bluuebunny/crossref_metadata_2025_split huggingface dataset:
Non‐specific immune response of turbot, Scophthalmus maximus (L.), experimentally infected with a pathogenic Vibrio pelagius
Authors: Villamil L , Figueras A , Aranguren R , Novoa B 
Published: June 2003

AbstractThe effect of a pathogenic Vibrio pelagius, isolated during a mass mortality of turbot larvae, on the non‐specific immune response of turbot, Scophthalmus maximus (L.), macrophages was studied both in vitro and in vivo. The in vitro treatment of head kidney (HK) macrophages with viable V. pelagius caused a significant inhibition of the chemiluminescence (CL) response in comparison with untreated macrophages, while incubation with heat‐killed bacteria did not affect this response. In vivo, the intraperitoneal injection of V. pelagius resulted in a significant inhibition of the CL response in infected fish at days 1 and 4 post‐infection compared with the control fish response. The HK macrophage nitric oxide (NO) production was enhanced by in vitro incubation with intermediate doses of viable V. pelagius (5 × 103 and 5 × 104 bacteria mL−1) and higher doses of the heat‐killed bacteria (5 × 104–5 × 106 bacteria mL−1). In both cases, the NO inhibitorN‐ω ‐nitro‐L‐arginine was capable of down‐regulating the specific NO induction caused by incubation with the bacterial treatments. In contrast, incubation with ECPs at higher doses caused a reduction in NO production. In vivo, a significant enhancement in NO production was also observed in macrophage supernatants at day 10 post‐infection. Lysozyme concentration in the serum was also significantly increased in the experimentally infected fish at days 4 and 10 post‐injection. In addition, viable V. pelagius and its ECPs significantly reduced HK macrophage viability in vitro, whereas no significant differences in viability were observed during the incubation with heat‐killed bacteria. As NO production was enhanced in the experimentally infected fish, the inhibitory effect of the NO donor, S‐nitroso‐acetyl‐penicillamine (SNAP), was tested in vitro in a cell‐free assay. The results showed that growth of V. pelagius was significantly inhibited using SNAP at a high concentration (1 mm).
A single‐dose pharmacokinetic study of oxolinic acid and vetoquinol, an oxolinic acid ester, in cod, Gadus morhua L., held in sea water at 8 °C and in vitro antibacterial activity of oxolinic acid against Vibrio anguillarum strains isolated from diseased cod
Authors: Samuelsen O B , Bergh Ø , Ervik A 
Published: June 2003

AbstractThe pharmacokinetic properties of the antibacterial agent oxolinic acid and vetoquinol, the carbitol ester of oxolinic acid, were studied after intravenous (i.v.) and oral (p.o.) administration to 100–150 g cod, Gadus morhua L., held in sea water at 8 °C. Following i.v. injection, the plasma drug concentration‐time profile showed two distinct phases. The distribution half‐life (t1/2α) was estimated at 1.3 h, the elimination half‐life (t1/2β) as 84 h and the total body clearance (ClT) as 0.047 L kg−1 h−1. The volume of distribution at steady state, Vd(ss) was calculated to be 5.5 L kg−1, indicating good tissue penetration of oxolinic acid in cod. Following p.o. administration of oxolinic acid or vetoquinol, the peak plasma concentrations (Cmax) of oxolinic acid and the time to peak plasma concentrations (Tmax) were estimated to be 1.2 and 2.5 μg mL−1, and 24 and 12 h, respectively. The bioavailabilities of oxolinic acid following p.o. administration of oxolinic acid and vetoquinol were calculated to be 55 and 72%, respectively. The in vitro minimum inhibitory concentration (MIC) values of oxolinic acid against three strains of Vibrio anguillarum isolated from diseased cod were 0.016 μg mL−1 (HI‐610), 0.250 μg mL−1 (HI‐618) and 0.250 μg mL−1 (HI‐A21). Based on a MIC value of 0.016 μg mL−1 a single p.o. administration of 25 mg kg−1 of oxolinic acid maintains plasma levels in excess of 0.064 μg mL−1, corresponding to four times the MIC‐value, for approximately 12 days. The analogous value for a single p.o. dose of 25 mg kg−1 of oxolinic acid administered as vetoquinol was 13 days.
Putative virulence factors of atypical Aeromonas salmonicida isolated from Arctic charr, Salvelinus alpinus (L.), and European grayling, Thymallus thymallus (L.)
Authors: Madetoja J , Pylkkö P , Pohjanvirta T , Schildt L , Pelkonen S 
Published: June 2003

