bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of complex cardiovascular flow with three‐component acceleration‐encoded MRI
Authors: Barker Alex J. , Staehle Felix , Bock Jelena , Jung Bernd A. , Markl Michael 
Published: May 2011

AbstractFunctional information regarding cardiac performance, pressure gradients, and local flow derangement are available from blood acceleration fields. Thus, this study examines a 2D and 3D phase contrast sequence optimized to efficiently encode three‐directional, time‐resolved acceleration in vitro and in vivo. Stenosis phantom acceleration measurements were compared to acceleration derived from standard velocity encoded phase contrast‐magnetic resonance imaging (i.e., “velocity‐derived acceleration”). For in vivo analysis, three‐directional 2D acceleration maps were compared to velocity‐derived acceleration using regions proximal and distal to the aortic valve in six healthy volunteers at 1.5 and 3.0 T (voxel size = 1.4 × 2.1 × 8 mm, temporal resolution = 16–20 ms). In addition, a 4D acceleration sequence was evaluated for feasibility in a healthy volunteer and postrepair biscuspid aortic valve patient with an ascending aortic aneurysm. The phantom magnetic resonance acceleration measurements were more accurate (nonturbulent root mean square error = 2.2 vs. 5.1 m/s2 for phase contrast‐magnetic resonance imaging) and 10 times less noisy (nonturbulent σ = 0.9 vs. 13.6 m/s2 for phase contrast‐magnetic resonance imaging) than velocity‐derived acceleration. Acceleration mapping of the left ventricular outflow tract and aortic arch exhibited signal voids colocated with complex flow events such as vortex formation and high order motion. 4D acceleration data, visualized in combination with the velocity data, may provide new insight into complex flow phenomena. Magn Reson Med 67:50–61, 2012. © 2011 Wiley Periodicals, Inc.
Optimized double inversion recovery for reduction of T1 weighting in fluid‐attenuated inversion recovery
Authors: Madhuranthakam Ananth J. , Sarkar Subhendra N. , Busse Reed F. , Bakshi Rohit , Alsop David C. 
Published: May 2011

AbstractFluid‐attenuated inversion recovery (FLAIR) is a routinely used technique in clinical practice to detect long T2 lesions by suppressing the cerebrospinal fluid. Concerns remain, however, that the inversion pulse in FLAIR imparts T1 weighting that can decrease the detectability and mischaracterize some lesions. Hence, FLAIR is usually acquired in conjunction with a standard T2 to guard against these concerns. Recently, double inversion recovery (DIR) preparations have highlighted certain types of lesions by suppressing both cerebrospinal fluid and white matter but produce even stronger T1 contrast than FLAIR. This work shows that the inversion times in a DIR sequence can be optimized to minimize unwanted T1 weighting, enabling the acquisition of cerebrospinal fluid‐suppressed images with pure T2 weighting. This technique is referred to as T1‐nulled DIR. The theory to determine the optimized inversion times is discussed and the results are shown by simulations, normal volunteer studies, and multiple sclerosis patient studies. T1‐nulled DIR provides equivalent or superior contrast between gray and white matters as well as white matter and multiple sclerosis lesion at the same repetition time. Multiple sclerosis lesions appeared sharper on T1‐nulled DIR compared to FLAIR. T1‐nulled DIR has the potential to replace the combination of standard T2 and FLAIR acquisitions in many clinical protocols. Magn Reson Med, 2011. © 2011 Wiley‐Liss, Inc.
Probing mouse brain microstructure using oscillating gradient diffusion MRI
Authors: Aggarwal Manisha , Jones Melina V. , Calabresi Peter A. , Mori Susumu , Zhang Jiangyang 
Published: May 2011

