bluuebunny/crossref_metadata_2025_split huggingface dataset:
Surface applicator calibration and commissioning of an electronic brachytherapy system for nonmelanoma skin cancer treatmenta)
Authors: Rong Yi , Welsh James S. 
Published: September 2010

Purpose:The Xoft Axxent® x‐ray source has been used for treating nonmelanoma skin cancer since the surface applicators became clinically available in 2009. The authors report comprehensive calibration procedures for the electronic brachytherapy (eBx) system with the surface applicators.Methods:The Xoft miniature tube (model S700) generates 50 kVp low‐energy x rays. The new surface applicators are available in four sizes of 10, 20, 35, and 50 mm in diameter. The authors’ tests include measurements of dose rate, air‐gap factor, output stability, depth dose verification, beam flatness and symmetry, and treatment planning with patient specific cutout factors. The TG‐61 in‐air method was used as a guideline for acquiring nominal dose‐rate output at the skin surface. A soft x‐ray parallel‐plate chamber (PTW T34013) and electrometer was used for the output commissioning. GafChromic® EBT films were used for testing the properties of the treatment fields with the skin applicators. Solid water slabs were used to verify the depth dose and cutout factors. Patients with basal cell or squamous cell carcinoma were treated with eBx using a calibrated Xoft system with the low‐energy x‐ray source and the skin applicators.Results:The average nominal dose‐rate output at the skin surface for the 35 mm applicator is 1.35 Gy/min with ±5% variation for 16 sources. The dose‐rate output and stability (within ±5% variation) were also measured for the remaining three applicators. For the same source, the output variation is within 2%. The effective source‐surface distance was calculated based on the air‐gap measurements for four applicator sizes. The field flatness and symmetry are well within 5%. Percentage depth dose in water was provided by factory measurements and can be verified using solid water slabs. Treatment duration was calculated based on the nominal dose rate, the prescription fraction size, the depth dose percentage, and the cutout factor. The output factor needs to be measured for each case with varying shapes of cutouts.Conclusions:Together with TG‐61, the authors’ methodology provides comprehensive calibration procedures for medical physicists for using the Xoft eBx system and skin applicators for nonmelanoma skin cancer treatments.
Quantitative comparison of thermal dose models in normal canine brain
Authors: Yung Joshua P. , Shetty Anil , Elliott Andrew , Weinberg Jeffrey S. , McNichols Roger J. , Gowda Ashok , Hazle John D. , Stafford R. Jason 
Published: September 2010

Purpose:Minimally invasive thermal ablative therapies as alternatives to conventional surgical management of solid tumors and other pathologies is increasing owing to the potential benefits of performing these procedures in an outpatient setting with reduced complications and comorbidity. Magnetic resonance temperature imaging (MRTI) measurement allows existing thermal dose models to use the spatiotemporal temperature history to estimate the thermal damage to tissue. However, the various thermal dose models presented in the literature employ different parameters and thresholds, affecting the reliability of thermal dosimetry. In this study, the authors quantitatively compared three thermal dose models (Arrhenius rate process,, and threshold temperature) using the dice similarity coefficient (DSC).Methods:The DSC was used to compare the spatial overlap between the region of thermal damage as predicted by the models forin vivo normal canine brain during thermal therapy to the region of thermal damage as revealed by contrast‐enhanced T1‐weighted images acquired immediately after therapy . The outer edge of the hyperintense rim of the ablation region was used as the surrogate marker for the limits of thermal coagulation. The DSC was also used to investigate the impact of varying the thresholds on each models’ ability to predict the zone of thermal necrosis.Results:At previously reported thresholds, the authors found that all three models showed good agreement (defined as) with post‐treatment imaging. All three models examined across the range of commonly applied thresholds consistently showed highly accurate spatial overlap, low variability, and little dependence on temperature uncertainty. DSC values corresponding to cited thresholds were not significantly different from peak DSC values.Conclusions:Thus, the authors conclude that the all three thermal dose models can be used as a reliable surrogate for postcontrast tissue damage verification imaging in rapid ablation procedures and can also be used to enhance the capability of MRTI to control thermal therapy in real time.
Iterative reconstruction of Fourier‐rebinned PET data using sinogram blurring function estimated from point source scans
Authors: Tohme Michel S. , Qi Jinyi 
Published: September 2010

