bluuebunny/crossref_metadata_2025_split huggingface dataset:
Routine use of a rapid test to detect bacteria at the time of issue for nonleukoreduced, whole blood–derived platelets
Authors: Harm Sarah K. , Delaney Meghan , Charapata Michael , AuBuchon James P. , Triulzi Darrell J. , Yazer Mark H. 
Published: July 2012

BACKGROUND: The Pan Genera detection (PGD) test is used to screen platelet (PLT) products for bacterial contamination. We report the experience of using the PGD test on whole blood–derived PLTs (WBPs) at two large centralized transfusion services (CTS).STUDY DESIGN AND METHODS: Records of PGD test results were retrospectively reviewed. The PGD test was performed on individual WBP units or pools of WBPs ranging in size from 2 to 6 units at the time of issue. Bacterial culture was performed on PLT products with positive PGD tests, and at one CTS, the available cocomponents.RESULTS: A total of 70,561 WBP pools were screened with the PGD test. There were seven true‐positive PGD tests and 242 false‐positive tests (positive predictive value of PGD test, 2.81%). The overall contamination rate was 99 per 106 WBP pools (1:10,080; 95% confidence interval [CI], 40‐204), and the false‐positive rate was 3430 per 106 WBP pools (1:292; 95% CI, 3011‐3890). All seven bacterial isolates were Gram positive. The median age of the individual WBP units in the seven contaminated pools was 5 days (range, 3‐5 days) compared to 4 days (range, 1‐5 days) in the false‐positive pools (p = 0.0012). The same bacteria isolated from a positive PLT pool also grew in one red blood cell cocomponent.CONCLUSION: After testing more than 70,000 WBP pools at two large CTSs, the rate of contaminated WBP pools detected by the PGD test was 99 per 106 pools (1:10,080).
Synthesis and Luminescence Properties of Mg–Si Co‐doped Tb3Al5O12:Ce3+ Phosphors with Blue Excitation for White LEDs
Authors: Luo Hongde , Liu Jie , Zheng Xiao , Xu Bo , Lu Yiming , Han Lixian , Ren Kuaixia , Yu Xibin 
Published: July 2012

Tb2.94MgxAl5−2xSixO12:Ce3+0.06 (TMASG: Ce) were synthesized by high temperature Solid‐State Reaction (SSR) at different temperatures from 1650°C to 1550°C. Samples with x = 0.1, 0.2, 0.3, 0.6 were fabricated and characterized using powder X‐ray diffraction (XRD) and room‐temperature photoluminescence spectroscopy. In this work, the excitation and emission spectra indicate that the phosphor can be excited effectively by the blue light (450–550 nm) and exhibit a satisfactory orange–yellow emission from 550 to 575 nm. The reasons of the red‐shift of the phosphor have been discussed. A crystal field analysis of the Ce3+ 5d energy levels is conducted to explain the correlation between the TMASG:Ce lattice expansion and the Ce3+ energy level changes. The chromaticity coordinates of the phosphors are tuned from (0.465, 0.527) to (0.512, 0.483). This indicates a prospective for application of this novel phosphor in white light emitting diodes (LEDs).
Critical size defect regeneration using PEG‐mediated BMP‐2 gene delivery and the use of cell occlusive barrier membranes – the osteopromotive principle revisited
Authors: Wehrhan Falk , Amann Kerstin , Molenberg Aart , Lutz Rainer , Neukam Friedrich W. , Schlegel Karl A. 
Published: July 2012

