bluuebunny/crossref_metadata_2025_split huggingface dataset:
Macroeconomic Linkages and Regional Monetary Cooperation: Steps Ahead*
Authors: De BROUWER Gordon , RAMAYANDI Arief , TURVEY David 
Published: November 2006

There is a growing appetite for economic cooperation in East Asia. Although the region has forums to facilitate this, economic cooperation has focussed largely on discussion of issues and policies − cooperative action is confined to functional cooperation in finance. There is scope for further cooperation in strengthening markets and institutions, with a view to accelerating convergence and stability in the region and deepening shared preferences about policy objectives, including on monetary and exchange rate issues. Although monetary policy in East Asia is generally focussed on controlling inflation, differences remain in economic structure and preferences about policy trade‐offs, markets, and institutions.
Partnerships between older people and their carers in the management of medication
Authors: Francis Sally‐Anne , Smith Felicity , Gray Nicola , Denham Michael 
Published: November 2006

Background.  Responsibility for medication can be an integral part of the informal caring role.Aims and objectives.  To explore partnerships between older people and their carers in the management of medication and consider the implications for health professionals.Methods.  Older people and their carers were identified through community pharmacies in four randomly selected areas of England. Data regarding their activities, responsibilities and experiences of managing medication were collected in semi‐structured interviews conducted in respondents’ own homes. Ninety‐four transcripts relating to 47 older people and their associated carers were analysed using a qualitative approach.Results.  Responsibility for medication was shared to varying extents between older people and their carers, and different patterns of partnership were identified. Differing perspectives between older people and their carers regarding the role, purpose and need for medication were revealed. Underlying these perspectives were issues concerning the sharing/concealment of information, autonomy and control. Caring was also described as a dynamic process. Older people and carers commented on how sharing responsibilities for medication varied on a day‐to‐day basis, as well as expressing concern regarding the changing needs of the older person and the carer's capacity to cope.Conclusions:  Older people and their carers work together in diverse and sometimes complex ways to manage medication. Problems included dilemmas relating to the sharing of information, patient determination, disputes about the control of medication and concerns about the future.Relevance to practice:  These patterns of partnership need to be recognized and taken into account by health professionals when providing information, advice and support. They need to listen for indications of differing perspectives and be aware of their possible implications for adherence to medication regimens. In caring for older people, health professionals need to find a balance that respects their autonomy whilst providing support for carers to enable them to be effective in their roles.
Upregulation of hemolymph and tissue ferritin by dietary HgCl2 in the wax moth Galleria mellonella
Authors: CHOI Chi‐Won , SEO Dong‐Hwan , YUK Ji‐Eun , PARK Jong‐Bae , HWANG Seock‐Yeon , KOH Sang Kyun , YUN Chi‐Young 
Published: November 2006

AbstractThe effect of Hg treatment on hemolymph and tissue ferritin in the wax moth Galleria mellonella was examined by western blotting. At 48 h after feeding HgCl2, the level of hemolymph ferritin increased approximately 1.8‐fold over that of control insects that were not fed HgCl2, while there was a small increase in tissue ferritin. Time series experiments showed that tissue ferritin had a typically saturated pattern, with a maximum level from 24 to 72 h, although it decreased 12 h following HgCl2 feeding, while hemolymph ferritin first decreased but subsequently increased. Tissue ferritin in the fat body, gut and Malpighian tubules, the main tissues of ferritin expression, was upregulated over time following treatment with Hg, and in particular, tissue ferritin in the gut increased by a large amount at 12–48 h. The results suggest that in G. mellonella, the ferritin‐inducible mechanisms following treatment with HgCl2 are different for hemolymph and tissue ferritin, as are their biochemical properties.
Identification of Non-dot/icmSuppressors of theLegionella pneumophilaΔdotLLethality Phenotype
Authors: Vincent Carr D. , Buscher Benjamin A. , Friedman Jonathan R. , Williams Lee Anne , Bardill Patrick , Vogel Joseph P. 
Published: November 2006

