bluuebunny/crossref_metadata_2025 huggingface dataset:
Insular shifts in body size of rice frogs in the Zhoushan Archipelago, China
Authors: WU ZHENGJUN , LI YIMING , MURRAY BRAD R.
Published: June 2006

Differences in body size between mainland and island populations have been reported for reptiles, birds and mammals. Despite widespread recognition of insular shifts in body size in these taxa, there have been no reports of such body size shifts in amphibians.

We provide the first evidence of an insular shift in body size for an amphibian species, the rice frog Rana limnocharis. We found significant increases in body size of rice frogs on most sampled islands in the Zhoushan archipelago when compared with neighbouring mainland China.

Large body size in rice frogs on islands was significantly related to increased population density, in both breeding and non‐breeding seasons. Increases in rice frog density were significantly related to higher resource availability on islands. Increased resource availability on islands has led to higher carrying capacities, which has subsequently facilitated higher densities and individual growth rates, resulting in larger body size in rice frogs. We also suggest that large body size has evolved on islands, as larger individuals are competitively superior under conditions of harsh intraspecific competition at high densities.

Increases in body size in rice frogs were not related to several factors that have been implicated previously in insular shifts in body size in other taxa. We found no significant relationships between body size of rice frogs and prey size, number of larger or smaller frog species, island area or distance of islands from the mainland.

Our findings contribute to the formation of a broad, repeatable ecological generality for insular shifts in body size across a range of terrestrial vertebrate taxa, and provide support for recent theoretical work concerning the importance of resource availability for insular shifts in body size.
Maternal antibodies in a wild altricial bird: effects on offspring immunity, growth and survival
Authors: PIHLAJA MARJO , SIITARI HELI , ALATALO RAUNO V.
Published: June 2006

In many animals immunity is not fully developed until adulthood but the young still need protection against various sets of pathogens. Thus, bird nestlings are highly dependent on antibodies received from their mother (in the eggs) during their rapid early growth period. The relationship between maternal immunity and the development of neonates’ own immunity has been poorly studied.

It has been suggested that immune function plays an important part in mediating resource competition between different life‐history traits, e.g. growth and reproduction. Maternal investment of antibodies has potentially permanent effects on offspring phenotype. Thus, the trade‐offs between the immune function and other important life‐history traits in the offspring will also affect the fitness of the mother.

Our supplemental feeding experiment in the magpiePica picaindicates that the immunoglobulin levels of offspring at hatching are dependent on a mother's nutritional condition. In addition, the amount of maternal immunoglobulins transferred to offspring increases along the laying order within a nest.

We also found that at the age of 8–10 days the immunoglobulin production of the offspring has already begun. Furthermore, the maternal immunoglobulin levels of the offspring at hatching were positively related to their immunoglobulin levels on day 10.

Maternal immunoglobulins did not significantly affect offspring growth, but there was a negative relationship between self‐produced immunoglobulins and growth over the first 10 days, indicating a trade‐off between these traits. Nestlings’ weight, however, had a positive relationship with immunoglobulin production suggesting that the observed trade‐off between growth and immunoglobulin production is due to catch‐up growth of nestlings with a low hatching weight. We found that within nests nestlings with higher maternal antibody levels had higher survival rate until day 20, but between nests there was an opposite relationship.

Evidently, there is a trade‐off, in magpies, between maternal resources, immune function and growth, shaping the evolution of maternal investment in offspring immunity.
The impact of role discrepancy on nurses’ intention to quit their jobs
Authors: Takase Miyuki , Maude Phillip , Manias Elizabeth
Published: June 2006

Aims and objective.  The purpose of this study was to investigate the impact of role discrepancy on nurses’ intention to quit their jobs.

Background.  Nurses experience role discrepancy, which refers to incompatibility between the roles nurses desire and expect to take, and the roles they actually engage in at work. However, there is a paucity of information as to how this role discrepancy affects nurses’ intention to quit their jobs.

Design.  A correlational design was used to investigate the impact of role discrepancy on nurses’ intention to quit their jobs.

Methods.  A total of 346 Australian nurses participated in this study by completing questionnaires. The results were analysed by t‐test, polynomial regression and response surface analysis.

Results.  Nurses tended to experience role discrepancy, in particular, in decision making with hospital policies and provision of patient education. The overall results show that this role discrepancy contributes to nurses’ intention to quit their jobs. Nurses’ intention to quit their jobs also increased when they had a low desire to engage in nursing roles and when they only performed a few roles. When specific dimensions of nursing roles were examined, a role discrepancy in the use of nursing skills, such as participation in decision making and providing patient education and emotional support, had little impact on their turnover intention. On the contrary, a role discrepancy in task delegation practice showed a significant association with nurses’ intention to leave their jobs.

Conclusions.  Role discrepancy has been experienced by many nurses, and this discrepancy partially contributes to nurses’ intention to quit their jobs.