Purpose:The accuracy of the system model that governs the transformation from the image space to the projection space in positron emission tomography (PET) greatly affects the quality of reconstructed images. For efficient computation in iterative reconstructions, the system model in PET can be factored into a product of geometric projection and sinogram blurring function. To further speed up reconstruction, fully 3D PET data can be rebinned into a stack of 2D sinograms and then be reconstructed using 2D iterative algorithms. The purpose of this work is to develop a method to estimate the sinogram blurring function to be used in reconstruction of Fourier‐rebinned data.Methods:In a previous work, the authors developed an approach to estimating the sinogram blurring function of nonrebinned PET data from experimental scans of point sources. In this study, the authors extend this method to the estimation of sinogram blurring function for Fourier‐rebinned PET data. A point source was scanned at a set of sampled positions in the microPET II scanner. The sinogram blurring function is considered to be separable between the transaxial and axial directions. A radially and angularly variant 2D blurring function is estimated from Fourier‐rebinned point source scans to model the transaxial blurring with consideration of the detector block structure of the scanner; a space‐variant 1D blurring kernel along the axial direction is estimated separately to model the correlation between neighboring planes due to detector intrinsic blurring and Fourier rebinning. The estimated sinogram blurring function is incorporated in a 2D maximuma posteriori (MAP) reconstruction algorithm for image reconstruction.Results:Physical phantom experiments were performed on the microPET II scanner to validate the proposed method. The authors compared the proposed method to 2D MAP reconstruction without sinogram blurring model and 2D MAP reconstruction with a Monte Carlo based blurring model. The results show that the proposed method produces images with improved contrast and spatial resolution. The reconstruction time is unaffected by the new method since the blurring component takes a relatively negligible part of the overall reconstruction time.Conclusions:The proposed method can estimate sinogram blurring matrix for Fourier‐rebinned PET data and can be used to improve contrast and spatial resolution of reconstructed images. The method can be applied to other human and animal scanners.
Multiplex Assay Detection of Immunoglobulin G Antibodies That RecognizeGiardia intestinalisandCryptosporidium parvumAntigens
Authors: Priest Jeffrey W. , Moss Delynn M. , Visvesvara Govinda S. , Jones Cara C. , Li Anna , Isaac-Renton Judith L. 
Published: September 2010

ABSTRACTGiardiasis and cryptosporidiosis are common enteric parasitic diseases that have similar routes of transmission. In this work, we have identified epitopes within theGiardiavariant-specific surface protein (VSP) sequences that are recognized by IgG antibodies from 13 of 14 (93%) sera from patients with stool-confirmed giardiasis. The conserved epitopes are shared among VSPs from both of the assemblages that commonly infect humans, and they are likely to be structural, as both sodium dodecyl sulfate treatment and dithiothreitol reduction decrease antibody recognition. In a multiplex bead assay (MBA), we used three VSP fragments from an assemblage AGiardiastrain, three VSP fragments from assemblage B strains, and the α-1 giardin structural antigen to detect IgG antibodies toGiardiaand used the recombinant 17- and 27-kDa antigens to simultaneously detect IgG antibodies toCryptosporidium. The MBA differentiated between sera fromGiardiaandCryptosporidiumoutbreaks and also identified a giardiasis outbreak that may have included cryptosporidiosis cases. Approximately 40% of cryptosporidiosis outbreak samples had high MBA responses for both the 27- and 17-kDa antigens, while <10% of nonoutbreak and giardiasis outbreak samples had high responses. At least 60% of giardiasis outbreak samples were positive for antibodies to multipleGiardiaantigens, while ≤12% of nonoutbreak samples and samples from U.S. and British Columbia cryptosporidiosis outbreaks met our definition forGiardiaseropositivity. A MBA using multiple parasite antigens may prove useful in the epidemiologic analysis of future waterborne or food-borne outbreaks of diarrheal disease.
Preexisting Antibody Response against 2009 Pandemic Influenza H1N1 Viruses in the Taiwanese Population
Authors: Chi Chia-Yu , Liu Ching-Chuan , Lin Chia-Chun , Wang Hsuan-Chen , Cheng Yung-Tsung , Chang Chung-Ming , Wang Jen-Ren 
Published: September 2010

