bluuebunny/crossref_metadata_2025_split huggingface dataset:
The affinity of the FimH fimbrial adhesin is receptor‐driven and quasi‐independent of Escherichia coli pathotypes
Authors: Bouckaert Julie , Mackenzie Jenny , De Paz José L. , Chipwaza Beatrice , Choudhury Devapriya , Zavialov Anton , Mannerstedt Karin , Anderson Jennifer , Piérard Denis , Wyns Lode , Seeberger Peter H. , Oscarson Stefan , De Greve Henri , Knight Stefan D. 
Published: August 2006

SummaryType‐1 fimbriae are important virulence factors for the establishment of Escherichia coli urinary tract infections. Bacterial adhesion to the high‐mannosylated uroplakin Ia glycoprotein receptors of bladder epithelium is mediated by the FimH adhesin. Previous studies have attributed differences in mannose‐sensitive adhesion phenotypes between faecal and uropathogenic E. coli to sequence variation in the FimH receptor‐binding domain. We find that FimH variants from uropathogenic, faecal and enterohaemorrhagic isolates express the same specificities and affinities for high‐mannose structures. The only exceptions are FimHs from O157 strains that carry a mutation (Asn135Lys) in the mannose‐binding pocket that abolishes all binding. A high‐mannose microarray shows that all substructures are bound by FimH and that the largest oligomannose is not necessarily the best binder. Affinity measurements demonstrate a strong preference towards oligomannosides exposing Manα1‐3Man at their non‐reducing end. Binding is further enhanced by the β1‐4‐linkage to GlcNAc, where binding is 100‐fold better than that of α‐d‐mannose. Manα1‐3Manβ1‐4GlcNAc, a major oligosaccharide present in the urine of α‐mannosidosis patients, thus constitutes a well‐defined FimH epitope. Differences in affinities for high‐mannose structures are at least 10‐fold larger than differences in numbers of adherent bacteria between faecal and uropathogenic strains. Our results imply that the carbohydrate expression profile of targeted host tissues and of natural inhibitors in urine, such as Tamm‐Horsfall protein, are stronger determinants of adhesion than FimH variation.
Multiple large filament bundles observed in Caulobacter crescentus by electron cryotomography
Authors: Briegel Ariane , Dias D. Prabha , Li Zhuo , Jensen Rasmus B. , Frangakis Achilleas S. , Jensen Grant J. 
Published: August 2006

SummaryWhile the absence of any cytoskeleton was once recognized as a distinguishing feature of prokaryotes, it is now clear that a number of different bacterial proteins do form filaments in vivo. Despite the critical roles these proteins play in cell shape, genome segregation and cell division, molecular mechanisms have remained obscure in part for lack of electron microscopy‐resolution images where these filaments can be seen acting within their cellular context. Here, electron cryotomography was used to image the widely studied model prokaryote Caulobacter crescentus in an intact, near‐native state, producing three‐dimensional reconstructions of these cells with unprecedented clarity and fidelity. We observed many instances of large filament bundles in various locations throughout the cell and at different stages of the cell cycle. The bundles appear to fall into four major classes based on shape and location, referred to here as ‘inner curvature’, ‘cytoplasmic’, ‘polar’ and ‘ring‐like’. In an attempt to identify at least some of the filaments, we imaged cells where crescentin and MreB filaments would not be present. The inner curvature and cytoplasmic bundles persisted, which together with their localization patterns, suggest that they are composed of as‐yet unidentified cytoskeletal proteins. Thus bacterial filaments are frequently found as bundles, and their variety and abundance is greater than previously suspected.
Requirement for the acetyl phosphate pathway in Escherichia coli ATP‐dependent proteolysis
Authors: Mizrahi Itzhak , Biran Dvora , Ron Eliora Z. 
Published: August 2006