AbstractHigh resolution diffusion tensor images of the mouse brain were acquired using the pulsed gradient spin echo sequence and the oscillating gradient spin echo sequence. The oscillating gradient spin echo tensor images demonstrated frequency‐dependent changes in diffusion measurements, including apparent diffusion coefficient and fractional anisotropy, in major brain structures. Maps of the rate of change in apparent diffusion coefficient with oscillating gradient frequency revealed novel tissue contrast in the mouse hippocampus, cerebellum, and cerebral cortex. The observed frequency‐dependent contrasts resembled neuronal soma‐specific Nissl staining and nuclei‐specific 4′,6‐diamidino‐2‐phenylindole (DAPI) staining in the mouse brain, which suggests that the contrasts might be related to key features of cytoarchitecture in the brain. In the mouse cuprizone model, oscillating gradient spin echo‐based diffusion MRI revealed significantly higher frequency‐dependence of perpendicular diffusivity (λ⊥) in the demyelinated caudal corpus callosum at 4 weeks after cuprizone treatment when compared with control mice and mice at 6 weeks after cuprizone treatment. The elevated frequency‐dependence of λ⊥coincided with the infiltration of activated microglia/macrophages and disruption of axons during acute demyelination in the caudal corpus callosum. The results demonstrate the potential of oscillating gradient spin echo‐based diffusion MRI for providing tissue contrasts complimentary to conventional pulsed gradient spin echo‐based diffusion MRI. Magn Reson Med 67:98–109, 2012. © 2011 Wiley Periodicals, Inc.
Fast whole‐body magnetic resonance angiography in mice
Authors: Lefrançois William , Thiaudière Eric , Ben Hassen Wadie , Sanchez Stéphane , Franconi Jean‐Michel , Miraux Sylvain 
Published: May 2011

AbstractHigh‐throughput magnetic resonance imaging (MRI) tools are required for the longitudinal investigation of vascular diseases in mouse models. Angiographic data from various anatomic regions may be needed in a single experiment. This study involves a three‐dimensional (3D) time‐of‐flight (TOF) magnetic resonance angiography (MRA) method using sequential acquisitions of four data sets corresponding to the head, the thorax, the abdomen, and the hind limbs of a mouse. After repositioning the animal, each anatomic region was acquired in 2 min, and the TOF effect was provided by the spatial selectivity of the radio frequency (RF) resonator. No slab selection was needed and whole‐body MRA was performed in a total experiment time of 10 min. The voxel size was equal to or greater than 131 × 195 × 188 μm3. To suppress the signal arising from stationary tissues, both inversion recovery and interspersed saturation, used as magnetization preparations, were compared from a theoretical and an experimental perspective. The arterial tree (carotid, aortic, iliac, renal, and smaller arteries) was well visualized by this method, both in control healthy mice and in mice with common carotid artery ligation. The potential interest of this method for evaluating arterial diseases is discussed. Magn Reson Med, 2011. © 2011 Wiley‐Liss, Inc.
In utero phenotyping of mouse embryonic vasculature with MRI
Authors: Berrios‐Otero Cesar A. , Nieman Brian J. , Parasoglou Prodromos , Turnbull Daniel H. 
Published: May 2011

AbstractThe vasculature is the earliest developing organ in mammals and its proper formation is critical for embryonic survival. MRI approaches have been used previously to analyze complex three‐dimensional vascular patterns and defects in fixed mouse embryos. Extending vascular imaging to an in utero setting with potential for longitudinal studies would enable dynamic analysis of the vasculature in normal and genetically engineered mouse embryos, in vivo. In this study, we employed an in utero MRI approach that corrects for motion, using a combination of interleaved gated acquisition and serial coregistration of rapidly acquired three‐dimensional images. We tested the potential of this method by acquiring and analyzing images from wildtype and Gli2 mutant embryos, demonstrating a number of Gli2 phenotypes in the brain and cerebral vasculature. These results show that in utero MRI can be used for in vivo phenotype analysis of a variety of mutant mouse embryos. Magn Reson Med, 2011. © 2011 Wiley‐Liss, Inc.
Lagrangean decomposition/relaxation for the routing and wavelength assignment problem
Authors: Thiongane Babacar 
Published: May 2011

AbstractThis work deals with solving the Routing and Wavelength Assignment problem where the number of accepted connections is to be maximized. Lagrangean decomposition as well as Lagrangean relaxation are studied for both node‐arc formulations and arc‐path formulation. It is shown that relaxing the demand constraints yields an edge‐disjoint path problem with profits that is NP‐hard, while the Lagrangean problem obtained when the clash constraints are relaxed becomes a shortest path problem or a 0–1 linear knapsack problem, depending on the formulation used. Moreover, it is shown that the Lagrangean decomposition is not stronger than the Lagrangean relaxation of the demand constraints. We also propose a subgradient algorithm to solve the Lagrangean dual obtained by relaxing the clash constraints. Numerical results demonstrate a high quality of Lagrangean dual bounds with fast computation time. © 2011 Wiley Periodicals, Inc. NETWORKS, 2012
The complexity of welfare maximization in congestion games
Authors: Meyers Carol A. , Schulz Andreas S. 
Published: May 2011

