bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development of a model for evaluating the effects of environmental temperature and thermal behaviour on biological control of locusts and grasshoppers using pathogens
Authors: Klass Justine I. , Blanford Simon , Thomas Matthew B. 
Published: March 2007

Abstract1 Recent years have seen an upsurge in locust and grasshopper populations in many parts of the world. Environmentally sustainable approaches to locust and grasshopper control may be possible through the use of biopesticides based on entomopathogenic fungi. Unfortunately, the performance of these biopesticides is highly variable with environmental temperature and host thermoregulatory behaviour critically determining the pattern and extent of mortality after applications. Here, we present a temperature‐dependent model that enables us to predict the field performance of Metarhizium anisopliae var. acridum, the key fungal pathogen used in locust biopesticides.2 The model was constructed using mortality rate data generated across a range of temperatures in the laboratory and is driven by environmental temperature data linked through host body temperature models.3 Model predictions were validated against empirical field data obtained for five species, Locustana pardalina, Oedaleus senegalensis, Zonocerus variegatus, Nomadacris septemfasciata and Chortoicetes terminifera. Mortality predictions were accurate to a 2‐day error in every 10 days. This level of resolution is satisfactory to guide operational use of the biopesticide.4 The model was subsequently used for a prospective evaluation of the performance of M. anisopliae var. acridum against two additional pest species, Dociostaurus maroccanus and Calliptamus italicus in Spain. Results suggest that this pathogen would work reasonably well against these species as long as early instars are targeted.5 The model could provide a useful tool to assist in interpreting effectiveness of control operations, develop improved application strategies to optimize the performance of the biopesticide and identify appropriate target species and environments.
Diversity of root‐associated fluorescent pseudomonads as affected by ferritin overexpression in tobacco
Authors: Robin Agnès , Mazurier Sylvie , Mougel Christophe , Vansuyt Gérard , Corberand Thérèse , Meyer Jean‐Marie , Lemanceau Philippe 
Published: March 2007

SummaryA transgenic tobacco overexpressing ferritin (P6) was recently shown to accumulate more iron than the wild type (WT), leading to a reduced availability of iron in the rhizosphere and shifts in the pseudomonad community. The impact of the transgenic line on the community of fluorescent pseudomonads was assessed. The diversity of 635 isolates from rhizosphere soils, rhizoplane + root tissues, and root tissues of WT and P6, and that of 98 isolates from uncultivated soil was characterized. Their ability to grow under iron stress conditions was assessed by identifying their minimal inhibitory concentrations of 8‐hydroxyquinoline for each isolate, pyoverdine diversity by isoelectrofocusing and genotypic diversity by random amplified polymorphism DNA. The antagonistic activity of representative isolates and of some purified pyoverdines against a plant pathogen (Pythium aphanidermatum Op4) was tested in vitro. In overall, isolates taken from P6 tobacco showed a greater ability to grow in iron stress conditions than WT isolates. The antagonism by some of the representative isolates was only expressed under iron stress conditions promoting siderophore synthesis and their pyoverdines appeared to have a specific structure as assessed by mass spectrometry. For other isolates, antagonism was still expressed in the presence of iron, suggesting the involvement of metabolites other than siderophores. Altogether, these data indicate that the transgenic tobacco that over‐accumulates iron selected fluorescent pseudomonads, less susceptible to iron depletion and more antagonistic to the tested plant pathogen than those selected by the tobacco WT.
Protein kinase A‐dependent recruitment of RNA polymerase II, C/EBPβ and NF‐Y to the rat GTP cyclohydrolase I proximal promoter occurs without alterations in histone acetylation
Authors: Kapatos Gregory , Vunnava Prashanthi , Wu Yanning 
Published: March 2007