ABSTRACT
A novel pandemic influenza H1N1 (pH1N1) virus spread rapidly across the world in 2009. Due to the important role of antibody-mediated immunity in protection against influenza infection, we used an enzyme-linked immunosorbent assay-based microneutralization test to investigate cross-reactive neutralizing antibodies against the 2009 pH1N1 virus in 229 stored sera from donors born between 1917 and 2008 in Taiwan. The peak of cumulative geometric mean titers occurred in donors more than 90 years old and declined sharply with decreasing age. Sixteen of 27 subjects (59%) more than 80 years old had cross-reactive antibody titers of 160 or more against the 2009 pH1N1 virus, whereas none of the donors from age 9 to 49 had an antibody titer of 160 or more. Interestingly, 2 of 51 children (4%) from 6 months to 9 years old had an antibody titer of 40. We further tested the antibody responses in 9 of the 51 pediatric sera to three endemic seasonal influenza viruses isolated in 2006 and 2008 in Taiwan, and the results showed that only the 2 sera from children with antibody responses to the 2009 pH1N1 virus had high titers of neutralizing antibody against recent seasonal influenza virus strains. Our study shows the presence of some level of cross-reactive antibody in Taiwanese persons 50 years old or older, and the elderly subjects who may already have been exposed to the 1918 virus had high titers of neutralizing antibody to the 2009 pH1N1 virus. Our data also indicate that natural infection with the Taiwan 2006 and 2008 seasonal H1N1 viruses may induce a cross-reactive antibody response to the 2009 pH1N1 virus.
The effect on collisions with injuries of a reduction in traffic citations issued by police officers
Authors: Blais Étienne , Gagné Marie-Pier 
Published: September 2010

ObjectiveTo assess the effect on collisions with injuries of a 61% reduction in the number of traffic citations issued by police officers over a 21-month period.MethodsUsing descriptive analyses as well as ARIMA intervention time-series analyses, this study estimated the impact of this reduction in citations issued for traffic violations on the monthly number of collisions with injuries.ResultsSimple descriptive analysis reveals that the 61% reduction in the number of citations issued for traffic violations during the experimental period coincided with an increase in collisions with injuries. Results from the interrupted time-series analyses reveal that, on average, eight additional collisions with injuries occurred every month during which the number of tickets issued for traffic violations was lower than normal. As this pressure tactic was applied for 21 months, it is estimated that this situation was associated with approximately 184 additional collisions with injuries: equivalent to 239 traffic injuries (either deaths, minor or serious injuries).ConclusionIn the province of Quebec, police officers are an important component of road safety policy. Issuing citations prevents drivers from adopting reckless driving habits such as speeding, running red lights and failing to fasten their seat belt.
The association of road safety knowledge and risk behaviour with paediatric road traffic injury in Guangzhou, China
Authors: Dong Xiaomei , Peek-Asa Corinne , Yang Jingzhen , Wang Shengyong , Chen Xiongfei , Chi Guibo , Ramirez Marizen 
Published: September 2010

BackgroundThis study describes road traffic injuries among school-aged children in Guangzhou, China, and examines the effect of road safety knowledge and risk behaviours on road traffic injuries.MethodsA stratified cluster sample of 3747 children from six primary schools and six middle schools in Guangzhou, China, was surveyed. Data were collected on sociodemographic factors and road traffic injuries during the past year. Knowledge about road safety rules was assessed using a 14-item road safety knowledge index, and risky road safety behaviours were measured using a 25-item road safety behaviour index.ResultsA total of 403 (10.8%) students reported having at least one road traffic injury during the past 12 months. A high proportion of injuries was found among children who were boys, in primary school and from the suburbs. Bicycle-related injuries were the most common (46.0% of all injuries). Motor vehicle-related injuries had higher hospitalisation rates and worse psychological impact than bicycle or pedestrian injuries. Children with low and medium road safety knowledge had 1.5 to 3 times the odds of injury compared with students with high road safety knowledge. Students with high scores on the risky road behaviour index had twice the odds of injury (OR 2.04, 95% CI 1.47 to 2.84) compared with students with low scores.ConclusionBetter road safety knowledge and the avoidance of walking or cycling-related risk behaviours are protective factors for road traffic injuries among Chinese school children. More injury prevention programmes are needed to improve road safety knowledge and reduce risk behaviours.
Child pedestrian injuries and urban change
Authors: Yiannakoulias Nikolaos , Scott Darren M , Rowe Brian H , Voaklander Donald C 
Published: September 2010

