bluuebunny/crossref_metadata_2025_split huggingface dataset:
Complex phylogeography and historical hybridization between sister taxa of freshwater sculpin (Cottus)
Authors: Baumsteiger Jason , Kinziger Andrew P. , Reid Stewart B. , Aguilar Andres 
Published: April 2014

AbstractSpecies ranges that span different geographic landscapes frequently contain cryptic species‐ or population‐level structure. Identifying these possible diversification factors can often be accomplished under a comparative phylogeographic framework. However, comparisons suffer if previous studies are limited to a particular group or habitat type. In California, a complex landscape has led to several phylogeographic breaks, primarily in terrestrial species. However, two sister taxa of freshwater fish, riffle sculpin (Cottus gulosus) and Pit sculpin (Cottus pitensis), display ranges based on morphological identifications that do not coincide with these breaks. Using a comprehensive sampling and nuclear, mitochondrial and microsatellite markers, we hypothesized that proposed species ranges are erroneous based on potential hybridization/gene flow between species. Results identified a phylogeographic signature consistent with this hypothesis, with breaks at the Coast Range Mountains and Sacramento/San Joaquin River confluence. Coastal locations ofC. gulosusrepresent a unique lineage, and ‘true’C. gulosuswere limited to the San Joaquin basin, both regions under strong anthropogenic influence and potential conservation targets.C. pitensislimits extended historically throughout the Sacramento/Pit River basin but currently are restricted to the Pit River. Interestingly, locations in the Sacramento River contained low levels of ancestral hybridization and gene flow fromC. gulosusbut now appear to be a distinct population. The remaining population structure was strongly correlated with Sierra Nevada presence (high) or absence (low). This study stresses the importance of testing phylogeographic breaks across multiple taxa/habitats before conservation decisions are made, but also the potential impact of different geographic landscapes on evolutionary diversification.
Unexpected ancestry of Populus seedlings from a hybrid zone implies a large role for postzygotic selection in the maintenance of species
Authors: Lindtke Dorothea , Gompert Zachariah , Lexer Christian , Buerkle C. Alex 
Published: April 2014

AbstractIn the context of potential interspecific gene flow, the integrity of species will be maintained by reproductive barriers that reduce genetic exchange, including traits associated with prezygotic isolation or poor performance of hybrids. Hybrid zones can be used to study the importance of different reproductive barriers, particularly when both parental species and hybrids occur in close spatial proximity. We investigated the importance of barriers to gene flow that act early vs. late in the life cycle of European Populus by quantifying the prevalence of homospecific and hybrid matings within a mosaic hybrid zone. We obtained genotypic data for 11 976 loci from progeny and their maternal parents and constructed a Bayesian model to estimate individual admixture proportions and hybrid classes for sampled trees and for the unsampled pollen parent. Matings that included one or two hybrid parents were common, resulting in admixture proportions of progeny that spanned the whole range of potential ancestries between the two parental species. This result contrasts strongly with the distribution of admixture proportions in adult trees, where intermediate hybrids and each of the parental species are separated into three discrete ancestry clusters. The existence of the full range of hybrids in seedlings is consistent with weak reproductive isolation early in the life cycle of Populus. Instead, a considerable amount of selection must take place between the seedling stage and maturity to remove many hybrid seedlings. Our results highlight that high hybridization rates and appreciable hybrid fitness do not necessarily conflict with the maintenance of species integrity.
Dual DNA binding and coactivator functions of Aspergillus nidulans TamA, a Zn(II)2Cys6 transcription factor
Authors: Downes Damien J. , Davis Meryl A. , Wong Koon Ho , Kreutzberger Sara D. , Hynes Michael J. , Todd Richard B. 
Published: April 2014