ABSTRACTLegionella pneumophila, a causative agent of bacterial pneumonia, survives inside phagocytic cells by avoiding rapid targeting to the lysosome. This bacterium utilizes a type IVB secretion system, encoded by thedot/icmgenes, to replicate inside host cells. DotL, a critical component of the Dot/Icm secretion apparatus, functions as the type IV coupling protein. In contrast to mostdot/icmgenes, which are dispensable for growth on bacteriological media,dotLis required for the viability of wild-typeL. pneumophila. Previously we reported that ΔdotLlethality could be suppressed by inactivation of the Dot/Icm complex via mutations in otherdot/icmgenes. Here we report the isolation of non-dot/icmsuppressors of this phenotype. These ΔdotLsuppressors include insertions that disrupt the function of theL. pneumophilahomologs ofcpxR,djlA,lysS, and two novel open reading frames, lpg0742 and lpg1594, that we have namedldsAandldsBforlethality of ΔdotL suppressor. In addition to suppressing ΔdotLlethality, inactivation of these genes in a wild-type strain background causes a range of defects inL. pneumophilavirulence traits, including intracellular growth, implicating these factors in the proper function of the Dot/Icm complex. Consistent with previous data showing a role for thecpxsystem in regulating expression of severaldot/icmgenes, thecpxRinsertion mutant produced decreased levels of three Dot/Icm proteins, DotA, IcmV, and IcmW. The remaining four suppressors did not affect the steady-state levels of any Dot/Icm protein and are likely to represent the first identified factors necessary for assembly and/or activation of the Dot/Icm secretion complex.
The
algT
Gene of
Pseudomonas syringae
pv. glycinea andNew Insights into the Transcriptional Organization of the
algT-muc
Gene Cluster
Authors: Schenk Alexander , Berger Michael , Keith Lisa M. , Bender Carol L. , Muskhelishvili Georgi , Ullrich Matthias S. 
Published: November 2006

ABSTRACT

The phytopathogenic bacterium
Pseudomonas syringae
pv. glycinea
infects soybean plants and causes bacterial blight. In addition to
P. syringae
, the human pathogen
Pseudomonas
aeruginosa
and the soil bacterium
Azotobacter vinelandii
produce the exopolysaccharide alginate, a copolymer of
d
-mannuronic and
l
-guluronic acids. Alginate
production in
P. syringae
has been associated with increased
fitness and virulence in planta. Alginate biosynthesis is tightly
controlled by proteins encoded by the
algT-muc
regulatory gene
cluster in
P. aeruginosa
and
A. vinelandii
. These
genes encode the alternative sigma factor AlgT
(σ
22
), its anti-sigma factors MucA and MucB, MucC, a
protein with a controversial function that is absent in
P.
syringae
, and MucD, a periplasmic serine protease and homolog of
HtrA in
Escherichia coli
. We compared an alginate-deficient
algT
mutant of
P. syringae
pv. glycinea with an
alginate-producing derivative in which
algT
is intact. The
alginate-producing derivative grew significantly slower in vitro growth
but showed increased epiphytic fitness and better symptom development
in planta. Evaluation of expression levels for
algT
,
mucA
,
mucB
,
mucD
, and
algD
, which
encodes an alginate biosynthesis gene, showed that
mucD
transcription is not dependent on AlgT in
P. syringae
in
vitro. Promoter mapping using primer extension experiments confirmed
this finding. Results of reverse transcription-PCR demonstrated that
algT
,
mucA
, and
mucB
are cotranscribed as an
operon in
P. syringae
. Northern blot analysis revealed that
mucD
was expressed as a 1.75-kb monocistronic mRNA in
P.
syringae
.
Detection of
Coccidioides
Species in Clinical Specimens by Real-Time PCR
Authors: Binnicker M. J. , Buckwalter S. P. , Eisberner J. J. , Stewart R. A. , McCullough A. E. , Wohlfiel S. L. , Wengenack N. L. 
Published: November 2006

