bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of Antibiotic Exposure Patterns on Selection of Community-Associated Methicillin-Resistant Staphylococcus aureus in Hospital Settings
Authors: Kardaś-Słoma Lidia , Boëlle Pierre Yves , Opatowski Lulla , Brun-Buisson Christian , Guillemot Didier , Temime Laura 
Published: July 2011

ABSTRACT

Community-associated methicillin-resistant
S. aureus
(CA-MRSA) is increasingly common in hospitals, with potentially serious consequences. The aim of this study was to assess the impact of antibiotic prescription patterns on the selection of CA-MRSA within hospitals, in a context of competition with other circulating staphylococcal strains, including methicillin-sensitive (MSSA) and hospital-associated methicillin-resistant (HA-MRSA) strains. We developed a computerized agent-based model of
S. aureus
transmission in a hospital ward in which CA-MRSA, MSSA, and HA-MRSA strains may cocirculate. We investigated a wide range of antibiotic prescription patterns in both intensive care units (ICUs) and general wards, and we studied how differences in antibiotic exposure may explain observed variations in the success of CA-MRSA invasion in the hospitals of several European countries and of the United States. Model predictions underlined the influence of antibiotic prescription patterns on CA-MRSA spread in hospitals, especially in the ICU, where the endemic prevalence of CA-MRSA carriage can range from 3% to 20%, depending on the simulated prescription pattern. Large antibiotic exposure with drugs effective against MSSA but not MRSA was found to promote invasion by CA-MRSA. We also found that, should CA-MRSA acquire fluoroquinolone resistance, a major increase in CA-MRSA prevalence could ensue in hospitals worldwide. Controlling the spread of highly community-prevalent CA-MRSA within hospitals is a challenge. This study demonstrates that antibiotic exposure strategies could participate in this control. This is all the more important in wards such as ICUs, which may play the role of incubators, promoting CA-MRSA selection in hospitals.
Functional and Phenotypic Characteristics of Alternative Activation Induced in Human Monocytes by Interleukin-4 or the Parasitic Nematode Brugia malayi
Authors: Semnani Roshanak Tolouei , Mahapatra Lily , Moore Vanessa , Sanprasert Vivornpun , Nutman Thomas B. 
Published: July 2011

ABSTRACTHuman monocytes from patients with patent filarial infections are studded with filarial antigen and express markers associated with alternative activation of macrophages (MΦ). To explore the role of filaria-derived parasite antigen in differentiation of human monocytes, cells were exposed to microfilariae (mf) ofBrugia malayi, and their phenotypic and functional characteristics were compared with those of monocytes exposed to factors known to generate either alternatively (interleukin-4 [IL-4]) or classically (macrophage colony-stimulating factor [MCSF]) activated MΦ. IL-4 upregulated mRNA expression of CCL13, CCL15, CCL17, CCL18, CCL22, CLEC10A, MRC1, CADH1, CD274, and CD273 associated with alternative activation of MΦ but not arginase 1. IL-4-cultured monocytes had a diminished ability to promote proliferation of both CD4+and CD8+T cells compared to that of unexposed monocytes. Similar to results with IL-4, exposure of monocytes to live mf induced upregulation of CCL15, CCL17, CCL18, CCL22, CD274, and CD273 and downregulation of Toll-like receptor 3 (TLR3), TLR5, and TLR7. In contrast to results with MCSF-cultured monocytes, exposure of monocytes to mf resulted in significant inhibition of the phagocytic ability of these cells to the same degree as that seen with IL-4. Our data suggest that short exposure of human monocytes to IL-4 induces a phenotypic characteristic of alternative activation and that secreted filarial products skew monocytes similarly.
Coinfection with Enterohepatic Helicobacter Species Can Ameliorate or Promote Helicobacter pylori-Induced Gastric Pathology in C57BL/6 Mice
Authors: Ge Zhongming , Feng Yan , Muthupalani Sureshkumar , Eurell Laura Lemke , Taylor Nancy S. , Whary Mark T. , Fox James G. 
Published: July 2011

