bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distribution and microhabitats of native and non‐native gammarids (Amphipoda, Crustacea) in Brittany, with particular reference to the endangered endemic sub‐species Gammarus duebeni celticus
Authors: Piscart Christophe , Manach Alain , Copp Gordon H. , Marmonier Pierre 
Published: October 2006

AbstractAim  To assess temporal changes in gammarid distribution in Brittany and microhabitat‐use overlap between the endangered endemic Gammarus duebeni celticusStock & Pinkster, 1970, the expanding natives G. pulex (Linnaeus, 1758) and Echinogammarus berilloni (Catta, 1878), and the introduced G. tigrinus Sexton, 1939.Location  Brittany and adjacent regions in western France.Methods  The spatial and temporal patterns in distribution of gammarids at the scale of Brittany were studied using 351 sites. Longitudinal distributions (from the source to the estuary of the river) and microhabitat‐use (substratum type and water velocity) were also considered in selected rivers.Results  At the regional scale, all species occurred together less often than expected statistically, with significant deviations from expected for G. pulex vs. both G. duebeni celticus and G. tigrinus, and for E. berilloni vs. both G. duebeni celticus and G. tigrinus. However, at the microhabitat scale, E. berilloni occurred significantly more often than expected with the endemic G. duebeni celticus, and this appears to be due to similar substratum and water velocity preferences, although at both the regional and microhabitat scales E. berilloni prefers wider streams than G. duebeni celticus. This study reveals a decline in the endangered G. duebeni celticus since 1970.Main conclusions  The longitudinal and local distributions of G. duebeni celticus, and the higher‐than‐expected co‐occurrence of the species with G. pulex, suggest that the decline of the endemic species may be due to changes in the environment and/or interference from native G. pulex, which is expanding its range in Brittany. The results are discussed as regards to the consequences for regional biodiversity.
Clinical nurse specialists as entrepreneurs: constrained or liberated
Authors: Austin Lynn , Luker Karen , Ronald Martin 
Published: October 2006

Aims.  This qualitative study explored the experiences of two groups of clinical nurse specialists – continence advisors and tissue viability nurses – working in primary care in the UK. In particular, the study focused on how clinical nurse specialists’ relationships with other health‐care professionals had an impact on their role.Background.  Clinical nurse specialists are recognized worldwide as having expertise in a given field, which they use to develop the practice of others. Additionally, clinical nurse specialists share many of the characteristics of entrepreneurs, which they use to develop services related to their speciality. However, little research has been conducted in relation to clinical nurse specialists’ experiences as they attempt to diversify nursing practice.Design/methods.  An ethnographic approach was adopted comprising many elements of Glaserian grounded theory. Data were collected via participant observation and face‐to‐face interviews with 22 clinical nurse specialists.Findings.  Services provided by clinical nurse specialists were not static, clinical nurse specialists being the main drivers for service developments. However, clinical nurse specialists encountered difficulties when introducing new ideas. Given their role as advisors, clinical nurse specialists lacked authority to bring about change and were dependent on a number of mechanisms to bring about change, including ‘cultivating relationships’ with more powerful others, most notably the speciality consultant.Conclusions.  The UK government has pledged to ‘liberate the talents of nurses’ so that their skills can be used to progress patient services. This study highlights the fact that a lack of collaborative working practices between health‐care professionals led to clinical nurse specialists being constrained.Relevance to clinical practice.  Health‐care organizations need to provide an environment in which the entrepreneurial skills of clinical nurse specialists may be capitalized on. In the absence of an outlet for their ideas regarding service developments, clinical nurse specialists may remain dependent on the mechanisms witnessed in this study for some time.
Carer reports of health status among adults with intellectual/developmental disabilities in Taiwan living at home and in institutions
Authors: Wang K.‐Y. , Hsieh K. , Heller T. , Davidson P. W. , Janicki M. P. 
Published: October 2006