Relevance to clinical practice.  To reduce nursing turnover, it is important to create a work environment where nurses are inspired to engage in various nursing roles and their work desires are reinforced by existing work opportunities.
Pdr1 regulates multidrug resistance in Candida glabrata: gene disruption and genome‐wide expression studies
Authors: Vermitsky John‐Paul , Earhart Kelly D. , Smith W. Lamar , Homayouni Ramin , Edlind Thomas D. , Rogers P. David
Published: June 2006

Candida glabrata emerged in the last decade as a common cause of mucosal and invasive fungal infection, in large part due to its intrinsic or acquired resistance to azole antifungals such as fluconazole. In C. glabrata clinical isolates, the predominant mechanism behind azole resistance is upregulated expression of multidrug transporter genes CDR1 and PDH1. We previously reported that azole‐resistant mutants (MIC ≥ 64 μg ml−1) of strain 66032 (MIC = 16 μg ml−1) similarly show coordinate CDR1‐PDH1 upregulation, and in one of these (F15) a putative gain‐of‐function mutation was identified in the single homologue of Saccharomyces cerevisiae transcription factors Pdr1–Pdr3. Here we show that disruption of C. glabrata PDR1 conferred equivalent fluconazole hypersensitivity (MIC = 2 μg ml−1) to both F15 and 66032 and eliminated both constitutive and fluconazole‐induced CDR1‐PDH1 expression. Reintroduction of wild‐type or F15 PDR1 fully reversed these effects; together these results demonstrate a role for this gene in both acquired and intrinsic azole resistance. CDR1 disruption had a partial effect, reducing fluconazole trailing in both strains while restoring wild‐type susceptibility (MIC = 16 μg ml−1) to F15. In an azole‐resistant clinical isolate, PDR1 disruption reduced azole MICs eight‐ to 64‐fold with no effect on sensitivity to other antifungals. To extend this analysis, C. glabrata microarrays were generated and used to analyse genome‐wide expression in F15 relative to its parent. Homologues of 10 S. cerevisiae genes previously shown to be Pdr1–Pdr3 targets were upregulated (YOR1, RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself) or downregulated (PDR12); roles for these genes include small molecule transport and transcriptional regulation. However, expression of 99 additional genes was specifically altered in C. glabrata F15; their roles include transport (e.g. QDR2, YBT1), lipid metabolism (ATF2, ARE1), cell stress (HSP12, CTA1), DNA repair (YIM1, MEC3) and cell wall function (MKC7, MNT3). These azole resistance‐associated changes could affect C. glabrata tissue‐specific virulence; in support of this, we detected differences in F15 oxidant, alcohol and weak acid sensitivities. C. glabrata provides a promising model for studying the genetic basis of multidrug resistance and its impact on virulence.
Neisseria meningitidis NhhA is a multifunctional trimeric autotransporter adhesin
Authors: Scarselli Maria , Serruto Davide , Montanari Paolo , Capecchi Barbara , Adu‐Bobie Jeannette , Veggi Daniele , Rappuoli Rino , Pizza Mariagrazia , Aricò Beatrice
Published: June 2006

NhhA, Neisseriahia/hsf homologue, or GNA0992, is an oligomeric outer membrane protein of Neisseria meningitidis, recently included in the family of trimeric autotransporter adhesins. In this study we present the structural and functional characterization of this protein. By expressing in Escherichia coli the full‐length gene, deletion mutants and chimeric proteins of NhhA, we demonstrated that the last 72 C‐terminal residues are able to allow trimerization and localization of the N‐terminal protein domain to the bacterial surface. In addition, we investigated on the possible role of NhhA in bacterial–host interaction events. We assessed in vitro the ability of recombinant purified NhhA to bind human epithelial cells as well as laminin and heparan sulphate. Furthermore, we shown that E. coli strain expressing NhhA was able to adhere to epithelial cells, and observed a reduced adherence in a meningococcal isogenic MC58ΔNhhA mutant. We concluded that this protein is a multifunctional adhesin, able to promote the bacterial adhesion to host cells and extracellular matrix components. Collectively, our results underline a putative role of NhhA in meningococcal pathogenesis and ascertain its structural and functional belonging to the emerging group of bacterial autotransporter adhesins with trimeric architecture.
PtxR modulates the expression of QS‐controlled virulence factors in the Pseudomonas aeruginosa strain PAO1
Authors: Carty Nancy L. , Layland Nancy , Colmer‐Hamood Jane A. , Calfee M. Worth , Pesci Everett C. , Hamood Abdul N.
Published: June 2006

The production of several virulence factors by Pseudomonas aeruginosa is regulated through the hierarchical cell‐density dependent quorum sensing (QS) systems las and rhl. A third component of the QS hierarchy, the Pseudomonas quinolone signal PQS, also controls the expression of several genes. We previously described P. aeruginosa PtxR as a transcriptional activator of the exotoxin A gene toxA. Here, we provide evidence that PtxR regulates the production of other virulence factors. Mutation of ptxR in PAO1 increased pyocyanin production. This increase was reduced in the presence of a ptxR plasmid. Throughout the growth cycle, PtxR reduced the expression of the pyocyanin operon phzA1‐G1 but not phzA2‐G2. As pyocyanin production is stringently controlled by QS, we examined the effect of PtxR on QS‐related genes in PAO1. PtxR also reduced the expression of the PQS synthesis operon pqsABCDE. ptxR mutation increased the expression of the rhamnolipid synthesis gene rhlA but decreased lasB expression. The expression of the RhlI synthase gene rhlI and the production of the C4‐HSL autoinducer were increased in the ptxR mutant, while the expression of the LasI synthase gene lasI and the production of 3OC12‐HSL were reduced. These results suggest that PtxR negatively regulates the expression of the rhamnolipid and pyocyanin genes through rhlI and the pqsABCDE operon while it positively regulates the expression of lasB through lasI.
Shutdown decay of mRNA
Authors: Condon Ciarán
Published: June 2006

