bluuebunny/crossref_metadata_2025 huggingface dataset:
Psychopathology and Pediatric Complex Partial Seizures: Seizure‐related, Cognitive, and Linguistic Variables
Authors: Caplan Rochelle , Siddarth Prabha , Gurbani Suresh , Ott Derek , Sankar Raman , Shields W. Donald
Published: September 2004

Summary: Purpose:This study examined the role of cognition, language, seizure‐related, and demographic variables in the psychopathology of children with complex partial seizure disorder (CPS) of average intelligence.

Methods:One‐hundred one CPS and 102 normal children, aged 5.1 to 16.9 years, had a structured psychiatric interview and cognitive and language testing. Parents provided demographic, perinatal, and seizure‐related information, as well as behavioral information through the Child Behavior Checklist (CBCL) and a structured psychiatric interview about the child.

Results:Significantly more CPS patients had psychopathology, cognitive deficits, and linguistic deficits than did those in the normal group. Among the patients, Verbal IQ predicted the presence of a psychiatric diagnosis, as well as CBCL scores in the borderline/clinical range. Seizure, linguistic, and demographic variables were unrelated to psychopathology. The cognitive and linguistic deficits of the CPS group, however, were predicted by seizure factors (e.g., prolonged seizures/febrile convulsions; seizure frequency/number of antiepileptic drugs) and demographic factors (e.g., minority status).

Conclusions:Because subtle verbal cognitive deficits predict behavioral disturbances in pediatric CPSs, the study's findings highlight the importance of assessing behavior, cognition, and language in these children. They also underscore the negative impact of prolonged seizures, febrile convulsions, seizure frequency, and antiepileptic drug polytherapy on cognition and language in pediatric CPSs.
Metabolic Acidosis and Malnutrition in Dialysis Patients
Authors: Szeto Cheuk‐Chun , Chow Kai‐Ming
Published: September 2004

Acidosis is a classic uremic toxin that causes protein catabolism, mainly by selective breakdown of skeletal muscle protein. However, the importance of acidosis is often overlooked in dialysis patients. In the presence of acidosis, there is activation of the ubiquitin‐proteasome machinery as well as the branched‐chain keto acid dehydrogenase, resulting in catabolism of muscle protein. Acidosis acts synergistically with other catabolic factors, such as inflammatory cytokines and insulin resistance, in inducing protein catabolism. There is ample laboratory evidence showing that correction of acidosis prevents the up‐regulation of the ubiquitin‐proteasome machinery and reduces protein degradation. Randomized control trials further show that acidosis in dialysis patients can be treated successfully by a higher dialysate bicarbonate or lactate concentration, or by oral bicarbonate supplement. Correction of mild acidosis in dialysis patients is effective in improving nutritional status and reducing the duration of hospitalization.
Measuring Quality of Dying in End‐Stage Renal Disease
Authors: Spital Aaron , Cohen Lewis M. , Germain Michael J.
Published: September 2004

Palliative medicine operates under the presumption that it is possible to improve the quality of a patient's death. Nephrology has justifiably taken pride in its reliance on internal benchmarking and the use of quality targets to shape clinical practice innovations, and this article discusses the efforts that are being made to measure end‐of‐life care of dialysis patients. A tool called the Dialysis Quality of Dying Apgar is described that examines five domains (pain, nonpain symptoms, advance care planning, peacefulness, and time) which are scored and then summed. A recent interdisciplinary workgroup of renal professionals has commissioned a series of focus groups that have attempted to ascertain patient and family values and preferences for the management of terminal situations. The results are summarized, and they should hopefully form a basis for the development of additional research and clinical measurement tools.
Special Article: Improving Outcomes in CKD and ESRD Patients: Carrying the Torch from Training to Practice
Authors: Nissenson Allen R. , Agarwal Rajiv , Allon Michael , Cheung Alfred K. , Clark William , Depner Tom , Diaz‐Buxo Jose A. , Kjellstrand Carl , Kliger Alan , Martin Kevin J. , Norris Keith , Ward Richard , Wish Jay
Published: September 2004

Practicing nephrologists are spending more time caring for end‐stage renal disease (ESRD) and chronic kidney disease (CKD) patients. Despite this focus, and considerable advances in the understanding of those aspects of care that impact on clinical outcomes, morbidity, mortality, and quality of life for these patients has not improved substantially over the past decade. One of the possible explanations for this lack of progress is the structure of current nephrology training programs, where ESRD and CKD patient care is not emphasized. To address this issue, we developed a short preceptorship for second‐year nephrology fellows, including didactic lectures and workshops. Of 67 participating fellows, 50% were from programs offering 3 or fewer months of exposure to outpatient hemodialysis, and 25% reported no exposure to peritoneal dialysis. Of more concern, 25% reported no “official rounds” with an attending nephrologist on dialysis patients. If nephrologists are to take their appropriate place as leaders of the care delivery team, nephrology fellowships must be restructured with appropriate emphasis placed on the comprehensive care of ESRD and CKD patients.
Use of Low Molecular Weight Heparins and Glycoprotein IIb/IIIa Inhibitors in Patients with Chronic Kidney Disease
Authors: Perazella Mark A. , Mosenkis Ari , Berns Jeffrey S.
Published: September 2004