SummaryTranscription factors containing DNA binding domains generally regulate transcription by direct interaction with DNA. For most transcription factors, including the fungal Zn(II)2Cys6 zinc binuclear cluster transcription factors, the DNA binding motif is essential for function. However, Aspergillus nidulans TamA and the related Saccharomyces cerevisiae Dal81p protein contain Zn(II)2Cys6 motifs shown to be dispensable for function. TamA acts at several promoters as a coactivator of the global nitrogen GATA transcription factor AreA. We now show that TamA is the major transcriptional activator of gdhA, encoding the key nitrogen metabolism enzyme NADP‐glutamate dehydrogenase. Moreover, activation of gdhA by TamA occurs primarily by a mechanism requiring the TamA DNA binding motif. We show that the TamA DNA binding motif is required for DNA binding of FLAG‐epitope‐tagged TamA to the gdhA promoter. We identify a conserved promoter element required for TamA activation, and show that TamA and AreA are reciprocally required for full binding at the gdhA promoter under conditions where AreA is inactive at most promoters but active at gdhA. Therefore TamA has dual functions as a DNA‐binding transcription factor and a non‐DNA‐binding coactivator. Dual DNA‐binding and coactivator functions provide an additional level of combinatorial control to mediate gene‐specific expression.
Bovine pancreatic trypsin inhibitor is a new antifungal peptide that inhibits cellular magnesium uptake
Authors: Bleackley Mark R. , Hayes Brigitte M. , Parisi Kathy , Saiyed Tamana , Traven Ana , Potter Ian D. , van der Weerden Nicole L. , Anderson Marilyn A. 
Published: April 2014

SummaryAntimicrobial peptides (AMPs) are promising agents for control of bacterial and fungal infections. Traditionally, AMPs were thought to act through membrane disruption but recent experiments have revealed a diversity of mechanisms. Here we describe a novel antifungal activity for bovine pancreatic trypsin inhibitor (BPTI). BPTI has several features in common with a subset of antimicrobial proteins in that it is small, cationic and stabilized by disulphide bonds. BPTI inhibits growth of Saccharomyces cerevisiae and the human pathogen Candida albicans. Screening of the yeast heterozygous essential deletion collection identified the magnesium transporter Alr1p as a potential BPTI target. BPTI treatment of wild type cells resulted in a lowering of cellular Mg2+ levels. Populations treated with BPTI had fewer cells in S‐phase of the cell cycle and a corresponding increase of cells in G0/G1 and G2 phases. The same patterns of cell cycle arrest obtained with BPTI were also obtained with the magnesium channel inhibitor hexamine(III)cobalt chloride. Analysis of the growth inhibition of C. albicans revealed that BPTI is inhibiting growth via the same mechanism in the two yeast species. Inhibition of magnesium uptake by BPTI represents a novel mechanism of action for AMPs.
Components of priming‐induced resistance to Fusarium head blight in wheat revealed by two distinct mutants of Fusarium graminearum
Authors: Ravensdale Michael , Rocheleau Hélène , Wang Li , Nasmith Charles , Ouellet Thérèse , Subramaniam Rajagopal 
Published: April 2014

SummaryTwo mutants (tri6Δ and noxABΔ) of the fungal pathogen Fusarium graminearum were assessed for their ability to prime immune responses in wheat (cv. Roblin) against challenge with pathogenic F. graminearum. Priming treatments generated Fusarium head blight (FHB)‐resistant wheat phenotypes and reduced the accumulation of fungal mycotoxins in infected tissues. Microarray analysis identified 260 transcripts that were differentially expressed during the priming period. Expression changes were observed in genes associated with immune surveillance systems, signalling cascades, antimicrobial compound production, oxidative burst, secondary metabolism, and detoxification and transport. Specifically, genes related to jasmonate, gibberellin and ethylene biosynthesis exhibited differential expression during priming. In addition, the induction of the phenylpropanoid pathways that lead to flavonoid, coumarin and hydroxycinnamic acid amide accumulation was also observed. This study highlights the utility of nonpathogenic mutants to both elicit and delineate stages of defence responses in wheat.
Patellins 3 and 6, two members of thePlantPatellin family, interact with the movement protein ofAlfalfa mosaic virusand interfere with viral movement
Authors: Peiro Ana , Izquierdo‐Garcia Ana Cristina , Sanchez‐Navarro Jesus Angel , Pallas Vicente , Mulet Jose Miguel , Aparicio Frederic 
Published: April 2014