AbstractWe investigate issues of complexity related to welfare maximization in congestion games. In particular, we provide a full classification of complexity results for the problem of finding a minimum cost solution to a congestion game, under the model of Rosenthal. We consider both network and general congestion games, and we examine several variants of the problem concerning the structure of the game and the properties of its associated cost functions. Many of these problem variants turn out to be NP‐hard, and some are hard to approximate to within any finite factor, unless P = NP. We also identify several versions of the problem that are solvable in polynomial time. © 2011 Wiley Periodicals, Inc. NETWORKS, 2012
A ΔRaf1–ER‐inducible oncogenic zebrafish liver cell model identifies hepatocellular carcinoma signatures
Authors: He Shuning , Krens SF Gabby , Zhan Huiqing , Gong Zhiyuan , Hogendoorn Pancras CW , Spaink Herman P , Snaar‐Jagalska B Ewa 
Published: May 2011

AbstractAlthough the underlying molecular mechanism of hepatocellular carcinoma remains unclear, signalling pathways essential in cell survival and growth are altered, including the Raf–MEK–MAPK pathway. This pathway can be activated by hepatitis B or C virus infections and the ectopic expression of the Raf‐1 oncogene is frequently seen in hepatocellular carcinomas. In addition, the Raf–MEK–MAPK pathway was also shown to be deregulated in zebrafish liver tumours. Based on the genetic conservation between zebrafish and human liver tumours, the zebrafish was used as an animal model to better understand the molecular basis of hepatocellular carcinoma. Here we establish an inducible oncogenic zebrafish cell model, in which oncogenic human Raf‐1(ΔRaf1) can be post‐transcriptionally activated in zebrafish liver cells by administration of 4‐hydroxytamoxifen (4HT). The ΔRaf1 activation resulted in the hyperactivation of the zebrafish MEK–ERK cascade, promoted cell growth and proliferation, and inhibited apoptosis. The mitogenic transformation of the ZFL–ΔRaf1–ER cells was confirmed by in vivo allo‐transplantation and in silico microarray analyses. Gene expression profiling of cells treated with 4HT and a MEK‐inhibitor identified a Raf–MEK‐dependent signature set. This transcriptome response was compared to zebrafish and human liver cancer transcriptomes. We identified, and validated by quantitative PCR, a set of genes transcriptionally regulated by hyperactive MAPK signalling in ZFL–ΔRaf1–ER cells, zebrafish liver tumours and human liver tumours, suggesting that the in vitro zebrafish liver cell model can be used for further study of the molecular basis of human hepatocellular carcinoma. The molecular targeting of the commonly regulated hepatocellular carcinoma genes using the ZFL–ΔRaf1–ER cell model can be applied for high‐throughput preclinical target discovery. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Osteoclast formation and function in pigmented villonodular synovitis
Authors: Taylor Richard , Kashima Takesh G , Knowles Helen , Gibbons C L Max H , Whitwell Duncan , Athanasou Nicholas A 
Published: May 2011

AbstractPigmented villonodular synovitis (PVNS) is a synovial tumour‐like lesion that frequently causes osteolysis. PVNS contains numerous macrophages and osteoclast‐like giant cells. In this study, we have analysed the cytochemical and functional characteristics of mononuclear and multinucleated cells in PVNS and determined the cellular and humoral mechanisms underlying giant cell formation and resorption in PVNS. Giant cells and CD14+ and CD14− mononuclear cell populations were isolated from PVNS synovial tissue and cultured alone or in the presence and absence of the osteoclastogenic factors, RANKL and M‐CSF. Osteoclast formation and activity was assessed by expression of TRAP and evidence of lacunar resorption. Giant cells in PVNS expressed an osteoclast‐phenotype (CD51+, TRAP+, CD14−, HLA‐DR−) and were formed only in cultures of mononuclear cells that expressed the macrophage marker CD14. Osteoclast formation required RANKL and occurred in both the presence and absence of exogenous M‐CSF. CD14− cells in PVNS expressed RANKL. Lacunar resorption by PVNS‐derived giant cells was abolished by the addition of the bisphosphonate, zoledronate. Our findings indicate that osteoclasts form by a RANKL‐dependent mechanism from CD14+ mononuclear phagocytes in PVNS. Osteoclast formation occurred even in the absence of exogenous M‐CSF, a finding which is in keeping with over‐expression of M‐CSF playing a pathogenic role in this condition. Anti‐osteoclast resorptive treatment may be useful to control osteolysis in PVNS. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Influence of whole arm loss of chromosome 16q on gene expression patterns in oestrogen receptor‐positive, invasive breast cancer
Authors: Hungermann Daniela , Schmidt Hartmut , Natrajan Rachel , Tidow Nicola , Poos Kathrin , Reis‐Filho Jorge S , Brandt Burkhard , Buerger Horst , Korsching Eberhard 
Published: May 2011

