bluuebunny/crossref_metadata_2025_split huggingface dataset:
Novel interneuronal network in the mouse posterior piriform cortex
Authors: Zhang Chunzhao , Szabó Gábor , Erdélyi Ferenc , Rose James D. , Sun Qian‐Quan 
Published: October 2006

AbstractThe neural circuits of the piriform cortex mediate field potential oscillations and complex functions related to integrating odor cues with behavior, affective states, and multisensory processing. Previous anatomical studies have established major neural pathways linking the piriform cortex to other cortical and subcortical regions and major glutamatergic and GABAergic neuronal subtypes within the piriform circuits. However, the quantitative properties of diverse piriform interneurons are unknown. Using quantitative neural anatomical analysis and electrophysiological recording applied to a GAD65‐EGFP transgenic mouse expressing GFP (green fluorescent protein) under the control of the GAD65 promoter, here we report a novel inhibitory network that is composed of neurons positive for GAD65‐EGFP in the posterior piriform cortex (PPC). These interneurons had stereotyped dendritic and axonal properties that were distinct from basket cells or interneurons expressing various calcium‐binding proteins (parvalbumin, calbindin, and calretinin) within the PPC. The GAD65‐GFP neurons are GABAergic and outnumbered any other interneurons (expressing parvalbumin, calbindin, and calretinin) we studied. The firing pattern of these interneurons was highly homogenous and is similar to the regular‐spiking nonpyramidal (RSNP) interneurons reported in primary sensory and other neocortical regions. Robust dye coupling among these interneurons and expression of connexin 36 suggested that they form electrically coupled networks. The predominant targets of descending axons of these interneurons were the dendrites of Layer III principal cells. Additionally, synapses were found on dendrites and somata of deep Layer II principal neurons and Layer III basket cells. A similar interneuronal subtype was also found in GAD65‐EGFP‐negative mouse. The extensive dendritic bifurcation at superficial lamina IA among horizontal afferent fibers and unique axonal targeting pattern suggests that these interneurons may play a role in direct feedforward inhibitory and disinhibitory olfactory processing. We conclude that the GAD65‐GFP neurons may play distinct roles in regulating information flow and olfactory‐related oscillation within the PPC in vivo. J. Comp. Neurol. 499:1000–1015, 2006. © 2006 Wiley‐Liss, Inc.
Follow‐up of an exercise‐based treatment for children with reading difficulties
Authors: Reynolds David , Nicolson Roderick I. 
Published: October 2006

AbstractThis study reports the results of a long‐term follow‐up of an exercise‐based approach to dyslexia‐related disorders (Reynolds, Nicolson, & Hambly, Dyslexia, 2003; 9(1): 48–71). In the initial study, children at risk of dyslexia were identified in 3 years of a junior school. One half then undertook a 6 month, home‐based exercise programme. Evaluation after 6 months indicated that the exercise group improved significantly more than the controls on a range of cognitive and motor skills. Critics had suggested that the improvement might be attributable to artifactual issues including Hawthorne effects; an initial literacy imbalance between the groups; and inclusion of non‐dyslexic participants. The present study evaluated the issue of whether the gains were maintained over the following 18 months, and whether they were in some sense artifactual as postulated by critics of the original study. Comparison of (age‐adjusted) initial and follow‐up performance indicated significant gains in motor skill, speech/language fluency, phonology, and working memory. Both dyslexic and non‐dyslexic low achieving children benefited. There was also a highly significant reduction in the incidence of symptoms of inattention. Interestingly there were no significant changes in speeded tests of reading and spelling, but there was a significant improvement in (age‐adjusted) reading (NFER). It is concluded that the gains were indeed long‐lasting, and that the alternative hypotheses based on potential artifacts were untenable, and that the exercise treatment therefore achieved its applied purpose. Further research is needed to determine the underlying reasons for the benefits. Possible (and potentially synergistic) explanations include: improved cerebellar function (neural level); improved learning ability and/or attentional ability (cognitive level); improved self‐esteem and self‐efficacy (affective level); and improved parental/familial support (social level). Copyright © 2006 John Wiley & Sons, Ltd.
STAT1 signaling is associated with acquired crossresistance to doxorubicin and radiation in myeloma cell lines
Authors: Fryknäs Mårten , Dhar Sumeer , Öberg Fredrik , Rickardson Linda , Rydåker Maria , Göransson Hanna , Gustafsson Mats , Pettersson Ulf , Nygren Peter , Larsson Rolf , Isaksson Anders 
Published: October 2006