AbstractObjectiveThe objective of this study was to investigate if osseous regeneration can be accelerated by involvement of periosteal tissue. Bone defect regeneration could be accelerated by the involvement of periosteal tissue if osteogenic cell signalling is maintained within the defect. It was questioned if local cell‐mediated BMP‐2 gene delivery makes a cell occlusive membrane dispensable during bone critical size defect regeneration.MethodsPEG matrix (degradation time 10 days) and PEG membrane (degradation time 120 days) were used in the pig calvarial model. Cylindrical (1 × 1 cm) critical size defects (CSD) (9 per animal; 20 animals) were filled with: (i) particulated autologous bone, covered with PEG membrane (group 1); (ii) HA/TCP, covered with PEG membrane (group 2); (iii) HA/TCP, mixed with PEG matrix (group 3); and (iv) HA/TCP mixed with BMP‐2‐transfected osteoblasts and PEG matrix (group 4). BMP‐2/4 gene transfer: liposomal in vitro transfection of BMP‐2/V5‐tag fusion‐protein. Quantitative histomorphometry (toluidine blue staining) after 2, 4 and 12 weeks assessed bone formation. Semiquantitative immunohistochemistry estimated the expression of BMP‐2, V5‐tag, Runx‐2 and Sox9.ResultsPEG matrix embedded BMP‐2 expressing cells presented higher bone formation (P < 0.05) than HA/TCP + PEG matrix defect filling or PEG membrane covering (HA/TCP filling) after 12 weeks. Highest expression of BMP‐2, Runx‐2 and lowest expression of fibrous tissue marker Sox9 was seen in the BMP‐2 group.ConclusionPEG matrix embedded BMP‐2 expressing cells are capable to maintain osteogenic signalling and to accelerate osseous defect regeneration in absence of a cell occlusive membrane.
The impact of hospitalization on dental plaque accumulation: an observational study
Authors: Needleman Ian , Hyun‐Ryu Jung , Brealey David , Sachdev Mishal , Moskal‐Fitzpatrick Donna , Bercades Georgia , Nagle Janette , Lewis Katherine , Agudo Elisa , Petrie Aviva , Suvan Jean , Donos Nikos , Singer Mervyn 
Published: July 2012

AbstractAimTo investigate the effect of hospitalization on oral health as assessed by dental plaque.Materials and MethodsObservational study in a critical care unit (CCU). Participants were recruited within 24 h of admission. Dental plaque amount was assessed at baseline, 1 and 2 weeks using the Debris index‐soft deposits (Greene & Vermillion 1960).ResultsFifty participants were recruited with 36 available for outcome assessment at 1 week and 10 at 2 weeks. The principal reason for losses was early discharge with no evidence of a difference between patients present only at baseline and those present at 1 week. The median value for dental plaque at baseline was 4 (95% CI: 4, 6). The median dental plaque increase from baseline to week 1 was 1.5 (95% CI: −1, 4), and this was statistically significant (p = 0.04). The median increase from week 1 to week 2 was 1.0 (95% CI −8, 6) and not statistically significant (p = 0.68).ConclusionsOral health as assessed by dental plaque deteriorates following hospitalization in CCU. Such change could lead to impairment of quality of life and well‐being as well as to increasing the risk of important healthcare‐associated infections such as nosocomial pneumonia.
Effects of different manual periodontal probes on periodontal measurements
Authors: Holtfreter Birte , Alte Dietrich , Schwahn Christian , Desvarieux Moïse , Kocher Thomas 
Published: July 2012

AbstractAimTo quantify the digit preference effect for three manual periodontal probes and to calculate correction values to enable comparison of studies with equal recording protocols, but different periodontal probes.Material and MethodsA prospective in vivo crossover study was conducted with a six‐sequence three‐period design. Six examiners assessed attachment loss (AL), probing pocket depth (PD) and gingiva height (GH) at four surfaces, full‐mouth, in six generally healthy subjects using three manual probes: PCP11 (3‐3‐3‐2 mm increments), PCP2 (2 mm increments), and PCPUNC15 (1 mm increments).ResultsDistributions of AL, PD and GH differed between probes (p < 0.001). Compared with PCPUNC15, periodontal measurements coinciding with probe markings of PCP11 and PCP2, respectively, were preferentially named by examiners. Digit preference was most pronounced for PD, but less for AL and GH. In multilevel models, PD differed significantly between all three probes (p < 0.05); probe‐ and examiner‐related effects were also observed for AL and GH. Correction values for pairwise combinations of probes were determined.ConclusionsWe provided empirical evidence and quantified the effect of probe type on periodontal measurements. Differences in probe type should be considered when comparing periodontal data within and between epidemiological studies and appropriate corrections, provided here, should be applied.
Arbuscular mycorrhizal fungi in a wetland constructed for benzene‐, methyl tert‐butyl ether‐ and ammonia‐contaminated groundwater bioremediation
Authors: Fester Thomas 
Published: July 2012