Although plasmid‐borne and chromosomal toxin–antitoxin (TA) operons have been known for some time, the recent identification of mRNA as the target of at least two different classes of toxins has led to a dramatic renewal of interest in these systems as mediators of stress responses. Members of the MazF/PemK family, the so‐called mRNA interferases, are ribonucleases that inhibit translation by destroying cellular mRNAs under stress conditions, while the founder member of the RelE family promotes cleavage of mRNAs through the ribosome. Detailed structures of these enzymes, often in complex with their inhibitors, have provided vital clues to their mechanisms of action. The primary role and regulation of these systems has been the subject of some controversy. One model suggests they play a beneficial role by wiping the slate clean and preventing wasteful energy consumption by the translational apparatus during adaptation to stress conditions, while another favours the idea that their main function is programmed cell death. The two models might not be mutually exclusive if a side‐effect of prolonged exposure to toxic RNase activity without de novo synthesis of the inhibitor were a state of dormancy for which we do not yet understand the key to recovery. In this review, I discuss the recent developments in the rapidly expanding field of what I refer to as bacterial shutdown decay.
In vivo, fliC expression by Salmonella enterica serovar Typhimurium is heterogeneous, regulated by ClpX, and anatomically restricted
Authors: Cummings Lisa A. , Wilkerson W. David , Bergsbaken Tessa , Cookson Brad T.
Published: June 2006

FliC is a natural antigen recognized by the innate and adaptive immune systems during Salmonella infection in mice and humans; however, the regulatory mechanisms governing its expression in vivo are incompletely understood. Here, we use flow cytometry to quantify fliC gene expression in single bacteria. In vitro, fliC transcription was not uniformly positive; a viable fliC‐negative subpopulation was also identified. Intracellular Salmonella repressed transcription of fliC and its positive regulator fliA, but constitutively transcribed the master regulator flhD; fliC repression required ClpXP protease, known to degrade FlhD. In orally infected mice, fliC transcription was anatomically restricted: Salmonella transcribed fliC in the Peyer's Patches (PP) but not in the mesenteric lymph nodes and spleen. The intracellularly transcribed pagC promoter was upregulated by Salmonella in all tissues, defining the infected PP as a unique environment that initiates expression of intracellularly induced genes and yet permits transcription of fliC. Because a single bacterium can escape the GI tract to colonize deeper tissues, heterogeneous gene expression may have important implications for Salmonella pathogenesis: FliC‐positive bacteria in the PP could stimulate inflammation and facilitate the priming of FliC‐specific immune responses, while FliC‐negative bacteria escape host detection in the gut and spread to systemic sites of replication.
Identification of the lipopolysaccharide modifications controlled by the Salmonella PmrA/PmrB system mediating resistance to Fe(III) and Al(III)
Authors: Nishino Kunihiko , Hsu Fong‐Fu , Turk John , Cromie Michael J. , Wösten Marc M. S. M. , Groisman Eduardo A.
Published: June 2006

Iron is an essential metal but can be toxic in excess. While several homeostatic mechanisms prevent oxygen‐dependent killing promoted by Fe(II), little is known about how cells cope with Fe(III), which kills by oxygen‐independent means. Several Gram‐negative bacterial species harbour a regulatory system – termed PmrA/PmrB – that is activated by and required for resistance to Fe(III). We now report the identification of the PmrA‐regulated determinants mediating resistance to Fe(III) and Al(III) in Salmonella enterica serovar Typhimurium. We establish that these determinants remodel two regions of the lipopolysaccharide, decreasing the negative charge of this major constituent of the outer membrane. Remodelling entails the covalent modification of the two phosphates in the lipid A region with phosphoethanolamine and 4‐aminoarabinose, which has been previously implicated in resistance to polymyxin B, as well as dephosphorylation of the Hep(II) phosphate in the core region by the PmrG protein. A mutant lacking the PmrA‐regulated Fe(III) resistance genes bound more Fe(III) than the wild‐type strain and was defective for survival in soil, suggesting that these PmrA‐regulated lipopolysaccharide modifications aid Salmonella's survival and spread in non‐host environments.
Cysteine peptidases CPA and CPB are vital for autophagy and differentiation in Leishmania mexicana
Authors: Williams Roderick A. , Tetley Laurence , Mottram Jeremy C. , Coombs Graham H.
Published: June 2006