AbstractThe myeloma cell line RPMI 8226/S and its doxorubicin resistant subline 8226/Dox40 were used as models to explore the potential importance of the STAT1 signaling pathway in drug and radiation resistance. The 40‐fold doxorubicin resistant subline 8226/Dox40 was found to be crossresistant to single doses of 4 and 8 Gy of radiation. A genome‐wide mRNA expression study comparing the 8226/Dox40 cell line to its parental line was performed to identify the underlying molecular mechanisms. Seventeen of the top 50 overexpressed genes have previously been implicated in the STAT1 signaling pathway. STAT1 was over expressed both at the mRNA and protein level. Moreover, analyses of nuclear extracts showed higher abundance of phosphorylated STAT1 (Tyr 701) in the resistant subline. Preexposure of the crossresistant cells to the STAT1 inhibiting drug fludarabine reduced expression of overexpressed genes and enhanced the effects of both doxorubicin and radiation. These results show that resistance to doxorubicin and radiation is associated with increased STAT1 signaling and can be modulated by fludarabine. The data support further development of therapies combining fludarabine and radiation. © 2006 Wiley‐Liss, Inc.
Low daytime pulse oximetry reading is associated with nocturnal desaturation and obstructive sleep apnea in children with sickle cell anemia
Authors: Spivey John F. , Uong Elizabeth C. , Strunk Robert , Boslaugh Sarah E. , DeBaun Michael R. 
Published: October 2006

AbstractA retrospective medical record review was established to test the hypothesis that in children with sickle cell anemia (SCA), a daytime oxygen saturation (SpO2) ≤94% is associated with nocturnal desaturation with or without obstructive sleep apnea (OSA). Twenty children had a resting SpO2 ≤94% and an abnormal polysomnogram (PSG). Seven patients had OSA and thirteen patients had nocturnal desaturation. The average daytime SpO2 correlated with the average nighttime SpO2 (Spearman correlation coefficient = 0.453; P = 0.045). Our results indicate that in children with SCA, a daytime SpO2 ≤94% is a reasonable threshold to recommend a pulmonary evaluation, including a PSG. Pediatr Blood Cancer 2008;50:359–362. © 2006 Wiley‐Liss, Inc.
Smooth semiparametric receiver operating characteristic curves for continuous diagnostic tests
Authors: Wan Shuwen , Zhang Biao 
Published: October 2006

AbstractWe propose a semiparametric kernel distribution function estimator, based on which a new smooth semiparametric estimator of the receiver operating characteristic (ROC) curve is constructed. We derive the asymptotic bias and variance of the newly proposed distribution function estimator and show that it is more efficient than the traditional non‐parametric kernel distribution estimator. We also derive the asymptotic bias and variance of our new ROC curve estimator and show that it is more efficient than the smooth non‐parametric ROC curve estimator proposed by Zou et al. (Stat. Med. 1997; 16:2143–2156) and Lloyd (J. Am. Stat. Assoc. 1998; 93:1356–1364). For our proposed estimators, we derive data‐based methods for bandwidth selection. In addition, we present some results on the analysis of two real data sets. Finally, a simulation study is presented to show that our estimators are better than the non‐parametric counterparts in terms of bias, standard error, and mean‐square error. Copyright © 2006 John Wiley & Sons, Ltd.
Impaired growth and neurological abnormalities in branched-chain α-keto acid dehydrogenase kinase-deficient mice
Authors: Joshi Mandar A. , Jeoung Nam Ho , Obayashi Mariko , Hattab Eyas M. , Brocken Eric G. , Liechty Edward A. , Kubek Michael J. , Vattem Krishna M. , Wek Ronald C. , Harris Robert A. 
Published: October 2006