AbstractCyclic‐AMP stimulation of GTP cyclohydrolase I (GCH1) gene transcription was investigated in PC12 cells, the protein kinase A‐deficient PC12 cell line 126‐1B2 and C6 cells using transient transfection assays of proximal promoter reporter constructs and wild type or dominant negative proteins, chromatin immunoprecipitation and real‐time quantitative PCR. These studies show that protein kinase A is necessary and sufficient for cAMP‐dependent transcription conferred by both the cAMP regulatory element and the adjacent CCAAT‐box. In intact cells these cis‐elements were shown to bind cAMP response element binding protein, CCAAT‐enhancer binding protein beta and nuclear factor‐Y, with each protein controlling a different aspect of the cAMP response. Cyclic‐AMP acting through protein kinase A stimulated promoter recruitment of CCAAT‐enhancer binding protein beta, nuclear factor‐Y and RNA polymerase II while depleting the promoter of cyclic‐AMP response element binding protein. Stimulation of transcription by cAMP was not associated with increased acetylation of histones H3 and H4 at proximal promoter nucleosomes, indicating that histone acetyltransferases are not involved in this response. Nonetheless, pharmacological inhibition of histone deacetylase activity did increase histone H4 acetylation and the recruitment of RNA polymerase II, indicating that histone acetyltransferases are normally associated with the proximal promoter. Only in C6 cells, however, did inhibition of histone deacetylases stimulate transcription and synergize with cAMP. These experiments provide the first glimpse of the GCH1 gene promoter functioning within intact cells and supply evidence for the involvement of histone acetyltransferase‐containing complexes in GCH1 gene transcription.
Donepezil induces a cholinergic sprouting in basocortical degeneration
Authors: Ginestet Laure , Ferrario Juan E. , Raisman‐Vozari Rita , Hirsch Etienne C. , Debeir Thomas 
Published: March 2007

AbstractOne of the few currently approved therapies for Alzheimer’s disease (AD) consists in the administration of acetylcholinesterase inhibitors, which enhances the lifetime of the neurotransmitter acetylcholine. Despite numerous studies on the symptomatic effect of acetylcholinesterase inhibitors, there is as yet no direct morphological evidence to indicate that they have a neurorestorative action. We investigated the effect of the acetylcholinesterase inhibitor donepezil administered subcutaneously in a rat model of partial unilateral cortical devascularization that induces a loss of the cortical cholinergic terminal network and a retrograde degeneration of the cholinergic projections that originate in the nucleus basalis. For 6 weeks, lesioned and sham‐operated rats received a subcutaneous infusion of donepezil (2 mg/kg/day) or vehicle, delivered by osmotic minipumps implanted 2 weeks before the cortical devascularization. In lesioned rats, donepezil treatment increased the number and the size of vesicular acetylcholine transporter immunoreactive boutons in comparison to vehicle treatment. Donepezil had no observable effect on any of these parameters in sham‐operated animals. These results show that donepezil mitigates cholinergic neuronal degeneration in vivo. This suggests a neuroplastic activity of this drug and provides evidence for a potential use of donepezil as a disease modifier in neurodegenerative diseases such as AD.
Cdk5–p39 is a labile complex with the similar substrate specificity to Cdk5–p35
Authors: Yamada Mari , Saito Taro , Sato Yutaka , Kawai Yusei , Sekigawa Akio , Hamazumi Yuko , Asada Akiko , Wada Mitsuhito , Doi Hirofumi , Hisanaga Shin‐ichi 
Published: March 2007

AbstractCyclin‐dependent kinase 5 (Cdk5) is a proline‐directed Ser/Thr kinase that plays important roles in various neuronal activities, including neuronal migration, synaptic activity, and neuronal cell death. Cdk5 is activated by association with a neuron‐specific activator, p35 or its isoform p39, but little is known about the kinase activity of Cdk5–p39. In fact, kinase‐active Cdk5–p39 was not prepared from rat brain extracts nor from HEK293 cells expressing Cdk5 and p39 by immunoprecipitation in the presence of non‐ionic detergent, under conditions with which active Cdk5–p35 could be isolated. p39 dissociated from Cdk5 in the presence of detergent, indicating that p39 has a lower binding affinity for Cdk5 than p35. We developed a method for purifying kinase‐active Cdk5–p39 from Sf9 cells infected with baculovirus encoding Cdk5 and p39. The purified Cdk5–p39 complex showed similar substrate specificity to that of Cdk5–p35, but with opposite sensitivity to detergent. Cdk5–p39 was inactivated by Triton X‐100, whereas Cdk5–p35 was activated. The N‐terminal deletion from p35 and p39, the amino acid sequences of which are different, did not change the stability or substrate specificity of either Cdk5 complex. The different stability between Cdk5–p35 and Cdk5–p39 suggests their distinct roles under different regulation mechanisms in neurons.
Glutamate‐dependent transcriptional regulation of GLAST/EAAT1: a role for YY1
Authors: Rosas Sandra , Vargas Miguel A. , López‐Bayghen Esther , Ortega Arturo 
Published: March 2007