ABSTRACT

To investigate how different enterohepatic
Helicobacter
species (EHS) influence
Helicobacter pylori
gastric pathology, C57BL/6 mice were infected with
Helicobacter hepaticus
or
Helicobacter muridarum
, followed by
H. pylori
infection 2 weeks later. Compared to
H. pylori
-infected mice, mice infected with
H. muridarum
and
H. pylori
(HmHp mice) developed significantly lower histopathologic activity index (HAI) scores (
P
< 0.0001) at 6 and 11 months postinoculation (MPI). However, mice infected with
H. hepaticus
and
H. pylori
(HhHp mice) developed more severe gastric pathology at 6 MPI (
P
= 0.01), with a HAI at 11 MPI (
P
= 0.8) similar to that of
H. pylori
-infected mice.
H. muridarum
-mediated attenuation of gastritis in coinfected mice was associated with significant downregulation of proinflammatory Th1 (interlukin-1beta [
Il-1β
], gamma interferon [
Ifn-γ
], and tumor necrosis factor-alpha [
Tnf-α
]) cytokines at both time points and Th17 (
Il-17A
) cytokine mRNA levels at 6 MPI in murine stomachs compared to those of
H. pylori
-infected mice (
P
< 0.01). Coinfection with
H. hepaticus
also suppressed
H. pylori
-induced elevation of gastric Th1 cytokines
Ifn-γ
and
Tnf-α
(
P
< 0.0001) but increased Th17 cytokine mRNA levels (
P
= 0.028) at 6 MPI. Furthermore, mRNA levels of
Il-17A
were positively correlated with the severity of helicobacter-induced gastric pathology (HhHp>
H. pylori
>HmHp) (at 6 MPI,

r
2

= 0.92,
P
< 0.0001; at 11 MPI,

r
2

= 0.82,
P
< 0.002). Despite disparate effects on gastritis, colonization levels of gastric
H. pylori
were increased in HhHp mice (at 6 MPI) and HmHp mice (at both time points) compared to those in mono-
H. pylori
-infected mice. These data suggest that despite consistent downregulation of Th1 responses, EHS coinfection either attenuated or promoted the severity of
H. pylori
-induced gastric pathology in C57BL/6 mice. This modulation was related to the variable effects of EHS on gastric interleukin 17 (IL-17) responses to
H. pylori
infection.
Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells
Authors: Weinkauf Craig , Salvador Ryan , PereiraPerrin Mercio 
Published: July 2011

ABSTRACT

Trypanosoma cruzi
, the agent of Chagas' disease, infects a variety of mammalian cells in a process that includes multiple cycles of intracellular division and differentiation starting with host receptor recognition by a parasite ligand(s). Earlier work in our laboratory showed that the neurotrophin-3 (NT-3) receptor TrkC is activated by
T. cruzi
surface
trans
-sialidase, also known as parasite-derived neurotrophic factor (PDNF). However, it has remained unclear whether TrkC is used by
T. cruzi
to enter host cells. Here, we show that a neuronal cell line (PC12-NNR5) relatively resistant to
T. cruzi
became highly susceptible to infection when overexpressing human TrkC but not human TrkB. Furthermore,
trkC
transfection conferred an ∼3.0-fold intracellular growth advantage. Sialylation-deficient Chinese hamster ovarian (CHO) epithelial cell lines Lec1 and Lec2 also became much more permissive to
T. cruzi
after transfection with the
trkC
gene. Additionally, NT-3 specifically blocked
T. cruzi
infection of the TrkC-NNR5 transfectants and of naturally permissive TrkC-bearing Schwann cells and astrocytes, as did recombinant PDNF. Two specific inhibitors of Trk autophosphorylation (K252a and AG879) and inhibitors of Trk-induced MAPK/Erk (U0126) and Akt kinase (LY294002) signaling, but not an inhibitor of insulin-like growth factor 1 receptor, abrogated TrkC-mediated cell invasion. Antibody to TrkC blocked
T. cruzi
infection of the TrkC-NNR5 transfectants and of cells that naturally express TrkC. The TrkC antibody also significantly and specifically reduced cutaneous infection in a mouse model of acute Chagas' disease. TrkC is ubiquitously expressed in the peripheral and central nervous systems, and in nonneural cells infected by
T. cruzi
, including cardiac and gastrointestinal muscle cells. Thus, TrkC is implicated as a functional PDNF receptor in cell entry, independently of sialic acid recognition, mediating broad
T. cruzi
infection both
in vitro
and
in vivo
.
Changes in specific leaf area and photosynthetic nitrogen-use efficiency associated with physiological acclimation of two hybrid poplar clones to intraclonal competition
Authors: Benomar Lahcen , DesRochers Annie , Larocque Guy R. 
Published: July 2011

