bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantification of dose perturbations induced by external and internal accessories in ocular proton therapy and evaluation of their dosimetric impact
Authors: Carnicer A. , Angellier G. , Thariat J. , Sauerwein W. , Caujolle J. P. , Hérault J. 
Published: May 2013

Purpose:Proton scattering on beam shaping devices and protons slowing down on media with different densities within the treatment volume may produce dose perturbations and range variations that are not predicted by treatment planning systems. The aim of this work was to assess the dosimetric impact of elements present in ocular proton therapy treatments that may disturb the prescribed treatment plan. Both distal beam shaping devices and intraocular elements were considered.Methods:A wedge filter, tantalum fiducial marker, hemispherical compensator, two intraocular endotamponades (densities 0.97 and 1.92 g cm−3) and an intraocular eye lens (IOL) were considered in the study. For these elements, longitudinal dose distributions were measured and/or calculated in water in beam alignment for a clinical spread‐out Bragg peak. Under the same conditions, the unperturbed dose distributions were similarly measured and/or calculated in the absence of the element. The dosimetric impact was assessed by comparison of unperturbed and perturbed dose distributions. Measurements and calculations were carried out with two methods. Measurements are based on EBT3 films with dedicated software, which makes use of a calibration curve and correction for the quenching effect. Calculations are based on the Monte Carlo (MC) code MCNPX and reproduce the experimental conditions. Both dose maps are obtained with a resolution of 300 dpi.Results:The degree of disturbance of distal beam shaping devices is low for the wedge filter (2% overdose ripple all along the central axis) and moderate for the hemispherical compensator (two bands of variable overdose of up to 10% downstream the compensator lateral edges and −5% underdose on the plateau at off‐axis distance of 5 cm). Tantalum clips produce important dose shadows (−20% behind the clip parallel to the beam and range reduction of 1.1 mm) and bands of overdose (15%). The presence of endotamponades modifies the dose distribution very significantly (−5% underdose on the plateau and 3 mm range prolongation for the tamponade with density 0.97 g cm−3 and −15% underdose on plateau and 8 mm range reduction for that with density 1.92 g cm−3). No dose perturbations were found for the IOL. The high performance of EBT3 film and MC tools used was confirmed and good agreement was found between them (percentage of pixels passing the gamma test >87%).Conclusions:The degree of disturbance by external beam shaping devices remains low in ocular proton therapy and can be reduced by bringing accessories closer to the eye. Tantalum fiducial markers must be located in such a way that dose perturbation is not projected on the tumor. The treatment of patients with intraocular endotamponades must be carefully managed. It is fundamental that radiation oncologists and medical physicists are informed about the presence of such substances prior to the treatment.
Genome Sequence of Burkholderia pseudomallei NCTC 13392
Authors: Sahl Jason W. , Stone Joshua K. , Gelhaus H. Carl , Warren Richard L. , Cruttwell Caroline J. , Funnell Simon G. , Keim Paul , Tuanyok Apichai 
Published: May 2013

ABSTRACT

Here, we describe the draft genome sequence of
Burkholderia pseudomallei
NCTC 13392. This isolate has been distributed as K96243, but distinct genomic differences have been identified. The genomic sequence of this isolate will provide the genomic context for previously conducted functional studies.
Draft Genome Sequence of Haemophilus parasuis gx033, a Serotype 4 Strain Isolated from the Swine Lower Respiratory Tract
Authors: Li Jun , Peng Hao , Xu Li-gan , Xie Yu-zhou , Xuan Xiong-biao , Ma Chun-xia , Hu Shuai , Chen Ze-xiang , Yang Wei , Xie Yong-ping , Pan Yan , Tao Li 
Published: May 2013

ABSTRACT

Haemophilus parasuis
serotype 4 is a Gram-negative pathogen that is the most prevalent
H. parasuis
serovar in the world, but its genome sequence information has not yet been reported. Thus, we determined the genome of
H. parasuis
strain gx033, a serovar 4 strain isolated from a lung specimen of a diseased piglet in southwestern China. Here, we present the first draft genome sequence of this species.
Draft Genome Sequence of Desulfotignum phosphitoxidans DSM 13687 Strain FiPS-3
Authors: Poehlein Anja , Daniel Rolf , Simeonova Diliana D. 
Published: May 2013