SummaryMovement proteins (MPs) encoded by plant viruses interact with host proteins to facilitate or interfere with intra‐ and/or intercellular viral movement. Using yeast two‐hybrid and bimolecular fluorescence complementation assays, we herein presentin vivoevidence for the interaction betweenAlfalfa mosaic virus(AMV)MPand ArabidopsisPatellin 3 (atPATL3) andPatellin 6 (atPATL6), two proteins containing aSec14 domain. Proteins withSec14 domains are implicated in membrane trafficking, cytoskeleton dynamics, lipid metabolism and lipid‐mediated regulatory functions. Interestingly, the overexpression ofatPATL3and/oratPATL6interfered with the plasmodesmata targeting ofAMV MPand correlated with reduced infection foci size. Consistently, the viralRNAlevels increased in the single and double Arabidopsis knockout mutants foratPATL3andatPATL6. Our results indicate that, in general,MP–PATLinteractions interfere with the correct subcellular targeting ofMP, thus rendering the intracellular transport of viralMP‐containing complexes less efficient and diminishing cell‐to‐cell movement.
Neuroprotective effects of enriched environment housing after transient global cerebral ischaemia are associated with the upregulation of insulin‐like growth factor‐1 signalling
Authors: Wadowska Magdalena , Woods Julie , Rogozinska Magdalena , Briones Teresita L. 
Published: April 2014

AimsUse of enriched environment (EE) housing has been shown to promote recovery from cerebral ischaemic injury but the underlying mechanisms of their beneficial effects remains unclear. Here we examined whether the beneficial effects of EE housing on ischaemia‐induced neurodegeneration and cognitive impairment are associated with increased insulin‐like growth factor‐1 (IGF‐1) signalling in the hippocampus.MethodsForty‐two adult male Wistar rats were included in the study and received either ischaemia or sham surgery. Rats in each group were further randomized to either: EE or standard laboratory cage housing (control). Rats were placed in their assigned housing condition immediately after recovery from anaesthesia. Behavioural testing in the cued learning and discrimination learning tasks were conducted 2 weeks after ischaemia. Rats were euthanized after behavioural testing and the hippocampus was analysed for IGF‐1 level, IGF‐1 receptor (IGF‐1R) activation, protein kinase B (Akt) pathway activation, neurone loss and caspase 3 expression.ResultsOur data showed that EE housing: (1) mitigated ischaemia‐induced neuronal loss; (2) attenuated ischaemia‐induced increase in caspase 3 immunoreactivity in the hippocampus; (3) ameliorated ischaemia‐induced cognitive impairments; and (4) increased IGF‐1R activation and signalling through the Akt pathway after ischaemic injury.ConclusionUltimately, these findings suggest the possibility that IGF‐1 signalling may be one of the underlying mechanisms involved in the beneficial effects of EE in optimizing recovery following cerebral ischaemic injury.
Gene expression signatures in motor neurone disease fibroblasts reveal dysregulation of metabolism, hypoxia‐response and RNA processing functions
Authors: Raman Rohini , Allen Scott P , Goodall Emily F , Kramer Shelley , Ponger Lize‐Linde , Heath Paul R. , Milo Marta , Hollinger Hannah C. , Walsh Theresa , Highley J Robin , Olpin Simon , McDermott Christopher J. , Shaw Pamela J. , Kirby Janine 
Published: April 2014

AimsAmyotrophic lateral sclerosis (ALS) and primary lateral sclerosis (PLS) are two syndromic variants within the motor neurone disease spectrum. As PLS and most ALS cases are sporadic (SALS), this limits the availability of cellular models for investigating pathogenic mechanisms and therapeutic targets. The aim of this study was to use gene expression profiling to evaluate fibroblasts as cellular models for SALS and PLS, to establish whether dysregulated biological processes recapitulate those seen in the central nervous system and to elucidate pathways that distinguish the clinically defined variants of SALS and PLS.MethodsMicroarray analysis was performed on fibroblast RNA and differentially expressed genes identified. Genes in enriched biological pathways were validated by quantitative PCR and functional assays performed to establish the effect of altered RNA levels on the cellular processes.ResultsGene expression profiling demonstrated that whilst there were many differentially expressed genes in common between SALS and PLS fibroblasts, there were many more expressed specifically in the SALS fibroblasts, including those involved in RNA processing and the stress response. Functional analysis of the fibroblasts confirmed a significant decrease in miRNA production and a reduced response to hypoxia in SALS fibroblasts. Furthermore, metabolic gene changes seen in SALS, many of which were also evident in PLS fibroblasts, resulted in dysfunctional cellular respiration.ConclusionsThe data demonstrate that fibroblasts can act as cellular models for ALS and PLS, by establishing the transcriptional changes in known pathogenic pathways that confer subsequent functional effects and potentially highlight targets for therapeutic intervention.
Loss of nuclear TDP‐43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones
Authors: Highley J. Robin , Kirby Janine , Jansweijer Joeri A. , Webb Philip S. , Hewamadduma Channa A. , Heath Paul R. , Higginbottom Adrian , Raman Rohini , Ferraiuolo Laura , Cooper‐Knock Johnathan , McDermott Christopher J. , Wharton Stephen B. , Shaw Pamela J. , Ince Paul G. 
Published: April 2014