AbstractBackground  The aim of the present study was to assess the health status of a cohort of adults with intellectual/developmental disabilities (I/DD) residing in family homes or institutions in Taiwan and to examine whether morbidity varied with age, sex, existing diagnosis [Down syndrome (DS), seizures, cerebral palsy (CP), intellectual disability (ID) level] and residential status.Methods  Systematic randomization based on geographic areas was employed for sampling selection. Primary carers were interviewed to provide health‐related information on individuals with I/DD aged 33 years or older living in institutions (n = 614) or living with their family (n = 514) in Taiwan.Results  Cardiovascular, neurological, visual and hearing impairments increased with age; while gastrointestinal, endocrine, infectious and dermatological diseases did not, after adjusting for sex, level of ID, presence of DS, seizures or CP, across settings. Institution cohorts were more likely to have infectious diseases, skin diseases, hepatitis or to be hepatitis carriers, and to have psychiatric disorders.Conclusions  Organ system morbidity increased with age and generally was influenced by the same factors as have been reported for cohorts in western countries. The results also suggest that disease/condition outcomes may vary or be influenced differentially by residential setting.
Dispersal ecology versus host specialization as determinants of ectoparasite distribution in brood parasitic indigobirds and their estrildid finch hosts
Authors: BALAKRISHNAN CHRISTOPHER N. , SORENSON MICHAEL D. 
Published: October 2006

AbstractBrood parasitic birds offer a unique opportunity to examine the ecological and evolutionary determinants of host associations in avian feather lice (Phthiraptera). Brood parasitic behaviour effectively eliminates vertical transfer of lice between parasitic parents and offspring at the nest, while at the same time providing an opportunity for lice associated with the hosts of brood parasites to colonize the brood parasites as well. Thus, the biology of brood parasitism allows a test of the relative roles of host specialization and dispersal ecology in determining the host–parasite associations of birds and lice. If the opportunity for dispersal is the primary determinant of louse distributions, then brood parasites and their hosts should have similar louse faunas. In contrast, if host‐specific adaptations limit colonization ability, lice associated with the hosts of brood parasites may be unable to persist on the brood parasites despite having an opportunity for colonization. We surveyed lice on four brood parasitic finch species (genus Vidua), their estrildid finch host species, and a few ploceid finches. While Brueelia lice were found on both parasitic and estrildid finches, a molecular phylogeny showed that lice infesting the two avian groups belong to two distinct clades within Brueelia. Likewise, distinct louse lineages within the amblyceran genus Myrsidea were found on estrildid finches and the parasitic pin‐tailed whydah (Vidua macroura), respectively. Although common on estrildid finches, Myrsidea lice were entirely absent from the brood parasitic indigobirds. The distribution and relationships of louse species on brood parasitic finches and their hosts suggest that host‐specific adaptations constrain the ability of lice to colonize new hosts, at least those that are distantly related.
Topoisomerases of kinetoplastid parasites: why so fascinating?
Authors: Das Benu Brata , Sengupta Tanushri , Ganguly Agneyo , Majumder Hemanta K. 
Published: October 2006

SummaryDNA topoisomerases are the key enzymes involved in carrying out high precision DNA transactions inside the cells. However, they are detrimental to the cell when a wide variety of topoisomerase‐targeted drugs generate cytotoxic lesions by trapping the enzymes in covalent complexes on the DNA. The discovery of unusual heterodimeric topoisomerase I in kinetoplastid family added a new twist in topoisomerase research related to evolution, functional conservation and their preferential sensitivity to Camptothecin. On the other hand, structural and mechanistic studies on kinetoplastid topoisomerase II delineate some distinguishing features that differentiate the parasitic enzyme from its prokaryotic and eukaryotic counterparts. This review summarizes the recent advances in research in kinetoplastid topoisomerases, their evolutionary significance and the death of the unicellular parasite Leishmania donovani induced by topoisomerase I inhibitor camptothecin.
Specificity of Streptococcus pyogenes NAD+ glycohydrolase in cytolysin‐mediated translocation
Authors: Ghosh Joydeep , Caparon Michael G. 
Published: October 2006