ABSTRACT

We report the 5.008-Mbp assembled draft genome sequence of
Desulfotignum phosphitoxidans
strain FiPS-3 (DSM 13687), which gains metabolic energy from the oxidation of phosphite to phosphate. Its genome provides insights into the composition and architecture of the phosphite-utilizing and energy-transducing systems required to live with phosphite as electron donor.
Genome Sequence of Lactobacillus plantarum Strain UCMA 3037
Authors: Naz Saima , Tareb Raouf , Bernardeau Marion , Vaisse Melissa , Lucchetti-Miganeh Celine , Rechenmann Mathias , Vernoux Jean-Paul 
Published: May 2013

ABSTRACT

Nucleic acid of the strain
Lactobacillus plantarum
UCMA 3037, isolated from raw milk camembert cheese in our laboratory, was sequenced. We present its draft genome sequence with the aim of studying its functional properties and relationship to the cheese ecosystem.
Draft Genome Sequence of
Botrytis cinerea
BcDW1, Inoculum for Noble Rot of Grape Berries
Authors: Blanco-Ulate Barbara , Allen Greg , Powell Ann L. T. , Cantu Dario 
Published: May 2013

ABSTRACT

Botrytized wines are produced from grape berries infected by
Botrytis cinerea
under specific environmental conditions. Here, we report the draft genome sequence of
B. cinerea
BcDW1, a strain isolated from Sémillon grapes in Napa Valley in 1992 that is used with the intent to induce noble rot for botrytized wine production.
Draft Genome Sequence of the Moderately Halophilic Bacterium Pseudoalteromonas ruthenica Strain CP76
Authors: de la Haba Rafael R. , Sánchez-Porro Cristina , León María José , Papke R. Thane , Ventosa Antonio 
Published: May 2013

ABSTRACT

Pseudoalteromonas ruthenica
strain CP76, isolated from a saltern in Spain, is a moderately halophilic bacterium belonging to the
Gammaproteobacteria
. Here we report the draft genome sequence, which consists of a 4.0-Mb chromosome, of this strain, which is able to produce the extracellular enzyme haloprotease CPI.
Draft Genome Sequence of Avibacterium paragallinarum Strain 221
Authors: Xu Fuzhou , Miao Deyuan , Du Yu , Chen Xiaoling , Zhang Peijun , Sun Huiling 
Published: May 2013

ABSTRACT

Avibacterium paragallinarum
is the causative agent of infectious coryza. Here we report the draft genome sequence of reference strain 221 of
A. paragallinarum
serovar A. The genome is composed of 135 contigs for 2,685,568 bp with a 41% G+C content.
The Microbiology of Malting and Brewing
Authors: Bokulich Nicholas A. , Bamforth Charles W. 
Published: May 2013

SUMMARYBrewing beer involves microbial activity at every stage, from raw material production and malting to stability in the package. Most of these activities are desirable, as beer is the result of a traditional food fermentation, but others represent threats to the quality of the final product and must be controlled actively through careful management, the daily task of maltsters and brewers globally. This review collates current knowledge relevant to the biology of brewing yeast, fermentation management, and the microbial ecology of beer and brewing.
A managed multidisciplinary programme on multi-resistantKlebsiella pneumoniaein a Danish university hospital
Authors: Andersen Stig Ejdrup , Knudsen Jenny Dahl ,   for the Bispebjerg Intervention Group
Published: May 2013

BackgroundBacteria-producing extended spectrum β-lactamase (ESBL) enzymes are resistant to commonly used antimicrobials. In 2008, routine monitoring revealed a clonal hospital outbreak of ESBL-producingKlebsiella pneumoniae(ESBL-KP).MethodsAt a 510-bed Danish university hospital, a multidisciplinary change project inspired by Kotter'sEight Steps of Changewas designed. In addition to revision of antimicrobial guidelines and restriction of selected antimicrobials, the complex, managed, multi-faceted intervention comprised training and education, enhanced isolation precautions, and a series of actions to improve the infection control measures and standardise procedures across the hospital. A prospective interrupted time series design was used to analyse data collected at hospital level from January 2008 through December 2011.ResultsThough overall antimicrobial consumption remained unaffected, the intervention led to intended, immediate and sustained reduction in the use of cefuroxime, and an increase in the use of ertapenem, piperacillin/tazobactam and β-lactamase sensitive penicillin. Moreover, a postintervention reduction in the rate of ESBL-KP in diagnostic samples and in the incidence of ESBL-KP infections was observed. The intervention may also have reduced the need for isolation precautions and may have shortened each isolation period.ConclusionsThe results indicate that an immediate and sustained change in the antimicrobial consumption and a decreasing rate of ESBL-KP are achievable through the application of a managed, multi-faceted intervention that does not require ongoing antibiotic stewardship.
Does the quality of chest compressions deteriorate when the chest compression rate is above 120/min?
Authors: Lee Soo Hoon , Kim Kyuseok , Lee Jae Hyuk , Kim Taeyun , Kang Changwoo , Park Chanjong , Kim Joonghee , Jo You Hwan , Rhee Joong Eui , Kim Dong Hoon 
Published: May 2013