AimsLoss of nuclear TDP‐43 characterizes sporadic and most familial forms of amyotrophic lateral sclerosis (ALS). TDP‐43 (encoded by TARDBP) has multiple roles in RNA processing. We aimed to determine whether (1) RNA splicing dysregulation is present in lower motor neurones in ALS and in a motor neurone‐like cell model; and (2) TARDBP mutations (mtTARDBP) are associated with aberrant RNA splicing using patient‐derived fibroblasts.MethodsAffymetrix exon arrays were used to study mRNA expression and splicing in lower motor neurones obtained by laser capture microdissection of autopsy tissue from individuals with sporadic ALS and TDP‐43 proteinopathy. Findings were confirmed by quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR) and in NSC34 motor neuronal cells following shRNA‐mediated TDP‐43 depletion. Exon arrays and immunohistochemistry were used to study mRNA splicing and TDP‐43 expression in fibroblasts from patients with mtTARDBP‐associated, sporadic and mutant SOD1‐associated ALS.ResultsWe found altered expression of spliceosome components in motor neurones and widespread aberrations of mRNA splicing that specifically affected genes involved in ribonucleotide binding. This was confirmed in TDP‐43‐depleted NSC34 cells. Fibroblasts with mtTARDBP showed loss of nuclear TDP‐43 protein and demonstrated similar changes in splicing and gene expression, which were not present in fibroblasts from patients with sporadic or SOD1‐related ALS.ConclusionLoss of nuclear TDP‐43 is associated with RNA processing abnormalities in ALS motor neurones, patient‐derived cells with mtTARDBP, and following artificial TDP‐43 depletion, suggesting that splicing dysregulation directly contributes to disease pathogenesis. Key functional pathways affected include those central to RNA metabolism.
Mitochondrial and inflammatory changes in sporadic inclusion body myositis
Authors: Rygiel Karolina A. , Miller James , Grady John P. , Rocha Mariana C. , Taylor Robert W. , Turnbull Doug M. 
Published: April 2014

AimsSporadic inclusion body myositis (sIBM) is the most common late onset muscle disease causing progressive weakness. In light of the lack of effective treatment, we investigated potential causes underlying muscle wasting. We hypothesized that accumulation of mitochondrial respiratory deficiency in muscle fibres may lead to fibre atrophy and degeneration, contributing to muscle mass reduction.MethodsHistochemical and immunohistochemical analyses were performed on muscle biopsies from 16 sIBM patients to detect activity of mitochondrial enzymes and expression of mitochondrial respiratory chain proteins along with inflammatory markers respectively. Mitochondrial DNA mutations were assessed in single muscle fibres using real‐time PCR.ResultsWe identified respiratory‐deficient fibres at different stages of mitochondrial dysfunction, with downregulated expression of complex I of mitochondrial respiratory chain being the initial feature. We detected mitochondrial DNA rearrangements in the majority of individual respiratory‐deficient muscle fibres. There was a strong correlation between number of T lymphocytes and macrophages residing in muscle tissue and the abundance of respiratory‐deficient fibres. Moreover, we found that respiratory‐deficient muscle fibres were more likely to be atrophic compared with respiratory‐normal counterparts.ConclusionsOur findings suggest that mitochondrial dysfunction has a role in sIBM progression. A strong correlation between the severity of inflammation, degree of mitochondrial changes and atrophy implicated existence of a mechanistic link between these three parameters. We propose a role for inflammatory cells in the initiation of mitochondrial DNA damage, which when accumulated, causes respiratory dysfunction, fibre atrophy and ultimately degeneration of muscle fibres.
Immune‐mediated monofocal motor neuropathy: Report of two cases with long‐term follow up and review of six published cases
Authors: Adeyemo Bamidele O , Andriotakis James , Dreyer Michael , Pavlakis Pantelis P , Siao Peter 
Published: April 2014