SummaryProtein degradation is a central component of the protein quality control system. Here we show that efficient proteolysis in Escherichia coli requires the active acetyl phosphate pathway. Deletion of this pathway, leading to depletion of acetyl phosphate, results in temperature sensitivity and reduced rate of ATP‐dependent proteolysis. The effect on proteolysis is general, as can be seen from the slowing down of the degradation of unstable proteins, including puromycin‐derived peptides. In addition, reduced intracellular concentrations of acetyl phosphate brings about an increase in the levels of protein aggregates, which contain a wide range of proteins, as expected if a broad spectrum of substrates are involved. Additional outcomes of acetyl phosphate deficiency are elevation in the transcript levels of heat shock genes and increased thermotolerance. In E. coli the acetyl phosphate pathway is the only source of acetyl phosphate, which is a key metabolic compound involved in major cellular processes. In this communication we present evidence for the general role of the acetyl phosphate pathway in protein degradation.
Type IV pili‐mediated secretion modulates Francisella virulence
Authors: Hager Anthony J. , Bolton Diana L. , Pelletier Mark R. , Brittnacher Mitchell J. , Gallagher Larry A. , Kaul Rajinder , Skerrett Shawn J. , Miller Samuel I. , Guina Tina 
Published: August 2006

Summary Francisella tularensis are the causative agent of the zoonotic disease, tularaemia. Among four F. tularensis subspecies, ssp. novicida (F. novicida) is pathogenic only for immunocompromised individuals, while all four subspecies are pathogenic for mice. This study utilized proteomic and bioinformatic approaches to identify seven F. novicida secreted proteins and the corresponding Type IV pilus (T4P) secretion system. The secreted proteins were predicted to encode two chitinases, a chitin binding protein, a protease (PepO), and a β‐glucosidase (BglX). The transcription of F. novicida pepO and bglX was regulated by the virulence regulator MglA. Intradermal infection of mice with F. novicida mutants defective in T4P secretion system or PepO resulted in enhanced F. novicida spread to systemic sites. Infection with F. novicida pepO mutants also resulted in increased neutrophil infiltration into the mouse airways. PepO is a zinc protease that is homologous to mammalian endothelin‐converting enzyme ECE‐1. Therefore, secretion of PepO likely results in increased production of endothelin and increased vasoconstriction at the infection site in skin that limits the F. novicida spread. Francisella human pathogenic strains contain a mutation in pepO predicted to abolish its secretion. Loss of PepO function may have contributed to evolution of highly virulent Francisellae.
Interdigital skin lesions of the lower limbs among patients with lymphoedema in an area endemic for bancroftian filariasis
Authors: Dreyer Gerusa , Addiss David , Gadelha Patricia , Lapa Eduardo , Williamson John , Dreyer Annelies 
Published: August 2006

SummaryObjectives  An estimated 15 million persons suffer from lymphoedema of the leg in filariasis‐endemic areas of the world. A major factor in the progression of lymphoedema severity is the incidence of acute dermatolymphangioadenitis (ADLA), which is triggered by bacteria that gain entry through damaged skin, especially in the toe web spaces (‘interdigital skin lesions’). Little is known about the epidemiology of these skin lesions or about patients’ awareness of them.Methods  We interviewed and examined 119 patients (89% women) with lymphoedema of the leg in Recife, Brazil, an area endemic for bancroftian filariasis.Results  We detected 412 interdigital skin lesions in 115 (96.6%) patients (mean, 3.5 lesions per patient, range 0–8). The number of interdigital skin lesions was significantly associated with lymphoedema stage (P < 0.001) and frequency of ADLA (P < 0.0001). Only 20 (16.8%) patients detected their own interdigital skin lesions or considered them abnormal. Patients reported a mean of 3.6 ADLA episodes during the previous 12 months (range, 0–20); reported ADLA incidence was associated with lymphoedema stage (P < 0.0001) and the number of interdigital skin lesions detected by the examining physician (P < 0.0001).Conclusions  These data suggest that interdigital skin lesions are a significant risk factor for ADLA and that persons with lymphoedema in filariasis‐endemic areas are unaware of their presence or importance. Prevention of ADLA through prompt recognition and treatment of interdigital skin lesions will require that patients be taught to identify lesions, especially between the toes and to recognize them as abnormal.
Pituitary–gonadal hormones and interleukin patterns in leprosy
Authors: Leal Ângela M. O. , Magalhães Patrícia K. R. , Souza Cacilda S. , Foss Norma T. 
Published: August 2006