In the past, ultrastructural investigations of Leishmania mexicana amastigotes revealed structures that were tentatively identified as autophagosomes. This study has now provided definitive data that autophagy occurs in the parasite during differentiation both to metacyclic promastigotes and to amastigotes, autophagosomes being particularly numerous during metacyclic to amastigote form transformation. Moreover, the results demonstrate that inhibiting two major lysosomal cysteine peptidases (CPA and CPB) or removing their genes not only interferes with the autophagy pathway but also prevents metacyclogenesis and transformation to amastigotes, thus adding support to the hypothesis that autophagy is required for cell differentiation. The study suggests that L. mexicana CPA and CPB perform similar roles to the aspartic peptidase PEP4 and the serine peptidase PRB1 in Saccharomyces cerevisiae. The results also provide an explanation for why L. mexicana CPA/CPB‐deficient mutants transform to amastigotes very poorly and lack virulence in macrophages and mice.
Lethal fragmentation of bacterial chromosomes mediated by DNA gyrase and quinolones
Authors: Malik Muhammad , Zhao Xilin , Drlica Karl
Published: June 2006

When DNA gyrase is trapped on bacterial chromosomes by quinolone antibacterials, reversible complexes form that contain DNA ends constrained by protein. Two subsequent processes lead to rapid cell death. One requires ongoing protein synthesis; the other does not. The prototype quinolone, nalidixic acid, kills wild‐type Escherichia coli only by the first pathway; fluoroquinolones kill by both. Both lethal processes correlated with irreversible chromosome fragmentation, detected by sedimentation and viscosity of DNA from quinolone‐treated cells. However, only fluoroquinolones fragmented purified nucleoids when incubated with gyrase purified from wild‐type cells. A GyrA amino acid substitution (A67S) expected to perturb a GyrA–GyrA dimer interface allowed nalidixic acid to fragment chromosomes and kill cells in the absence of protein synthesis; moreover, it made a non‐inducible lexA mutant hypersusceptible to nalidixic acid, a property restricted to fluoroquinolones with wild‐type cells. The GyrA variation also facilitated immunoprecipitation of DNA fragments by GyrA antiserum following nalidixic acid treatment of cells. The ability of changes in both gyrase and quinolone structure to enhance protein synthesis‐independent lethality and chromosome fragmentation is explained by drug‐mediated destabilization of gyrase–DNA complexes. Instability of type II topoisomerase–DNA complexes may be a general phenomenon that can be exploited to kill cells.
pH‐dependent pore‐forming activity of OmpATb from Mycobacterium tuberculosis and characterization of the channel by peptidic dissection
Authors: Molle Virginie , Saint Nathalie , Campagna Sylvie , Kremer Laurent , Lea Edward , Draper Philip , Molle Gérard
Published: June 2006

Mycobacteria are characterized by an unusual cell wall that controls nutrient and small hydrophilic compound permeability. Porin‐like proteins are necessary to ensure the transport of molecules into the cell. Here, we investigated the pore‐forming properties of OmpATb, a porin from Mycobacterium tuberculosis, in lipid bilayers. Multi‐channel experiments showed an asymmetric behaviour with channel closures at negative critical voltages (Vc) and a strong decrease in Vc at acidic pH. Single‐channel experiments gave conductance values of about 850 ± 80 pS in 1 M KCl and displayed a weak cationic selectivity in 4–8 pH range. The production and characterization of a series of truncated OmpATb proteins, showed that the central domain (OmpATb73−220) was sufficient to induce the ion channel properties of the native protein in lipid bilayers, i.e. asymmetric insertion, pH‐dependent voltage closure, cationic selectivity and similar conductance values in 1 M KCl. Western blot analysis suggests that the presence of OmpATb is only restricted to certain pathogenic species. Therefore, the propensity of channels of native OmpATb to close at low pH may represent an intrinsic property allowing pathogenic mycobacteria to adapt and survive to mildly acidic conditions, such as those encountered within the macrophage phagosome.
Interaction between two murein (peptidoglycan) synthases, PBP3 and PBP1B, in Escherichia coli
Authors: Bertsche Ute , Kast Thomas , Wolf Benoît , Fraipont Claudine , Aarsman Mirjam E. G. , Kannenberg Kai , Von Rechenberg Moritz , Nguyen‐Distèche Martine , Den Blaauwen Tanneke , Höltje Joachim‐Volker , Vollmer Waldemar
Published: June 2006

The murein (peptidoglycan) sacculus is an essential polymer embedded in the bacterial envelope. The Escherichia coli class B penicillin‐binding protein (PBP) 3 is a murein transpeptidase and essential for cell division. In an affinity chromatography experiment, the bifunctional transglycosylase‐transpeptidase murein synthase PBP1B was retained by PBP3‐sepharose when a membrane fraction of E. coli was applied. The direct protein–protein interaction between purified PBP3 and PBP1B was characterized in vitro by surface plasmon resonance. The interaction was confirmed in vivo employing two different methods: by a bacterial two‐hybrid system, and by cross‐linking/co‐immunoprecipitation. In the bacterial two‐hybrid system, a truncated PBP3 comprising the N‐terminal 56 amino acids interacted with PBP1B. Both synthases could be cross‐linked in vivo in wild‐type cells and in cells lacking FtsW or FtsN. PBP1B localized diffusely and in foci at the septation site and also at the side wall. Statistical analysis of the immunofluorescence signals revealed that the localization of PBP1B at the septation site depended on the physical presence of PBP3, but not on the activity of PBP3. These studies have demonstrated, for the first time, a direct interaction between a class B PBP (PBP3) and a class A PBP (PBP1B) in vitro and in vivo, indicating that different murein synthases might act in concert to enlarge the murein sacculus during cell division.
Southern GEMS groups – I. Dynamical properties
Authors: Brough Sarah , Forbes Duncan A. , Kilborn Virginia A. , Couch Warrick
Published: June 2006

