bluuebunny/crossref_metadata_2025_split huggingface dataset:
The genus Stauroneis (Bacillariophyceae) in the Antarctic region
Authors: Van de Vijver Bart , Gremmen Niek J. M. , Beyens Louis 
Published: September 2005

AbstractAim  To provide a detailed biogeography of the diatom genus Stauroneis in the Antarctic and sub‐Antarctic regions and to establish the biogeographical relationships between the different constituent locations to test the application of a precise and refined taxonomy in generating accurate polar biogeographies.Location  The Antarctic and sub‐Antarctic region comprising the islands South Georgia, Crozet, Kerguelen, Marion, Heard and the Antarctic Peninsula.Methods  Diatom samples from different habitats in a large part of the sub‐Antarctic and Antarctic region were investigated for their Stauroneis content. Presence/absence data were investigated using Sørensen's similarity index. An additional 500 samples from Arctic locations were used to provide a bipolar comparison. Using reliable literature data, gaps in the distribution of the Stauroneis taxa were filled.Results  The Stauroneis flora of the Antarctic and sub‐Antarctic regions is quite distinct from its Arctic equivalent, with only five species (out of 60) common to both areas. Within the (sub‐)Antarctic group, the islands of the Indian Ocean have the most diverse Stauroneis composition, which is clearly separated from the rest of the region. The South Georgia Stauroneis composition has some affinities with the Antarctic Peninsula but the latter has far fewer species. These results are in clear contrast to older data showing no biogeographical difference between the Arctic and Antarctic regions.Main conclusions  Using only a single genus, a clear biogeography of the (sub‐)Antarctic region can be produced that separates the Indian Ocean islands from other sampling locations. When based on a precise taxonomy, biogeographical relationships between locations in the region become much more reliable. Contrary to previous work, there is almost no similarity in the diatom floras of the Arctic and Antarctic regions.
The sensitivity of the premature infant pain profile – PIPP to measure pain in hospitalized neonates
Authors: Jonsdottir Rakel Bjorg , Kristjansdottir G. 
Published: September 2005

AbstractAim  The present study uses an Icelandic translation of the original version of the Premature Infant Pain Profile (PIPP) in order to assess its accuracy and sensitivity to the measure of pain in hospitalized neonates in Iceland. The PIPP is a composite tool developed to assess acute pain in preterm and term neonates.Methods  A crossover design, with a sample of 24 neonates, was used on three, routinely occurring events in the neonatal intensive care unit, where neonates were their own controls. The three events were baseline, non‐pain and pain event. Neonates were independently assessed for their pain, using the Icelandic translation of the PIPP, at the bedside.Results  Repeated measures analysis yielded a statistically significant main effect for the three events (pain, non‐pain and baseline), thus differentiating pain from non‐pain and baseline events (F = 57.11; P < 0.0001). Pair‐wise comparisons were subsequently carried out and the results show that PIPP scores at the pain event (11.72) were significantly lower (P < 0.0001) than that at the non‐pain event (6.04) and that at the baseline event (3.54; P < 0.0001). The PIPP scores at the non‐pain event were also significantly higher than that at the baseline event (P < 0.0001). These results suggest that the PIPP measure is sensitive to a painful event and differentiates between stress and pain in a clinical context across linguistic barriers. The findings also revealed almost a complete correlation between the PIPP scores of the two independent nurse raters at all events (P < 0.0001). Conclusion  Therefore the authors conclude that the Icelandic translation of the PIPP qualifies as a satisfying measure of pain responses in Icelandic neonates and can be recommended for use by clinicians and researchers. More research is, however, needed to further the accuracy and validity of the PIPP measure in general to assess pain in neonates in comparison to other pain measures.
Publishing outcome data: is it an effective approach?
Authors: Mason Anne , Street Andrew 
Published: September 2005

