolving. This review delineates the diversity of the cell types found in the intervertebral disc, with emphasis on human, but with reference to other species. The cells of the NP appear rounded and express a proteoglycan‐rich matrix, whereas the more elongated AF cells are embedded in a collagen fibre matrix and the CEPs represent a layer of cartilage. Even though all disc cells have often been referred to as ‘intervertebral disc chondrocytes’, distinct phenotypical differences in comparison with articular chondrocytes exist and have been reported recently. The availability of more specific markers has also improved our understanding of progenitor cell differentiation towards an IVD cell phenotype. Ultimately, new cell‐ and tissue‐engineering approaches to regenerative therapies will only be successful if the specific characteristics of the individual tissues and their context in the function of the whole organ, are taken into consideration.
Evolution of the mammalian middle ear and jaw: adaptations and novel structures
Authors: Anthwal Neal , Joshi Leena , Tucker Abigail S. 
Published: June 2012

AbstractHaving three ossicles in the middle ear is one of the defining features of mammals. All reptiles and birds have only one middle ear ossicle, the stapes or columella. How these two additional ossicles came to reside and function in the middle ear of mammals has been studied for the last 200 years and represents one of the classic example of how structures can change during evolution to function in new and novel ways. From fossil data, comparative anatomy and developmental biology it is now clear that the two new bones in the mammalian middle ear, the malleus and incus, are homologous to the quadrate and articular, which form the articulation for the upper and lower jaws in non‐mammalian jawed vertebrates. The incorporation of the primary jaw joint into the mammalian middle ear was only possible due to the evolution of a new way to articulate the upper and lower jaws, with the formation of the dentary‐squamosal joint, or TMJ in humans. The evolution of the three‐ossicle ear in mammals is thus intricately connected with the evolution of a novel jaw joint, the two structures evolving together to create the distinctive mammalian skull.
The impact of live trapping and trap model on the stress profiles of North American red squirrels
Authors: Bosson C.O. , Islam Z. , Boonstra R. 
Published: June 2012

AbstractLive‐capture is a necessary component for the scientific study and management of most mammals, but it may negatively affect their health and physiology. We compared blood parameters related to the stress response (nominal base levels) from red squirrels Tamiasciurus hudsonicus after capture of up to 4.5 h in five different live trap models (Hava‐hart, Sherman, Tomahawk 102, Tomahawk 103 and ‘Special Squirrel’ trap) with true base levels (obtained in less than three minutes). In addition, we evaluated the capture rate in the five trap models. We found that (1) prolonged time in live traps altered stress hormone concentrations compared with true base levels, but maximum corticosteroid‐binding capacity was unaffected; (2) squirrels captured in a trap model with reduced visibility (a roof cover – Hava‐hart) had significantly lower (c. 50%) mean free cortisol levels compared with those captured in a trap model with full visibility (Tomahawk 102), but all other blood parameters were similar; (3) cortisol levels and white blood cell counts (mainly neutrophil counts) were positively related to duration of capture; (4) a non‐covered trap (Tomahawk 102) was most effective and fully covered trap (Sherman) was least effective at capturing squirrels. We discuss the use of effective, yet less stress‐inducing trap models to mitigate the stress caused by live‐capture on these animals. We conclude that covered traps such as the Hava‐hart may reduce trap‐induced stress in red squirrels, but at the same time also reduces their capture rates.
Opportunities for improving phosphorus‐use efficiency in crop plants
Authors: Veneklaas Erik J. , Lambers Hans , Bragg Jason , Finnegan Patrick M. , Lovelock Catherine E. , Plaxton William C. , Price Charles A. , Scheible Wolf‐Rüdiger , Shane Michael W. , White Philip J. , Raven John A. 
Published: June 2012

SummaryLimitation of grain crop productivity by phosphorus (P) is widespread and will probably increase in the future. Enhanced P efficiency can be achieved by improved uptake of phosphate from soil (P‐acquisition efficiency) and by improved productivity per unit P taken up (P‐use efficiency). This review focuses on improved P‐use efficiency, which can be achieved by plants that have overall lower P concentrations, and by optimal distribution and redistribution of P in the plant allowing maximum growth and biomass allocation to harvestable plant parts. Significant decreases in plant P pools may be possible, for example, through reductions of superfluous ribosomal RNA and replacement of phospholipids by sulfolipids and galactolipids. Improvements in P distribution within the plant may be possible by increased remobilization from tissues that no longer need it (e.g. senescing leaves) and reduced partitioning of P to developing grains. Such changes would prolong and enhance the productive use of P in photosynthesis and have nutritional and environmental benefits. Research considering physiological, metabolic, molecular biological, genetic and phylogenetic aspects of P‐use efficiency is urgently needed to allow significant progress to be made in our understanding of this complex trait.