Here, we present an investigation of the properties of 16 nearby galaxy groups and their constituent galaxies. The groups are selected from the Group Evolution Multiwavelength Study (GEMS) and all have X-ray as well as wide-field neutral hydrogen (H i) observations. Group membership is determined using a friends-of-friends algorithm on the positions and velocities from the 6-degree Field Galaxy Survey and NASA/IPAC Extragalactic Database. For each group we derive their physical properties using this membership, including: velocity dispersions (σv), virial masses (MV), total K-band luminosities [LK(Tot)] and early-type fractions (fearly) and present these data for the individual groups. We find that the GEMS X-ray luminosity is proportional to the group velocity dispersions and virial masses: LX(r500) ∝σ3.11±0.59v and LX(r500) ∝M1.13±0.27V, consistent with the predictions of self-similarity between group and clusters. We also find that MV∝LK(Tot)2.0±0.9, i.e. mass grows faster than light and that the fraction of early-type galaxies in the groups is correlated with the group X-ray luminosities and velocity dispersions. We examine the brightest group galaxies (BGGs), finding that, while the luminosity of the BGG correlates with its total group luminosity, the fraction of group luminosity contained in the BGG decreases with increasing total group luminosity. This suggests that BGGs grow by mergers at early times in group evolution while the group continues to grow by accreting infalling galaxies. We form a composite galaxy group in order to examine the properties of the constituent galaxies and compare their properties with those of field galaxies. There are clear radial trends, with group galaxies becoming fainter, bluer and morphologically later types with increasing radius from the group centre, reaching field levels at radii >r500(>0.7r200). We divide the composite group-by-group X-ray luminosity and find that galaxies in high X-ray luminosity groups [log10LX(r500) ≥ 41.7 erg s−1] are redder with a higher giant-to-dwarf ratio and are more likely to be early-type galaxies than are those galaxies in low X-ray luminosity groups. We conclude that harassment and ram-pressure stripping processes are unlikely to cause these differences. The differences are more likely to be due to galaxy–galaxy mergers and possibly some further mechanism such as strangulation. If mergers are the dominant mechanism then the properties of galaxies in the higher X-ray luminosity groups are a result of mergers at earlier epochs in smaller mass groups that have since merged to become the structures we observe today, while lower X-ray luminosity groups are still undergoing mergers today.
The role of NADPH oxidase and MAP kinase phosphatase in UV‐B‐dependent gene expression in Arabidopsis
Authors: KALBINA IRINA , STRID ÅKE
Published: June 2006

Plant responses to supplementary UV‐B irradiation have been reported to include formation of reactive oxygen species (ROS), hydrogen peroxide, in particular, and regulation by mitogen‐activated protein kinase (MAPK) cascades which in turn are fine‐tuned by MAPK phosphatases (MKPs). Here we present direct genetic evidence for the involvement of plasma membrane NADPH oxidase, a source of superoxide and hydrogen peroxide in the apoplasts, in UV‐B signalling in Arabidopsis thaliana, by analysis of gene expression of the UV‐B molecular markers in NADPH oxidase (atrbohD, F and DF) and MAP kinase phosphatase 1 (MKP1) knockout mutants (mkp1). Whereas the NADPH oxidase mutants were affected in UV‐B‐dependent CHS, PYROA and MEB5.2 gene expression, the mkp1 mutant was affected in the general expression pattern of the pathogenesis‐related (PR) and PDF1.2 genes. The results indicate involvement of MKP1 in repressive action on gene expression of more general stress response pathways, similar to those activated by pathogen attack, while NADPH oxidase is involved in quantitative (rather than absolute) regulation of more UV‐B‐specific genes. The expressions of the molecular markers in the knockout mutant mkp1 and in its complemented lines (lines 6 and 10) were similar, as opposed to the responses of the corresponding wild‐type Wassilewskija‐4 (Ws‐4). Lines 6 and 10 showed much higher MKP1 mRNA than Ws‐4 but did not complement the mutant. This suggests a complex dependency of the MAPK phosporylation level of the PR and PDF1.2 genes. Both NADPH oxidase mutants and the mkp1 mutant phenotypically responded to UV‐B by growth retardation.
Changes in C uptake in populations of Chlamydomonas reinhardtii selected at high CO2
Authors: COLLINS SINÉAD , SÜLTEMEYER DIETER , BELL GRAHAM
Published: June 2006

Estimates of the effect of increased global atmospheric CO2 levels on oceanic primary productivity depend on the physiological responses of contemporary phytoplankton populations. However, microalgal populations will possibly adapt to rising CO2 levels in such a way that they become genetically different from contemporary populations. The unknown properties of these future populations introduce an undefined error into predictions of C pool dynamics, especially the presence and size of the biological C pump. To address the bias in predictions introduced by evolution, we measured the kinetics of CO2 uptake in populations of Chlamydomonas reinhardtii that had been selected for growth at high CO2 for 1000 generations. Following selection at high CO2, the populations were unable to induce high‐affinity CO2 uptake, and one line had a lower rate of net CO2 uptake. We attribute this to conditionally neutral mutations in genes affecting the C concentrating mechanism (CCM). Lower affinity CO2 uptake, in addition to smaller population sizes, results in a significant reduction in net CO2 uptake of about 38% relative to contemporary populations under the same conditions. This shows how predictions about the properties of communities in the future can be influenced by the effect of natural selection.
Living on the edge: feeding of subtropical open ocean copepods
Authors: Paffenhöfer Gustav‐Adolf , Mazzocchi Maria Grazia , Tzeng Mimi W.
Published: June 2006