AbstractRationale, aims and objectives  The publication of health outcome data – rather than merely the measurement and collection – is being given increasing consideration. Publication reflects society's increasing emphasis on a general ‘right to know’, as well as being a means of informing consumer choice. In theory, publication may help to promote public trust, support patient choice, and stimulate action to improve the quality of care whilst controlling costs.Methods  Drawing on a literature review, this paper overviews the strategies employed in the UK and US to publish outcome data. The focus is on outcomes, and certain related process measures, that measure the performance of hospitals or surgeons.Results and conclusions  Presenting the limited evidence that exists, we review the potential beneficial and harmful effects of publishing hospital outcome data. We also consider the risks of making incorrect inferences based on these data and the potential for dysfunctional consequences. Recognizing that the public largely mistrusts currently published health outcome data, we offer some recommendations for the future direction of strategies for publication.
Exploring the continuum: medical information to effective clinical practice*. Paper I: the translation of knowledge into clinical practice
Authors: Genuis Shelagh K. , Genuis Stephen J. 
Published: September 2005

AbstractThis paper investigates the translation of medical information into clinical practice and the role of thoughtful dissent by exploring the influence of sociological factors on change, the impact of evidence‐based medicine (EBM), and the role of industry. Changing practice related to hormone therapy for menopausal and post‐menopausal women provides context for this discussion. Medical change involves diffusion of ideas to potential users and ongoing reconciliation of new information with old ideas; this process is influenced by sociological factors including values and experiences, interpersonal relationships and local context. While EBM has alerted doctors to the importance of high quality research and theoretically provides a tool for translating research into practice, there are important problems with its application: (1) it has resulted in a reductionist approach to research and illness; (2) there is a considerable gap between research findings and the complex environment of clinical practice; and (3) EBM has been appropriated by experts, thus corporately developed ‘standard‐of‐care’ documents have become instruments of external regulation, and EBM has ceased to be a tool in the hand of individual clinicians. In addition, industry impacts the translation of knowledge by significantly influencing academia, researchers, medical publications, consensus conferences, and practising doctors. While questioning doctrinaire practices or directives is a daunting prospect for individual clinicians, the translation of knowledge into practice and evolution of medical thought is dependent on the progressive role of thoughtful dissent.
Exploring the continuum: medical information to effective clinical practice*. Paper II. Towards aetiology‐centred clinical practice
Authors: Genuis Stephen J. , Genuis Shelagh K. 
Published: September 2005

AbstractContemporary clinical practice increasingly functions within a disease management paradigm aimed at finding and implementing therapeutic interventions that demonstrate efficacy in clinical trials. Disease prevention, elucidation of illness aetiology and proactive health promotion have taken a back seat. Current clinical care often includes a ‘fast‐food’ type of medical encounter, which frequently neglects disease causality. The medical community is presently challenged by unique administrative and professional adversities as well as undue commercial influence; these factors contribute to a lethargic response to escalating rates of chronic illness and to mainstream medicine's relative inattention to emerging research about disease aetiology. Individual medical practitioners and the medical establishment must strategically seek to advance patient health and maintain professional relevancy by a renewed emphasis on the following principles: patient‐based clinical care, aetiology‐centred medicine, and proactive health promotion.
Do case‐generic measures of queue performance for bypass surgery accurately reflect the waiting‐list experiences of those most urgent?
Authors: Burstein Jason , Lee Douglas S. , Alter David A. 
Published: September 2005

AbstractBackground  Queue performance is typically assessed using generic measures, which capture the queue in aggregate. The objective of this study was to examine whether case‐generic measures of queue performance appropriately reflected the waiting‐list experiences of those patients with greatest disease  severity. Methods  We examined the queue for isolated coronary artery bypass grafting (CABG) in Ontario between April 1993 and March 2000 using data obtained from the Cardiac Care Network. Our primary measure of queue performance was the proportion of patients who received their bypass surgery within their recommended maximum waiting times (%RMWTs) in any given month. We compared case‐generic measures of queue performance to case‐specific measures of queue performance stratified  by  urgency  level.Results  The queue was largely comprised of elective cases ranging from 73% (1993) to 57%(1999). Urgent patients comprised the minority of the queue ranging from 14% (1993) to 20% (1999). Case‐generic month‐to‐month variations in the percentage of cases completed within RMWTs (an aggregated waiting list measure encompassing the characteristics of all patients in the queue) closely resembled the experiences of elective patients (R2 = 0.81), but conversely, bore little relationship to the waiting‐list experiences of those most urgent (R2 = 0.15).Interpretation  Case‐generic measures of queue performance for bypass surgery in Ontario were not reflective of the waiting‐list experiences of those most urgent. Our results reinforce the concept that urgency‐specific waiting list monitoring systems are required to best evaluate and appropriately respond to fluctuations in queue performance.
Strengthening the case for disease management effectiveness: un‐hiding the hidden bias
Authors: Linden Ariel , Adams John L. , Roberts Nancy 
Published: September 2005