BackgroundThe health impacts of rapid changes in urban environments due to economic growth and/or retraction are not widely known. This study looks at the effects of urban change on the risk of child pedestrian injury in Edmonton, Alberta, a city that has experienced large economic and population growth following the expansion of the oil and gas industry in Canada.MethodsA longitudinal ecological study design was used to model the relationships between several built and social environmental variables and the risk of child pedestrian injury and severe child pedestrian injury between 1996 and 2007.ResultsThe incidence of child pedestrian injury was stable, but the incidence of severe injury increased over the study period. Areas with higher proportions of families on low incomes had higher injury incidence. While new residential development is associated with a lower incidence of injury in most areas, in poor areas, new residential development is associated with a higher incidence, even after controlling for urban planning features and traffic intensity.ConclusionWhile suburban areas have a lower incidence of child pedestrian injury, residential development in poorer areas is associated with a higher child pedestrian injury risk. Child pedestrians may be less able to adapt to changes in the urban environment due to rapid growth and increasing income, and as a result, may be at greater risk of injury.
Aerobic Glycolysis Suppresses p53 Activity to Provide Selective Protection from Apoptosis upon Loss of Growth Signals or Inhibition of BCR-Abl
Authors: Mason Emily F. , Zhao Yuxing , Goraksha-Hicks Pankuri , Coloff Jonathan L. , Gannon Hugh , Jones Stephen N. , Rathmell Jeffrey C. 
Published: September 2010

Abstract
Unlike the growth factor dependence of normal cells, cancer cells can maintain growth factor–independent glycolysis and survival through expression of oncogenic kinases, such as BCR-Abl. Although targeted kinase inhibition can promote cancer cell death, therapeutic resistance develops frequently, and further mechanistic understanding is needed. Cell metabolism may be central to this cell death pathway, as we have shown that growth factor deprivation leads to decreased glycolysis that promotes apoptosis via p53 activation and induction of the proapoptotic protein Puma. Here, we extend these findings to show that elevated glucose metabolism, characteristic of cancer cells, can suppress protein kinase Cδ (PKCδ)–dependent p53 activation to maintain cell survival after growth factor withdrawal. In contrast, DNA damage–induced p53 activation was PKCδ independent and was not metabolically sensitive. Both stresses required p53 Ser18 phosphorylation for maximal activity but led to unique patterns of p53 target gene expression, showing distinct activation and response pathways for p53 that were differentially regulated by metabolism. Consistent with oncogenic kinases acting to replace growth factors, treatment of BCR-Abl–expressing cells with the kinase inhibitor imatinib led to reduced metabolism and p53- and Puma-dependent cell death. Accordingly, maintenance of glucose uptake inhibited p53 activation and promoted imatinib resistance. Furthermore, inhibition of glycolysis enhanced imatinib sensitivity in BCR-Abl–expressing cells with wild-type p53 but had little effect on p53-null cells. These data show that distinct pathways regulate p53 after DNA damage and metabolic stress and that inhibiting glucose metabolism may enhance the efficacy of and overcome resistance to targeted molecular cancer therapies. Cancer Res; 70(20); 8066–76. ©2010 AACR.
Tumor Antigen Acrosin Binding Protein Normalizes Mitotic Spindle Function to Promote Cancer Cell Proliferation
Authors: Whitehurst Angelique W. , Xie Yang , Purinton Scott C. , Cappell Kathryn M. , Swanik Jackie T. , Larson Brittany , Girard Luc , Schorge John O. , White Michael A. 
Published: September 2010

Abstract
Cancer cells manage to divide in the context of gross chromosomal abnormalities. These abnormalities can promote bypass of normal restraints on cell proliferation but at a cost of mitotic vulnerabilities that can be attacked by chemotherapy. Determining how cancer cells balance these issues may permit chemotherapeutic sensitivity to be leveraged more efficiently. From a pan-genomic small interfering RNA screen for modifiers of chemoresponsiveness, we identified the tumor antigen acrosin binding protein (ACRBP)/OY-TES-1 as a specifier of paclitaxel resistance. ACRBP expression is normally restricted to the testes but is detected in a wide variety of cancers, including most ovarian cancers. We found that ACRBP is both necessary and sufficient for paclitaxel resistance in ovarian cancer cell lines and ovarian tumor explants. Moreover, high ACRBP expression correlated with reduced survival time and faster relapse among ovarian cancer patients. We identified the mitotic spindle protein NuMA as an ACRBP-interacting protein that could account for the effects of ACRBP on paclitaxel sensitivity. In cancer cells, ACRBP restricted a NuMA-dependent abrogation of a mitotic spindle assembly that is otherwise pathologic. As a consequence, ACRBP depletion resulted in mitotic errors and reduced proliferative fitness that could be rescued by NuMA codepletion. We propose that the codependent relationship of ACRBP and NuMA in cancer cells reflects their passage through a selection bottleneck during tumor evolution, one which requires the acquisition of traits that normalize mitotic perturbations that originally drove the plasticity of a preneoplastic genome. The molecular definition of such traits as defined by the ACRBP-NuMA complex may represent conceptually ideal intervention targets based on the wide therapeutic windows they may offer. Cancer Res; 70(19); 7652–61. ©2010 AACR.
Fibroblast Growth Factor Receptor 4 Regulates Tumor Invasion by Coupling Fibroblast Growth Factor Signaling to Extracellular Matrix Degradation
Authors: Sugiyama Nami , Varjosalo Markku , Meller Pipsa , Lohi Jouko , Hyytiäinen Marko , Kilpinen Sami , Kallioniemi Olli , Ingvarsen Signe , Engelholm Lars H. , Taipale Jussi , Alitalo Kari , Keski-Oja Jorma , Lehti Kaisa 
Published: September 2010