The objective of this study was to provide quantitative information on environmental feeding rates of warm water oceanic epipelagic copepods. We determined clearance rates at 23 °C for various particle size ranges in shipboard studies in the western oligotrophic subtropical Atlantic Ocean for females of the calanoid species Clausocalanus furcatus and Mecynocera clausii. These in situ clearance rates were then applied to the various particle size ranges of environmental particle spectra of auto‐ and heterotrophs at different depths from three stations in the western Atlantic. After calculating the metabolic demands of each of these two copepod species and applying an assimilation efficiency of 90%, we determined that C. furcatus meets its metabolic demands in all six cases, and M. clausii in two of six cases. Clausocalanus furcatus would also meet its energy demands at 25 °C, where it is often found, while M. clausii at 20 °C, where it is regularly found, would cover its metabolic needs in four of six cases. It is hypothesized that these species, and most likely most of the other co‐occurring copepod species, are limited in their abundance by food availability, or, better said, are ‘living on the edge’ in relation to food abundance.
Anaerobic ammonium oxidation in a tropical freshwater system (Lake Tanganyika)
Authors: Schubert Carsten J. , Durisch‐Kaiser Edith , Wehrli Bernhard , Thamdrup Bo , Lam Phyllis , Kuypers Marcel M. M.
Published: June 2006

Here we provide the first direct evidence for the anammox process (anaerobic ammonium oxidation) in a lacustrine system, Lake Tanganyika, the second largest lake in the world. Incubations with 15N labelled nitrate showed that anammox occurred in the suboxic water layer at 100–110 m water depth. Anammox rates up to 10 nM N2 h−1 are comparable to those reported for the marine water column. Up to ∼13% of produced N2 could be attributed to the anammox process whereas the remainder was related to denitrification. Typical lipid biomarkers characteristic of anammox bacteria were found in filtered water from the depths where anammox occurred, thus supporting the presence of anammox bacteria. Further evidence is provided by fluorescence in situ hybridization (FISH), revealing up to 13 000 anammox bacteria cells per ml or 1.4% of all DAPI (4′‐6‐Diamidino‐2‐phenylindole)‐stained cells. Phylogenetic analyses of partial 16S rRNA genes indicated the presence of sequences most closely related to the known anammox bacterium Candidatus‘Scalindua brodae’ (95.7% similarity). Using the incubation results, a total loss of 0.2 Tg N2 per year linked to anammox was estimated for the Northern basin of Lake Tanganyika.
The Disintegrating Effects of Equality: A Study of a Failed International Merger
Authors: Meyer Christine B. , Altenborg Ellen
Published: June 2006

In the literature on M&A and social justice, equality is regarded as an important principle to facilitate social integration. This article debates what happens when the equality principle is operationalized; from intentions in the pre‐merger process to the distribution of resources and decision‐making rules in the post‐merger process. In a merger between two state‐owned telecoms corporations in the Scandinavian countries, we found that the principle of equality had the reverse effects on social integration to that predicted in the literature. Instead of facilitating the social integration process, the equality principle led to perceptual and structural fallacies negatively influencing social integration. We suggest that these disintegrating effects were particularly strong because this was an international merger between two state‐owned firms of unequal size.
Rate‐of‐return Parity in Experimental Asset Markets*
Authors: Childs Jason , Mestelman Stuart
Published: June 2006

This paper applies experimental methods to evaluate the completeness of arbitrage and rate‐of‐return parity in simultaneous asset markets in which the assets are denominated in different currencies. Two assets, which return uncertain, but known, dividends in each trading period, are traded over 20 periods, after which the asset has no value. Results indicate that risk‐neutral rate‐of‐return parity is a strong predictor of relative asset prices when assets have common expected dividends and the expected dividends have common variances. The predictive power of risk‐neutral rate‐of‐return parity is reduced as the assets become differentiated.
Misleading Inferences from Panel Unit Root Tests: a Comment
Authors: Ford George S. , Jackson John D. , Kline Audrey D.
Published: June 2006

In their 2001 paper, Breuer, McNown, and Wallace argue that panel unit root tests are flawed in that the “all or nothing nature of these procedures may lead to serious misinterpretations of tests applied to mixed panels” (2001, p. 483). The authors propose an alternative test, the SURADF test, which allows for and estimates heterogeneous rates of convergence. We show that SURADF test results are highly sensitive to the selection of panel members. As such, application of the SURADF test seems to require a sound basis for panel member selection and a caveat that all results are panel‐specific.
Food Protection for Sale*
Authors: Lopez Rigoberto A. , Matschke Xenia
Published: June 2006