Photosynthesis is the most important process driving productivity, and its acclimation to intraclonal competition is not well understood in hybrid poplars. The aim of this study was to examine the physiological response of the crown of two hybrid poplar clones, BT747215 ( Populus balsamifera L. × Populus trichocarpa Torr. & A. Gray) and MB915319 ( Populus maximowiczii A. Henry × P. balsamifera ), to intraclonal competition. We measured light-saturated photosynthesis (Amax), leaf N content on an area basis (Narea), specific leaf area (SLA), and photosynthetic N-use efficiency (PNUE) for three successive growing seasons on trees planted at three spacings (1 m × 1 m, 3 m × 3 m, and 5 m × 5 m). Crowns were sampled at 10 locations corresponding to vertical and horizontal subdivisions. Significant changes took place at the crown level in the closest spacing (1 m × 1 m) compared with the wider spacings (3 m × 3 m and 5 m × 5 m): (i) 30% decrease in Narea, (ii) 20% increase in SLA, and (iii) 40% increase in PNUE. The slope of the Amax–Narea curve was greatest in the closest spacing, indicating a greater change in Amax per unit change in Narea. The two hybrid poplar clones had a similar morphophysiological response to changes of spacing. Both clones showed physiological acclimation of their foliage in response to intraclonal competition through modulation of SLA and PNUE.
Comprehensive Genome Methylation Analysis in Bladder Cancer: Identification and Validation of Novel Methylated Genes and Application of These as Urinary Tumor Markers
Authors: Reinert Thomas , Modin Charlotte , Castano Francisco M. , Lamy Philippe , Wojdacz Tomasz K. , Hansen Lise Lotte , Wiuf Carsten , Borre Michael , Dyrskjøt Lars , Ørntoft Torben F. 
Published: July 2011

Abstract
Purpose: Epigenetic alterations are common and can now be addressed in a parallel fashion. We investigated the methylation in bladder cancer with respect to location in genome, consistency, variation in metachronous tumors, impact on transcripts, chromosomal location, and usefulness as urinary markers.
Experimental Design: A microarray assay was utilized to analyze methylation in 56 samples. Independent validation was conducted in 63 samples by a PCR-based method and bisulfite sequencing. The methylation levels in 174 urine specimens were quantified. Transcript levels were analyzed using expression microarrays and pathways were analyzed using dedicated software.
Results: Global methylation patterns were established within and outside CpG islands. We validated methylation of the eight tumor markers genes ZNF154 (P &lt; 0.0001), HOXA9 (P &lt; 0.0001), POU4F2 (P &lt; 0.0001), EOMES (P = 0.0005), ACOT11 (P = 0.0001), PCDHGA12 (P = 0.0001), CA3 (P = 0.0002), and PTGDR (P = 0.0110), the candidate marker of disease progression TBX4 (P &lt; 0.04), and other genes with stage-specific methylation. The methylation of metachronous tumors was stable and targeted to certain pathways. The correlation to expression was not stringent. Chromosome 21 showed most differential methylation (P &lt; 0.0001) and specifically hypomethylation of keratins, which together with keratin-like proteins were epigenetically regulated. In DNA from voided urine, we detected differential methylation of ZNF154 (P &lt; 0.0001), POU4F2 (P &lt; 0.0001), HOXA9 (P &lt; 0.0001), and EOMES (P &lt; 0.0001), achieving 84% sensitivity and 96% specificity.
Conclusions: We initiated a detailed mapping of the methylome in metachronous bladder cancer. Novel genes with tumor, chromosome, as well as pathway-specific differential methylation in bladder cancer were identified. The methylated genes were promising cancer markers for early detection of bladder cancer. Clin Cancer Res; 17(17); 5582–92. ©2011 AACR.
Mobile Thrombus on Device Leads in Patients Undergoing Ablation
Authors: Supple Gregory E. , Ren Jian-Fang , Zado Erica S. , Marchlinski Francis E. 
Published: July 2011

Background—
Mobile thrombi, not routinely recognized on transthoracic echocardiography, are frequently identified on cardiovascular implantable electronic device leads with intracardiac echocardiography (ICE) during ablation procedures. Their incidence, characteristics, and consequences have not yet been defined.