AbstractBackground and AimThere are rare cases of multifocal motor neuropathy (MMN) with single nerve involvement published. The aim of the present study was to describe two cases of MMN with single nerve involvement and long‐term follow up. The first consisted of an isolated wrist drop, which developed conduction block later in the course of the disease. The second presented with longstanding left thumb weakness and near complete radial conduction block. Both responded to intravenous immunoglobulin.MethodsThe clinical and electrodiagnostic findings of two cases with long–term follow up are discussed, and six cases published in the literature are reviewed.ResultsBoth patients responded to intravenous immunoglobulin. One developed conduction block later in the course of the disease.ConclusionMonofocal motor neuropathy, a pure motor immune–mediated mononeuropathy, is a rare disorder, which responds to intravenous immunoglobulin. Although it might resemble MMN, some of its features lead us to consider it as a distinct entity.
Pain in the acute phase of Guillain–Barré syndrome
Authors: Kinboshi Masato , Inoue Manabu , Kojima Yasuhiro , Ono Michio , Nakagawa Tomokazu , Kanda Masutaro , Shibasaki Hiroshi 
Published: April 2014

AbstractBackground and AimPain has not been recognized as a main feature of Guillain–Barré syndrome (GBS) in its acute phase. The pathophysiology of pain and its effect on the prognostic outcome of GBS have not been fully evaluated. The aim of the present study was to report the clinical features and prognosis of GBS patients presenting with pain in the acute phase.MethodsThis was a retrospective study of 34 consecutive patients with GBS. We compared clinical profiles and laboratory findings between the GBS patients with pain and those without pain.ResultsA total of 29% of GBS patients had pain in the acute phase. Among others, low back pain was most common. GBS patients with pain were significantly younger than those without pain. In GBS patients with pain, the time of admission, the time for starting treatment and the time of discharge from the hospital were significantly delayed as compared with those without pain. However, there was no difference in the preceding infections, laboratory findings, or disability at the time of nadir and discharge.ConclusionPain is relatively common in the acute phase of GBS. Young GBS patients are especially susceptible to pain. Pain in the acute phase of GBS delays the time for reaching the correct diagnosis, and prolongs the duration of hospital stay and recovery, although it does not influence the functional prognosis.
Selenium deficiency presenting visual disturbance and myelopathy
Authors: Fujita Koji , Furukawa Takahiro , Matsuoka Takashi , Osaki Yusuke , Izumi Yuishin , Kaji Ryuji 
Published: April 2014

AbstractThe neurological features of selenium deficiency are poorly understood, and deserve more recognition for early diagnosis and treatment. Here, we report a 63‐year‐old parenteral nutrition‐dependent woman with Crohn's disease who presented with visual loss, myelopathy and macrocytic anemia. It was found that the selenium level was below the sensitivity limit in the serum. On selenium supplementation, which ameliorated anemia, her consciousness slightly improved, but vision and sensation did not. We suggest that visual disturbance and myelopathy after anemia can be warning signs of selenium deficiency.
Ultra‐early intravenous thrombolytic therapy for recurrent ischemic stroke after transient ischemic attack
Authors: Kobayashi Junpei , Ohara Tomoyuki , Sato Kazuaki , Uehara Toshiyuki , Minematsu Kazuo , Toyoda Kazunori 
Published: April 2014

AbstractAn 89‐year‐old woman was admitted to our stroke care unit because of transient ischemic attack caused by cardioembolic occlusion of the right internal carotid artery. She developed recurrent ischemic stroke shortly after hospitalization. She was very quickly treated with intravenous tissue plasminogen activator, because she had been just hospitalized, and had a favorable outcome. Earlier thrombolysis to patients with ischemic stroke is associated with better outcomes. Hospitalization in a stroke care unit is useful for close observation of patients with transient ischemic attack, and allows timely administration of tissue plasminogen activator.
Meralgia paresthetica secondary to abdominal desmoid tumor
Authors: Rattray Kyle , Schaeffer John 
Published: April 2014

AbstractMeralgia paresthetica is a mononeuropathy of the lateral femoral cutaneous nerve that supplies sensation to the anterolateral portion of the thigh. Compression of this nerve can lead to paresthesias and neuropathic pain. It is commonly associated with pregnancy, obesity, trauma or diabetes mellitus. Here we present a case of meralgia paresthetica in a 26‐year‐old woman secondary to nerve compression by a desmoid tumor within the internal oblique muscle tissue. Desmoid tumors are fibrous neoplasms originating from musculoaponeurotic structures, and can be locally aggressive and recurrent.