SummaryThe functional status of pituitary–gonadal hormones and their relationship to the pattern of inflammatory cytokines in the lepromatous (LL/BL) and tuberculoid (TT/BT) poles of leprosy were investigated. Gonadotropins [luteinizing hormone (LH) and follicle‐stimulating hormone (FSH)], interleukin (IL)‐1β, IL‐6, tumour necrosis factor (TNF)‐α and C‐reactive protein (CRP) concentrations and erythrocyte sedimentation rate (ESR) were significantly higher in LL/BL leprosy patients than in controls and were not different from controls in TT/BT patients. LH and FSH were positively correlated with IL‐1β, IL‐6 and TNF‐α, and CRP concentrations and ESR. Testosterone plasma levels were significantly decreased in LL/BL patients and not different in TT/BT patients compared with controls. In addition, testosterone levels were inversely correlated with IL‐6 and TNF‐α. Prolactin plasma levels of both LL/BL and TT/BT patients were not different when compared with those of controls. There was a significant positive correlation between IL‐6 and TNF‐α plasma levels and ESR and CRP concentrations. IL‐1β was positively correlated with ESR but not with CRP. The significant correlations between gonadotropins and testosterone and cytokines in leprosy patients suggest that cytokines may have a direct influence at testicular level and may be of pathogenetic significance in leprosy and in other inflammatory states involving reproductive dysfunction.
Potential Risk Factors Associated with Bovine Spongiform Encephalopathy in Cattle from Schleswig‐Holstein, Germany
Authors: Pottgießer C. , Ovelhey A. , Ziller M. , Kramer M. , Selhorst T. , Conraths F. J. 
Published: August 2006

SummarySince the first detection of bovine spongiform encephalopathy (BSE) in homebred cattle in Germany on 26 November 2000, 382 cases have been confirmed until 30 September 2005. Thirty‐two of these cases were reported from the Federal State of Schleswig‐Holstein (SH). There are hypotheses on the routes of infection for German cattle, but only few efforts have been made to assess potential risk factors by epidemiological studies. The purpose of this study was to identify potential risk factors at the farm level for the occurrence of BSE in cattle in SH. By applying the method of indirect standardization, the prevalence of various structural and management parameters of BSE‐affected farms in SH was compared with the prevalence of these parameters in a standard population of cattle farms from SH. The data describing the standard population were obtained by a cross‐sectional study performed in SH in 2003. Data of the BSE case population were available from the central German BSE case database. A possible association of the occurrence of BSE with the feeding of milk replacers to calves was observed. There was a clear indication that the occurrence of BSE was associated with the presence of pigs and/or poultry on the farm. This finding suggests that cross‐contamination of feed or cross‐exposition may have occurred in SH. The results obtained using the indirect standardization analysis were validated by multiple logistic regression. This study indicates that the feedborne path has been the principal route of transmission for the BSE agent in SH.
Myotropic Avian Leukosis Virus subgroup J Infection in a Chicken
Authors: Sironi G. , Manarolla G. , Pisoni G. , Recordati C. , Rampin T. 
Published: August 2006

SummaryThe study describes a highly productive myotropic avian leukosis virus infection (ALV) in a 3‐month‐old female chicken. At necropsy, ascites, hepatic fibrosis and cardiomegaly were seen. Histologically, the most striking lesion was the presence of cytoplasmic basophilic inclusions in myocardial fibers. Immunostaining for ALV group specific antigen p27 revealed a diffuse presence of virus antigen in cardiac myofibers, in smooth muscle fibers of most of the organs, and in rare, pancreatic and ovarian theca cells. Ultrastructurally, myocardial inclusions consisted of clusters of 50–60 nm round particles with interspersed ribosome‐like granules. Numerous C‐type particles were found in intercellular spaces of ALV p27 positive tissues. PCR analyses revealed the presence of both ALV‐E and ALV‐J related sequences. In chicken genome, ALV‐E is usually present as endogenous provirus therefore, the pathological findings observed in this case are considered to be related with the ALV‐J infection. The results of this report further confirm that ALV‐J may be responsible for highly productive myotropic infections.
Distribution and Abundance of Bluetongue Vectors in Sardinia: Comparison of Field Data with Prediction Maps
Authors: Pili E. , Ciuccè S. , Culurgioni J. , Figus V. , Pinna G. , Marchi A. 
Published: August 2006