ObjectivesThe quality of chest compressions along with defibrillation is the cornerstone of cardiopulmonary resuscitation (CPR), which is known to improve the outcome of cardiac arrest. We aimed to investigate the relationship between the compression rate and other CPR quality parameters including compression depth and recoil.MethodsA conventional CPR training for lay rescuers was performed 2 weeks before the ‘CPR contest’. CPR anytime training kits were distributed to respective participants for self-training on their own in their own time. The participants were tested for two-person CPR in pairs. The quantitative and qualitative data regarding the quality of CPR were collected from a standardised check list and SkillReporter, and compared by the compression rate.ResultsA total of 161 teams consisting of 322 students, which includes 116 men and 206 women, participated in the CPR contest. The mean depth and rate for chest compression were 49.0±8.2 mm and 110.2±10.2/min. Significantly deeper chest compression depths were noted at rates over 120/min than those at any other rates (47.0±7.4, 48.8±8.4, 52.3±6.7, p=0.008). Chest compression depth was proportional to chest compression rate (r=0.206, p<0.001), but there were significantly more incomplete chest recoils at the rate of over 120/min than at any other rates (9.8%, 6.3%, 25.6%, p=0.011).ConclusionsThe study showed conflicting results in the quality of chest compression including chest compression depth and chest recoil by chest compression rate. Further evaluation regarding the upper limit of the chest compression rate is needed to ensure complete full chest wall recoil while maintaining an adequate chest compression depth.
The MET Oncogene in Glioblastoma Stem Cells: Implications as a Diagnostic Marker and a Therapeutic Target
Authors: Boccaccio Carla , Comoglio Paolo M. 
Published: May 2013

Abstract
The MET oncogene, a crucial regulator of the genetic program known as “invasive growth” or “epithelial–mesenchymal transition,” has recently emerged as a functional marker of glioblastoma stem cells. Here, we review findings that associate MET expression and activity with a specific, genetically defined glioblastoma stem cell subtype, and data showing how MET sustains the stem cell phenotype in glioblastoma and other tumors. Finally, we discuss issues related to identification of tumorigenic clones driven by MET in the context of genetically heterogeneous tumors and strategies aimed at eradicating cancer stem cells. Cancer Res; 73(11); 3193–9. ©2013 AACR.
Autophagy Plays a Critical Role in the Degradation of Active RHOA, the Control of Cell Cytokinesis, and Genomic Stability
Authors: Belaid Amine , Cerezo Michaël , Chargui Abderrahman , Corcelle–Termeau Elisabeth , Pedeutour Florence , Giuliano Sandy , Ilie Marius , Rubera Isabelle , Tauc Michel , Barale Sophie , Bertolotto Corinne , Brest Patrick , Vouret-Craviari Valérie , Klionsky Daniel J. , Carle Georges F. , Hofman Paul , Mograbi Baharia 
Published: May 2013

Abstract
Degradation of signaling proteins is one of the most powerful tumor-suppressive mechanisms by which a cell can control its own growth. Here, we identify RHOA as the molecular target by which autophagy maintains genomic stability. Specifically, inhibition of autophagosome degradation by the loss of the v-ATPase a3 (TCIRG1) subunit is sufficient to induce aneuploidy. Underlying this phenotype, active RHOA is sequestered via p62 (SQSTM1) within autolysosomes and fails to localize to the plasma membrane or to the spindle midbody. Conversely, inhibition of autophagosome formation by ATG5 shRNA dramatically increases localization of active RHOA at the midbody, followed by diffusion to the flanking zones. As a result, all of the approaches we examined that compromise autophagy (irrespective of the defect: autophagosome formation, sequestration, or degradation) drive cytokinesis failure, multinucleation, and aneuploidy, processes that directly have an impact upon cancer progression. Consistently, we report a positive correlation between autophagy defects and the higher expression of RHOA in human lung carcinoma. We therefore propose that autophagy may act, in part, as a safeguard mechanism that degrades and thereby maintains the appropriate level of active RHOA at the midbody for faithful completion of cytokinesis and genome inheritance. Cancer Res; 73(14); 4311–22. ©2013 AACR.
c-Src Modulates Estrogen-Induced Stress and Apoptosis in Estrogen-Deprived Breast Cancer Cells
Authors: Fan Ping , Griffith Obi L. , Agboke Fadeke A. , Anur Pavana , Zou Xiaojun , McDaniel Russell E. , Creswell Karen , Kim Sung Hoon , Katzenellenbogen John A. , Gray Joe W. , Jordan V. Craig 
Published: May 2013