Methods and Results—

We used ICE to examine leads for thrombi and to measure the pulmonary artery systolic pressure in patients with a cardiovascular implantable electronic device presenting for ablation. Patient clinical characteristics, device type, and lead characteristics were correlated with presence of thrombi. Most patients had congestive heart failure (84%), with an average left ventricular ejection fraction of 40%. Thrombi were seen with ICE in 26 of 86 patients (30%) but were seen on transthoracic echocardiography in only 1 of the 26 patients. Thrombi on ICE were mobile, averaged 18±5.9 mm long by 4.4±2.3 mm wide, and were more commonly identified in the right atrium (n=25) than in the right ventricle (n=5). Thrombi were associated with higher pulmonary artery systolic pressure: 39±9 mm Hg with thrombi versus 33±7 mm Hg without thrombi (odds ratio, 1.11; 95% confidence interval, 1.03 to 1.20;
P
=0.01). No other characteristic assessed was associated with a significant difference in the presence of lead thrombi.

Conclusions—
Mobile thrombi on cardiovascular implantable electronic device leads are present in 30% of patients undergoing ablation and are readily identified with ICE despite being underrecognized with transthoracic echocardiography. Further study is warranted to determine whether lead thrombi are a clinically relevant source of pulmonary emboli in some patients with cardiovascular implantable electronic devices.
Innate signals overcome acquired TCR signaling pathway regulation and govern the fate of human CD161hi CD8α+ semi-invariant T cells
Authors: Turtle Cameron J. , Delrow Jeff , Joslyn Rochelle C. , Swanson Hillary M. , Basom Ryan , Tabellini Laura , Delaney Colleen , Heimfeld Shelly , Hansen John A. , Riddell Stanley R. 
Published: July 2011

Abstract
Type 17 programmed CD161hiCD8α+ T cells contribute to mucosal immunity to bacteria and yeast. In early life, microbial colonization induces proliferation of CD161hi cells that is dependent on their expression of a semi-invariant Vα7.2+ TCR. Although prevalent in adults, CD161hiCD8α+ cells exhibit weak proliferative and cytokine responses to TCR ligation. The mechanisms responsible for the dichotomous response of neonatal and adult CD161hi cells, and the signals that enable their effector function, have not been established. We describe acquired regulation of TCR signaling in adult memory CD161hiCD8α+ T cells that is absent in cord CD161hi cells and adult CD161lo cells. Regulated TCR signaling in CD161hi cells was due to profound alterations in TCR signaling pathway gene expression and could be overcome by costimulation through CD28 or innate cytokine receptors, which dictated the fate of their progeny. Costimulation with IL-1β during TCR ligation markedly increased proinflammatory IL-17 production, while IL-12–induced Tc1-like function and restored the response to TCR ligation without costimulation. CD161hi cells from umbilical cord blood and granulocyte colony stimulating factor-mobilized leukaphereses differed in frequency and function, suggesting future evaluation of the contribution of CD161hi cells in hematopoietic stem cell grafts to transplant outcomes is warranted.
Polydatin up-regulates clara cell secretory protein to suppress phospholipase A2 of lung induced by LPS in vivo and in vitro
Authors: Shiyu Shu , Zhiyu Ling , Mao Ye , Lin Bo , Lijia Wang , Tianbao Zhang , Jie Chen , Tingyu Li 
Published: July 2011

Abstract

Background
Lung injury induced by lipopolysaccharide (LPS) remains one of the leading causes of morbidity and mortality in children. The damage to membrane phospholipids leads to the collapse of the bronchial alveolar epithelial barrier during acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Phospholipase A2 (PLA2), a key enzyme in the hydrolysis of membrane phospholipids, plays an important traumatic role in pulmonary inflammation, and Clara cell secretory protein (CCSP) is an endogenous inhibitor of PLA2. Our previous study showed that polydatin (PD), a monocrystalline extracted from a traditional Chinese medicinal herb (Polygonum cuspidatum Sieb, et Zucc), reduced PLA2 activity and sPLA2-IIA mRNA expression and mitigated LPS-induced lung injury. However, the potential mechanism for these effects has not been well defined. We have continued to investigate the effect of PD on LPS-induced expression of CCSP mRNA and protein in vivo and in vitro.

