bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hodological characterization of the septum in anuran amphibians: I. Afferent connections
Authors: Roden Katja , Endepols Heike , Walkowiak Wolfgang 
Published: February 2005

AbstractOn the basis of Nissl‐stained sections, we subdivided the septum of the gray treefrog Hyla versicolor in the lateral, central, and medial septal complex. The afferent projections of the different septal nuclei were studied by combined retrograde and anterograde tracing with biotin ethylendiamine (Neurobiotin). The central and medial septal complex receives direct input from regions of the olfactory bulb and from all other limbic structures of the telencephalon (e.g., amygdalar regions, nucleus accumbens), whereas projections to the lateral septal complex are absent or less extensive. The medial pallium projects to all septal nuclei. In the diencephalon, the anterior thalamic nucleus provides the main ascending input to all subnuclei of the anuran septum, which can be interpreted as a limbic/associative pathway. The ventromedial thalamic nucleus projects to the medial and lateral septal complex and may thereby transmit multisensory information to the limbic system. Anterior preoptic nucleus, suprachiasmatic nucleus, and hypothalamic nuclei innervate the central and lateral septal complex. Only the nuclei of the central septal complex receive input from the brainstem. Noteworthy is the relatively strong projection from the nucleus raphe to the central septal complex, but not to the other septal nuclei. J. Comp. Neurol. 483:415–436, 2005. © 2005 Wiley‐Liss, Inc.
Cellular and network properties of the subiculum in the pilocarpine model of temporal lobe epilepsy
Authors: Knopp Andreas , Kivi Anatol , Wozny Christian , Heinemann Uwe , Behr Joachim 
Published: February 2005

AbstractThe subiculum was recently shown to be crucially involved in the generation of interictal activity in human temporal lobe epilepsy. Using the pilocarpine model of epilepsy, this study examines the anatomical substrates for network hyperexcitability recorded in the subiculum. Regular‐ and burst‐spiking subicular pyramidal cells were stained with fluorescence dyes and reconstructed to analyze seizure‐induced alterations of the dendritic and axonal system. In control animals burst‐spiking cells outnumbered regular‐spiking cells by about two to one. Regular‐ and burst‐spiking cells were characterized by extensive axonal branching and autapse‐like contacts, suggesting a high intrinsic connectivity. In addition, subicular axons projecting to CA1 indicate a CA1‐subiculum‐CA1 circuit. In the subiculum of pilocarpine‐treated rats we found an enhanced network excitability characterized by spontaneous rhythmic activity, polysynaptic responses, and all‐or‐none evoked bursts of action potentials. In pilocarpine‐treated rats the subiculum showed cell loss of about 30%. The ratio of regular‐ and burst‐spiking cells was practically inverse as compared to control preparations. A reduced arborization and spine density in the proximal part of the apical dendrites suggests a partial deafferentiation from CA1. In pilocarpine‐treated rats no increased axonal outgrowth of pyramidal cells was observed. Hence, axonal sprouting of subicular pyramidal cells is not mandatory for the development of the pathological events. We suggest that pilocarpine‐induced seizures cause an unmasking or strengthening of synaptic contacts within the recurrent subicular network. J. Comp. Neurol. 483:476–488, 2005. © 2005 Wiley‐Liss, Inc.
Performance‐based middleware for Grid computing
Authors: Nudd G. R. , Jarvis S. A. 
Published: February 2005

AbstractThis paper describes a stateful service‐oriented middleware infrastructure for the management of scientific tasks running on multi‐domain heterogeneous distributed architectures. Allocating scientific workload across multiple administrative boundaries is a key issue in Grid computing and as a result a number of supporting services including match‐making, scheduling and staging have been developed. Each of these services allows the scientist to utilize the available resources, although a sustainable level of service in such shared environments cannot always be guaranteed. A performance‐based middleware infrastructure is described in which prediction data for each scientific task are calculated, stored and published through a Globus‐based performance information service. Distributing these data allows additional performance‐based middleware services to be built, two of which are described in this paper: an intra‐domain predictive co‐scheduler and a multi‐domain workload steering system. These additional facilities significantly improve the ability of the system to meet task deadlines, as well as enhancing inter‐domain load‐balancing and system‐wide resource utilization. Copyright © 2005 John Wiley & Sons, Ltd.
ASKALON: a tool set for cluster and Grid computing
Authors: Fahringer Thomas , Jugravu Alexandru , Pllana Sabri , Prodan Radu , Seragiotto Clovis , Truong Hong‐Linh 
Published: February 2005