AbstractAtypical Aeromonas salmonicida (AAS) causes generalized lethal infections in farmed Arctic charr, Salvelinus alpinus (L.), and European grayling, Thymallus thymallus (L.), and is thus a serious threat for culture of these fish species. Virulence factors were studied among isolates of AAS from Arctic charr (n = 20), European grayling (n = 19) and other fish species (n = 20), of which 48 were of Finnish and 11 of Swedish origin. All isolates produced an A‐layer. Extracellular products (ECP) of the AAS isolates did not produce detectable gelatinase and caseinase activity in test assays. Analysis of the same ECP preparations with substrate sodium dodecyl sulphate–polyacrylamide gel electrophoresis showed weak proteolytic activity, indicating the different sensitivity of the detection methods used. The ECP from AAS isolates showed low cytotoxic activity against cultured cells. However, the ECP did not induce mortality in challenged Arctic charr. The results suggest that toxic components, like ECP, secreted by the bacterium may not be the major virulence factor in AAS‐infection in Arctic charr and European grayling, and hence the pathogenesis also differs from the pathogenesis of AAS‐infection in Atlantic salmon, Salmo salar L.
A UK Consensus Group on management of glucocorticoid‐induced osteoporosis: an update
Authors: Eastell R. , Reid D. M. , Compston J. , Cooper C. , Fogelman I. , Francis R. M. , Hosking D. J. , Purdie D. W. , Ralston S. H. , Reeve J. , Russell R. G. G. , Stevenson J. C. , Torgerson D. J. 
Published: June 2003

Abstract. Eastell R, Reid DM, Compston J, Cooper C, Fogelman I, Francis RM, Hosking DJ, Purdie DW, Ralston SH, Reeve J, Russell RGG, Stevenson JC, Torgerson DJ (University of Sheffield Medical School, Sheffield; University of Aberdeen, Aberdeen; University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge; Southampton General Hospital, Southampton; Guy's Hospital, London; Freeman Hospital, Newcastle upon Tyne; Nottingham City Hospital, Nottingham; Hull Royal Infirmary, Hull; Wynn Institute for Metabolic Research, London; and the University of York, York, UK). A UK Consensus Group on management of glucocorticoid‐induced osteoporosis: an update (Review). J Intern Med 1998; 244: 271–292.In the UK, over 250 000 patients take continuous oral glucocorticoids (GCs), yet no more than 14% receive any therapy to prevent bone loss, a major complication of GC treatment. Bone loss is rapid, particularly in the first year, and fracture risk may double. This review, based wherever possible on clinical evidence, aims to provide easy‐to‐use guidance with wide applicability. A treatment algorithm is presented for adults receiving GC doses of 7.5 mg day−1 or more for 6 months or more. General measures, e.g. alternative GCs and routes of administration, and therapeutic interventions, e.g. cyclical etidronate and hormone replacement, are recommended.
Field evaluation of a lethal ovitrap against dengue vectors in Brazil
Authors: Perich M. J. , Kardec A. , Braga I. A. , Portal I. F. , Burge R. , Zeichner B. C. , Brogdon W. A. , Wirtz R. A. 
Published: June 2003

Abstract. Field evaluation of a ‘lethal ovitrap’ (LO) to control dengue vector Aedes mosquitoes (Diptera: Culicidae), was undertaken in two Brazilian municipalities, Areia Branca and Nilopolis, in the State of Rio de Janeiro. The LO is designed to kill Aedes via an insecticide‐treated ovistrip (impregnated with deltamethrin). In each municipality, the intervention was applied to a group of 30 houses (10 LOs/house) and compared to 30 houses without LOs in the same neighbourhood. Five LOs were put outside and five LOs inside each treated house.Three methods of monitoring Aedes density were employed: (i) percentage of containers positive for larvae and/or pupae; (ii) total pupae/house; (iii) total adult females/house collected by aspirator indoors. Weekly mosquito surveys began during the month before LO placement, by sampling from different groups of 10 houses/week for 3 weeks pre‐intervention (i.e. 30 houses/month) and for 3 months post‐intervention in both treated and untreated areas.Prior to LO placement at the end of February 2001, Aedes aegypti (L) densities were similar among houses scheduled for LO treatment and comparison (untreated control) at each municipality. Very few Ae. albopictus (Skuse) were found and this species was excluded from the assessment. Post‐intervention densities of Ae. aegypti were significantly reduced for most comparators (P < 0.01), as shown by fewer positive containers (4–5 vs. 10–18) and pupae/house (0.3–0.7 vs. 8–10) at LO‐treated vs. untreated houses, 3 months post‐treatment at both municipalities. Numbers of adult Ae. aegypti females indoors were consistently reduced in LO‐treated houses at Areia Branca (3.6 vs. 6.8/house 3 months post‐intervention) but not at Niloplis (∼3/house, attributed to immigration). These results demonstrate sustained impact of LOs on dengue vector population densities in housing conditions of Brazilian municipalities.
Mosquito larval consumption of toxic arborescent leaf‐litter, and its biocontrol potential
Authors: David J. P. , Tilquin M. , Rey D. , Ravanel P. , Meyran J. C. 
Published: June 2003