This article tests the Protection for Sale (PFS) model using detailed data from US food‐processing industries under alternative import‐demand specifications. All empirical results support the PFS model predictions and previous empirical work qualitatively. However, a surprising result is that we obtain weights between 2.6 and 3.6 for domestic welfare using import slopes or elasticities derived from domestic demand and supply functions. In contrast, results based on directly specified import demands (including the Armington model) yield the usual, unrealistically large estimates for the domestic welfare weight. We contend that this empirical paradox arises mainly because the explanatory variables tend to be extremely large for industries with low import ratios and/or low import elasticities (or slopes) resulting from relatively volatile import prices. The results with derived import parameters point to a much stronger role of campaign contributions within the PFS model than previously found.
Foreign Direct Investment: Flows, Volatility, and the Impact on Growth*
Authors: Lensink Robert , Morrissey Oliver
Published: June 2006

This paper contributes to the literature on FDI and economic growth. We deviate from previous studies by introducing measures of the volatility of FDI inflows. As introduced into the model, these are predicted to have a negative effect on growth. We estimate the standard model using cross‐section, panel data, and instrumental variable techniques. Whilst all results are not entirely robust, there is a consistent finding that volatility of FDI has a negative impact on growth. The evidence for a positive effect of FDI levels on growth is not robust, nor is that for any effect of human capital.
Making Sense of the Comparative Advantage Gains from Trade: Comment on Batra
Authors: Bernhofen Daniel M.
Published: June 2006

This paper addresses Ravi Batra’s (2002) criticism of the basic comparative advantage gains‐from‐trade model. While Batra’s criticism is based on the selection view interpretation of real income, the gains from trade can only be properly understood from the options view interpretation of real income. I also show how a recent empirical implementation of the gains‐from‐trade model defies Batra’s claim that “the consumption gain . . . is not subject to measurement” (2002, p. 642).
Gaussian Maximum Likelihood Estimation For ARMA Models. I. Time Series
Authors: Yao Qiwei , Brockwell Peter J.
Published: June 2006

Abstract.  We provide a direct proof for consistency and asymptotic normality of Gaussian maximum likelihood estimators for causal and invertible autoregressive moving‐average (ARMA) time series models, which were initially established by Hannan [Journal of Applied Probability (1973) vol. 10, pp. 130–145] via the asymptotic properties of a Whittle's estimator. This also paves the way to establish similar results for spatial processes presented in the follow‐up article by Yao and Brockwell [Bernoulli (2006) in press].
Parental Separation and Children's Educational Attainment: A Siblings Analysis on Swedish Register Data
Authors: BJÖRKLUND ANDERS , SUNDSTRÖM MARIANNE
Published: June 2006

This paper analyses whether the commonly found negative relationship between parental separation in childhood and educational outcomes is causal or due mainly to selection. We use data on about 100,000 Swedish full biological siblings, born in 1948–63, and perform cross‐section and sibling‐difference estimations. Outcomes are measured as educational attainment in 1996. Our cross‐section analysis shows the expected negative and significant relationship, while the relationship is not significant, though precisely estimated, in the sibling‐difference analysis. This finding was robust to the sensitivity tests performed and is consistent with selection, rather than causation, being the explanation for the negative relationship.
Market Design with Correlated Valuations
Authors: CHEN YONGMIN , WANG RUQU
Published: June 2006

The effects of information on market design are explored in a simple setting where firms have private information about their correlated fixed costs and the government aims to maximize its expected revenue conditional on achieving efficient allocations. Government revenues are higher when the costs are less correlated (or are more of a private value). The reduced correlation increases the firms' information rents, but a change in the information structure also changes the expected market structures with positive effects on government revenues. If the government faces the no‐deficit constraint, there are situations where efficient allocations are achieved under asymmetric information but not under symmetric information.
Multiple promoter elements required for leukemia inhibitory factor‐stimulated M2 muscarinic acetylcholine receptor promoter activity
Authors: Laszlo George S. , Rosoff Marc L. , Amieux Paul S. , Nathanson Neil M.
Published: June 2006

Treatment of neuronal cells with leukemia inhibitory factor (LIF) results in increased M2 muscarinic acetylcholine receptor promoter activity. We demonstrate here that multiple promoter elements mediate LIF stimulation of M2 gene transcription. We identify a LIF inducible element (LIE) in the M2 promoter with high homology to a cytokine‐inducible ACTG‐containing sequence in the vasoactive intestinal peptide promoter. Mutagenesis of both a STAT (signal transducers and activators of transcription) element and the LIE in the M2 promoter is required to attenuate stimulation of M2 promoter activity by LIF completely. Mobility shift assays indicate that a LIF‐stimulated complex binds to a 70 base pair M2 promoter fragment. Furthermore, a STAT element within this fragment can bind to LIF‐stimulated nuclear STAT1 homodimers in vitro. Mutagenesis experiments show that cytokine‐stimulated activation of M2 promoter activity requires tyrosine residues on glycoprotein 130 (gp130) that are also required for both STAT1 and STAT3 activation. Dominant negative STAT1 or STAT3 can block LIF‐stimulated M2 promoter activity. Real‐time RT‐PCR analysis indicates that LIF‐stimulated induction of M2 mRNA is partially dependent on protein synthesis. These results show that regulation of M2 gene transcription in neuronal cells by LIF occurs through a complex novel mechanism that is dependent on LIE, STAT and de novo protein synthesis.
Trichomonas gallinae in wintering Common Wood Pigeons Columba palumbus in Spain
Authors: VILLANÚA DIEGO , HÖFLE URSULA , PÉREZ‐RODRÍGUEZ LORENZO , GORTÁZAR CHRISTIAN
Published: June 2006