Results
Our results suggested that the CCSP mRNA level was consistent with its protein expression. CCSP expression was decreased in lung after LPS challenge. In contrast, PD markedly increased CCSP expression in a concentration-dependent manner. In particular, CCSP expression in PD-pretreated rat lung was higher than in rats receiving only PD treatment.

Conclusion
These results indicated that up-regulation of CCSP expression causing inhibition of PLA2 activation may be one of the crucial protective mechanisms of PD in LPS-induced lung injury.
Cognitive behaviour therapy in medication-treated adults with ADHD and persistent Symptoms: A randomized controlled trial
Authors: Emilsson Brynjar , Gudjonsson Gisli , Sigurdsson Jon F , Baldursson Gisli , Einarsson Emil , Olafsdottir Halldora , Young Susan 
Published: July 2011

Abstract

Background
Attention deficit hyperactivity disorder (ADHD) in adulthood is not fully treated by psychopharmacological treatment alone. The main aim of the current study was to evaluate a newly developed cognitive behaviour therapy (CBT) based group programme, the Reasoning and Rehabilitation for ADHD Youths and Adults (R&R2ADHD), using a randomized controlled trial.

Methods
54 adults with ADHD already receiving psychopharmacological treatment were randomly allocated to an experimental (CBT/MED) treatment condition (n = 27) and a 'treatment as usual' (TAU/MED) control condition (n = 27) that did not receive the CBT intervention. The outcome measures were obtained before treatment (baseline), after treatment and at three month follow-up and included ADHD symptoms and impairments rated by independent assessors, self-reported current ADHD symptoms, and comorbid problems.

Results
The findings suggested medium to large treatment effects for ADHD symptoms, which increased further at three month follow-up. Additionally, comorbid problems also improved at follow-up with large effect sizes.

Conclusions
The findings give support for the effectiveness of R&R2ADHD in reducing ADHD symptoms and comorbid problems, an improving functions associated with impairment. The implications are that the benefits of R&R2ADHD are multifaceted and that combined psychopharmacological and CBT based treatments may add to and improve pharmacological interventions.

Trial registration

ACTRN12611000533998 (http://www.ANZCTR.org.au/ACTRN12611000533998.aspx)
Evaluating target silencing by short hairpin RNA mediated by the group I intron in cultured mammalian cells
Authors: Noguchi Kousei , Ishitu Yoshio , Takaku Hiroshi 
Published: July 2011

Abstract

Background
The group I intron, a ribozyme that catalyzes its own splicing reactions in the absence of proteins in vitro, is a potential target for rational engineering and attracted our interest due to its potential utility in gene repair using trans-splicing. However, the ribozyme activity of a group I intron appears to be facilitated by RNA chaperones in vivo; therefore, the efficiency of self-splicing could be dependent on the structure around the insert site or the length of the sequence to be inserted. To better understand how ribozyme activity could be modulated in cultured mammalian cells, a group I intron was inserted into a short hairpin RNA (shRNA), and silencing of a reporter gene by the shRNA was estimated to reflect self-splicing activity in vivo. In addition, we appended a theophylline-binding aptamer to the ribozyme to investigate any potential effects caused by a trans-effector.

Results
shRNA-expression vectors in which the loop region of the shRNA was interrupted by an intron were constructed to target firefly luciferase mRNA. There was no remarkable toxicity of the shRNA-expression vectors in Cos cells, and the decrease in luciferase activity was measured as an index of the ribozyme splicing activity. In contrast, the expression of the shRNA through intron splicing was completely abolished in 293T cells, although the silencing induced by the shRNA-expressing vector alone was no different from that in the Cos cells. The splicing efficiency of the aptamer-appended intron also had implications for the potential of trans-factors to differentially promote self-splicing among cultured mammalian cells.

Conclusions
Silencing by shRNAs interrupted by a group I intron could be used to monitor self-splicing activity in cultured mammalian cells, and the efficiency of self-splicing appears to be affected by cell-type specific factors, demonstrating the potential effectiveness of a trans-effector.