Abstract.  Previously we described the mosquito larvicidal properties of decomposed leaf‐litter from deciduous trees, especially the alder Alnus glutinosa (L) Gaertn., due to toxic polyphenols and other secondary compounds. To further examine the biocontrol potential of toxic leaf‐litter for mosquito control, feeding rates of third‐instar mosquito larvae were assessed for examples of three genera: Anopheles stephensi Liston, Aedes aegypti (L) and Culex pipiens L. (Diptera: Culicidae).When immersed in a suspension of non‐toxic leaf‐litter particles (∼0.4 mm), pre‐starved larvae of all three species ingested sufficient material in 30 min to fill the anterior gut lumen (thorax plus two to three abdominal segments). Gut filling peaked after 1–2 h ingestion time, filling the intestine up to six to seven abdominal segments for Ae. aegypti, but maxima of five abdominal segments for Cx. pipiens and An. stephensi.Using three methods to quantify consumption of three materials by third‐instar larvae of Ae. aegypti, the average amount of leaf‐litter (non‐toxic 0.4 mm particles) ingested during 3 h was determined as ∼20 µg/larva (by dry weight and by lignin spectrophotometric assay). Consumption of humine (∼100 µm particles extracted from leaf‐litter) during 3 h was ∼80 µg/larva for Ae. aegypti, but only ∼30 µg/larva for Cx. pipiens and 15 µg/larva for An. stephensi, with good concordance of determinations by dry weight and by radiometric assay. Cellulose consumption by Ae. aegypti was intermediate: ∼40 µg/larva determined by radiometric assay. Apparent differences between the amounts of these materials ingested by Ae.aegypti larvae (humine four‐fold, cellulose two‐fold more than leaf‐litter) may be attributed to contrasts in palatability (perhaps related to particle size or form), rather than technical discrepancies, because there was good concordance between results of both methods used to determine the amounts of humine and leaf‐litter ingested.Bioassays of toxic leaf‐litter (decomposed 10 months) with 4‐h exposure period (ingestion time) ranked the order of sensitivity: Ae. aegypti (LC50 < 0.03 g/L) > An. stephensi (LC50 = 0.35 g/L) > Cx. pipiens (LC20 > 0.4 g/L). When immersed in the high concentration of 0.5 g/L toxic leaf‐litter (0.4 mm particles), as little as 15–30 min ingestion time (exposure period) was sufficient to kill the majority of larvae of all three species, as soon as the gut lumen was filled for only the first few abdominal segments. Possibilities for mosquito larval control with toxic leaf‐litter products and the need for standardized ingestion bioassays of larvicidal particles are discussed.
Horizontal transfer of the insect growth regulator pyriproxyfen to larval microcosms by gravid Aedes albopictus and Ochlerotatus triseriatus mosquitoes in the laboratory
Authors: Dell Chism B. , Apperson C. S. 
Published: June 2003