Despite aggressive intervention, cardiac causes of death, including acute coronary syndrome (ACS), continue to be a major source of mortality in patients with chronic kidney disease (CKD), including end‐stage renal disease (ESRD). Multiple large prospective trials have demonstrated the clinical benefits of both low molecular weight heparin (LMWH) and glycoprotein (Gp) IIb/IIIa inhibitors in treating patients with ACS. Unfortunately patients with significant impairment of kidney function have generally been excluded from these major clinical trials. Consequently relatively little is known about the pharmacokinetics, appropriate dosing, efficacy, and safety of these medications in patients with CKD of various stages. This article examines the available literature regarding the pharmacokinetics, dosing, efficacy, and safety of LMWH and Gp IIb/IIIa inhibitors in patients with CKD.
American Society of Diagnostic and Interventional Nephrology Section Editor: Stephen Ash: Peritoneal Dialysis Access‐Related Procedures by Nephrologists
Authors: Asif Arif
Published: September 2004

Traditionally the placement of a peritoneal dialysis (PD) catheter in a patient with end‐stage renal disease (ESRD) has been accomplished by a surgeon and using general anesthesia. This approach often introduces delays in starting PD, incurs additional costs in utilizing an operating room as well as anesthesia services, and introduces the mortality risk associated with general anesthesia. Recent data have emphasized that interventional nephrologists can safely and successfully perform PD access procedures. In this context, operating room facilities and staff and anesthesia services are not required and catheter insertion can be performed in a procedure room using local anesthesia, thereby reducing costs and completely bypassing the mortality risk associated with general anesthesia. When performed by a nephrologist, the catheter insertion can be accomplished swiftly and dialysis therapy initiated in a timely manner. Once begun, the success of PD hinges on reliable and long‐term access to the peritoneal cavity. Prospective randomized and nonrandomized studies have shown that PD catheters peritoneoscopically placed by nephrologists have fewer complications (infection, exit site leak) and longer catheter survival rates than those inserted surgically. Although PD offers a variety of advantages, it remains an underutilized form of renal replacement therapy. To counteract PD underutilization, at least two separate centers have demonstrated a positive impact on the growth of the PD population when catheter insertion is performed by nephrologists. This article presents PD access‐related procedures currently performed by interventional nephrologists. Furthermore, some of the complicating issues (bowel perforation, catheter migration, prior abdominal surgery) related to PD catheter insertion and management are also discussed.
Review article: anti‐reflux surgery and endoluminal therapies
Authors: Sonnenberg A.
Published: September 2004

In the short term, fundoplication and antisecretory medication are equally effective in the management of gastro‐oesophageal reflux disease. However, over the long term, the fundoplication wrap tends to become loose, and many surgical patients continue to take antisecretory medication after surgery. The operation is technically complex and takes a long time to learn. Inexperience of the individual surgeon is a major factor contributing to the occurrence of postsurgical complications. Fundoplication does not prevent the occurrence of Barrett's oesophagus nor its progression to oesophageal adenocarcinoma. There is no evidence to suggest that the procedure is less costly or more cost‐effective than long‐term maintenance therapy with antisecretory medications, especially if surgical failures and postsurgical complications are taken into account. Fundoplication represents an alternative to medical therapy in patients with gastro‐oesophageal reflux disease who cannot or do not want to be on long‐term maintenance therapy with antisecretory medication. Endoluminal procedures, such as radiofrequency ablation, endoscopic suturing and injection at the gastro‐oesophageal junction, work only in mild forms of reflux disease. They fail to provide complete relief of reflux symptoms and do not heal erosive oesophagitis. All endoluminal procedures would have to undergo major technological improvements before they could become comparable with fundoplication or antisecretory therapy.
Practical examples: trials and conclusions — an interactive segment
Authors: Talley N. J.
Published: September 2004

There is a requirement for a critical review of the literature published in the field of reflux disease management, particularly when the literature is used as a basis for the adoption of specific interventions into everyday practice. Numerous published studies are valid and robust, but many are not. Particularly common is the over‐interpretation of positive studies based on small patient numbers, which may be subject to publication bias. Claims of equivalence are invalid without a pre‐specified level of equivalence and adequate power to measure this. More generally, a lack of pre‐defined primary end‐points, clinically relevant and measured appropriately, is a common feature of reflux trial methodology.
Review article: gastric pH — the most relevant predictor of benefit in reflux disease?
Authors: Armstrong D.
Published: September 2004

In patients with gastro‐oesophageal reflux disease, the pH of refluxed gastric contents has a direct bearing on disease severity and oesophageal damage. A pH of 4 has been defined as a threshold below which refluxed gastric contents become injurious to the oesophagus. Studies in patients with erosive oesophagitis have shown that the 8‐week healing rates produced by acid suppressive therapy are related to the duration of time over a 24‐h period that the intragastric pH > 4. The most effective agents, providing more hours with gastric pH > 4 and higher healing rates in erosive oesophagitis patients, are the proton pump inhibitors. The intragastric pH is often used to gauge the efficacy of acid suppressive therapies. There are several factors, however, that may affect the clinical relevance of such data, and these should be taken into account when comparing the effectiveness of different therapies. Firstly, because of inter‐individual variation, studies comparing therapies should be of a crossover design, so that responses to therapy are measured in the same individuals. Secondly, the Helicobacter pylori status of the individual should be known, as H. pylori infection has been shown to increase intragastric pH readings when examining the effect of acid suppressive therapy. Other factors, such as positioning of the pH electrode and the duration of previous therapy, also need to be standardized when using intragastric pH to assess the efficacy of different therapies. Crossover studies comparing standard doses of different proton pump inhibitors have shown that esomeprazole 40 mg produces a significantly greater amount of time at intragastric pH > 4 on day 5 of treatment than standard doses of other proton pump inhibitors. The correlation between greater efficacy in acid suppression and clinical benefit is supported by the findings that esomeprazole 40 mg is the only proton pump inhibitor to provide greater 8‐week healing rates in patients with erosive oesophagitis than both omeprazole and lansoprazole. These data all suggest strongly that intragastric pH monitoring is an effective surrogate marker and a relevant predictor of outcome in gastro‐oesophageal reflux disease.
Review article: towards the optimization of symptom evaluation in reflux disease
Authors: Dent J.
Published: September 2004