Abstract
Aberrant expression and polymorphism of fibroblast growth factor receptor 4 (FGFR4) has been linked to tumor progression and anticancer drug resistance. We describe here a novel mechanism of tumor progression by matrix degradation involving epithelial-to-mesenchymal transition in response to membrane-type 1 matrix metalloproteinase (MT1-MMP, MMP-14) induction at the edge of tumors expressing the FGFR4-R388 risk variant. Both FGFR4 and MT1-MMP were upregulated in tissue biopsies from several human cancer types including breast adenocarcinomas, where they were partially coexpressed at the tumor/stroma border and tumor invasion front. The strongest overall coexpression was found in prostate carcinoma. Studies with cultured prostate carcinoma cell lines showed that the FGFR4-R388 variant, which has previously been associated with poor cancer prognosis, increased MT1-MMP–dependent collagen invasion. In this experimental model, knockdown of FGFR4-R388 or MT1-MMP by RNA interference blocked tumor cell invasion and growth in collagen. This was coupled with impaired phosphorylation of FGFR substrate 2 and Src, upregulation of E-cadherin, and suppression of cadherin-11 and N-cadherin. These in vitro results were substantiated by reduced MT1-MMP content and in vivo growth of prostate carcinoma cells after the FGFR4-R388 gene silencing. In contrast, knockdown of the alternative FGFR4-G388 allele enhanced MT1-MMP and invasive tumor cell growth in vivo and within three-dimensional collagen. These results will help to explain the reported association of the FGFR4-R388 variant with the progression and poor prognosis of certain types of tumors. Cancer Res; 70(20); 7851–61. ©2010 AACR.
Activation-Induced Cytidine Deaminase Accelerates Clonal Evolution in BCR-ABL1–Driven B-Cell Lineage Acute Lymphoblastic Leukemia
Authors: Gruber Tanja Andrea , Chang Mi Sook , Sposto Richard , Müschen Markus 
Published: September 2010

Abstract
Activation-induced cytidine deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center (GC) B cells. Occasionally, AID can target non-Ig genes and thereby promote GC B-cell lymphomagenesis. We recently showed that the oncogenic BCR-ABL1 kinase induces aberrant expression of AID in pre-B acute lymphoblastic leukemia (ALL) and lymphoid chronic myelogenous leukemia blast crisis. To elucidate the biological significance of aberrant AID expression, we studied loss of AID function in a murine model of BCR-ABL1 ALL. Mice transplanted with BCR-ABL1–transduced AID−/− bone marrow had prolonged survival compared with mice transplanted with leukemia cells generated from AID+/+ bone marrow. Consistent with a causative role of AID in genetic instability, AID−/− leukemia had a lower frequency of amplifications and deletions and a lower frequency of mutations in non-Ig genes, including Pax5 and Rhoh compared with AID+/+ leukemias. AID−/− and AID+/+ ALL cells showed a markedly distinct gene expression pattern, and AID−/− ALL cells failed to downregulate a number of tumor-suppressor genes including Rhoh, Cdkn1a (p21), and Blnk (SLP65). We conclude that AID accelerates clonal evolution in BCR-ABL1 ALL by enhancing genetic instability and aberrant somatic hypermutation, and by negative regulation of tumor-suppressor genes. Cancer Res; 70(19); 7411–20. ©2010 AACR.