SummaryFollowing the spread of Bluetongue virus (BTV) in many Mediterranean countries during the last 5 years, presence of the main BTV vector, Culicoides imicola Kieffer (Diptera: Ceratopogonidae), was recorded in the region, including the island of Sardinia where the first BT epidemic originally started in the year 2000. Several models were also designed based on climate variables and satellite imaging in order to predict the presence and abundance of BTV vectors across Europe. A 3 years entomological survey (2001–2003) was conducted in the southern part of Sardinia confirming the widespread presence of C. imicola. However, substantial differences in terms of relative abundance were observed between field data and prediction maps based on satellite‐derived climate variables. Distribution of other potential BT vectors, belonging to Culicoides obsoletus Meigen and Culicoides pulicaris Linnaeus groups was also not congruent with model‐based predictions. These results stress the need of taking into account additional environmental factors (such as soil type, land usage, etc.) and local microclimatic conditions, especially related to breeding site requirements of Culicoides species, in order to predict the presence and abundance of BT vectors and to design reliable prediction maps on a local scale.
Neural representation of olfactory mixtures in the honeybee antennal lobe
Authors: Deisig Nina , Giurfa Martin , Lachnit Harald , Sandoz Jean‐Christophe 
Published: August 2006

AbstractNatural olfactory stimuli occur as mixtures of many single odors. We studied whether the representation of a mixture in the brain retains single‐odor information and how much mixture‐specific information it includes. To understand mixture representation in the honeybee brain, we used in vivo calcium imaging at the level of the antennal lobe, and systematically measured odor‐evoked activity in 24 identified glomeruli in response to four single odorants and all their possible binary, ternary and quaternary mixtures. Qualitatively, mixture‐induced activity patterns always contained glomeruli belonging to the pattern of at least one of the components, suggesting a high conservation of component information in olfactory mixtures. Quantitatively, glomerular activity saturated quickly and increasing the number of components resulted in an increase of cases in which the response of a glomerulus to the mixture was lower than that to the strongest component (‘suppression’). This shows global inhibition in the antennal lobe, probably acting as overall gain control. Single components were not equally salient (in terms of number of active glomeruli) and mixture activity patterns were always more similar to the more salient components, in a way that could be predicted linearly. Thus, although a gain control system in the honeybee antennal lobe prevents saturation of the olfactory system, mixture representation follows essentially elemental rules.
Spinal cord injury‐induced up‐regulation of AHNAK, expressed in cells delineating cystic cavities, and associated with neoangiogenesis
Authors: Von Boxberg Ysander , Salim Claudio , Soares Sylvia , Baloui Hasna , Alterio Jeanine , Ravaille‐Veron Michèle , Nothias Fatiha 
Published: August 2006

AbstractTo investigate the molecular basis for the poor regenerative capacity of the mammalian central nervous system (CNS) after injury, we searched for genes whose expression was affected by an adult rat spinal cord hemi‐section. Differential screening of a rat spinal cord expression library was performed using polyclonal antibodies raised against lesioned spinal cord tissue. A striking overexpression was found for ahnak, encoding a 700‐kDa protein, in normal CNS present only in the blood–brain barrier (BBB) forming vascular endothelial cells. Indeed, very early after spinal cord injury (SCI), high levels of membrane‐associated AHNAK are observed on non‐neuronal cells invading the lesion site. With time, AHNAK distribution spreads rostrally and caudally concomitant with the process of tissue inflammation and axon degeneration, delineating the interior surface of cystic cavities, mainly in front of barrier‐forming astrocytes. Strong overexpression is also observed on vascular endothelial cells reacting to BBB breakdown. Based on our detailed analysis of its spatiotemporal and cellular expression, and its previously described function in BBB, we suggest that AHNAK expression is associated with cell types displaying tissue–protective barrier properties. Our study may thus contribute to the elucidation of the precise molecular and cellular events that eventually render traumatic spinal cord tissue non‐permissive for regeneration.
Paraventricular–coerulear interactions: role in hypertension induced by prenatal undernutrition in the rat
Authors: Pérez H. , Ruiz S. , Núñez H. , White A. , Gotteland M. , Hernández A. 
Published: August 2006