A recent workshop has taken stock of the processes used for the evaluation of reflux disease symptoms. Such evaluations are vital both for routine clinical practice and for the critical assessment and comparison of therapeutic options. The workshop endorsed the importance of the assessment of symptom patterns for the diagnosis of reflux disease. Patient self‐report symptom questionnaires were considered to be potentially valuable instruments, but have been researched relatively little in reflux disease. On the basis of a survey of the literature and data from generic methodological research, the workshop concluded that virtually all trials of the therapy of reflux disease have used too few response options for a sensitive definition of symptom status, and recommended that six to seven response options be used. Modified Likert scales with defined individual response options and structured patient self‐report, rather than physician assessment, were considered to be the best approaches. These views on symptom status assessment are not reflected fully in the current practice of reflux disease clinical trials. Furthermore, the terminology used to describe symptom status is frequently ambiguous or tautological. Quality of life measures were acknowledged as valid and useful secondary measures of therapeutic benefit. By contrast, evaluation of the state of the art of assessment of patient satisfaction with therapy led to the conclusion that the methodology for this particular assessment was still in its infancy. The outputs of the workshop revealed many aspects of the assessment of reflux disease that would benefit from further research and development. A report on the detailed outputs of the workshop has been published recently.
Positive supercoiling is generated in the presence of Escherichia coli SeqA protein
Authors: Klungsøyr Hege Kjellesvik , Skarstad Kirsten
Published: September 2004

In Escherichia coli, the SeqA protein is known as a negative regulator of chromosome replication. This protein is also suggested to have a role in chromosome organization. SeqA preferentially binds to hemi‐methylated DNA and is by immunofluorescence microscopy seen as foci situated at the replication factories. Loss of SeqA leads to increased negative supercoiling of the DNA. We show that purified SeqA protein bound to fully methylated, covalently closed or nicked circular DNA generates positive supercoils in vitro in the presence of topoisomerase I or ligase respectively. This means that binding of SeqA changes either the twist or the writhe of the DNA. The ability to affect the topology of DNA suggests that SeqA may take part in the organization of the chromosome in vivo. The topology change performed by SeqA occurred also on unmethylated plasmids. It is, however, reasonable to suppose that in vivo the major part of such activity is performed on hemi‐methylated DNA at the replication factories and presumably forms the basis for the characteristic SeqA foci observed by fluorescence microscopy.
Identification of ComW as a new component in the regulation of genetic transformation in Streptococcus pneumoniae
Authors: Luo Ping , Li Haiying , Morrison Donald A.
Published: September 2004

Regulation of competence for genetic transformation in Streptococcus pneumoniae depends on a quorum‐sensing system, genes involved in DNA uptake and recombination and a link between these two gene sets. The alternative sigma factor ComX provides this link. ComE, the response regulator of the quorum‐sensing system, is required for expression of ComX and other early genes. However, an unknown ComE‐dependent regulator is also required for competence when comX is expressed under control of the raffinose‐responsive promoter of the aga operon. The gene comW (SP0018) is required for a high level of competence and is regulated by the quorum‐sensing system, but its function is unknown. To explore its role further, comW was cloned into the multicopy plasmid pMSP3535, under the control of a nisin‐inducible promoter (PN), and transformed into pneumococcal strains containing a raffinose‐inducible comX gene (PR::comX). Further introduction of a comE deletion blocked the endogenous CSP signal transduction pathway. In the resulting strain, competence was independent of CSP but depended on treatment with both nisin and raffinose, showing that coexpression of comW and comX complemented the comE deficiency. ComX protein accumulation and expression of a late competence gene in the above strain support the conclusion that ComW is a new positive factor involved in competence regulation.
RNase HI overproduction is required for efficient full‐length RNA synthesis in the absence of topoisomerase I in Escherichia coli
Authors: Baaklini Imad , Hraiky Chadi , Rallu Fabien , Tse‐Dinh Yuk‐Ching , Drolet Marc
Published: September 2004

It has long been known that Escherichia coli cells deprived of topoisomerase I (topA null mutants) do not grow. Because mutations reducing DNA gyrase activity and, as a consequence, negative supercoiling, occur to compensate for the loss of topA function, it has been assumed that excessive negative supercoiling is somehow involved in the growth inhibition of topA null mutants. However, how excess negative supercoiling inhibits growth is still unknown. We have previously shown that the overproduction of RNase HI, an enzyme that degrades the RNA portion of an R‐loop, can partially compensate for the growth defects because of the absence of topoisomerase I. In this article, we have studied the effects of gyrase reactivation on the physiology of actively growing topA null cells. We found that growth immediately and almost completely ceases upon gyrase reactivation, unless RNase HI is overproduced. Northern blot analysis shows that the cells have a significantly reduced ability to accumulate full‐length mRNAs when RNase HI is not overproduced. Interestingly, similar phenotypes, although less severe, are also seen when bacterial cells lacking RNase HI activity are grown and treated in the same way. All together, our results suggest that excess negative supercoiling promotes the formation of R‐loops, which, in turn, inhibit RNA synthesis.
New enzymes involved in aerobic benzoate metabolism in Azoarcus evansii
Authors: Zaar Annette , Gescher Johannes , Eisenreich Wolfgang , Bacher Adelbert , Fuchs Georg
Published: September 2004