AbstractA whole chromosome arm loss of 16q belongs to the most frequent and earliest chromosomal alterations in invasive and in situ breast cancers of all common subtypes. Besides E‐cadherin, several putative tumour suppressor genes residing on 16q in breast cancer have been investigated. However, the significance of these findings has remained unclear. Thus, other mechanisms leading to gene loss of function (eg haploinsufficiency, or distortion of multiple regulative subnetworks) remain to be tested as a hypothesis. To define the effect on gene expression of whole‐arm loss of chromosome 16q in invasive breast cancer, we performed global gene expression analysis on a series of 18 genetically extensively characterized invasive ductal breast carcinomas and verified the results by quantitative real‐time PCR (qRT–PCR). The distribution of the differential genes across the genome and their expression status was studied. A second approach by qRT–PCR in an independent series of 30 breast carcinomas helped to narrow down the observed effect. Whole‐arm chromosome 16q losses, irrespective of other chromosomal changes, are associated with decreased expression of a number of candidate genes located on 16q (eg CDA08, CGI‐128, SNTB2, NQO1, SF3B3, KIAA0174, ATBF1, GABARAPL2, KARS, GCSH, MBTPS1 and ZDHHC7) in breast carcinomas with a low degree of genetic instability. qRT–PCR provided evidence to suggest that the expression of these genes was reduced in a gene dosage‐dependent manner. The differential expression of the candidate genes according to the chromosomal 16q‐status vanished in genetically advanced breast cancer cases and changed ER status. These results corroborate previous reports about the importance of whole‐arm loss of chromosome 16q in breast carcinogenesis and give evidence for the first time that haploinsufficiency, in the sense of a gene dosage effect, might be an important contributing factor in the early steps of breast carcinogenesis. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Spermatocytic seminoma: toward further understanding of pathogenesis
Authors: Looijenga Leendert HJ 
Published: May 2011

AbstractHuman germ cell tumours comprise a heterogeneous group of neoplasms which, based on pathobiological, genetic and clinical characteristics, can be subdivided into different entities. One of these subgroups relates to the so‐called spermatocytic seminomas, benign tumours only found in the testis, preferentially in elderly men. Various developmental models for this type of germ cell tumour have been proposed and it is clear that spermatocytic seminoma has a pathogenesis independent from that of seminoma. A recent study examining expression of spermatogonial markers shows that spermatocytic seminomas are a heterogeneous group of tumours, with a supposed difference in origin, ie the majority from A$_{\rm{pale}}$ or B spermatogonia, and a minority from A$_{\rm{dark}}$ spermatogonia. However, this does not exclude an earlier cell of origin, possibly explaining the unique properties of this type of human germ cell tumour, with various counterparts in animals. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sustained response to intrathecal rituximab in EBV associated Post‐transplant lymphoproliferative disease confined to the central nervous system following haematopoietic stem cell transplant
Authors: Bonney Denise K. , Htwe Ei E. , Turner Andrew , Kelsey Anna , Shabani Abdu , Hughes Stephen , Hughes Imelda , Wynn Robert F. 
Published: May 2011