AbstractThe emergence of anti-estrogen resistance in breast cancer is an important clinical phenomenon affecting long-term survival in this disease. Identifying factors that convey cell survival in this setting may guide improvements in treatment. Estrogen (E2) can induce apoptosis in breast cancer cells that have been selected for survival after E2 deprivation for long periods (MCF-7:5C cells), but the mechanisms underlying E2-induced stress in this setting have not been elucidated. Here, we report that the c-Src kinase functions as a key adapter protein for the estrogen receptor (ER, ESR1) in its activation of stress responses induced by E2 in MCF-7:5C cells. E2 elevated phosphorylation of c-Src, which was blocked by 4-hydroxytamoxifen (4-OHT), suggesting that E2 activated c-Src through the ER. We found that E2 activated the sensors of the unfolded protein response (UPR), IRE1α (ERN1) and PERK kinase (EIF2AK3), the latter of which phosphorylates eukaryotic translation initiation factor-2α (eIF2α). E2 also dramatically increased reactive oxygen species production and upregulated expression of heme oxygenase HO-1 (HMOX1), an indicator of oxidative stress, along with the central energy sensor kinase AMPK (PRKAA2). Pharmacologic or RNA interference–mediated inhibition of c-Src abolished the phosphorylation of eIF2α and AMPK, blocked E2-induced ROS production, and inhibited E2-induced apoptosis. Together, our results establish that c-Src kinase mediates stresses generated by E2 in long-term E2-deprived cells that trigger apoptosis. This work offers a mechanistic rationale for a new approach in the treatment of endocrine-resistant breast cancer. Cancer Res; 73(14); 4510–20. ©2013 AACR.
Declining Rates of High-Grade Cervical Lesions in Young Women in Connecticut, 2008–2011
Authors: Niccolai Linda M. , Julian Pamela J. , Meek James I. , McBride Vanessa , Hadler James L. , Sosa Lynn E. 
Published: May 2013

Abstract
Vaccines that prevent infection with human papillomavirus (HPV) types 16 and 18 that are known to cause cervical cancer have been available in the United States since 2006. High-grade cervical lesions are important for monitoring early vaccine impact because they are strong surrogates for cancer yet can develop within years after infection as opposed to decades. Trends in high-grade cervical lesions including cervical intraepithelial neoplasia grades 2, 2/3, and 3 and adenocarcinoma in situ among women ages 21 to 39 years old were examined using a statewide surveillance registry in Connecticut from 2008 to 2011. During this time period, HPV vaccine initiation increased among adolescent females from 45% to 61%. Analyses were stratified by age, according to census tract measures of proportion of population Black, Hispanic, living in poverty, and by urban/nonurban counties. The annual rate per 100,000 females ages 21 to 24 years declined from 834 in 2008 to 688 in 2011 (Ptrend &lt; 0.001). No significant declines were observed among women ages 25 to 39 years. Significant declining trends also occurred in census tracts with lower proportions of the population being Black, Hispanic, or living below the federal poverty level. Declines in high-grade cervical lesions have occurred among young women during 2008 to 2011. This is the first report of declines in cervical neoplasia in the United States since HPV vaccines became available. Continued surveillance is needed to measure vaccine impact and monitor health disparities. Cancer Epidemiol Biomarkers Prev; 22(8); 1446–50. ©2013 AACR.
An Assessment of the Shared Allelic Architecture between Type II Diabetes and Prostate Cancer
Authors: Yu Oriana Hoi Yun , Foulkes William D. , Dastani Zari , Martin Richard M. , Eeles Rosalind ,   for the PRACTICAL Consortium and the CRUK GWAS Investigators, Richards J. Brent 
Published: May 2013