A new principle of aerobic aromatic metabolism has been postulated, which is in contrast to the known pathways. In various bacteria the aromatic substrate benzoate is first converted to its coenzyme A (CoA) thioester, benzoyl‐CoA, which is subsequently attacked by an oxygenase, followed by a non‐oxygenolytic fission of the ring. We provide evidence for this hypothesis and show that benzoyl‐CoA conversion in the bacterium Azoarcus evansii requires NADPH, O2 and two protein components, BoxA and BoxB. BoxA is a homodimeric 46 kDa iron‐sulphur‐flavoprotein, which acts as reductase. In the absence of BoxB, BoxA catalyses the benzoyl‐CoA stimulated artificial transfer of electrons from NADPH to O2 via free FADH2 to produce H2O2. Physiologically, BoxA uses NADPH to reduce BoxB, a monomeric 55 kDa iron‐protein that acts as benzoyl‐CoA oxygenase. The product of benzoyl‐CoA oxidation was identified by NMR spectroscopy as its dihydrodiol derivative, 2,3‐dihydro‐2,3‐dihydroxybenzoyl‐CoA. This suggests that BoxBA act as a benzoyl‐CoA dioxygenase/reductase. Unexpectedly, benzoyl‐CoA transformation by BoxBA was greatly stimulated when another enoyl‐CoA hydratase/isomerase‐like protein, BoxC, was added that catalysed the further transformation of the dihydrodiol product formed from benzoyl‐CoA. The benzoyl‐CoA oxygenase system has very low similarity to known (di)oxygenase systems and is the first member of a new enzyme family.
Positioning of the MinE binding site on the MinD surface suggests a plausible mechanism for activation of the Escherichia coli MinD ATPase during division site selection
Authors: Ma Luyan , King Glenn F. , Rothfield Lawrence
Published: September 2004

Division site selection in Escherichia coli requires that the MinD protein interact with itself and with MinC and MinE. MinD is a member of the NifH‐ArsA‐Par‐MinD subgroup of ATPases. The MinE–MinD interaction results in activation of MinD ATPase activity in the presence of membrane vesicles. The sites within MinD responsible for its interaction with MinC and MinE were studied by site‐directed mutagenesis and yeast two‐hybrid analysis, guided by the known three‐dimensional structure of MinD proteins. This provided evidence that MinC and MinE bind to overlapping sites on the MinD surface. The results also suggested that MinE and the invariant Lys11 residue in the ATPase P‐loop of MinD compete for binding to a common site within the MinD structure, thereby providing a plausible structural basis for the ability of MinE to activate the ATPase activity of MinD.
Molecular pathogenesis of neonatal group B streptococcal infection: no longer in its infancy
Authors: Doran Kelly S. , Nizet Victor
Published: September 2004

The process of human infection by group B Streptococcus (GBS) is complex and multifactorial. While this bacterium has adapted well to asymptomatic colonization of adult humans, it remains a potentially devastating pathogen to susceptible infants. Advances in molecular techniques and refinement of in vitro and in vivo model systems have elucidated key elements of the pathogenic process, from initial attachment to the maternal vaginal epithelium to penetration of the newborn blood–brain barrier. Sequencing of two complete GBS genomes has provided additional context for interpretation of experimental data and comparison to other well‐studied pathogens. Here we review recent discoveries regarding GBS virulence mechanisms, many of which are revealed or magnified by the unique circumstances of the birthing process and the deficiencies of neonatal immune defence. Appreciation of the formidable array of GBS virulence factors underscores why this bacterium remains at the forefront of neonatal pathogens.
Role of the GGDEF protein family in Salmonella cellulose biosynthesis and biofilm formation
Authors: García Begoña , Latasa Cristina , Solano Cristina , Portillo Francisco García‐del , Gamazo Carlos , Lasa Iñigo
Published: September 2004

Salmonella enterica serovar Typhimurium is capable of producing cellulose as the main exopolysaccharide compound of the biofilm matrix. It has been shown for Gluconacetobacter xylinum that cellulose biosynthesis is allosterically regulated by bis‐(3′,5′) cyclic diguanylic acid, whose synthesis/degradation depends on diguanylate cyclase/phosphodiesterase enzymatic activities. A protein domain, named GGDEF, is present in all diguanylate cyclase/phosphodiesterase enzymes that have been studied to date. In this study, we analysed the molecular mechanisms responsible for the failure of Salmonella typhimurium strain SL1344 to form biofilms under different environmental conditions. Using a complementation assay, we were able to identify two genes, which can restore the biofilm defect of SL1344 when expressed from the plasmid pBR328. Based on the observation that one of the genes, STM1987, contains a GGDEF domain, and the other, mlrA, indirectly controls the expression of another GGDEF protein, AdrA, we proceeded on a mutational analysis of the additional GG[DE]EF motif containing proteins of S. typhimurium. Our results demonstrated that MlrA, and thus AdrA, is required for cellulose production and biofilm formation in LB complex medium whereas STM1987 (GGDEF domain containing protein A, gcpA) is critical for biofilm formation in the nutrient‐deficient medium, ATM. Insertional inactivation of the other six members of the GGDEF family (gcpB‐G) showed that only deletion of yciR (gcpE) affected cellulose production and biofilm formation. However, when provided on plasmid pBR328, most of the members of the GGDEF family showed a strong dominant phenotype able to bypass the need for AdrA and GcpA respectively. Altogether, these results indicate that most GGDEF proteins of S. typhimurium are functionally related, probably by controlling the levels of the same final product (cyclic di‐GMP), which include among its regulatory targets the cellulose production and biofilm formation of S. typhimurium.
Food vacuole‐associated lipid bodies and heterogeneous lipid environments in the malaria parasite, Plasmodium falciparum
Authors: Jackson Katherine E. , Klonis Nectarios , Ferguson David J. P. , Adisa Akinola , Dogovski Con , Tilley Leann
Published: September 2004