AbstractPerformance engineering of parallel and distributed applications is a complex task that iterates through various phases, ranging from modeling and prediction, to performance measurement, experiment management, data collection, and bottleneck analysis. There is no evidence so far that all of these phases should/can be integrated into a single monolithic tool. Moreover, the emergence of computational Grids as a common single wide‐area platform for high‐performance computing raises the idea to provide tools as interacting Grid services that share resources, support interoperability among different users and tools, and, most importantly, provide omnipresent services over the Grid. We have developed the ASKALON tool set to support performance‐oriented development of parallel and distributed (Grid) applications. ASKALON comprises four tools, coherently integrated into a service‐oriented architecture. SCALEA is a performance instrumentation, measurement, and analysis tool of parallel and distributed applications. ZENTURIO is a general purpose experiment management tool with advanced support for multi‐experiment performance analysis and parameter studies. AKSUM provides semi‐automatic high‐level performance bottleneck detection through a special‐purpose performance property specification language. The PerformanceProphet enables the user to model and predict the performance of parallel applications at the early stages of development. In this paper we describe the overall architecture of the ASKALON tool set and outline the basic functionality of the four constituent tools. The structure of each tool is based on the composition and sharing of remote Grid services, thus enabling tool interoperability. In addition, a data repository allows the tools to share the common application performance and output data that have been derived by the individual tools. A service repository is used to store common portable Grid service implementations. A general‐purpose Factory service is employed to create service instances on arbitrary remote Grid sites. Discovering and dynamically binding to existing remote services is achieved through registry services. The ASKALON visualization diagrams support both online and post‐mortem visualization of performance and output data. We demonstrate the usefulness and effectiveness of ASKALON by applying the tools to real‐world applications. Copyright © 2005 John Wiley & Sons, Ltd.
Automatic performance analysis tools for the Grid
Authors: Gerndt M. 
Published: February 2005

AbstractApplications on Grids require scalable and online performance analysis tools. The execution environment of such applications includes a large number of processors. In addition, some of the resources such as the network will be shared with other applications. This requires applications to adapt dynamically to resource changes. The article presents the requirements of Grid application classes for performance analysis tools. It introduces a new analysis environment currently being developed for teraflop computers within the Peridot project at Technische Universität München. This environment applies a distributed automatic performance analysis approach. It is based on a formal specification of performance properties in the APART specification language. It uses a hierarchy of analysis agents that obtain performance data from a configurable monitoring system. This scalable design allows performance analysis for large Grid applications. Copyright © 2005 John Wiley & Sons, Ltd.
Streamlined analysis of pooled genotype data in SNP‐based association studies
Authors: Moskvina Valentina , Norton Nadine , Williams Nigel , Holmans Peter , Owen Michael , O'Donovan Michael 
Published: February 2005

AbstractSeveral groups have developed methods for estimating allele frequencies in DNA pools as a fast and cheap way for detecting allelic association between genetic markers and disease. To obtain accurate estimates of allele frequencies, a correction factor k for the degree to which measurement of allele‐specific products is biased is generally applied. Factor k is usually obtained as the ratio of the two allele‐specific signals in samples from heterozygous individuals, a step that can significantly impair throughput and increase cost. We have systematically investigated the properties of k through the use of empirical and simulated data. We show that for the dye terminator primer extension genotyping method we have applied, the correction factor k is substantially influenced by the dye terminators incorporated, but also by the terminal 3′ base of the extension primer. We also show that the variation in k is large enough to result in unacceptable error rates if association studies are conducted without regard to k. We show that the impact of ignoring k can be neutralized by applying a correction factor kmax that can be easily derived, but this at the potential cost of an increase in type I error. Finally, based upon observed distributions for k we derive a method allowing the estimation of the probability pooled data reflects significant differences in the allele frequencies between the subjects comprising the pools. By controlling the error rates in the absence of knowledge of the appropriate SNP‐specific correction factors, each approach enhances the performance of DNA pooling, while considerably streamlining the method by reducing time and cost. Genet. Epidemiol. © 2005 Wiley‐Liss, Inc.
Impact of young age on prognosis for head and neck cancer: A matched‐pair analysis
Authors: Gilroy Jeffrey S. , Morris Christopher G. , Amdur Robert J. , Mendenhall William M. 
Published: February 2005