Abstract.  The insect growth regulator (IGR) pyriproxyfen is highly active against mosquitoes (Diptera: Culicidae). Through continuous emersion of large larvae (instars 3–4) the concentration causing 50% inhibition of adult emergence (EI50) was determined as 0.200 p.p.b. for Aedes albopictus (Skuse) and 3.5 to 7 times less for Ochlerotatus triseriatus (Say): IE50 0.0288 p.p.b.As a possible method of application to larval microscosms of these species that oviposit in water containers and phytotelmata, the horizontal transfer of pyriproxyfen to larval microcosms by adult mosquitoes was evaluated under laboratory conditions. Gravid females were forced to walk on surfaces treated with pyriproxyfen (tarsal contact exposure) and then allowed to oviposit in larval microcosms. Using replicate bioassay cages, each with an oviposition container, and a factorial experimental design, we assessed Ae. albopictus for the effects of (i) pyriproxyfen concentration (0.2, 0.3 and 0.4 mg/cm2) contacted by gravid females, and (ii) the number of treated gravid females added to bioassay cages (one, three or five females/cage), on the mortality of larvae in oviposition containers. Only 0.2 mg/cm2 treatment rate was tested on Oc. triseriatus.A significant (P < 0.05) curvilinear response in inhibition of emergence (IE) was achieved on both species. Densities of one or three treated Oc. triseriatus females/cage yielded IE rates of only 21–27%, whereas five treated females/cage resulted in 70% inhibition. With Ae. albopictus, densities of three or five treated females/cage yielded 48–67% and 59–73% IE, respectively, whereas one treated female/cage gave only 4–30% inhibition.Use of IGR‐treated oviposition containers to achieve horizontal transfer of pyriproxyfen to mosquito oviposition sites could be a field management technique based on mosquito biology and behaviour. In binary choice tests with Ae. albopictus, horizontal transfer of pyriproxyfen from a container with a treated ovistrip (0.3 or 0.4 mg/cm2) to an untreated microcosm resulted in 14–38% inhibition. In larval bioassays, pyriproxyfen activity declined markedly within 10 days. Forcibly exposing gravid female mosquitoes to pyriproxyfen‐treated paper surface did not affect their fecundity. However, from the 1st to 2nd gonotrophic cycles the egg hatch rate declined by 30% (P < 0.05). Some variation of results could be due to interactions between females at the oviposition site, possibly causing disproportionate transfer of pyriproxyfen to larval microcosms. Comparative studies of the oviposition behaviour of each mosquito are warranted and would potentially provide information needed to improve the technique.
A mechanism by which nitric oxide accelerates the rate of oxidative DNA damage in Escherichia coli
Authors: Woodmansee Anh N. , Imlay James A. 
Published: June 2003

SummaryThe presence of nitric oxide (NO) greatly accelerates the rate at which hydrogen peroxide (H2O2) kills Escherichia coli. Workers have suggested that this effect may be important in the process of bacteriocide by phagocytes. The goal of this study was to determine the mechanism of this synergism. The filamentation of the dead cells, and their protection by cell‐permeable iron chelators, indicated that NO/H2O2 killed cells by damaging their DNA through the Fenton reaction. Indeed, the number of DNA lesions was far greater when NO was present during H2O2 exposure. In the Fenton reaction, free intracellular iron transfers electrons from adventitious donors to H2O2, producing hydroxyl radicals. Although NO damaged the [Fe‐S] clusters of dehydratases, this did not increase the amount of free iron and was therefore not the reason for acceleration of Fenton chemistry. However, NO also blocked respiration, an event that previous studies have shown can stimulate oxidative DNA damage. The resultant accumulation of NADH accelerates the reduction of free flavins by flavin reductase, and these reduced flavins drive Fenton chemistry by transferring electrons to free iron. Indeed, mutants lacking the respiratory quinol oxidases were sensitive to H2O2, and NO did not have any further effect. Further, mutants that lack flavin reductase were resistant to NO/H2O2, and overproducing strains were hypersensitive. We discuss the possibility that H2O2 and NO synergize when macrophages attack captive bacteria.
The interaction of Slt2 MAP kinase with Knr4 is necessary for signalling through the cell wall integrity pathway in Saccharomyces cerevisiae
Authors: Martin‐Yken Helene , Dagkessamanskaia Adilia , Basmaji Fadi , Lagorce Arnaud , Francois Jean 
Published: June 2003