AbstractAs is the case with most health care program evaluations, disease management (DM) programs typically follow an observational study design, indicating that randomization to treatment or control was not performed. The foremost limitation of observational studies, compared to randomized studies, is that the only biases that can be controlled for are those associated with observed variables. Hidden bias refers to all those unobserved covariates that may distort the conclusions of the study. This paper introduces a sensitivity analysis that is used to determine the magnitude of hidden bias necessary to alter the conclusion that a DM program intervention was indeed effective.
Two proteins with 6‐cys motifs are required for malarial parasites to commit to infection of the hepatocyte
Authors: Ishino Tomoko , Chinzei Yasuo , Yuda Masao 
Published: September 2005

SummaryMany intracellular pathogens have host cells suitable for their proliferation, and selectively invade them using specific host–parasite interactions. Malarial sporozoites, the liver‐invasive forms, are effectively targeted to hepatocytes and proliferate in them. So far, however, sporozoite molecules that mediate the specific infection of hepatocytes remain unknown. Here we report that two proteins, Pbs36p and Pbs36, belonging to the plasmodium 6‐cys domain protein family, carry out this function. We found that these molecules are specifically produced in liver‐infective sporozoites. Target disruption of the respective genes nearly abolished sporozoite infectivity in the mammalian host. Invasion assays revealed that the mutant parasites could not commit to infection, even when they encounter with hepatocytes, resulting in continuous traversal of hepatocytes. These results suggest that these proteins are necessary for sporozoites to recognize hepatocytes and commit to infection. This finding might lead to novel anti‐malarial strategies that prevent sporozoite infection of the hepatocyte.
DNA polymerase II as a fidelity factor in chromosomal DNA synthesis in Escherichia coli
Authors: Banach‐Orlowska Magdalena , Fijalkowska Iwona J. , Schaaper Roel M. , Jonczyk Piotr 
Published: September 2005

Summary Escherichia coli DNA polymerase III holoenzyme (HE) is the main replicase responsible for replication of the bacterial chromosome. E. coli contains four additional polymerases, and it is a relevant question whether these might also contribute to chromosomal replication and its fidelity. Here, we have investigated the role of DNA polymerase II (Pol II) (polB gene product). Mismatch repair‐defective strains containing the polBex1 allele – encoding a polymerase‐proficient but exonucleolytically defective Pol II – displayed a mutator activity for four different chromosomal lac mutational markers. The mutator effect was dependent on the chromosomal orientation of the lacZ gene. The results indicate that Pol II plays a role in chromosomal replication and that its role is not equal in leading‐ versus lagging‐strand replication. In particular, the role of Pol II appeared larger in the lagging strand. When combined with dnaQ or dnaE mutator alleles, polBex1 showed strong, near multiplicative effects. The results fit a model in which Pol II acts as proofreader for HE‐produced misinsertion errors. A second role of Pol II is to protect mismatched 3′ termini against the mutagenic action of polymerase IV (dinB product). Overall, Pol II may be considered a main player in the polymerase trafficking at the replication fork.
A role for topoisomerase III in a recombination pathway alternative to RuvABC
Authors: Lopez Christopher R. , Yang Shirley , Deibler Richard W. , Ray Starlight A. , Pennington Jeanine M. , DiGate Russell J. , Hastings P. J. , Rosenberg Susan M. , Zechiedrich E. Lynn 
Published: September 2005