AbstractGlutamate is the major excitatory transmitter in the vertebrate brain and its extracellular levels are tightly regulated to prevent excitotoxic effects. The Na+‐dependent glutamate/aspartate transporter GLAST/EAAT1 is regulated in the short and in the long term by glutamate. A receptors‐independent change in its membrane translocation rate, accounts for an acute modulation in GLAST/EAAT1 transport. In contrast, activation of the α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate subtype of glutamate receptors represses the transcription of the chick glast gene. A glutamate responsive element has been mapped to the promoter region of this gene containing a bonafide binding site for the transcription factor Ying‐Yang 1. Using cultured chick cerebellar Bergmann glia cells, glutamate elicited a time and dose‐dependent increase in Ying‐Yang 1 DNA binding consistent with the negative response generated in a reporter gene construct controlled for Ying‐Yang 1. Over‐expression of this transcription factor leads to a substantial reduction in GLAST/EAAT1 transporter uptake and an important decrease in mRNA levels, all associated with the transcriptional repression of the chick glast promoter activity. These results provide evidence for an involvement of Ying‐Yang 1 in the transcriptional response to glutamate in glial cells and favor the notion of a relevant role of this factor in GLAST/EAAT1 transcriptional control.
Membrane topology of the Drosophila vesicular glutamate transporter
Authors: Fei Hao , Karnezis Tara , Reimer Richard J. , Krantz David E. 
Published: March 2007

AbstractThe vesicular glutamate transporters (VGLUTs) are responsible for packaging glutamate into synaptic vesicles, and are part of a family of structurally related proteins that mediate organic anion transport. Standard computer‐based predictions of transmembrane domains have led to divergent topological models, indicating the need for experimentally derived predictions. Here we present data on the topology of the VGLUT ortholog from Drosophila melanogaster (DVGLUT). Using immunofluorescence assays of DVGLUT transiently localized to the plasma membrane of heterologously transfected cells, we have determined the accessibility of epitope tags inserted into the lumenal/extracellular face of the protein. Using immunoisolation, we have identified complementary tagged sites that face the cytoplasm. Our data show that DVGLUT contains 10 hydrophobic regions that completely span the membrane (TMs 1–10) and that the amino and carboxyl termini are cytosolic. Importantly, between TMs 4 and 5 is an unforeseen cytosolic loop of some 50 residues. Other domains exposed to the cytosol include loops between TMs 6–7 and 8–9, and regions C‐terminal to TM2 and N‐terminal to TM3. Between TM2 and 3 is a potentially hydrophobic, but topologically ambiguous region. Lumenal domains include sequences between TMs 1–2, 3–4, 5–6, 7–8 and 9–10. These data provide a basis for determining structure‐function relationships for DVGLUT and other related proteins.
Mutations in LRRK2/dardarin associated with Parkinson disease are more toxic than equivalent mutations in the homologous kinase LRRK1
Authors: Greggio Elisa , Lewis Patrick A. , Van Der Brug Marcel P. , Ahmad Rili , Kaganovich Alice , Ding Jinhui , Beilina Alexandra , Baker Acacia K. , Cookson Mark R. 
Published: March 2007

AbstractSeveral mutations have been found in the leucine‐rich repeat kinase 2 gene (LRRK2), encoding the protein dardarin, which are associated with autosomal dominant Parkinson disease. We have previously shown that mutant LRRK2/dardarin is toxic to neurons and neuron‐like cell lines in culture and that some mutations are also associated with an inclusion‐body phenotype. There is a homologous kinase, LRRK1, which has a similar domain structure but is not known to carry mutations causing Parkinson disease. In the current study, we introduced mutations at equivalent residues in both LRRK2 and LRRK1 to determine their effects in cells. We show that mutations in dardarin are more prone to form inclusion bodies in transfected cells and are more toxic than equivalent mutations in LRRK1. This work suggests that dardarin/LRRK2 is inherently more damaging than LRRK1.
Mammalian‐produced chondroitinase AC mitigates axon inhibition by chondroitin sulfate proteoglycans
Authors: Curinga Gabrielle M. , Snow Diane M. , Mashburn Charles , Kohler Katharina , Thobaben Rebecca , Caggiano Anthony O. , Smith George M. 
Published: March 2007