AbstractBackground.The purpose of this study was to review outcomes of young patients (age <40 years) treated with definitive radiotherapy alone for squamous cell carcinoma of the oropharynx, and larynx, and to compare these results with an older matched patient cohort.Methods.Since 1983, 30 previously untreated young patients underwent definitive radiotherapy at the University of Florida and were matched with an older group of patients (age >45 years) with respect to primary site, stage of disease, and sex.Results.There was no difference in cause‐specific survival, locoregional control, or long‐term complications between the two groups; however, there was a significant difference in overall survival favoring young patients (p = .0174). Older patients had twice as many second malignancies.Conclusion.Young age does not confer a worse prognosis in patients treated with definitive radiotherapy for squamous cell carcinoma of the oropharynx and larynx. © 2005 Wiley Periodicals, Inc. Head Neck 27: XXX–XXX, 2005
Threat perception distortions and psychopathological symptoms in typically developing children
Authors: Muris Peter , Meesters Cor , Smulders Lianne , Mayer Birgit 
Published: February 2005

AbstractThis study examined relationships between symptoms of anxiety, aggression, and depression, on the one hand, and threat perception distortions, on the other hand. A large sample of typically developing children aged 8–12 years (N=157) were interviewed with an instrument for assessing the main types of childhood psychopathology, and were then exposed to a series of ambiguous vignettes in order to measure threat perception. As all measures were obtained twice, some 8 weeks apart, it was also possible to study prospective relationships between threat perception distortions and psychopathological symptoms. Results showed that threat perception was associated with a broad range of psychopathological symptoms, although the connection with anxiety was the most robust. No support was found for the notion that threat perception scores were predictive for the persistence of psychopathological symptoms during the 8‐weeks period. Copyright © 2005 John Wiley & Sons, Ltd.
Exposure to childhood infections and risk of Epstein‐Barr virus–defined Hodgkin's lymphoma in women
Authors: Glaser Sally L. , Keegan Theresa H. M. , Clarke Christina A. , Trinh Muoi , Dorfman Ronald F. , Mann Risa B. , DiGiuseppe Joseph A. , Ambinder Richard F. 
Published: February 2005

AbstractThe role of Epstein‐Barr virus (EBV) in Hodgkin's lymphoma (HL) etiology remains unresolved as EBV is detected in only some HL tumors and few studies have tried to reconcile its presence with factors suggesting viral etiology (e.g., childhood social class, infection history). In a population‐based case‐control study of San Francisco Bay area women, we analyzed interview data by tumor EBV status. Among 211 young adult cases, EBV‐positive HL (11%) was associated with a single vs. shared bedroom at age 11 (OR = 4.0, 95% CI 1.1–14.4); risk was decreased for common childhood infections (OR = 0.3, 95% CI 0.1–1.0), including measles before age 10, but not with prior infectious mononucleosis (IM), which is delayed EBV infection. No study factors affected risk of young adult EBV‐negative HL. Among 57 older adult cases, EBV‐positive HL (23%) was unrelated to study factors; EBV‐negative HL was associated with a single bedroom at age 11 (OR = 3.6, 95% CI 1.5–9.1) and IM in family members (OR = 3.1, 95% CI 1.1–9.0). Thus, delayed exposure to infection may increase risk of EBV‐positive HL in young adults, but risk patterns differ in younger and older women for both EBV‐positive and ‐negative HL. Late EBV infection does not appear relevant to risk, suggesting that other pathogens impact HL etiology in affluent female populations. Inconsistency of findings with prior studies may reflect failure of study risk factors to proxy meaningful exposures, risk differences by gender, or selection or misclassification bias. Null findings for EBV‐negative HL indicate that etiologic models should be reconsidered for this common form. © 2005 Wiley‐Liss, Inc.
Absence of acute apoptotic response to genotoxic carcinogens in p53‐deficient mice is associated with increased susceptibility to azoxymethane‐induced colon tumours
Authors: Hu Ying , Le Leu Richard K. , Young Graeme P. 
Published: February 2005