SummaryThe physiological role of topoisomerase III is unclear for any organism. We show here that the removal of topoisomerase III in temperature sensitive topoisomerase IV mutants in Escherichia coli results in inviability at the permissive temperature. The removal of topoisomerase III has no effect on the accumulation of catenated intermediates of DNA replication, even when topoisomerase IV activity is removed. Either recQ or recA null mutations, but not helD null or lexA3, partially rescued the synthetic lethality of the double topoisomerase III/IV mutant, indicating a role for topoisomerase III in recombination. We find a bias against deleting the gene encoding topoisomerase III in ruvC53 or ΔruvABC backgrounds compared with the isogenic wild‐type strains. The topoisomerase III RuvC double mutants that can be constructed are five‐ to 10‐fold more sensitive to UV irradiation and mitomycin C treatment and are twofold less efficient in transduction efficiency than ruvC53 mutants. The overexpression of ruvABC allows the construction of the topoisomerase III/IV double mutant. These data are consistent with a role for topoisomerase III in disentangling recombination intermediates as an alternative to RuvABC to maintain the stability of the genome.
Transcriptional activation of the pathway‐specific regulator of the actinorhodin biosynthetic genes in Streptomyces coelicolor
Authors: Uguru Gabriel C. , Stephens Karen E. , Stead Jonathan A. , Towle Jane E. , Baumberg Simon , McDowall Kenneth J. 
Published: September 2005

SummaryThe Streptomyces produce a plethora of secondary metabolites including antibiotics and undergo a complex developmental cycle. As a means of establishing the pathways that regulate secondary metabolite production by this important bacterial genus, the model species Streptomyces coelicolor and its relatives have been the subject of several genetic screens. However, despite the identification and characterization of numerous genes that affect antibiotic production, there is still no overall understanding of the network that integrates the various environmental and growth signals to bring about changes in the expression of biosynthetic genes. To establish new links, we are taking a biochemical approach to identify transcription factors that regulate antibiotic production in S. coelicolor. Here we describe the identification and characterization of a transcription factor, designated AtrA, that regulates transcription of actII‐ORF4, the pathway‐specific activator of the actinorhodin biosynthetic gene cluster in S. coelicolor. Disruption of the corresponding atrA gene, which is not associated with any antibiotic gene cluster, reduced the production of actinorhodin, but had no detectable effect on the production of undecylprodigiosin or the calcium‐dependent antibiotic. These results indicate that atrA has specificity with regard to the biosynthetic genes it influences. An orthologue of atrA is present in the genome of Streptomyces avermitilis, the only other streptomycete for which there is a publicly available complete sequence. We also show that S. coelicolor AtrA can bind in vitro to the promoter of strR, a transcriptional activator unrelated to actII‐ORF4 that is the final regulator of streptomycin production in Streptomyces griseus. These findings provide further evidence that the path leading to the expression of pathway‐specific activators of antibiotic biosynthesis genes in disparate Streptomyces may share evolutionarily conserved components in at least some cases, even though the final activators are not related, and suggests that the regulation of streptomycin production, which serves an important paradigm, may be more complex than represented by current models.
Clustered genes required for synthesis and deposition of envelope glycolipids in Anabaena sp. strain PCC 7120
Authors: Fan Qing , Huang Guocun , Lechno‐Yossef Sigal , Wolk C. Peter , Kaneko Takakazu , Tabata Satoshi 
Published: September 2005