SummaryThe mechanism by which the cytolysin‐mediated translocation (CMT) pathway of the Gram‐positive pathogen Streptococcus pyogenes injects effector proteins into the cytosol of an infected host cell via the pore‐forming protein streptolysin O is unknown. Key questions include whether the pathway can discriminate between different substrates for translocation, and whether the effector protein plays an active or passive role in the translocation process. Here we show that CMT can discriminate between a known effector of the pathway, the S. pyogenes NAD+ glycohydrolase (SPN), and a second secreted protein, the mitogenic factor (MF), routing the former into the host cell cytosol and the latter into the extracellular milieu. Residues within the amino‐terminal 190 residues of SPN were essential for discrimination, as deletions within this domain produced proteins that retained full enzymatic activity, but were completely uncoupled from the translocation pathway. The enzymatic domain itself played a pivotal role in the discrimination as deletions within this domain also produced translocation incompetent proteins and the conversion of MF to a translocation‐competent form required fusion with both SPN domains in a contiguous orientation. These data establish that CMT is discriminatory, and that SPN is a multidomain protein that plays an active role in its translocation.
Lex marks the spot: the virulent side of SOS and a closer look at the LexA regulon
Authors: Kelley William L. 
Published: October 2006

SummaryThe SOS response that responds to DNA damage induces many genes that are under LexA repression. A detailed examination of LexA regulons using genome‐wide techniques has recently been undertaken in both Escherichia coli and Bacillus subtilis. These extensive and elegant studies have now charted the extent of the LexA regulons, uncovered many new genes, and exposed a limited overlap in the LexA regulon between the two bacteria. As more bacterial genomes are analysed, more curiosities in LexA regulons arise. Several notable examples include the discovery of a LexA‐like protein, HdiR, in Lactococcus lactis, organisms with two lexA genes, and small DNA damage‐inducible cassettes under LexA control. In the cyanobacterium Synechocystis, genetic and microarray studies demonstrated that a LexA paralogue exerts control over an entirely different set of carbon‐controlled genes and is crucial to cells facing carbon starvation. An examination of SOS induction evoked by common therapeutic drugs has shed new light on unsuspected consequences of drug exposure. Certain antibiotics, most notably fluoroquinolones such as ciprofloxacin, can induce an SOS response and can modulate the spread of virulence factors and drug resistance. SOS induction by β‐lactams in E. coli triggers a novel form of antibiotic defence that involves cell wall stress and signal transduction by the DpiAB two‐component system. In this review, we provide an overview of these new directions in SOS and LexA research with emphasis on a few themes: identification of genes under LexA control, the identification of new endogenous triggers, and antibiotic‐induced SOS response and its consequences.
FvVE1 regulates filamentous growth, the ratio of microconidia to macroconidia and cell wall formation in Fusarium verticillioides
Authors: Li Shaojie , Myung Kyung , Guse Diana , Donkin Brett , Proctor Robert H. , Grayburn W. Scott , Calvo Ana M. 
Published: October 2006

SummaryThe velvet gene, veA, co‐ordinates asexual and sexual development in the homothallic fungal species Aspergillus nidulans. Studies in Aspergillus parasiticus and Aspergillus fumigatus demonstrated that veA also regulates morphological differentiation in these species. Whether veA has the same role in morphogenesis in other fungal genera has not been investigated. In this work, we studied the role of the veA homologue, FvVE1, in the heterothallic fungus Fusarium verticillioides. Deletion of FvVE1 suppressed aerial hyphal growth and reduced colony surface hydrophobicity on solid media. In submerged cultures, FvVE1 deletion caused alterations in hyphal polarity, marked activation of conidiation and yeast‐like growth. The latter was promoted by shaking to increase aeration of cultures. In addition, FvVE1 deletion markedly increased the ratio of macroconidia to microconidia. Supplementation of osmotic stabilizers restored the wild‐type phenotype to deletion mutants, suggesting phenotypic alterations caused by FvVE1 deletion are related to cell wall defects. This is consistent with the hypersensitivity of FvVE1 deletion mutants to SDS and with the significant reduction in the mannoprotein content of mutants compared with the wild‐type strain. However, no dramatic cell wall alterations were observed when mutants were examined by transmission electron microscopy. Our data strongly suggest that FvVE1 is important for cell wall integrity, cell surface hydrophobicity, hyphal polarity and conidiation pattern.
Descriptive epidemiology of Down’s syndrome in Estonia
Authors: Reimand Tiia , Õunap Katrin , Zordania Riina , Ilus Tiiu , Uibo Oivi , Sitska Mari , Talvik Tiina 
Published: October 2006