The BCKDH (branched-chain α-keto acid dehydrogenase complex) catalyses the rate-limiting step in the oxidation of BCAAs (branched-chain amino acids). Activity of the complex is regulated by a specific kinase, BDK (BCKDH kinase), which causes inactivation, and a phosphatase, BDP (BCKDH phosphatase), which causes activation. In the present study, the effect of the disruption of the BDK gene on growth and development of mice was investigated. BCKDH activity was much greater in most tissues of BDK−/− mice. This occurred in part because the E1 component of the complex cannot be phosphorylated due to the absence of BDK and also because greater than normal amounts of the E1 component were present in tissues of BDK−/− mice. Lack of control of BCKDH activity resulted in markedly lower blood and tissue levels of the BCAAs in BDK−/− mice. At 12 weeks of age, BDK−/− mice were 15% smaller than wild-type mice and their fur lacked normal lustre. Brain, muscle and adipose tissue weights were reduced, whereas weights of the liver and kidney were greater. Neurological abnormalities were apparent by hind limb flexion throughout life and epileptic seizures after 6–7 months of age. Inhibition of protein synthesis in the brain due to hyperphosphorylation of eIF2α (eukaryotic translation initiation factor 2α) might contribute to the neurological abnormalities seen in BDK−/− mice. BDK−/− mice show significant improvement in growth and appearance when fed a high protein diet, suggesting that higher amounts of dietary BCAA can partially compensate for increased oxidation in BDK−/− mice. Disruption of the BDK gene establishes that regulation of BCKDH by phosphorylation is critically important for the regulation of oxidative disposal of BCAAs. The phenotype of the BDK−/− mice demonstrates the importance of tight regulation of oxidative disposal of BCAAs for normal growth and neurological function.
Arabidopsis thaliana RGXT1 and RGXT2 Encode Golgi-Localized (1,3)-α-d-Xylosyltransferases Involved in the Synthesis of Pectic Rhamnogalacturonan-II
Authors: Egelund Jack , Petersen Bent Larsen , Motawia Mohammed Saddik , Damager Iben , Faik Ahmed , Olsen Carl Erik , Ishii Tadashi , Clausen Henrik , Ulvskov Peter , Geshi Naomi 
Published: October 2006

Abstract
Two homologous plant-specific Arabidopsis thaliana genes, RGXT1 and RGXT2, belong to a new family of glycosyltransferases (CAZy GT-family-77) and encode cell wall (1,3)-α-d-xylosyltransferases. The deduced amino acid sequences contain single transmembrane domains near the N terminus, indicative of a type II membrane protein structure. Soluble secreted forms of the corresponding proteins expressed in insect cells showed xylosyltransferase activity, transferring d-xylose from UDP-α-d-xylose to l-fucose. The disaccharide product was hydrolyzed by α-xylosidase, whereas no reaction was catalyzed by β-xylosidase. Furthermore, the regio- and stereochemistry of the methyl xylosyl-fucoside was determined by nuclear magnetic resonance to be an α-(1,3) linkage, demonstrating the isolated glycosyltransferases to be (1,3)-α-d-xylosyltransferases. This particular linkage is only known in rhamnogalacturonan-II, a complex polysaccharide essential to vascular plants, and is conserved across higher plant families. Rhamnogalacturonan-II isolated from both RGXT1 and RGXT2 T-DNA insertional mutants functioned as specific acceptor molecules in the xylosyltransferase assay. Expression of RGXT1- and RGXT2-enhanced green fluorescent protein constructs in Arabidopsis revealed that both fusion proteins were targeted to a Brefeldin A–sensitive compartment and also colocalized with the Golgi marker dye BODIPY TR ceramide, consistent with targeting to the Golgi apparatus. Taken together, these results suggest that RGXT1 and RGXT2 encode Golgi-localized (1,3)-α-d-xylosyltransferases involved in the biosynthesis of pectic rhamnogalacturonan-II.
NPS6, Encoding a Nonribosomal Peptide Synthetase Involved in Siderophore-Mediated Iron Metabolism, Is a Conserved Virulence Determinant of Plant Pathogenic Ascomycetes
Authors: Oide Shinichi , Moeder Wolfgang , Krasnoff Stuart , Gibson Donna , Haas Hubertus , Yoshioka Keiko , Turgeon B. Gillian 
Published: October 2006

AbstractNPS6, encoding a nonribosomal peptide synthetase, is a virulence determinant in the maize (Zea mays) pathogen Cochliobolus heterostrophus and is involved in tolerance to H2O2. Deletion of NPS6 orthologs in the rice (Oryza sativa) pathogen, Cochliobolus miyabeanus, the wheat (Triticum aestivum) pathogen, Fusarium graminearum, and the Arabidopsis thaliana pathogen, Alternaria brassicicola, resulted in reduced virulence and hypersensitivity to H2O2. Introduction of the NPS6 ortholog from the saprobe Neurospora crassa to the Δnps6 strain of C. heterostrophus restored wild-type virulence to maize and tolerance to H2O2, demonstrating functional conservation in filamentous ascomycete phytopathogens and saprobes. Increased sensitivity to iron depletion was identified as a conserved phenotype of Δnps6 strains. Exogenous application of iron enhanced the virulence of Δnps6 strains of C. heterostrophus, C. miyabeanus, F. graminearum, and A. brassicicola to each host. NPS6 is responsible for the biosynthesis of extracellular siderophores by C. heterostrophus, F. graminearum, and A. brassicicola. Application of the extracellular siderophore of A. brassicicola restored wild-type virulence of the ΔAbnps6 strain to Arabidopsis. It is proposed that the role of extracellular siderophores in fungal virulence to plants is to supply an essential nutrient, iron, to their producers in planta and not to act as phytotoxins, depriving their hosts of iron.
Management of cutaneous angiomyolipoma and its association with tuberous sclerosis
Authors: DEBLOOM James R. , FRIEDRICHS Amanda , SWICK Brian L. , WHITAKER Duane C. 
Published: October 2006