Abstract
Background: To determine whether the alleles that influence type II diabetes risk and glycemic traits also influence prostate cancer risk.
Methods: We used a multiple single-nucleotide polymorphisms (SNP) genotypic risk score to assess the average effect of alleles that increase type II diabetes risk or worsen glycemic traits on risk of prostate cancer in 19,662 prostate cancer cases and 19,715 controls from the Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) consortium and 5,504 prostate cancer cases and 5,834 controls from the Cancer Research UK (CRUK) prostate cancer study.
Results: Calculating the average additive effect of type II diabetes or glycemic trait risk alleles on prostate cancer risk using a logistic model revealed no evidence of a shared allelic architecture between type II diabetes, or worsened glycemic status, with prostate cancer risk [OR for type II diabetes alleles: 1.00 (P = 0.58), fasting glycemia alleles: 1.00 (P = 0.67), HbA1c alleles: 1.00 (P = 0.93), 2-hour OGTT alleles: 1.01 (P = 0.14), and HOMA-B alleles: 0.99 (P = 0.57)].
Conclusions: Using genetic data from large consortia, we found no evidence for a shared genetic etiology of type II diabetes or glycemic risk with prostate cancer.
Impact: Our results showed that alleles influencing type II diabetes and related glycemic traits were not found to be associated with the risk of prostate cancer. Cancer Epidemiol Biomarkers Prev; 22(8); 1473–5. ©2013 AACR.
Telmisartan Exerts Pleiotropic Effects in Endothelial Cells and Promotes Endothelial Cell Quiescence and Survival
Authors: Siragusa Mauro , Sessa William C. 
Published: May 2013

Objective—
Telmisartan, an angiotensin II type 1 receptor blocker, and amlodipine, a calcium channel blocker, are antihypertensive agents clinically used as monotherapy or in combination. They exert beneficial cardiovascular effects independently of blood pressure lowering and classic mechanisms of action. In this study, we investigate molecular mechanisms responsible for the off-target effects of telmisartan and telmisartan–amlodipine in endothelial cells (ECs), using an unbiased genomic approach.

Approach and Results—
In human umbilical vein ECs, microarray analysis of gene expression followed by pathway enrichment analysis and quantitative polymerase chain reaction validation revealed that telmisartan modulates the expression of key genes responsible for cell cycle progression and apoptosis. Amlodipine’s effect was similar to control. ECs exposed to telmisartan, but not amlodipine, losartan, or valsartan, exhibited a dose-dependent impairment of cell growth and failed to enter the S-phase of the cell cycle. Similarly, telmisartan inhibited proliferation in COS-7 cells lacking the angiotensin II type 1 receptor. In telmisartan-treated ECs, phosphorylation and activation of Akt, as well as MDM2, were reduced, leading to accumulation of p53 in the nucleus, where it represses the transcription of cell cycle–promoting genes. Phosphorylation of glycogen synthase kinase-3β was also reduced, resulting in rapid proteolytic turnover of CyclinD1. Telmisartan induced downregulation of proapoptotic genes and protected ECs from serum starvation–induced and 7-ketocholesterol–induced apoptosis.

Conclusions—
Telmisartan exerts antiproliferative and antiapoptotic effects in ECs. This may account for the improved endothelial dysfunction observed in the clinical setting.
Plasmin Promotes Foam Cell Formation by Increasing Macrophage Catabolism of Aggregated Low-Density Lipoprotein
Authors: Haka Abigail S. , Grosheva Inna , Singh Rajesh K. , Maxfield Frederick R. 
Published: May 2013

Objective—
The plasmin/plasminogen system is involved in atherosclerosis. However, the mechanisms by which it stimulates disease are not fully defined. A key event in atherogenesis is the deposition of low-density lipoprotein (LDL) on arterial walls where it is modified, aggregated, and retained. Macrophages are recruited to clear the lipoproteins, and they become foam cells. The goal of this study was to assess the role of plasmin in macrophage uptake of aggregated LDL and foam cell formation.

Approach and Results—
Plasminogen treatment of macrophages catabolizing aggregated LDL significantly accelerated foam cell formation. Macrophage interaction with aggregated LDL increased the surface expression of urokinase-type plasminogen activator receptor and plasminogen activator activity, resulting in increased ability to generate plasmin at the cell surface. The high local level of plasmin cleaves cell-associated aggregated LDL, allowing a portion of the aggregate to become sequestered in a nearly sealed, yet extracellular, acidic compartment. The low pH in the plasmin-induced compartment allows lysosomal enzymes, delivered via lysosome exocytosis, greater activity, resulting in more efficient cholesteryl ester hydrolysis and delivery of a large cholesterol load to the macrophage, thereby promoting foam cell formation.

Conclusions—
These findings highlight a critical role for plasmin in the catabolism of aggregated LDL by macrophages and provide a new context for considering the atherogenic role of plasmin.