SummaryThe aim of the study was to investigate the livebirth prevalence of Down’s syndrome (DS) in Estonia during the past 14 years, create a DS database and observe the effectiveness of prenatal screening. This is a population‐based descriptive study. The study subjects were children with DS diagnosis born between the years 1990 and 2003. We collected data from genetic centres in Estonia, from the databases of DS support groups, from institutions for disabled children and from the registers of family doctors/paediatricians. Prenatal screening for chromosomal anomalies for women aged ≥35 years was started in Estonia in 1995. Therefore, we divided the DS children into two groups: 112 born between 1990 and 1994 comprise group I, and 127 born between 1995 and 2003 comprise group II. Group II was further divided into two subgroups: IIa, from 1995 to 1998, when screening of advanced maternal age (≥35 years) commenced, and IIb, from 1999 to 2003, when screening of second trimester maternal serum for younger women commenced. Prenatally, 68 cases of DS were diagnosed between 1995 and 2003 in the whole of Estonia, and all of these pregnancies were terminated. This represents 34.9% of all delivered and prenatally detected DS cases from this period.The overall livebirth prevalence was 1.17 per 1000 livebirths. The livebirth prevalence in group I was 1.25 and in group II was 1.09 per 1000 livebirths. The second trimester maternal serum screening with advanced maternal age screening was more effective than advanced maternal age screening alone. The livebirth prevalence in group IIa was 1.22 and in group IIb 0.99 per 1000 livebirths. Overall, regular trisomy was found in 90.4%, translocation in 6.3% and mosaicism in 2.9%. The overall male to female sex ratio of DS was 1.09.
Levels of IL‐15 in Serum and Cerebrospinal Fluid of Patients with Behçet's Disease
Authors: Hamzaoui K. , Hamzaoui A. , Ghorbel I. , Khanfir M. , Houman H. 
Published: October 2006

AbstractInterleukin‐15 (IL‐15) is a novel proinflammatory cytokine, involved in the pathogenesis of inflammatory/autoimmune disease. The objective of our study was to measure serum and cerebrospinal fluid (CSF) IL‐15 levels in patients with Behçet's disease (BD). CSF/serum IL‐15 ratio was introduced to assess the origin of elevated IL‐15 levels. We measured serum and CSF‐IL‐15 levels in 40 patients with BD (20 patients in active stage). Inflammatory and non‐inflammatory neurological disease patients acted as controls. Active BD patients have significantly higher serum IL‐15 levels (median 10.4 pg/ml; range 5.3–17.4) compared with BD in remission (6.05 pg/ml; 4–10.4) and healthy controls (4.65 pg/ml; 3.9–6.2). Similar serum IL‐15 levels were found in active neuro‐BD and inflammatory neurological disease (9.5 pg/ml; 5–13). Elevated levels of IL‐15 were observed in CSF samples from neuro‐BD patients (11 pg/ml; 8.5–15) and inflammatory neurological disease patients (10 pg/ml; 6.5–14) compared with patients with non‐inflammatory neurological disease (4 pg/ml; 4–5.5; P < 0.001). Vascular cerebral BD lesions were associated with high CSF/serum IL‐15 ratio. Our findings suggest that IL‐15 is involved in BD inflammatory process, particularly in vasculitis foci, as an elevated CSF/serum IL‐15 ratio characterizes vascular cerebral lesions.
Is the Activity of Partially Agonistic MHC:Peptide Ligands Dependent on the Quality of Immunological Help?
Authors: Uhlin M. , Masucci M. , Levitsky V. 
Published: October 2006