SummaryIn budding yeast, PKC1 plays an essential role in cell integrity and proliferation through a linear MAP (Mitogen Activated Protein) kinase phosphorylation cascade, which ends up with the activation of the Slt2‐MAP kinase by dual phosphorylation on two conserved threonine and tyrosine residues. In this phosphorylated form, Slt2p kinase activates by phosphorylation at least two known downstream targets: Rlm1p, which is implicated in the expression of cell wall‐related genes, and SBF, required for transcription activation of cell cycle‐regulated genes at the G1 to S transition. In this paper, we demonstrate by two‐hybrid, in vitro immunoprecipitation and tandem affinity purification (TAP) methods that Knr4p physically interacts with Slt2p. Moreover, we show that the absence of Knr4p alters proper signalling of Slt2p to its two known downstream targets. In a knr4 null mutant, the SLT2‐dependent activation of Rlm1p is strongly reduced and the transcriptional activity of Rlm1p is decreased, although the phosphorylated form of Slt2p is more abundant than in wild‐type cells. On the contrary, SBF is abnormally activated in this mutant, as shown by a more abundant phosphorylated form of Swi6p, by higher β‐galactosidase levels from a SCB‐lacZ gene fusion, and by deregulation of the cyclic behaviour of several cell cycle‐regulated genes. These results, taken together with our recent finding that Bck2p requires Knr4p to activate additively with Cln3‐Cdc28p SBF target genes, lead to a model in which Knr4p is involved in co‐ordinating the Slt2p‐mediated cell wall integrity pathway with progression of the cell cycle.
Identification of a novel iron regulated staphylococcal surface protein with haptoglobin‐haemoglobin binding activity
Authors: Dryla Agnieszka , Gelbmann Dieter , Von Gabain Alexander , Nagy Eszter 
Published: June 2003

Summary Staphylococcus aureus is an extremely adaptable pathogen causing a wide variety of infections. Staphylococcal surface proteins that directly interact with host extracellular proteins greatly contribute to virulence and are involved in adhesion, immune escape and nutrient acquisition. In our extensive search for highly immunogenic, in vivo‐expressed, staphylococcal proteins, previously, we identified a novel member of the family of Gram‐positive anchor motif proteins with a predicted 895 amino acid long sequence. In order to determine the ligand for this novel LPXTG cell wall protein, we employed affinity purification of human plasma using the recombinant form of the protein. Two‐dimensional electrophoresis of eluted plasma proteins identified haptoglobin as a specific binding partner. Importantly, we also observed this specific ligand binding when living S. aureus cells were exposed to biotin‐labelled haptoglobin (Hp) in a FACS‐based assay. Targeted deletion of the gene eliminated Hp‐binding, a function that has not been attributed to S. aureus before. Based on these data we specified the protein as the staphylococcal haptoglobin receptor A (HarA). Similarly to other haptoglobin receptors identified in Gram‐negative pathogens, HarA binds not only Hp, but also haptoglobin‐haemoglobin complexes with an even higher affinity, as demonstrated in in vitro binding assays. Employing specific deletion mutants, ligand binding was localized to two homologous regions with about 145 amino acid residues located within the N‐terminal part of the protein. In addition, we demonstrated that expression of HarA was strictly controlled by iron through the iron‐dependent transcriptional regulator Fur. Based on these data we propose that HarA can be added to the list of staphylococcal virulence factors with a most likely function related to iron acquisition.
Uropathogenic Escherichia coli use d‐serine deaminase to modulate infection of the murine urinary tract
Authors: Roesch Paula L. , Redford Peter , Batchelet Stephanie , Moritz Rebecca L. , Pellett Shahaireen , Haugen Brian J. , Blattner Frederick R. , Welch Rodney A. 
Published: June 2003

SummaryAlthough once thought to be unique to bacteria, d‐amino acids are also produced by mammals. For example, d‐serine is excreted in human urine at concentrations ranging from 3.0 to 40 µg ml−1. An epidemiological survey demonstrated that urine isolates of E. coli are more likely to catabolise d‐serine via expression of d‐serine deaminase, DsdA than enteric disease isolates. The urosepsis strain, CFT073, and an isogenic dsdA mutant have similar growth kinetics in minimal or complex media. However, relative to the wild type, the dsdA mutant has a pleiomorphic cell shape and a prolonged, 4–6 h lag phase when grown in human urine. This suggests that d‐serine catabolism provides a growth advantage in the urinary tract. Unexpectedly, in a direct competition model of urinary tract infection, the dsdA mutant was recovered 300‐times more frequently than the wild type in the bladders of mice 48 h after infection. A new model of E. coli uropathogenesis is proposed where growth and gene expression are modulated in response to environmental d‐serine levels. In support of this, the CFT073 dsdA mutant is hyperflagellated and more motile than the wild type indicating that intracellular levels of d‐serine may directly or indirectly influence the expression of regulons associated with E. coli uropathogenesis.