SummaryArbuscular mycorrhizal fungi (AMF), which are present in most natural environments, have demonstrated capacity to promote biodegradation of organic pollutants in the greenhouse. However, it is not certain whether AMF can spontaneously establish in phytoremediation systems constructed to decontaminate groundwater, because of the unusual conditions during the construction and operation of such systems. To assess this possibility, root samples from a wetland constructed for the phytoremediation of groundwater contaminated with benzene, methyl tert‐butyl ether and ammonia were analysed. Substantial AMF colonization was observed in plant roots sampled close to the inlet of a basin filled with fine gravel and planted with Phragmites australis. In addition, analysis of a fragment of the nuclear large ribosomal subunit, amplified by nested PCR, revealed the presence of AMF molecular operational taxonomic units closely related to Funneliformis mosseae and Rhizophagus irregularis in the samples. These findings demonstrate the capacity of generalist AMF strains to establish spontaneously, rapidly and extensively in groundwater bioremediation technical installations.
Commensal Escherichia coli strains in Guiana reveal a high genetic diversity with host‐dependant population structure
Authors: Lescat Mathilde , Clermont Olivier , Woerther Paul Louis , Glodt Jérémy , Dion Sara , Skurnik David , Djossou Felix , Dupont Claire , Perroz Gilles , Picard Bertrand , Catzeflis François , Andremont Antoine , Denamur Erick 
Published: July 2012

SummaryWe undertook a large‐scale epidemiological survey of commensal Escherichia coli in Trois‐Sauts, an isolated village located in the south of French Guiana where human population exchanges are restricted and source of antibiotics controlled. Stools from 162 Wayampi Amerindians and rectal swabs from 33 human associated and 198 wild animals were collected in the close proximity of the village. The prevalence of E. coli was decreasing from humans (100%) to human associated (64%) and wild (45%) animals. A clear genetic structure between these three E. coli populations was observed with human strains belonging very rarely to B2 phylogroup (3.7%), exhibiting few virulence genes and bacteriocins but being antibiotic resistant whereas wild animal strains were characterized by 46.1% of B2 phylogroup belonging, with very unique and infrequent sequence types, numerous extraintestinal genes and bacteriocins but no antibiotic resistance; the human‐associated animal strains being intermediate. Furthermore, an unexpected genetic diversity was observed among the strains, as the housekeeping gene nucleotide diversity per site of the Trois‐Sauts's strains was higher than the one of reference strains representative of the known species diversity. The existence of such E. coli structured phylogenetic diversity within various hosts of a single localization has never been reported.
Nuclear factor‐κB signalling and transcriptional regulation in skeletal muscle atrophy
Authors: Jackman Robert W. , Cornwell Evangeline W. , Wu Chia‐Ling , Kandarian Susan C. 
Published: July 2012

New findings
What is the topic for this review?An up‐to‐date analysis on the role of nuclear factor‐κB signaling and transcriptional control in adult skeletal muscle atrophy.
What advances does it highlight?Our analysis of the literature and research in our laboratory has allowed us to propose interpretations that have not previously been published. We believe these interpretations will be of interest to scientists studying the cellular control of adult skeletal muscle atrophy.
The nuclear factor‐κB (NF‐κB) signalling pathway is a necessary component of adult skeletal muscle atrophy resulting from systemic illnesses or disuse. Studies showing a role for the NF‐κB pathway in muscle disuse include unloading, denervation and immobilization, and studies showing a role for NF‐κB in systemic illnesses include cancer, chronic heart failure and acute septic lung injury. Muscle atrophy due to most of these triggers is associated with activation of NF‐κB transcriptional activity. With the exception of muscle unloading, however, there is a paucity of data on the NF‐κB transcription factors that regulate muscle atrophy, and little is known about which genes are targeted by NF‐κB transcription factors during atrophy. Interestingly, in some cases it appears that the amelioration of muscle atrophy by genetic inhibition of NF‐κB signalling proteins is due to effects that are independent of the downstream NF‐κB transcription factors. These questions are prime areas for investigation if we are to understand a key component of muscle wasting in adult skeletal muscle.
Cigarette smoke induces endoplasmic reticulum stress response and proteasomal dysfunction in human alveolar epithelial cells
Authors: Somborac‐Bačura Anita , van der Toorn Marco , Franciosi Lorenza , Slebos Dirk‐Jan , Žanić‐Grubišić Tihana , Bischoff Rainer , van Oosterhout Antoon J. M. 
Published: July 2012