The malaria parasite Plasmodium falciparum induces a sixfold increase in the phospholipid content of infected erythrocytes during its intraerythrocytic growth. We have characterized the lipid environments in parasitized erythrocyte using the hydrophobic probe, Nile Red. Spectral imaging with a confocal microscope revealed heterogeneous lipid environments in parasite‐infected erythrocytes. An insight into the nature of these environments was gained by comparing these spectra with those of triacylglycerol/phospholipid emulsions and phospholipid membranes. Using this approach, we identified a population of intensely stained particles of a few hundred nanometers in size that are closely associated with the digestive vacuole of the parasite and appear to be composed of neutral lipids. Electron microscopy and isolation of food vacuoles confirmed the size of these particles and their intimate association respectively. Lipid analysis suggests that these neutral lipid bodies are composed of di‐ and triacylgycerols and may represent storage organelles for lipid intermediates that are generated during digestion of phospholipids in the food vacuole. Mono‐, di‐ and triacylglycerol suspensions promote β‐haematin formation, suggesting that these neutral lipid bodies, or their precursors, may also be involved in haem detoxification. We also characterized other compartments of the infected erythrocyte that were stained less intensely with the Nile Red probe. Both the erythrocyte membrane and the parasite membrane network exhibit red shifts compared with the neutral lipid bodies that are consistent with cholesterol‐rich and cholesterol‐poor membranes respectively. Ratiometric imaging revealed more subtle variations in the lipid environments within the parasite membrane network.
Human Cryptosporidiosis: An Update With Special Emphasis on the Situation in Europe
Authors: Joachim A.
Published: September 2004

The genus Cryptosporidium consists of different species and genotypes which infect a wide range of hosts, including humans. The parasite is ubiquitous and lack of differentiation between the species and strains has made it difficult to track down sources of human and animal infections. Genetic analysis of strains and isolates has led to the redescription of Cryptosporidium with special consideration of the host specificity and possible ways of transmission to humans. Infection with the small oocysts usually occurs directly by faecal–oral transmission, water‐ or food–borne. In Europe water from different sources is frequently contaminated with oocysts. Generally, humans are most frequently infected with C. hominis in an anthroponotic cycle (especially in cases of infections imported from highly endemic (sub‐) tropical regions) and the animal genotype (type II) of C. parvum in a zoonotic cycle which seems to play a major role in autochthonous infections in Switzerland, the UK and probably other European countries. Other species (such as C. felis or the avian species C. meleagridis and C. baileyi) and genotypes are rare in humans and mostly restricted to immunocompromised individuals who are highly susceptible to serious opportunistic cryptosporidial infections.
Classical Swine Fever Virus Strain ‘C’. How Long is it Detectable After Oral Vaccination?
Authors: Kaden V. , Lange E. , Riebe R. , Lange B.
Published: September 2004

To determine the persistence period of C‐strain vaccine virus in immunized animals, domestic pigs and wild boars were vaccinated orally and killed on different days post vaccinationem (dpv). Tissue samples were taken at necropsy from both species for detection of C‐strain virus. From domestic pigs nasal swabs and faeces were also collected. During the investigation period (2–12 dpv) vaccine virus could never be detected in nasal secretions and in faeces of vaccinated domestic pigs. In contrast, C‐strain virus was found in organs until day 8 pv in domestic pigs and until day 9 pv in wild boars. Whereas in domestic pigs virus was detected in tonsils, Ln. mandibularis or in spleen, in wild boar it only was found in tonsils. We conclude that C‐strain vaccine virus is not detectable in wild boars longer than 10–12 days after intake of the vaccine baits.
Effects of Subinhibitory Concentrations of Florfenicol on Morphology, Growth, and Viability of Staphylococcus aureus
Authors: Blickwede M. , Valentin‐Weigand P. , Rohde M. , Schwarz S.
Published: September 2004

Staphylococcus aureus strain Newman was investigated for changes in its growth pattern, its morphology and its viability when grown in the presence of 3 μg/ml florfenicol (Ff). This concentration corresponds to the 0.75‐fold strain‐specific minimum inhibitory concentration (MIC). Under these conditions, S. aureus Newman showed a distinct retardation in its growth pattern and 20% dead cells were detected in a fluorescence microscopic viability assay. However, bactericidal activity – defined as a 3‐log drop in the staphylococcal population – was not recorded at this Ff concentration. Further analysis of the cell wall revealed a significant increase in cell wall thickness of S. aureus Newman when grown in the presence of 3 μg/ml Ff. This might result in a compression of the protoplast with subsequent disruption of single staphylococcal cells. Accordingly, 20% of the staphylococcal cells analysed by electron microscopy proved to be disrupted. These observations suggest that Ff can cause a thickening of the cell wall accompanied by impaired viability of the staphylococcal cells.
Virulence Genes of Escherichia coli Strains Isolated from Mastitic Milk
Authors: Bean A. , Williamson J. , Cursons R. T.
Published: September 2004