ABSTRACTAlthough typically presenting renally, angiomyolipomas can rarely present in the skin. The tumors are composed of an admixture of blood vessels, smooth muscle and adipose tissue and are often seen in the setting of tuberous sclerosis. We describe a case of angiomyolipoma presenting on the thigh of a 50‐year‐old white female. This is the 17th reported case of cutaneous angiomyolipoma. As with all previously described cases, our patient did not present with the stigmata of tuberous sclerosis. Angiomyolipoma should be considered within the differential for subcutaneous nodules and work‐up for tuberous sclerosis should not be pursued when presenting in the skin.
Meta‐analysis: anti‐viral therapy of hepatitis C virus‐related liver disease in renal transplant patients
Authors: FABRIZI F. , LUNGHI G. , DIXIT V. , MARTIN P. 
Published: October 2006

SummaryBackgroundThe efficacy and safety of interferon‐based therapy in renal transplant recipients with hepatitis C remains unclear, although a number of small clinical trials have been published addressing this issue.AimTo evaluate efficacy and safety of antiviral therapy with interferon (interferon alone or interferon plus ribavirin) in renal transplant patients with hepatitis C by performing a systematic review of the literature with a meta‐analysis of clinical trials.MethodsThe primary outcomes were sustained virological response (as a measure of efficacy) and/or drop‐out rate (as a measure of tolerability). We used the random‐effects model of DerSimonian and Laird, with heterogeneity and sensitivity analysis.ResultsWe identified 12 clinical trials (102 unique patients); there was one controlled study. The summary estimate for sustained virological response and drop‐out rate was 18.0% (95% CI 7.0–29.0%) and 35.0% (95% CI 20–50%), respectively. The most frequent side‐effect requiring interruption of treatment was graft dysfunction (n = 28; 71.7%). Meta‐regression analysis showed an inverse and significant association between reference year and drop‐out logit rate (P = 0.012); an inverse link between sustained virological response logit rate and frequency of hepatitis C virus genotype 1 (P = 0.067) and cirrhosis (P = 0.08) was found, even if no statistical significance was reached. No publication bias was observed.ConclusionsInterferon‐based therapy of hepatitis C has poor tolerance and safety after renal transplant. The optimal treatment of hepatitis C after renal transplant requires additional agents or alternative therapeutic approaches.
Genomic organisation and regulation of murine alpha haemoglobin stabilising protein by erythroid Kruppel‐like factor
Authors: Keys Janelle R. , Tallack Michael R. , Hodge Denise J. , Cridland Simon O. , David Rakesh , Perkins Andrew C. 
Published: October 2006

SummaryAlpha haemoglobin stabilising protein (AHSP) binds free α‐globin chains and plays an important role in the protection of red cells, particularly during β‐thalassaemia. Murine ASHP was discovered as a GATA‐1 target gene and human AHSP is directly regulated by GATA‐1. More recently, AHSP was rediscovered as a highly erythroid Kruppel‐like factor (EKLF) ‐dependent transcript. We have determined the organisation of the murine AHSP gene and compared it to orthologs. There are two CACC box elements in the proximal promoter. The proximal element is absolutely conserved, but does not bind EKLF as it is not a canonical binding site. In rodents, the distal element contains a 3 bp insertion that disrupts the typical EKLF binding consensus region. Nevertheless, EKLF binds this atypical site by gel mobility shift assay, specifically occupies the AHSP promoter in vivo in a chromatin immunoprecipitation assay, and transactivates AHSP through this CACC site in promoter–reporter assays. Our results suggest EKLF can occupy CACC elements in vivo that are not predictable from the consensus binding site inferred from structural studies. We also propose that absence of AHSP in EKLF‐null red cells exacerbates the toxicity of free α‐globin chains, which exist because of the defect in β‐globin gene activation.
Analysis of the Klebsiella pneumoniae ntrB gene by site‐directed in vitro mutagenesis
Authors: MacFarlane S. A. , Merrick M. J. 
Published: October 2006