AbstractRats submitted to fetal growth retardation by in utero malnutrition develop hypertension when adult, showing increased hypothalamic mRNA expression for corticotropin‐releasing hormone (CRH) and increased central noradrenergic activity. As hypothalamic CRH serves as an excitatory neurotransmitter within the locus coeruleus (LC) and coerulear norepinephrine plays a similar role within the paraventricular nucleus (PVN) of the hypothalamus, we studied, in both normal and prenatally undernourished 40‐day‐old anesthetized rats, the effects of intra‐LC microinjection of CRH and intra‐PVN microinjection of the α1‐adrenoceptor antagonist prazosin on multiunit neuronal activity recorded simultaneously from the two nuclei, as well as the effects on systolic pressure. Undernutrition was induced during fetal life by restricting the diet of pregnant mothers to 10 g daily, whereas mothers of control rats received the same diet ad libitum. At day 40 of postnatal life: (i) undernourished rats showed increased neuronal activity in the PVN and LC, as well as increased systolic pressure; (ii) intra‐LC CRH stimulated LC and PVN neurons and increased systolic pressure only in normal rats; (iii) intra‐PVN prazosin decreased LC and PVN neuronal activity and systolic pressure only in undernourished rats; and (iv) in normal rats, prazosin prevented the stimulatory effect of CRH only in PVN activity; in undernourished rats, prazosin allowed CRH to regain its stimulatory effects. The results point to the existence of an excitatory PVN–LC closed loop, which seems to be hyperactive in prenatally undernourished rats as a consequence of fetal programming; this loop could be responsible, in part, for the hypertension developed by these animals.
A deficiency in RFX3 causes hydrocephalus associated with abnormal differentiation of ependymal cells
Authors: Baas D. , Meiniel A. , Benadiba C. , Bonnafe E. , Meiniel O. , Reith W. , Durand B. 
Published: August 2006

AbstractCiliated ependymal cells play central functions in the control of cerebrospinal fluid homeostasis in the mammalian brain, and defects in their differentiation or ciliated properties can lead to hydrocephalus. Regulatory factor X (RFX) transcription factors regulate genes required for ciliogenesis in the nematode, drosophila and mammals. We show here that Rfx3‐deficient mice suffer from hydrocephalus without stenosis of the aqueduct of Sylvius. RFX3 is expressed strongly in the ciliated ependymal cells of the subcommissural organ (SCO), choroid plexuses (CP) and ventricular walls during embryonic and postnatal development. Ultrastructural analysis revealed that the hydrocephalus is associated with a general defect in CP differentiation and with severe agenesis of the SCO. The specialized ependymal cells of the CP show an altered epithelial organization, and the SCO cells lose their characteristic ultrastructural features and adopt aspects more typical of classical ependymal cells. These differentiation defects are associated with changes in the number of cilia, although no obvious ultrastructural defects of these cilia can be observed in adult mice. Moreover, agenesis of the SCO is associated with downregulation of SCO‐spondin expression as early as E14.5 of embryonic development. These results demonstrate that RFX3 is necessary for ciliated ependymal cell differentiation in the mouse.
Multiple risk reduction mechanisms: can dormancy substitute for dispersal?
Authors: Snyder Robin E. 
Published: August 2006

AbstractIn a spatiotemporally variable environment, plants use seed dispersal and dormancy to reduce risk. Intuition suggests that dormancy should be able to substitute for dispersal, so that dormancy will reduce the optimal mean dispersal distance, and previous theoretical studies using temporally uncorrelated environments have found this to be true. I show that in the presence of positive temporal correlations, dormancy instead increases dispersal: dormancy and dispersal are not interchangeable risk reduction mechanisms. Dispersal has both costs (seeds landing in unfavourable habitat) and benefits (seeds being in place to exploit newly favourable habitat). I discuss how the costs and benefits balance to determine optimal dispersal and how dormancy shifts this balance, causing dispersal to increase. I also find that an interaction between spatial and temporal correlations determines whether an evolutionarily stable dispersal distance exists at all and confirm the expectation that increasing the scale of spatial correlations causes dispersal to increase.