Escherichia coli, a Gram‐negative environmental pathogen associated with bovine mastitis was isolated from the milk of 34 symptomatic cows that had been diagnosed with clinical mastitis. Eighty isolates were obtained over a 17‐month period and these isolates were screened by DNA amplification for the following E. coli virulence genes: cnf1, cnf2, eaeA, eagg, einv, ltx1, stx1, stx2 and vt2e. Thirty of the bacterial isolates, obtained from 23 different cows, had toxin genes identified in their DNA. The most common virulence gene detected was stx1, with a prevalence of 31%, followed by cnf2 (7.5%), vt2e (6.25%) and eaeA (4%). The possession of different virulence genes by the bacterial isolates had no discernable impact on the health status of the cows as there was no correlation between the potential for toxin production by the E. coli isolates and the systemic clinical condition of the respective infected cows.
Characterization of Pathogenic Escherichia coli Isolated from Humans in Austria: Phenotypes, Toxin Gene Types and Epidemiology
Authors: Wagner M. , Allerberger F. , Manafi M. , Lindner G. , Friedrich A. W. , Sonntag A.‐K. , Foissy H.
Published: September 2004

One hundred and ten clinical Escherichia coli isolates of serovar O157 (n = 102) and O26 (n = 8) were characterized for the presence of putative virulence genes by PCR. All but one of these isolates contained the eae gene. The EHEC‐hly gene could be detected in all E. coli O157 and in 50% of E. coli O26 isolates. Forty‐five (40.9%) of the 110 E. coli were positive for both stx1 and stx2 genes, 2 (1.8%) isolates were positive for stx1 and 57 isolates (51.8%) were positive for stx2 only. Among the 102 stx2 positive isolates, 14 (13.7%) E. coli O157 contained also the stx2c variant gene. No other stx2 variant was identified. Six clinical isolates (five E. coli O157:H7 and one E. coli O26) did not contain stx genes. Ten non‐pathogenic E. coli isolates which were amplified as controls didn't contain any stx and eae gene but two of the ten strains contained the EHEC‐hly gene. By their growth on chromogenic media, all but two of 50 E. coli O157 could be differentiated from eight E. coli O26 and 10 non‐pathogenic E. coli. Sixty‐one of the O157:H7 isolates were further subjected to pulsed‐field gel electrophoresis (PFGE) which identified 49 distinguishable patterns. In five cases where contact infection among family members was suspected, indistinguishable PFGE patterns confirmed the epidemiological relatedness of the isolates. Moreover, two PFGE clusters were identified which comprised five and three strains, respectively. These findings indicate the occurrence of both family and diffuse outbreaks of E. coli O157 infections in Austria during recent years and demonstrate the need for molecular subtyping of these pathogens.
Lameness in Piglets. Abrasions in Nursing Piglets and Transfer of Protection towards Infections withStreptococcifrom Sow to Offspring
Authors: Zoric M. , Sjölund M. , Persson M. , Nilsson E. , Lundeheim N. , Wallgren P.
Published: September 2004

A group of 175 newborn piglets were monitored with respect to development of abrasions and lameness. Lameness was diagnosed in 10.9% of the piglets. About every second litter was affected and around 75% of these diagnoses took place during the first 3 weeks of life. Skin lesions were present already on day 3. They increased in magnitude until day 10 and thereafter declined. They were generally bilateral and most commonly observed as abrasions over the carpal joints. Hocks, face and tails were affected in a similar way, but at lower magnitudes. Sole bruising was observed in 87% of the piglets on the third day of life, and moderate to severe lesions dominated until day 10. Thereafter the incidence decreased, indicating healing with time. Still 39% of the piglets were affected at day 17. There was a significant positive correlation between skin lesions of carpus and hock within all examination days in selected piglets with known identity (n = 48). Between day 10 and 17 significant positive correlations were found within all examination sites with exception of abdomen and teats. The offspring of sows treated against mastitis expressed more abrasions then piglets delivered by healthy sows and the mortality during the first 17 days postpartum was significantly higher among piglets delivered by sows treated for mastitis. The level of serum antibodies toStreptococcus equisimilisin eight dams decreased during the last month of gestation and a declining maternal immunity toS. equisimiliswas demonstrated in all piglets (n = 47) during the first 5 weeks of life. During the first 2 weeks of life somewhat lower median levels of serum antibodies were recorded among the piglets that were treated against arthritis (n = 8).
Bottom‐current deposits in the Miocene–Pliocene Misaki Formation, Izu forearc area, Japan
Authors: LEE INTAE , OGAWA YUJIRO
Published: September 2004