AbstractCD8+ cytotoxic T lymphocytes (CTL) are important for the immunological control of infections and tumours. Engagement of the T‐cell receptor (TCR) with major histocompatibility complex (MHC) class I/peptide complexes on antigen‐presenting cells (APC) is the key interaction, which initiates the process of T‐cell activation. Depending on the affinity of this interaction, different arrays of signalling pathways and functional outcomes can be activated in the specific T cells. Molecular alterations in the peptide bound to the MHC class I can lead to a lower affinity of the MHC:TCR interaction resulting in incomplete or qualitatively different T‐cell responses. Altered peptide ligands (APL) exhibiting such activity are referred to as partial agonists and often occur naturally through genetic instability, which affects T‐cell epitopes derived from rapidly mutating viruses or tumour‐associated cellular antigens. Partial agonists are usually viewed as peptide variants, which escape efficient CTL recognition. Our recent data suggest that APL can not only trigger incomplete activation but also induce and modulate intrinsic T‐cell programmes leading to the shut‐off of specific CTL responses. This APL‐induced suppression appears to be more prominent in the absence of immunological help, suggesting that under conditions of immune deregulation APL may actively inhibit CTL responses against infectious agents or tumours. In this review, we discuss experimental data supporting this model and possible role of APL‐induced immunosuppression in different pathological conditions.
Two Neisseria meningitidis Strains with Different Ability to Stimulate Toll‐Like Receptor 4 Through the MyD88‐Independent Pathway
Authors: Mogensen T. H. , Paludan S. R. , Kilian M. , Østergaard L. 
Published: October 2006

Abstract Neisseria meningitidis causes acute severe diseases, including sepsis and meningitis, and more benign manifestations such as chronic meningococcemia or colonization of the upper respiratory tract. The inflammatory response, which contributes to the pathogenesis of meningococcal disease, is initiated by pattern recognition receptors, among which Toll‐like receptors (TLR)s have been ascribed a particularly important role. We have previously demonstrated that N. meningitidis induce proinflammatory cytokine expression through TLR2 and TLR4. Here we characterize the molecular basis for differential activation of the inflammatory response by two N. meningitidis strains. This difference was due to differential ability to activate signal transduction through TLR4, as HEK293 cells expressing TLR4 produced significantly different levels of interleukin‐8 in response to these strains. At the level of signal transduction, the two strains differed substantially in their ability to activate the pathway to nuclear factor κB in HEK293‐TLR4/MD2 cells at late, but not early, time points. TLR4 activates two signal transduction pathways: one dependent on the adaptor molecule MyD88 and one independent of MyD88, and these pathways induce distinct patterns of gene expression in response to TLR4 ligands. By using macrophages from TLR2−/− mice, we observed that the two strains differed in their ability to activate the TLR4‐induced MyD88‐independent pathway, but not the MyD88‐dependent pathway. This idea was further supported by experiments where either of the two pathways was inhibited and IL‐8 secretion was measured. These data therefore provide molecular insight into activation of the inflammatory response by N. meningitidis, which is one of the key events in the pathogenesis of meningococcal disease.
Clinical predictors of suicidal acts after major depression in bipolar disorder: a prospective study
Authors: Galfalvy Hanga , Oquendo Maria A , Carballo Juan J , Sher Leo , Grunebaum Michael F , Burke Ainsley , John Mann J 
Published: October 2006

Objective:  This study determined the clinical predictors of suicidal behavior during a 2‐year follow‐up of patients with bipolar disorder presenting with a major depressive episode (MDE).Method:  Sixty four patients with DSM‐III‐R bipolar disorder were assessed at presentation for treatment of an MDE. Correlates of past suicidal behavior were determined by comparing patients with and without a history of suicide attempts using a t‐test, Wilcoxon test or chi‐squared test of independence on individual explanatory variables. Putative predictors of attempts during the follow‐up period were tested separately using Cox proportional hazards regression analysis.Results:  Twelve of 64 patients had at least one suicide attempt in the follow‐up period, five of them attempted in the first 2 months and seven around or shortly after the 1‐year follow‐up visit. All attempters had a history of past suicide attempts. Most predictors of future suicidal behavior were correlates of past suicidal behavior. Family history of suicide acts and comorbid borderline personality disorder predicted early attempts, while younger age, high hostility scores, number of past attempts, subjective pessimism as reflected in depression and suicidal ideation, and few reported reasons for living predicted suicidal acts during the whole period.Conclusion:  In this data set of bipolar patients we noted an intriguing picture of two clusters of suicide attempts. Hostility was the strongest risk factor. These findings may have implications in both the identification of at‐risk patients and the timing of clinical interventions including aggressive pharmacotherapeutic prophylaxis to prevent relapse or recurrence of depressive symptomatology.