New findings
What is the central question of this study?The endoplasmic reticulum stress response caused by cigarette smoke may lead to excessive apoptosis with disruption of the epithelial barrier, thus contributing to chronic obstructive pulmonary disease. One way of promoting cell survival is to facilitate degradation of cigarette smoke‐induced protein damage through the ubiquitin–proteasome pathway. Direct effects of gas‐phase cigarette smoke on proteasomal activities have not been demonstrated previously.
What is the main finding and what is its importance?We show that cigarette smoke induces protein damage and triggers the endoplasmic reticulum stress response in human alveolar epithelial cells. A significant reduction of all three proteasomal activities was found. Ineffective degradation of damaged proteins could lead to a sustained epithelial stress response and development of chronic obstructive pulmonary disease.
Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease. Cigarette smoke (CS) causes oxidative stress and severe damage to proteins in the lungs. One of the main systems to protect cells from the accumulation of damaged proteins is the ubiquitin–proteasome pathway. In the present study, we aimed to find out whether exposure of alveolar epithelial cells to CS induces an endoplasmic reticulum (ER) stress response by accumulation of damaged proteins that are inefficiently degraded by the proteasomes. The hypothesis was tested in a human alveolar epithelial cell line (A549) exposed to gas‐phase CS. Exposure to gas‐phase CS for 5 min caused an increase in the amount of ubiquitin–protein conjugates within 4 h. Cigarette smoke exposure also induced the ER stress response marker eIF2α, followed by a significant reduction of nascent protein synthesis and increase in the level of free intracellular amino acids. Moreover, CS exposure significantly reduced all three proteasomal activities (caspase‐, trypsin‐ and chymotrypsin‐like activity) within 4 h, which was still present after 24 h. It can be concluded that gas‐phase CS induces ER stress in A549 alveolar epithelial cells, leading to inadequate protein turnover caused by an accumulation of damaged proteins, reduction in nascent protein synthesis and inhibition of the proteasome. We suggest that prolonged ER stress may lead to excessive cell death with disruption of the epithelial barrier, contributing to development of chronic obstructive pulmonary disease.
A characterization of robust radiation therapy treatment planning methods—from expected value to worst case optimization
Authors: Fredriksson Albin 
Published: July 2012

Purpose:To characterize a class of optimization formulations used to handle systematic and random errors in radiation therapy, and to study the differences between the methods within this class.Methods:The class of robust methods that can be formulated as minimax stochastic programs is studied. This class generalizes many previously used methods, ranging between optimization of the expected and the worst case objective value. The robust methods are used to plan intensity‐modulated proton therapy (IMPT) treatments for a case subject to systematic setup and range errors, random setup errors with and without uncertain probability distribution, and combinations thereof. As reference, plans resulting from a conventional method that uses a margin to account for errors are shown.Results:For all types of errors, target coverage robustness increased with the conservativeness of the method. For systematic errors, best case organ at risk (OAR) doses increased and worst case doses decreased with the conservativeness. Accounting for random errors of fixed probability distribution resulted in heterogeneous dose. The heterogeneities were reduced when uncertainty in the probability distribution was accounted for. Doing so, the OAR doses decreased with the conservativeness. All robust methods studied resulted in more robust target coverage and lower OAR doses than the conventional method.Conclusions:Accounting for uncertainties is essential to ensure plan quality in complex radiation therapy such as IMPT. The utilization of more information than conventional in the optimization can lead to robust target coverage and low OAR doses. Increased target coverage robustness can be achieved by more conservative methods.
Effect of Systemic Infection Induced by Pseudomonas aeruginosa on the Brain Uptake of Colistin in Mice
Authors: Jin Liang , Li Jian , Nation Roger L. , Nicolazzo Joseph A. 
Published: July 2012

ABSTRACT

In view of reports of colistin-induced neurotoxicity in infected patients, the aim of this study was to assess whether the integrity of the blood-brain barrier (BBB) and the brain uptake of colistin are altered in the presence of systemic
Pseudomonas aeruginosa
infection. Bacteremia was confirmed 8 h after intramuscular administration of
P. aeruginosa
ATCC 27853 to Swiss Outbred mice, at which time a single subcutaneous dose of colistin sulfate (40 mg/kg of body weight) or an intravenous dose of [
14
C]sucrose (2 μCi) was administered. Despite a substantial elevation in plasma levels of the proinflammatory cytokines tumor necrosis factor alpha, interleukin-1β, and interleukin-6 during bacterial infection, the brain uptake of colistin was similar between infected and noninfected mice with AUC
brain
/AUC
plasma
(where AUC
brain
is the area under the brain concentration-time curve and AUC
plasma
is the area under the plasma concentration-time curve) ratios of 0.023 and 0.024, respectively. Similarly, the brain-to-plasma ratios of [
14
C]sucrose were no different between infected and noninfected mice, consistent with a lack of effect of bacteremia on BBB integrity. To further correlate any relationship between BBB disruption and plasma levels of proinflammatory cytokines, BBB integrity, colistin brain uptake, and plasma proinflammatory cytokines were measured following the administration of
Salmonella enterica
lipopolysaccharide (LPS), an agent known to induce BBB disruption. Despite LPS inducing a 4-fold increase in colistin brain uptake and a significant (
P
< 0.05) 1.2-fold increase in [
14
C]sucrose BBB penetration, plasma cytokine levels were lower with LPS treatment relative to those obtained with bacterial infection with
P. aeruginosa
. This study demonstrates that the brain uptake of colistin is not increased in mice during
P. aeruginosa
-induced systemic bacteremia despite a significant increase in plasma levels of three proinflammatory cytokines.
A Mutation in the PP2C Phosphatase Gene in a Staphylococcus aureus USA300 Clinical Isolate with Reduced Susceptibility to Vancomycin and Daptomycin
Authors: Passalacqua Karla D. , Satola Sarah W. , Crispell Emily K. , Read Timothy D. 
Published: July 2012