Contents

Summary
306

I.
The need to use phosphorus efficiently
307

II.
P‐use efficiency and P dynamics in a growing crop
307

III.
P pools in plants
307

IV.
Phosphorus pools and growth rates
310

V.
Are crops different from other plants in their P concentration?
310

VI.
Phosphorus use and photosynthesis
311

VII.
Crop development and canopy P distribution
312

VIII.
Internal redistribution of P in a growing vegetative plant
313

IX.
Allocation of P to reproductive structures
314

X.
Constraints to P remobilisation
315

XI.
Do physiological or phylogenetic trade‐offs constrain traits that could improve PUE?
316

XII.
Identifying genetic loci associated with PUE
316

XIII.
Conclusions
317

Acknowledgements
317

References
317
The evolution of land plant cilia
Authors: Hodges Matthew E. , Wickstead Bill , Gull Keith , Langdale Jane A. 
Published: June 2012

SummaryEukaryotic cilia/flagella are ancient organelles with motility and sensory functions. Cilia display significant ultrastructural conservation where present across the eukaryotic phylogeny; however, diversity in ciliary biology exists and the ability to produce cilia has been lost independently on a number of occasions. Land plants provide an excellent system for the investigation of cilia evolution and loss across a broad phylogeny, because early divergent land plant lineages produce cilia, whereas most seed plants do not. This review highlights the differences in cilia form and function across land plants and discusses how recent advances in genomics are providing novel insights into the evolutionary trajectory of ciliary proteins. We propose a renewed effort to adopt ciliated land plants as models to investigate the mechanisms underpinning complex ciliary processes, such as number control, the coordination of basal body placement and the regulation of beat patterns.ContentsSummary526I.Introduction526II.Plant cilia: a model for evolution and development530III.Future perspectives:MarchantiaandCeratopterisas models for cilia research535Acknowledgements536References536
Hypometabolism precedes limbic atrophy and spontaneous recurrent seizures in a rat model of TLE
Authors: Jupp Bianca , Williams John , Binns David , Hicks Rodney J. , Cardamone Lisa , Jones Nigel , Rees Sandra , O’Brien Terence J. 
Published: June 2012

SummaryPurpose:  Temporal hypometabolism on fluorodeoxyglucose positron emission tomography (FDG‐PET) is a common finding in patients with drug‐resistant temporal lobe epilepsy (TLE). The pathophysiology underlying the hypometabolism, including whether it reflects a primary epileptogenic process, or whether it occurs later as result of limbic atrophy or as a result of chronic seizures, remains unknown. This study aimed to investigate the ontologic relationship among limbic atrophy, histological changes, and hypometabolism in rats.Methods:  Serial in vivo imaging with FDG‐PET and volumetric magnetic resonance imaging (MRI) was acquired before and during the process of limbic epileptogenesis resulting from kainic acid–induced status epilepticus in the rat. The imaging data were correlated with histologic measures of cell loss, and markers of astrogliosis (glial fibrillary acid protein [GFAP]), synaptogenesis (synaptophysin), glucose transporter 1 (Glut1) and energy metabolism (cytochrome oxidase C), on brains of the animals following the final imaging point.Key Findings:  Hippocampal hypometabolism on FDG‐PET was found to be present 24 h following status epilepticus, tending to lessen by 1 week and then become more marked again following the onset of spontaneous seizures. Atrophy of limbic structures was evident from 7 days post‐SE, becoming progressively more marked on serial MRI over subsequent weeks. No relationship was observed between the severity of MRI‐detected atrophy or CA1 pyramidal cell loss and the degree of the hypometabolism on FDG‐PET. However, an inverse relationship was observed between hypometabolism and increased expression of the Glut1 and synaptophysin in the hippocampus.Significance:  These findings demonstrate that hypometabolism occurs early in the processes of limbic epileptogenesis and is not merely a consequence of pyramidal cell loss or the progressive atrophy of limbic brain structures that follow. The hypometabolism may reflect cellular mechanisms occurring early during epileptogenesis in addition to any effects of the subsequent recurrent spontaneous seizures.
Focal neocortical epilepsy affects hippocampal volume, shape, and structural integrity: A longitudinal MRI and immunohistochemistry study in a rat model
Authors: Otte Willem M. , Bielefeld Pascal , Dijkhuizen Rick M. , Braun Kees P.J. 
Published: June 2012