SummaryPhotoreduction of dinitrogen by heterocyst‐forming cyanobacteria is of great importance ecologically and for subsistence rice agriculture. Their heterocysts must have a glycolipid envelope layer that limits the entry of oxygen if nitrogenase is to remain active to fix dinitrogen in an oxygen‐containing milieu (the Fox+ phenotype). Genes alr5354 (hglD), alr5355 (hglC) and alr5357 (hglB) of the filamentous cyanobacterium, Anabaena sp. strain PCC 7120, and hglE of Nostoc punctiforme are required for synthesis of heterocyst envelope glycolipids. Newly identified Fox– mutants bear transposons in nearby open reading frames (orfs) all5343, all5345–asr5349 and alr5351–alr5358. Complementation and other analysis provide evidence that at least orfs all5343 (or a co‐transcribed gene), all5345, all5347, alr5348, asr5350–alr5353 and alr5356, but not asr5349, are also required for a Fox+ phenotype. Lipid and sequence analyses suggest that alr5351–alr5357 encode the enzymes that biosynthesize the glycolipid aglycones. Electron microscopy indicates a role of all5345 through all5347 in the normal deposition of the envelope glycolipids.
Binding of the Streptococcus gordonii surface glycoproteins GspB and Hsa to specific carbohydrate structures on platelet membrane glycoprotein Ibα
Authors: Takamatsu Daisuke , Bensing Barbara A. , Cheng Hui , Jarvis Gary A. , Siboo Ian R. , López José A. , Griffiss J. McLeod , Sullam Paul M. 
Published: September 2005

SummaryGspB and Hsa are homologous serine‐rich surface glycoproteins of Streptococcus gordonii strains M99 and Challis, respectively, that mediate the binding of these organisms to platelet membrane glycoprotein (GP) Ibα. Both GspB and Hsa consist of an N‐terminal putative signal peptide, a short serine‐rich region, a region (BR) that is rich in basic amino acids, a longer serine‐rich region and a C‐terminal cell wall anchoring domain. To further assess the mechanisms for GspB and Hsa binding, we investigated the binding of the BRs of GspB and Hsa (expressed as glutathione S‐tranferase fusion proteins) to sialylated glycoproteins in vitro. Both fusion proteins showed significant levels of binding to sialylated moieties on fetuin and GPIbα. In contrast, the corresponding region of a GspB homologue of Streptococcus agalactiae, which is acidic rather than basic, showed no binding to either fetuin or GPIbα. As measured by surface plasmon resonance kinetic analysis, GspB‐ and Hsa‐derived fusion proteins had high affinity for GPIbα, but with somewhat different dissociation constants. Dot blot analysis using a panel of synthesized oligosaccharides revealed that the BR of Hsa can bind both α(2‐3) sialyllactosamine [NeuAcα(2‐3)Galβ(1‐4)GlcNAc] and sialyl‐T antigen [NeuAcα(2‐3)Galβ(1‐3)GalNAc], whereas the BR of GspB only bound sialyl‐T antigen. Moreover, far Western blotting using platelet membrane proteins revealed that GPIbα is the principal receptor for GspB and Hsa on human platelets. The combined results indicate that the BRs of GspB and Hsa are the binding domains of these adhesins. However, the subsets of carbohydrate structures on GPIbα recognized by the binding domains appear to be different between the two proteins.
Trypanosomes change their transferrin receptor expression to allow effective uptake of host transferrin
Authors: Van Luenen Henri G. A. M. , Kieft Rudo , Mußmann Rainer , Engstler Markus , Ter Riet Bas , Borst Piet 
Published: September 2005

SummaryIn its mammalian host, Trypanosoma brucei covers its iron requirements by receptor‐mediated uptake of host transferrin (Tf). The Tf‐receptor (Tf‐R) is a heterodimeric membrane protein encoded by expression site‐associated gene (ESAG) 6 and 7 located promoter‐proximal in a polycistronic expression site (ES). Each of the 20 ESs encodes a slightly different Tf‐R; these differences strongly affect the binding affinity for Tfs of different hosts. The Tf‐R encoded in the 221 ES has a low affinity for dog Tf. Transfer of trypanosomes with an active 221 ES to dilute dog serum leads to growth arrest, which they can overcome by switching to another ES encoding a Tf‐R with higher affinity for dog Tf. Here we show that trypanosomes can also adapt to dilute dog serum without switching but by replacing the ESAG7 gene in the 221 ES by one from another ES, by deleting ESAG7 from the 221 ES with concomitant upregulation of transcription of ESAG7 in ‘silent’ ESs, by grossly overproducing the 221 Tf‐R or by combinations of these alterations. Our results illustrate the striking genetic flexibility of trypanosomes.