AbstractChondroitin sulfate proteoglycans (CSPGs) are up‐regulated following spinal cord injury and are partly responsible for failed regeneration. Experimental paradigms in vivo that degrade chondroitin sulfate glycosaminoglycan chains with the bacterial enzyme, chondroitinase, greatly enhance the ability of axons to regenerate through the glial scar. Unfortunately, enthusiasm for this treatment paradigm is diminished by the lack of a minimally invasive and sustained delivery method. To address these deficits, we have engineered a Tet‐On adenoviral vector encoding chondroitinase AC and have characterized its enzymatic function in vitro. U373 human astrocytoma cells were transduced with adenovirus and subsequently induced with doxycycline to secrete enzymatically active chondroitinase as detected by western blot and kinetic analyses. Enzymatic activity demonstrated biological relevance in studies where neurite outgrowth into and across CSPG‐adsorbed regions pre‐treated with conditioned media from chondroitinase secreting astrocytes was significantly increased compared with untreated controls (p < 0.0001). We also measured important parameters of enzyme activity including: pH, temperature, and enzyme stability that are fundamental to harnessing the true therapeutic potential of this approach. The use of resident cells for continuous secretion of CSPG‐degrading enzymes at the site of the glial scar promises to be of greater clinical relevance than contemporary methods.
Wild‐type superoxide dismutase acquires binding and toxic properties of ALS‐linked mutant forms through oxidation
Authors: Ezzi Samer Abou , Urushitani Makoto , Julien Jean‐Pierre 
Published: March 2007

AbstractRecent studies suggest that superoxide dismutase (SOD1) may represent a major target of oxidative damage in neurodegenerative diseases. To test the possibility that oxidized species of wild‐type (WT) SOD1 might be involved in pathogenic processes, we analyzed the properties of the WT human SOD1 protein after its oxidation in vivo or in vitro by hydrogen peroxide (H2O2) treatment. Using transfected Neuro2a cells expressing WT or amyotrophic lateral sclerosis‐linked SOD1 species, we show that exposure to H2O2 modifies the properties of WT SOD1. Western blot analysis of immunoprecipitates from cell lysates revealed that, like mutant SOD1, oxidized WT SOD1 can be conjugated with poly‐ubiquitin and can interact with Hsp70. Chromogranin B, a neurosecretory protein that interacts with mutant SOD1 but not with WT SOD1, was co‐immunoprecipitated with oxidized WT SOD1 from lysates of Neuro2a cells treated with H2O2. Treatment of microglial cells (line BV2) with either oxidized WT SOD1 or mutant SOD1 recombinant proteins induced tumor necrosis factor‐α and inducible nitric oxide synthase. Furthermore, exposure of cultured motor neurons to oxidized WT SOD1 caused dose‐dependent cell death like mutant SOD1 proteins. These results suggest that WT SOD1 may acquire binding and toxic properties of mutant forms of SOD1 through oxidative damage.
Hepatitis B‐associated vasculitis in Alaska Natives: viral genotype, clinical and serologic outcome
Authors: Hurlburt Kathy J. , McMahon Brian J. , Simonetti Josephine P. , Livingston Stephen E. , Bulkow Lisa R. , Snowball Mary M. , Chulanov Vladimir P. , Nainan Omana P. , Williams James L. 
Published: March 2007

AbstractBackground: The highest incidence of hepatitis B virus (HBV)‐associated vasculitis in the world has been reported in Alaska Natives. We examined the incidence of HBV‐associated vasculitis before and after mass HBV vaccine immunization and the association between HBV genotype and vasculitis in a population‐based cohort study in Alaska natives chronically infected with HBV.Methods: Genotyping was performed in vasculitis cases and 644 hepatitis B‐positive controls without vasculitis using polymerase chain reaction and sequencing of the S gene. Occurrence of HBV vasculitis from 1974 to 2004 was calculated. HBV vasculitis patients and controls were also tested for basal core promoter and precore mutations.Results: Fifteen cases of HBV‐associated vasculitis were identified: 13 (86%) had genotype D and one each genotype A and F. Genotype D was more commonly found in patients with vasculitis than controls [odd ratio (OR)=5.9, confidence interval (95% CI) 1.2, 21.8; P<0.015).Conclusions: HBV‐associated vasculitis was associated with genotype D.
Analysis of the core gene of hepatitis B virus in Korean patients
Authors: Kim Hyung Joon , Lee Dong Ho , Gwak Geum‐Youn , Choi Moon Seok , Lee Joon Hyeok , Koh Kwang Cheol , Paik Seung Woon , Yoo Byung Chul 
Published: March 2007