ABSTRACT

Coccidioides
spp. are dimorphic fungal pathogens endemic to the semiarid regions of North, Central, and South America. Currently, direct smear and culture are the most common means of identifying
Coccidioides
spp. While these methods offer relatively sensitive and specific means of detecting
Coccidioides
spp., growth in culture may take up to 3 weeks, potentially delaying the diagnosis and initiation of appropriate antifungal therapy. In addition, growth of the organism represents a significant safety risk to laboratory personnel. The need for a rapid and safe means of diagnosing coccidioidomycosis prompted us to develop a real-time PCR assay to detect
Coccidioides
spp. directly from clinical specimens. Primers and fluorescent resonance energy transfer (FRET) probes were designed to target the internal transcribed spacer 2 region of
Coccidioides
. The assay's limit of detection is below 50 targets per reaction. An analysis of 40
Coccidioides
sp. clinical isolates grown in culture demonstrated 100% sensitivity of the assay. A cross-reactivity panel containing fungi, bacteria, mycobacteria, and viruses was tested and demonstrated 100% specificity for
Coccidioides
spp. An analysis of 266 respiratory specimens by LightCycler PCR demonstrated 100% sensitivity and 98.4% specificity for
Coccidioides
spp. compared with culture. Analysis of 66 fresh tissue specimens yielded 92.9% sensitivity and 98.1% specificity versus those of the culture method. The sensitivity of the assay testing 148 paraffin-embedded tissue samples is 73.4%. A rapid method for the detection of
Coccidioides
spp. directly from clinical material will greatly assist in the timely diagnosis and treatment of patients, while at the same time decreasing the risk of accidental exposure to laboratory personnel.
CTX-M β-Lactamase-Producing
Escherichia coli
in French Hospitals: Prevalence, Molecular Epidemiology, and Risk Factors
Authors: Lavigne Jean-Philippe , Marchandin Hélène , Delmas Julien , Moreau Jérôme , Bouziges Nicole , Lecaillon Evelyne , Cavalie Laurent , Jean-Pierre Hélène , Bonnet Richard , Sotto Albert 
Published: November 2006

ABSTRACT

In 2004, 65 CTX-M-producing
Escherichia coli
isolates were collected from infected patients in four French hospitals. The
bla
CTX-M-15
genes were predominant. Pulsed-field gel electrophoresis highlighted a clonal propagation of CTX-M-15-producing strains belonging to phylogenetic group B2, notably in the community. The main risk factors for acquiring these isolates were urinary tract infections or the presence of a urinary catheter in diabetic or renal failure patients.
N-Linked Glycosylation Status of Classical Swine Fever Virus Strain Brescia E2 Glycoprotein Influences Virulence in Swine
Authors: Risatti G. R. , Holinka L. G. , Fernandez Sainz I. , Carrillo C. , Lu Z. , Borca M. V. 
Published: November 2006

ABSTRACT
E2 is one of the three envelope glycoproteins of classical swine fever virus (CSFV). Previous studies indicate that E2 is involved in several functions, including virus attachment and entry to target cells, production of antibodies, induction of protective immune response in swine, and virulence. Here, we have investigated the role of E2 glycosylation of the highly virulent CSFV strain Brescia in infection of the natural host. Seven putative glycosylation sites in E2 were modified by site-directed mutagenesis of a CSFV Brescia infectious clone (BICv). A panel of virus mutants was obtained and used to investigate whether the removal of putative glycosylation sites in the E2 glycoprotein would affect viral virulence/pathogenesis in swine. We observed that rescue of viable virus was completely impaired by removal of all putative glycosylation sites in E2 but restored when mutation N185A reverted to wild-type asparagine produced viable virus that was attenuated in swine. Single mutations of each of the E2 glycosylation sites showed that amino acid N116 (N1v virus) was responsible for BICv attenuation. N1v efficiently protected swine from challenge with virulent BICv at 3 and 28 days postinfection, suggesting that glycosylation of E2 could be modified for development of classical swine fever live attenuated vaccines.
Failure To Open the Blood-Brain Barrier and Deliver Immune Effectors to Central Nervous System Tissues Leads to the Lethal Outcome of Silver-Haired Bat Rabies Virus Infection
Authors: Roy Anirban , Phares Timothy W. , Koprowski Hilary , Hooper D. Craig 
Published: November 2006