Sedimentary structures in the middle–late Miocene to early Pliocene Misaki Formation, Miura Group, Miura Peninsula, Central Japan, were studied, and paleocurrent data were interpreted as the result of deep‐sea bottom‐current flow. These current data were further compared with present‐day bottom currents in the northwestern Pacific region. The Misaki Formation is thought to be a forearc deposit within the Izu oceanic arc, and is composed of thick volcaniclastic beds interbedded with siliceous biogenic clayey sediments. Sedimentary structures showing paleocurrent directions are involved in the upper part of the volcaniclastic beds, in the pumiceous beds just above the volcaniclastic beds, and in the pelagic sediments. Based on paleomagnetic data suggesting considerable rotation of the beds, all the current directions were reconstructed to their original orientation. The paleocurrents are summarized into the following three groups. The first group in the volcaniclastic beds indicates southeast‐directed paleocurrent directions. The second group in the upper parts of volcaniclastic beds and in some pumiceous beds exhibits a southwest‐ and northeast‐directed paleoflow. The third group usually observed in the pumiceous beds with parallel lamination displays a northwest‐ or southeast‐directed paleocurrent. The origin of each group's paleoflow direction is attributed to turbidity current, internal tidal current, and contour current influences, respectively. Present‐day observations of the deep‐sea northwest Pacific suggest that most of the bottom‐current indicators in the Misaki Formation are related to North Pacific Deep Water, possibly Antarctic Bottom Water as well as a combination of tidal and local effects. It is concluded that the beds of the Misaki Formation were deposited in the proto‐Sagami basin ca 9 Ma and were formed under weak bottom currents in a wide and flat basin during colder climatic conditions, whereas the beds dated at ca 6 Ma were deposited under strong bottom‐current flow, and were then accreted to the Honshu arc.
Arc–arc collision in the Izu collision zone, central Japan, deduced from the Ashigara Basin and adjacent Tanzawa Mountains
Authors: SOH WONN , NAKAYAMA KAZUO , KIMURA TAKU
Published: September 2004

The Pleistocene Ashigara Basin and adjacent Tanzawa Mountains, Izu collision zone, central Japan, are examined to better understand the development of an arc–arc orogeny, where the Izu–Bonin – Mariana (IBM) arc collides with the Honshu Arc. Three tectonic phases were identified based on the geohistory of the Ashigara Basin and the denudation history of the Tanzawa Mountains. In phase I, the IBM arc collided with the Honshu Arc along the Kannawa Fault. The Ashigara Basin formed as a trench basin, filled mainly by thin‐bedded turbidites derived from the Tanzawa Mountains together with pyroclastics. The Ashigara Basin subsided at a rate of 1.7 mm/year, and the denudation rate of the Tanzawa Mountains was 1.1 mm/year. The onset of Ashigara Basin Formation is likely to be older than 2.2 Ma, interpreted as the onset of collision along the Kannawa Fault. Significant tectonic disruption due to the arc–arc collision took place in phase II, ranging from 1.1 to 0.7 Ma in age. The Ashigara Basin subsided abruptly (4.6 mm/year) and the accumulation rate increased to approximately 10 times that of phase I. Simultaneously, the Tanzawa Mountains were abruptly uplifted. A tremendous volume of coarse‐grained detritus was provided from the Tanzawa Mountains and deposited in the Ashigara Basin as a slope‐type fan delta. In phase III, 0.7–0.5 Ma, the entire Ashigara Basin was uplifted at a rate of 3.6 mm/year. This uplift was most likely caused by isostatic rebound resulting from stacking of IBM arc crust along the Kannawa Fault which is not active as the decollement fault by this time. The evolution of the Ashigara Basin and adjacent Tanzawa Mountains shows a series of the development of the arc–arc collision; from the subduction of the IBM arc beneath the Honshu Arc to the accretion of IBM arc crust onto Honshu. Arc–arc collision is not the collision between the hard crusts (massif) like a continent–continent collision, but crustal stacking of the subducting IBM arc beneath the Honshu Arc intercalated with very thick trench fill deposits.
Possible Miocene rifting of the Izu–Ogasawara (Bonin) arc deduced from magnetic anomalies
Authors: YAMAZAKI TOSHITSUGU , YUASA MAKOTO
Published: September 2004

A magnetic anomaly map of the northern part of the Philippine Sea plate shows two conspicuous north–south rows of long‐wavelength anomalies over the Izu–Ogasawara (Bonin) arc, which are slightly oblique to the present volcanic front. These anomalies are enhanced on reduced‐to‐pole and upward‐continued anomaly maps. The east row is associated with frontal arc highs (the Shinkurose Ridge), and the west row is accompanied by the Nishi‐Shichito Ridge. Another belt of long‐wavelength anomalies very similar to the former two occurs over the Kyushu–Palau Ridge. To explain the similarity of the magnetic anomalies, it is proposed that after the spreading of the Shikoku Basin separated the Izu–Ogasawara arc from the Kyushu–Palau Ridge, another rifting event occurred in the Miocene, which divided the Izu–Ogasawara arc into the Nishi‐Shichito and Shinkurose ridges. The occurrence of Miocene rifting has also been suggested from the geology of the collision zone of the Izu–Ogasawara arc against the Southwest Japan arc: the Misaka terrain yields peculiar volcanic rocks suggesting back‐arc rifting at ∼ 15 Ma. The magnetic anomaly belts over the Izu–Ogasawara arc do not extend south beyond the Sofugan Tectonic Line, suggesting a difference in tectonic history between the northern and southern parts of the Izu–Ogasawara arc. It is estimated that the Miocene extension was directed northeast–southwest, utilizing normal faults originally formed during Oligocene rifting. The direction is close to the final stage of the Shikoku Basin spreading. On a gravity anomaly relief map, northeast–southwest lineaments can be recognized in the Shikoku Basin as well as over the Nishi‐Shichito Ridge. We thus consider that lines of structural weakness connected transform faults of the Shikoku Basin spreading system and the transfer faults of the Miocene Izu–Ogasawara arc rifting. Volcanism on the Nishi‐Shichito Ridge has continued along the lines of weakness, which could have caused the en echelon arrangement of the volcanoes.
K–Ar ages from seamount chains in the back‐arc region of the Izu–Ogasawara arc
Authors: ISHIZUKA OSAMU , UTO KOZO , YUASA MAKOTO , HOCHSTAEDTER ALFREDG.
Published: September 2004