We studied the prevalence and potential subclinical effects of infestation by Trichomonas gallinae in 91 hunter‐harvested Common Wood Pigeons Columba palumbus from northern (n = 30) and southern (n = 61) Spain during the winter period. All animals were measured, sexed, aged, necropsied and their organs were weighed. Infestation with T. gallinae was diagnosed using three different methods: direct inspection for the presence of lesions, direct microscopic observation and culture. Of the sampled birds, 34.2% were positive for the presence of T. gallinae. Prevalence was significantly higher in adult Wood Pigeons than in the juvenile group, and prevalence was significantly lower in birds sampled from the north. No significant differences in prevalence were found between males and females. Culture was significantly more sensitive than the other methods of diagnosis. Parasitized birds were in poorer body condition, as revealed by their lower body mass and fat reserves. No significant variation could be detected in heart or spleen weight between parasitized and healthy birds. However, juvenile Wood Pigeons in which T. gallinae was detected had a significantly larger bursa of Fabricius. Variations in the prevalence of T. gallinae in Wood Pigeons could be related to migration as well as increased exposure through shared feed and water where these are artificially provided. We also discuss the potential effect of T. gallinae on body condition and the eventual risk for endangered predators through increased exposure to infected prey.
Naturally occurring genetic variation in the age‐specific immune response of Drosophila melanogaster
Authors: Lesser Karen J. , Paiusi Ioana C. , Leips Jeff
Published: June 2006

Immunosenescence, the age‐related decline in immune response, is a well‐known consequence of aging. To date, most studies of age‐related changes in immune response focused on the cellular and physiological bases of this decline; we have virtually no understanding of the genetic basis of age‐related changes in the immune system or if indeed such control exists. We used 25 chromosome substitution lines of Drosophila melanogaster derived from a natural population to address three questions: (i) How is the function of the innate immune system influenced by age? (ii) Is there a genetic basis for phenotypic variation in immune response at different ages? (iii) Is there a genetic basis for differences in the way that age influences the immune function? Virgin females from each line were assayed for immune response using clearance of infection with Escherichia coli at 1 and 4 weeks of age. We found significant genetic variation among lines in immune response at each age. Unexpectedly, when averaged across all lines, the immune response actually improved with age. However, there was significant variation in the effect of age on immune response with 11 lines showing improvement, nine lines showing no change and five exhibiting a decline with age. There was no genetic correlation of immune response across ages suggesting that different loci contribute to variation in immune response at each age. The genetic component of the variation in immune response increased with age, a pattern predicted by the mutation accumulation model of senescence. However, this increase in variation resulted in part from the improvement of the immune response in some lines with age. Thus the observed changes in genetic variation in immune function with age are not entirely explained by the mutation accumulation model.
Treatment and prognostic factors in patients with hepatocellular carcinoma
Authors: Martins A. , Cortez‐Pinto H. , Marques‐Vidal P. , Mendes N. , Silva S. , Fatela N. , Glória H. , Marinho R. , Távora I. , Ramalho F. , Carneiro de Moura M.
Published: June 2006

Abstract: Introduction: Hepatocellular carcinoma is a leading cause of death from cancer worldwide. Survival of patients depends on tumor extension and liver function, but yet there is no consensual prognostic model.

Aims: To evaluate the influence on survival of pretreatment parameters (clinico‐laboratorial, liver function, tumor extension, Okuda and Cancer of the Liver Italian program (CLIP) staging) and treatment modalities.

Methods: We retrospectively analyzed 207 patients, diagnosed between 1993 and 2003. The initial treatment was: surgery – six patients; radiofrequency ablation – 21; percutaneous ethanol injection – 29; transarterial chemoembolization – 49; tamoxifen – 49; supportive care alone – 53. Factors determining survival were assessed by Kaplan–Meier method and Cox regression models.

Results: Median survival was 24 months. In univariate analysis, Child–Pugh classification and Model for end‐stage liver disease (MELD) score, portal vein thrombosis (PVT), tumor size, number of lesions, Okuda and CLIP scores were all associated with prognosis (P<0.001). α‐Fetoprotein levels were not predictive of survival. Independent predictors of survival were ascites, bilirubin, PVT and therapeutic modalities (P<0.001). In early stage hepatocellular carcinoma (HCC), survival was similar for both percutaneous ablation modalities, either radiofrequency or ethanol injection (P=NS). In advanced HCC, survival was better in patients receiving tamoxifen than supportive care alone (P<0.001).

Conclusion: This study reinforces the importance of baseline liver function (Child–Pugh classification and MELD score) in the survival of patients with HCC, although staging systems allowed the stratification of patients in different prognostic groups. Ascites, bilirubin and PVT were independent pretreatment predictors of survival. All treatments influenced the patient's outcome, whether in early or advanced stages.