ABSTRACT

Methicillin-resistant
Staphylococcus aureus
(MRSA) strains with reduced susceptibility to vancomycin (MIC of 4 to 8 μg/ml) are referred to as vancomycin-intermediate
S. aureus
(VISA). In this study, we characterized two isogenic USA300
S. aureus
isolates collected sequentially from a single patient with endocarditis where the
S. aureus
isolate changed from being susceptible to vancomycin (VSSA) (1 μg/ml) to VISA (8 μg/ml). In addition, the VISA isolate lost beta-lactamase activity and showed increased resistance to daptomycin and linezolid. The two strains did not differ in growth rate, but the VISA isolate had a thickened cell wall and was less autolytic. Transcriptome sequencing (RNA-seq) analysis comparing the two isolates grown to late exponential phase showed significant differences in transcription of cell surface protein genes (
spa
, SBI [second immunoglobulin-binding protein of
S. aureus
], and fibrinogen-binding proteins), regulatory genes (
agrBCA
, RNAIII,
sarT
, and
saeRS
), and others. Using whole-genome shotgun resequencing, we identified 6 insertion/deletion mutations between the VSSA and VISA isolates. A protein phosphatase 2C (PP2C) family phosphatase had a 6-bp (nonframeshift) insertion mutation in a highly conserved metal binding domain. Complementation of the clinical VISA isolate with a wild-type copy of the PP2C gene reduced the vancomycin and daptomycin MICs and increased autolytic activity, suggesting that this gene contributed to the reduced vancomycin susceptibility phenotype acquired
in vivo
. Creation of
de novo
mutants from the VSSA strain resulted in different mutations, demonstrating that reduced susceptibility to vancomycin in USA300 strains can occur via multiple routes, highlighting the complex nature of the VISA phenotype.
Enterococcus faecalis Enhances Cell Proliferation through Hydrogen Peroxide-Mediated Epidermal Growth Factor Receptor Activation
Authors: Boonanantanasarn Kanitsak , Gill Ann Lindley , Yap YoonSing , Jayaprakash Vijayvel , Sullivan Maureen A. , Gill Steven R. 
Published: July 2012

ABSTRACT

Enterococcus faecalis
is a member of the intestinal and oral microbiota that may affect the etiology of colorectal and oral cancers. The mechanisms by which
E. faecalis
may contribute to the initiation and progression of these cancers remain uncertain. Epidermal growth factor receptor (EGFR) signaling is postulated to play a crucial role in oral carcinogenesis. A link between
E. faecalis
and EGFR signaling in oral cancer has not been elucidated. The present study aimed to evaluate the association between
E. faecalis
and oral cancer and to determine the underlying mechanisms that link
E. faecalis
to EGFR signaling. We report the high frequency of
E. faecalis
infection in oral tumors and the clinical association with EGFR activation. Using human oral cancer cells, we support the clinical findings and demonstrate that
E. faecalis
can induce EGFR activation and cell proliferation.
E. faecalis
activates EGFR through production of H
2
O
2
, a signaling molecule that activates several signaling pathways. Inhibitors of H
2
O
2
(catalase) and EGFR (gefitinib) significantly blocked
E. faecalis
-induced EGFR activation and cell proliferation. Therefore,
E. faecalis
infection of oral tumor tissues suggests a possible association between
E. faecalis
infection and oral carcinogenesis. Interaction of
E. faecalis
with host cells and production of H
2
O
2
increase EGFR activation, thereby contributing to cell proliferation.