AbstractBackground/Aims: As the core gene of hepatitis B virus (HBV) is a major immunological target, its mutation may evoke or evade immune clearance. We investigated the frequency and location of HBV core gene substitutions according to hepatitis B e antigen (HBeAg) status and viral replication status, and evaluated the association of these substitutions with the different stages of chronic HBV infection in Korean patients.Methods: The study population included 45 HBeAg‐positive/DNA‐positive patients (group I), 49 HBeAg‐negative/DNA‐positive patients (II) and 50 HBeAg‐negative/DNA‐negative patients (III). The HBV core gene was analysed by polymerase chain reaction (PCR) and sequencing.Results: The frequency of core gene substitutions increased from group I to group III. Substitutions were commonly detected at codons 87, 97, 112 and 130. The frequency of substitutions at codons 87 and 112 was higher in groups II/III than in group I. The frequency of the codon I97F substitutions was the highest in group III. However, the codon 130 substitution was more frequently found in groups I/II than in group III.Conclusion: Core gene substitutions were more frequently detected in HBeAg‐negative and/or HBV DNA‐negative patients. The substitutional hot spots were codons 87, 97, 112 and 130; substitutions at these codons might play a role in immune‐modulation during the course of chronic HBV infection.
Robust Resource Allocation Decisions in Resource‐Constrained Projects*
Authors: Deblaere Filip , Demeulemeester Erik , Herroelen Willy , Van de Vonder Stijn 
Published: March 2007

ABSTRACTThe well‐known deterministic resource‐constrained project scheduling problem involves the determination of a predictive schedule (baseline schedule or pre‐schedule) of the project activities that satisfies the finish–start precedence relations and the renewable resource constraints under the objective of minimizing the project duration. This baseline schedule serves as a baseline for the execution of the project. During execution, however, the project can be subject to several types of disruptions that may disturb the baseline schedule. Management must then rely on a reactive scheduling procedure for revising or reoptimizing the baseline schedule. The objective of our research is to develop procedures for allocating resources to the activities of a given baseline schedule in order to maximize its stability in the presence of activity duration variability. We propose three integer programming–based heuristics and one constructive procedure for resource allocation. We derive lower bounds for schedule stability and report on computational results obtained on a set of benchmark problems.
Decision Sciences Research in China: Current Status, Opportunities, and Propositions for Research in Supply Chain Management, Logistics, and Quality Management*
Authors: Zhao Xiande , Flynn Barbara B. , Roth Aleda V. 
Published: March 2007

ABSTRACTAs China becomes increasingly important to the global economy, it is critical to conduct high‐quality research on important decision sciences issues there. This article provides an extensive review and critique of the extant China‐based literature on supply chain management, logistics, and quality management, based on the foundation established by Zhao, Flynn, and Roth (2006). In general, decision sciences research in China is in its infancy. Although there have been some very interesting and well‐executed articles, the majority are descriptive and focus on status updates. We provide a set of propositions to guide future research in logistics, supply chain management, and quality management in China, as well as guidelines for dealing with some of the unique challenges of conducting empirical research in China.
The Severity of Supply Chain Disruptions: Design Characteristics and Mitigation Capabilities
Authors: Craighead Christopher W. , Blackhurst Jennifer , Rungtusanatham M. Johnny , Handfield Robert B. 
Published: March 2007

ABSTRACTSupply chain disruptions and the associated operational and financial risks represent the most pressing concern facing firms that compete in today's global marketplace. Extant research has not only confirmed the costly nature of supply chain disruptions but has also contributed relevant insights on such related issues as supply chain risks, vulnerability, resilience, and continuity. In this conceptual note, we focus on a relatively unexplored issue, asking and answering the question of how and why one supply chain disruption would be more severe than another. In doing so, we argue, de facto, that supply chain disruptions are unavoidable and, as a consequence, that all supply chains are inherently risky. Employing a multiple‐method, multiple‐source empirical research design, we derive novel insights, presented as six propositions that relate the severity of supply chain disruptions (i) to the three supply chain design characteristics of density, complexity, and node criticality and (ii) to the two supply chain mitigation capabilities of recovery and warning. These findings not only augment existing knowledge related to supply chain risk, vulnerability, resilience, and business continuity planning but also call into question the wisdom of pursuing such practices as supply base reduction, global sourcing, and sourcing from supply clusters.