SummaryA number of in‐frame insertion and deletion mutations have been constructed in vitro in the Klebsiella pneumoniae ntrB gene and the effects of each mutant NtrB protein on NtrC activity have been assessed after reintroduction of the ntrB mutation into the glnA ntrBC operon. These experiments suggest that the phosphorylation of NtrC catalysed by NtrB not only makes NtrC competent as a transcriptional activator but also improves the DNA‐binding properties and hence the negative control functions of NtrC. The variety of NtrB phenotypes obtained suggest a structure/function model for the protein.
A gene fusion approach to the study of pullulanase export and secretion in Eschenchia coli
Authors: D'Enfert C. , Pugsley A.P. 
Published: October 2006

SummaryA series of fusions between the gene for the Klebsiella pneumoniae secreted lipoprotein pullulanase (pulA) and the genes for cytoplasmic β‐galactosidase (lacZ) or periplasmic alkaline phosphatase (phoA) were created by transposon mutagenesis using mini‐Mudlt1681 or TnphoA, respectively. The hybrid genes were expressed in Escherichia coli K‐12 with or without the K. pneumoniae genes that promote pullulanase secretion in E. coli. We characterized seven different pulA‐lacZ gene fusions encoding hybrid polypeptides containing from 14 to c. 1060 residues of pro‐pullulanase. All but the smallest hybrid were fatty acylated and were toxic to producing cells, causing the accumulation of precursors of other exported proteins. Four different pulA‐phoA gene fusions encoded hybrids with alkallne phosphatase activity. All four hybrids were fatty acylated, but were not toxic. Although the hybrids were apparently membrane‐associated, they were not secreted into the medium either by E. coli carrying pullulanase secretion genes or by K. pneumoniae. Immunofluorescence tests indicated that the pullulanase secretion genes promoted the localization of one of these hybrids to the outer face of the E. coli outer membrane, which may have important implications for the design of live vaccine. strains and of immobilized enzymes.
Transcriptional activation of the Klebsiella pneumoniae nitrogenase promoter may involve DNA loop formation
Authors: Buck M. , Cannon W. , Woodcock J. 
Published: October 2006

SummaryTranscriptional activation of nitrogen fixation genes by Nrt A in Klebsiella pneumoniae requires an upstream Nif A binding site. We now report that the introduction of haif turns of the DNA helix into the DNA separating the upstream NifA binding site from the downstream promoter element of the nifH promoter decreases Nif A‐mediated activation to a greater extent than does the introduction of full helical turns. Reducing the spacing between the upstream and downstream elements of the nifH promoter also results in a promoter down phenotype. Introduction of a tight protein‐binding site, the lac operator, between the upstream and downstream promoter elements did not render activation of the nifH promoter sensitive to occupancy of this site by the lac repressor. These findings indicate that NifA‐mediated activation of transcription requires that NifA is bound upstream, and to the correct face of the DNA helix, in order to interact with downstream transcription factors. This implies that the interaction is brought about by the formation of a DNA loop between upstream and downstream promoter elements rather than by NifA sliding downstream.The authors wish to thank Ray Dixon, Martin Drummond, Mike Merrick, and John Postgate for their constructive comments on the manuscript, and Beryl Scutt for typing the manuscript.
Nucleotide sequence and transcriptional startpoint of the glpT gene of Escherichia coli: extensive sequence homology of the glycerol‐3‐phosphate transport protein with components of the hexose‐6‐phosphate transport system
Authors: Eiglmeier K. , Boos W. , Cole S. T. 
Published: October 2006

SummaryThe nucleotide sequences of the glpT gene of Escherichia coli and its regulatory region have been elucidated and the primary structure of the glycerot‐3‐phosphate transport protein deduced. Extensive amino acid sequence homology was found with two other cytoplasmic membrane proteins: the functionally related hexose‐6‐phosphate transport protein, and the UHPC protein involved in regulating hexose‐6‐phosphate uptake. Although no significant amino acid sequence homology was found with other transport proteins, such as the arabinose, citrate, glucose, melibiose, lactose or xylose transporters, all of these proteins share a common secondary structure arrangement with the GLP T protein as they apparently contain twelve membrane‐spanning alpha‐helical segments. The promoter for glpT was located by transcript mapping and shown to overlap a site to which cata‐bolite activator protein binds in vitro. These findings indicate how catabolite repression may be mediated but do not explain its physiological significance in glycerol metabolism.