ABSTRACT
Rabies is a lethal disease caused by neurotropic viruses that are endemic in nature. When exposure to a potentially rabid animal is recognized, prompt administration of virus-neutralizing antibodies, together with active immunization, can prevent development of the disease. However, once the nonspecific clinical symptoms of rabies appear conventional postexposure treatment is unsuccessful. Over the last decade, rabies viruses associated with the silver-haired bat (SHBRV) have emerged as the leading cause of human deaths from rabies in the United States and Canada as a consequence of the fact that exposure to these viruses is often unnoticed. The need to treat SHBRV infection following the development of clinical rabies has lead us to investigate why the immune response to SHBRV fails to protect at a certain stage of infection. We have established that measurements of innate and adaptive immunity are indistinguishable between mice infected with the highly lethal SHBRV and mice infected with an attenuated laboratory rabies virus strain. While a fully functional immune response to SHBRV develops in the periphery of infected animals, the invasion of central nervous system (CNS) tissues by immune cells is reduced and, consequently, the virus is not cleared. Our data indicate that the specific deficit in the SHBRV-infected animal is an inability to enhance blood-brain barrier permeability in the cerebellum and deliver immune effectors to the CNS tissues. Conceivably, at the stage of infection where immune access to the infected CNS tissues is limited, either the provision or the development of antiviral immunity will be ineffective.
Resistance training reduces whole-body protein turnover and improves net protein retention in untrained young males
Authors: Hartman Joseph W. , Moore Daniel R. , Phillips Stuart M. 
Published: November 2006

It is thought that resistance exercise results in an increased need for dietary protein; however, data also exists to support the opposite conclusion. The purpose of this study was to determine the impact of resistance exercise training on protein metabolism in novices with the hypothesis that resistance training would reduce protein turnover and improve whole-body protein retention. Healthy males (n = 8, 22 ± 1 y, BMI = 25.3 ± 1.8 kg·m–2) participated in a progressive whole-body split routine resistance-training program 5d/week for 12 weeks. Before (PRE) and after (POST) the training, oral [15N]-glycine ingestion was used to assess nitrogen flux (Q), protein synthesis (PS), protein breakdown (PB), and net protein balance (NPB = PS – PB). Macronutrient intake was controlled over a 5d period PRE and POST, while estimates of protein turnover and urinary nitrogen balance (Nbal = Nin – urine Nout) were conducted. Bench press and leg press increased 40% and 50%, respectively (p < 0.01). Fat- and bone-free mass (i.e., lean muscle mass) increased from PRE to POST (2.5 ± 0.8 kg, p < 0.05). Significant PRE to POST decreases (p <0.05) occurred in Q (0.9 ± 0.1 vs. 0.6 ± 0.1 g N·kg–1·d–1), PS (4.6 ± 0.7 vs. 2.9 ± 0.3 g·kg–1·d–1), and PB (4.3 ± 0.7 vs. 2.4 ± 0.2 g·kg–1·d–1). Significant training-induced increases in both NPB (PRE = 0.22 ± 0.13 g·kg–1·d–1; POST = 0.54 ± 0.08 g·kg–1·d–1) and urinary nitrogen balance (PRE = 2.8 ± 1.7 g N·d–1; POST = 6.5 ± 0.9 g N·d–1) were observed. A program of resistance training that induced significant muscle hypertrophy resulted in reductions of both whole-body PS and PB, but an improved NPB, which favoured the accretion of skeletal muscle protein. Urinary nitrogen balance increased after training. The reduction in PS and PB and a higher NPB in combination with an increased nitrogen balance after training suggest that dietary requirements for protein in novice resistance-trained athletes are not higher, but lower, after resistance training.
A Sequential Blockade Strategy for the Design of Combination Therapies to Overcome Oncogene Addiction in Chronic Myelogenous Leukemia
Authors: Chen Rong , Gandhi Varsha , Plunkett William 
Published: November 2006

Abstract
Some tumors are dependent on the continued activity of a single oncogene for maintenance of their malignant phenotype. The best-studied example is the Bcr-Abl fusion protein in chronic myelogenous leukemia (CML). Although the clinical success of the Abl kinase inhibitor imatinib against chronic-phase CML emphasizes the importance of developing therapeutic strategies aimed at this target, resistance to imatinib poses a major problem for the ultimate success of CML therapy by this agent. We hypothesized a sequential blockade strategy that is designed to decrease the expression of the Bcr-Abl protein, with the goal of complementing the action of imatinib on kinase activity. In this study, flavopiridol, an inhibitor of transcription, homoharringtonine (HHT), a protein synthesis inhibitor, and imatinib were used singly and in combination against the Bcr-Abl-positive human CML cell line K562. Flavopiridol alone inhibited phosphorylation of the RNA polymerase II COOH-terminal domain, specifically reduced RNA polymerase II–directed mRNA synthesis, and decreased the Bcr-Abl transcript levels. HHT inhibited protein synthesis and reduced the Bcr-Abl protein level. Imatinib directly inhibited the kinase activity of Bcr-Abl. The combinations of flavopiridol and HHT and flavopiridol and imatinib synergistically decreased clonogenicity as evaluated by the median-effect method. Greater synergy was observed when HHT and imatinib were given sequentially compared with simultaneous administration. Imatinib-resistant Ba/F3 cells that were transfected to express the E255K and T315I mutations of Bcr-Abl were not cross-resistant to flavopiridol and HHT. These results provided a rationale for the combination of inhibitors of transcription and/or translation with specific kinase inhibitors. (Cancer Res 2006; 66(22): 10959-66)
Epigenetic Regulation of Tumor Endothelial Cell Anergy: Silencing of Intercellular Adhesion Molecule-1 by Histone Modifications
Authors: Hellebrekers Debby M.E.I. , Castermans Karolien , Viré Emmanuelle , Dings Ruud P.M. , Hoebers Nicole T.H. , Mayo Kevin H. , oude Egbrink Mirjam G.A. , Molema Grietje , Fuks François , van Engeland Manon , Griffioen Arjan W. 
Published: November 2006