The Izu–Ogasawara arc contains, from east to west, a volcanic front, a back‐arc extensional zone (back‐arc knolls zone), and a series of across‐arc seamount chains that cross the extensional zone in an east‐northeast and west‐southwest direction and extend into the Shikoku Basin. K–Ar ages of dredged volcanic rocks from these across‐arc seamount chains and extension‐related edifices in the back‐arc region of the Izu–Ogasawara arc were measured to constrain the volcanic and tectonic history of the arc since the termination of spreading in the Shikoku Basin. K–Ar ages range between 12.5 and 1 Ma. Andesitic to dacitic rocks of 12.5–2.9 Ma occur mainly on the western part of the chains. The western part of the chains are the locus of volcanism behind the front which erupted mainly calc‐alkaline andesitic lavas. The youngest rocks (< 2.8 Ma), characterized by cpx‐ol basalt, occur along the western margin of the back‐arc knolls zone. Basaltic rocks of 12.5–2.9 Ma have relatively high concentrations of Na2O (> 2.0 wt%), Zr (> 50 p.p.m.) and Y (> 20 p.p.m.) and low CaO (< 12 wt%). On the other hand, basalts of 2.8–1 Ma have lower Na2O (< 1.8 wt%), Zr (< 50 p.p.m.) and Y (< 20 p.p.m.), but significantly higher CaO (> 12 wt%). The age inferred for the initiation of back‐arc rifting (∼ 2.35–2.9 Ma: Taylor 1992) behind the current volcanic arc coincides with the time that basalt chemistry changed drastically (eruption of the low‐Na2O and high‐CaO basalt). This implies that post‐2.8 Ma volcanism in the back‐arc knolls zone is associated with rifting. Similarly, the change in chemical composition might be explained by a different type of source mantle following rift initiation. Volcanism in the western seamounts ceased after the onset of rifting at ∼ 2.8 Ma.
Noble gases in pillow basalt glasses from the northern Mariana Trough back‐arc basin
Authors: IKEDA YASUO , NAGAO KEISUKE , STERN ROBERT J. , YUASA MAKOTO , NEWMAN SALLY
Published: September 2004

Noble gas concentrations and isotopic compositions have been measured in eight samples of pillow basalt glasses collected from seven different localities along 250 km of the Mariana Trough spreading and rifting axis. The samples have uniform and mid‐ocean ridge basalt (MORB)‐like 3He/4He values of 9–12 × 10–6 (6.4–8.6 times atmospheric) despite large variations in 4He. Concentrations of the noble gases Ne, Ar, Kr, and Xe show much smaller variations between samples, but larger variations in isotopic compositions of Ne, Ar, and Xe. Excess radiogenic 21Ne is observed in some samples. 40Ar/36Ar varies widely (atmospheric to 1880). Kr is atmospheric in composition for all samples. Some samples show a clear excess 129Xe, which is a well‐known MORB signature. Isotopic compositions of the heavier noble gases (Ar, Kr, and Xe) in some samples, however, show more atmospheric components. These data reflect the interaction of a MORB‐like magma with an atmospheric component such as seawater or of a depleted mantle source with a water‐rich component that was probably derived from the subducting slab.
Segmentation of the southern Mariana back‐arc spreading center
Authors: StÜben Doris , Neumann Thomas , Taibi Nasr‐Eddine , Glasby GeoffreyP.
Published: September 2004

SeaBeam multibeam bathymetry obtained during cruise SO‐69 of research vessel (R/V) Sonne defines the segmentation and structure of ∼ 300 km of the Mariana back‐arc spreading center south of the Pagan fracture zone at 17°33′N. Eight ridge segments, ranging from 14 to 64 km in length, are displaced as much as 2.7–14.5 km by both right‐ (predominantly) and left‐lateral offsets and transform faults. An axial ridge commonly occupies the middle portion of the rift valley and rises from 200 to 700 m above the adjacent sea floor, in places shoaling to a water depth of 3200 m. An exception is the 60‐km‐long segment between 16°58′ and 17°33′N where single peaks only a few tens of meters high punctuate the rift axis. Photographic evidence and rock samples reveal the presence of mostly pillow lavas outcropping on the axial ridges or peaks whereas the deeper parts of the rift valley floor (max. depth 4900 m) are heavily to totally sedimented. Abundant talus ramps along fault scarps testify to ongoing disruption of the crust. Lozenge‐shaped collapse structures are covered by layers of sediment up to tens of centimeters thick on the rift valley floor. The presence of discrete volcanic ridges in the southern Mariana back‐arc spreading region suggests that emplacement of oceanic crust at this slow spreading center occurs by `multi‐site' injection of magma. Along‐axis variations in length, crestal depth, and size of the axial ridges can be best explained by different stages in the cyclicity of magma supply along‐axis.