SummaryPurpose: Extratemporal epilepsy often coincides with cognitive decline, which may be associated with hippocampal dysfunction. Severe hippocampal sclerosis can be detected with conventional neuroimaging in some patients with chronic extrahippocampal epilepsy (so‐called dual pathology). However, subtle structural hippocampal changes may already develop at a much earlier phase, and in a larger number of patients. Our goal was to longitudinally characterize the development of bilateral hippocampal pathology in an experimental neocortical focal epilepsy model.Methods: Focal unilateral neocortical epilepsy was induced by microinjection of tetanus toxin in the primary motor cortex in adult male Sprague‐Dawley rats. Another group of age‐matched rats served as controls. In both groups, structural magnetic resonance imaging (MRI) was performed at 1, 3, 7, and 10 weeks of follow‐up. Bilateral hippocampi were outlined and macroscopically analyzed using a state‐of‐the‐art point‐based morphometry model. Hippocampal microstructural changes at the end of follow‐up, 10 weeks after epilepsy induction, were assessed with postmortem standard cresyl‐violet, Fluoro‐Jade, proteolipid protein 1, vimentin, glial fibrillary acidic protein, and ionized calcium binding adaptor molecule 1 stainings.Key Findings: All rats in the injected group developed seizures. The ipsilateral hippocampal volume was on average 8.76 (mean) ± 3.32% (standard deviation) smaller in the epileptic animals as compared to controls (p = 0.01) during the 10 weeks of follow‐up. The contralateral hippocampus showed a similar reduction of 8.49 (mean) ± 3.27% (standard deviation) in total volume (p = 0.02). Clear hippocampal shape differences were found between the two groups. The most affected areas after epilepsy induction were the bilateral dorso‐mediorostral, dorsolateral, and ventrolateral areas of the hippocampi. Normal developmental shape changes of the hippocampus, as detected in control rats, were largely absent in the ipsilateral hippocampus of epileptic rats. Quantitative histologic analysis revealed significant neuronal loss in the hippocampus, most pronounced in the hilar subregion, globally impaired myelination, reactive astrocytosis, and activated microglia. We found a weak but significant correlation between the number of neurons and hippocampal volume (r = 0.25, p = 0.0025).Significance: We found evidence of hippocampal pathology in both hemispheres following experimental focal neocortical epilepsy. The observed development of bilateral hippocampal pathology, with onset in the early stages of focal neocortical epilepsy, may be a significant factor in comorbidities, such as cognitive dysfunction, found in patients with extratemporal localization‐related epilepsy.
Topiramate increases the risk of valproic acid–induced encephalopathy
Authors: Noh Young , Kim Dong Wook , Chu Kon , Lee Soon‐Tae , Jung Keun‐Hwa , Moon Hye‐Jin , Lee Sang Kun 
Published: June 2012

SummaryMetabolic encephalopathy is a rare but serious complication of valproic acid (VPA) therapy that usually presents with impaired consciousness or increased seizure frequency. Although it has been suggested that topiramate (TPM) increases the risk of VPA‐induced encephalopathy, the additional risk in patients receiving TPM therapy has not been evaluated. We reviewed all adult patients who took VPA between January 2005 and February 2009 at the Seoul National University Hospital and identified patients with VPA‐induced encephalopathy based on clinical and electroencephalography (EEG) data. Information on sex, age, serum ammonia level, serum VPA level, liver function test, and EEG was collected from patient registry and medical data. We enrolled 8,372 patients who received VPA therapy and 1,236 patients who received VPA/TPM combination therapy. We identified 11 patients with VPA‐induced encephalopathy (0.13%), 7 of whom received a combination therapy of VPA and TPM. The odds ratio of VPA‐induced encephalopathy with TPM over that without TPM was 10.16. There were no significant differences in sex distribution, number of antiepileptic agents, ammonia level, VPA serum level, underlying diseases, dosage of VPA, duration of VPA treatment, treatment of encephalopathy, and outcomes between the two groups. Our study showed that the prevalence of VPA‐induced encephalopathy is approximately 0.1% among patients treated with VPA and that the risk of this condition, although still low, can increase by approximately 10 times in the presence of TPM therapy. Based on these results, we suggest that TPM should be carefully used in patients receiving VPA treatment.
Homozygous PLCB1 deletion associated with malignant migrating partial seizures in infancy
Authors: Poduri Annapurna , Chopra Sameer S. , Neilan Edward G. , Christina Elhosary P. , Kurian Manju A. , Meyer Esther , Barry Brenda J. , Khwaja Omar S. , Salih Mustafa A. M. , Stödberg Tommy , Scheffer Ingrid E. , Maher Eamonn R. , Sahin Mustafa , Wu Bai‐Lin , Berry Gerard T. , Walsh Christopher A. , Picker Jonathan , Kothare Sanjeev V. 
Published: June 2012

SummaryMalignant migrating partial seizures in infancy (MMPEI) is an early onset epileptic encephalopathy with few known etiologies. We sought to identify a novel cause of MMPEI in a child with MMPEI whose healthy parents were consanguineous. We used array comparative genomic hybridization (CGH) to identify copy number variants genome‐wide and long‐range polymerase chain reaction to further delineate the breakpoints of a deletion found by CGH. The proband had an inherited homozygous deletion of chromosome 20p13, disrupting the promoter region and first three coding exons of the gene PLCB1. Additional MMPEI cases were screened for similar deletions or mutations in PLCB1 but did not harbor mutations. Our results suggest that loss of PLCβ1 function is one cause of MMPEI, consistent with prior studies in a Plcb1 knockout mouse model that develops early onset epilepsy. We provide novel insight into the molecular mechanisms underlying MMPEI and further implicate PLCB1 as a candidate gene for severe childhood epilepsies. This work highlights the importance of pursuing genetic etiologies for severe early onset epilepsy syndromes.