Abstract
Tumors can escape from immunity by repressing leukocyte adhesion molecule expression on tumor endothelial cells and by rendering endothelial cells unresponsive to inflammatory activation. This endothelial cell anergy is induced by angiogenic growth factors and results in reduced leukocyte-vessel wall interactions, thereby attenuating infiltration of leukocytes into the tumor. This report describes a novel mechanism of endothelial cell anergy regulation. We recently reported that DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors have angiostatic activity. Here, we studied whether epigenetic mechanisms regulate this angiogenesis-mediated escape from immunity. We found that DNMT inhibitors 5-aza-2′-deoxycytidine and zebularine, as well as HDAC inhibitor trichostatin A, reexpressed intercellular adhesion molecule-1 (ICAM-1) on tumor-conditioned endothelial cells in vitro, resulting in restored leukocyte-endothelial cell adhesion. In addition, treatment with DNMT or HDAC inhibitors in vivo also restored ICAM-1 expression on tumor endothelial cells from two different mouse tumor models. Furthermore, leukocyte-vessel wall interactions in mouse tumors were increased by these compounds, as measured by intravital microscopy, resulting in enhanced leukocyte infiltration. We show that ICAM-1 down-regulation in tumor endothelial cells is associated with ICAM-1 promoter histone H3 deacetylation and loss of histone H3 Lys4 methylation but not with DNA hypermethylation. In conclusion, our data show that ICAM-1 is epigenetically silenced in tumor endothelial cells by promoter histone modifications, which can be overcome by DNMT and HDAC inhibitors, suggesting a new molecular mechanism based on which novel therapeutic approaches for cancer can be pursued. (Cancer Res 2006; 66(22): 10770-7)
Oncostatin M (OSM) Cytostasis of Breast Tumor Cells: Characterization of an OSM Receptor β–Specific Kernel
Authors: Underhill-Day Nicholas , Heath John K. 
Published: November 2006

AbstractThe interleukin-6 cytokine oncostatin M (OSM) induces potent growth-inhibitory and morphogenic responses in several different tumor cell types, highlighting the importance of OSM signaling mechanisms as targets for therapeutic intervention. The specific molecular pathways involved are not well understood, as OSM can signal through two separate heterodimeric receptor complexes, glycoprotein 130 (gp130)/leukemia inhibitory factor receptor (LIFR) α and gp130/OSM receptor β (OSMRβ). In this investigation, we used a LIFR antagonist to help resolve signaling responses and identify patterns of gene expression elicited by the different receptor complexes. OSM-induced biological effects on breast tumor–derived cell lines were specifically mediated through the gp130/OSMRβ complex. Each cytokine tested exhibited differential signaling capability and manifested both shared and unique patterns of gene activation, emphasizing compositional differences in activator protein-1 transcription factor activity and expression. In particular, OSM strongly activated the c-Jun NH2-terminal kinase (JNK) serine/threonine kinase and downstream components, including activating transcription factor (ATF)/cyclic AMP-responsive element binding protein family member, ATF3. JNK/stress-activated protein kinase kinase inhibition abrogated cell morphogenesis induced by OSM, indicating an important role for this pathway in OSM specificity. These findings identify a core signaling/transcriptional mechanism specific to the OSMRβ in breast tumor cells. (Cancer Res 2006; 66(22): 10891-901)