AbstractPost‐transplant lymphoproliferative disorder (PTLD) in the central nervous system (CNS) is a very rare complication of haematopoietic stem cell transplant (HSCT) and has a dismal prognosis. We report the successful treatment of this disorder with intrathecal rituximab therapy in two children who developed isolated CNS PTLD after HSCT. These children had failed to respond to standard chemotherapy, intravenous rituximab and EBV specific cellular therapy. Pediatr Blood Cancer 2012; 58: 459–461. © 2011 Wiley Periodicals, Inc.
Reporting health‐related quality of life scores to physicians during routine follow‐up visits of pediatric oncology patients: Is it effective?
Authors: Engelen Vivian , Detmar Symone , Koopman Hendrik , Maurice‐Stam Heleen , Caron Huib , Hoogerbrugge Peter , Egeler R. Maarten , Kaspers Gertjan , Grootenhuis Martha 
Published: May 2011

AbstractBackgroundThe aim of the current study is to investigate the effectiveness of an intervention that provides health‐related quality of life (HRQOL) scores of the patient (the QLIC‐ON PROfile) to the pediatric oncologist.ProcedureChildren with cancer participated in a sequential cohort intervention study: intervention N = 94, control N = 99. Primary outcomes of effectiveness were communication about HRQOL domains (t‐test, Mann–Whitney U‐test) and identification of HRQOL problems (chi‐squared test). Secondary outcomes were satisfaction (multilevel analysis), referrals (chi‐squared test), and HRQOL (multilevel analysis).ResultsThe QLIC‐ON PROfile increased discussion of emotional functioning (control M = 32.9 vs. intervention M = 47.4, P < 0.05) and psychosocial functioning (M = 56.9 vs. M = 63.8, P < 0.05). Additionally more emotional problems remained unidentified in the control compared to the intervention group, for example, anger (control 26% vs. intervention 3%, P < 0.01), fear (14% vs. 0%, P < 0.01), and sadness (26% vs. 0%, P < 0.001). The intervention had no effect on satisfaction and referrals, but did improve HRQOL of patients 5–7 years of age with respect to self‐esteem (P < 0.05), family activities (P < 0.05), and psychosocial functioning (P < 0.01).ConclusionsWe conclude that a PRO is a helpful tool for systematic monitoring HRQOL of children with cancer, without lengthening the duration of the consultation. It is recommended to be implemented in clinical practice. Pediatr Blood Cancer 2012; 58: 766–774. © 2011 Wiley Periodicals, Inc.
Autologous purified peripheral blood stem cell transplantation compare to chemotherapy in childhood acute lymphoblastic leukemia after low‐risk relapse
Authors: Balduzzi Adriana , Galimberti Stefania , Valsecchi Maria G. , Bonanomi Sonia , Conter Valentino , Barth Andrea , Rovelli Attilio , Henze Günter , Biondi Andrea , von Stackelberg Arend 
Published: May 2011

AbstractBackgroundThe treatment of childhood B‐cell precursor acute lymphoblastic leukemia (ALL) after isolated extramedullary or late relapse is mostly based on chemotherapy or allogeneic transplantation. The aim of this study is to provocatively assess the role of purified autologous transplantation compared with best chemotherapy results in the same setting.ProcedureWe reported a series of 30 pediatric patients who underwent purified peripheral blood autologous transplantation for ALL in CR2, after isolated extramedullary (7), or late medullary (23) relapse from January 1997 and March 2004. Among 246 patients treated with chemotherapy within Berlin–Frankfurt–Münster relapse protocols during the same period, we found 103 controls who matched our 30 cases, according to site of relapse, CR1 duration, time elapsed in CR2, and period of relapse.ResultsEvent‐free survival and survival at 5 years after relapse were 73.3% (SE 8.1) and 86.5% (SE 8.2) for auto‐transplanted cases and 40.0% (SE 9.7) and 62.5%(SE 9.6) for chemotherapy‐treated controls (P‐values: 0.012 and 0.025, respectively). The risk of relapse after auto‐transplantation at 1 and 4 years was approximately half and one‐fifth, respectively, of the same risk obtained with chemotherapy.ConclusionsThis matched analysis showed an advantage of purified autologous transplantation compared with chemotherapy in low‐risk relapsed ALL, possibly explained by the single‐center effect, the myeloablation of total body irradiation, the documented low tumor burden at mobilization and the stem cell isolation procedure. Pediatr Blood Cancer 2011; 57: 654–659. © 2011 Wiley‐Liss, Inc.