AbstractAcute apoptotic response to genotoxic carcinogens (AARGC) might be important for controlling the consequences of mutational load in the colon. It has been shown to occur in parallel with activation of DNA repair mechanisms. Inadequate AARGC might allow development of mutated clones with the potential to progress to cancer. In this study, we tested if p53 levels were important for AARGC in the colon and whether defective AARGC was associated with increased risk for colorectal oncogenesis. Apoptosis was measured in colonic epithelium of mice from each p53 genotype (p53−/−, p53+/−, wild‐type) without and 8 hr following a single injection of azoxymethane (AOM). To determine risk for carcinogen‐induced colorectal cancer (CRC), groups of mice from each p53 genotype received 3 weekly injections of AOM and colons were examined for tumour 20 weeks later. Rates of spontaneous apoptosis in colon were not affected by p53 level. However, AARGC was absent in p53−/− mice and reduced by 50% in p53+/− mice (both p < 0.01) compared to wild‐type mice. AOM induced tumours in 30% of wild‐type mice (average multiplicity 1.0 tumours/mouse) compared to 72% of p53+/− mice (2.0 tumours/mouse, p < 0.01) and 100% of p53−/− mice (2.8 tumours/mouse, p < 0.01). Without AOM, significantly fewer mice in all groups had tumours. Rates of apoptosis in tumours were independent of p53 status. p53 dysfunction puts intestinal epithelia at increased risk of genotoxin‐induced oncogenesis due to impairment of apoptotic response mechanisms. p53 levels do not appear, however, to be important for spontaneous apoptosis in normal epithelium or apoptosis in tumours. Subsequent studies are now warranted to test the converse, namely, that enhanced apoptotic response to carcinogen reduces risk for colorectal oncogenesis. © 2005 Wiley‐Liss, Inc.
Potential attenuation of p38 signaling by DDB2 as a factor in acquired TNF resistance
Authors: Sun Chun‐Ling , Chao Chuck C.‐K. 
Published: February 2005

AbstractOur previous study demonstrated that DDB2, a DNA repair protein, attenuates cell surface membrane‐associated death signal induced by UV or FasAb; DDB2 is overexpressed in cisplatin‐selected cells. However, the molecular mechanism underlying the protective role of DDB2 along the apoptotic pathway remains unknown. Our study identified the cross‐resistance of the cisplatin‐selected cells to tumor necrosis factor‐α (TNF‐α). Since knock‐down of the DDB2 level rendered cells (HR18) sensitive to the treatment, the cell sensitivity to TNF‐α appears inversely proportional to the cellular level of DDB2. Treatment of HeLa cells with TNF‐α transiently induced activation of p38MAPK signal, but this induction was significantly reduced in the resistant cells. Overexpression of DDB2 attenuated the activation of p38 in cells. TNF‐α‐induced apoptotic signals, represented by caspase‐8 and downstream substrate cleavage, were reduced in resistant cells compared to their sensitive counterparts. Inhibition of p38 signal by SB202190 clearly attenuated TNF‐α‐induced apoptotic signals. Moreover, overexpression of DDB2 in HR18 cells also attenuated TNF‐α induced caspase activation. These results suggest that p38MAPK activation may be a key upstream signal of TNF‐α‐induced apoptosis and that attenuation of p38 signal by DDB2 overexpression may be responsible for acquired TNF‐α resistance. © 2005 Wiley‐Liss, Inc.
Aberrant methylation of Reprimo in human malignancies
Authors: Takahashi Takao , Suzuki Makoto , Shigematsu Hisayuki , Shivapurkar Narayan , Echebiri Chinyere , Nomura Masaharu , Stastny Victor , Augustus Meena , Wu Chew‐Wun , Wistuba Ignacio I. , Meltzer Stephen J. , Gazdar Adi F. 
Published: February 2005

AbstractReprimo is a new candidate mediator of p53‐mediated cell cycle arrest at the G2 phase. Loss of Reprimo gene expression accompanied by its promoter methylation was identified in pancreatic and lung cancers. Our aim was to examine the methylation status of Reprimo in a broad range of cancers. We examined Reprimo expression by RT‐PCR and the DNA methylation status of the Reprimo promoter by MSP in 39 tumor cell lines. Loss or downregulation of Reprimo expression was frequent (62%), and we confirmed that transcriptional repression of Reprimo was caused by hypermethylation (overall concordance 92%). Treatment of expression‐negative cells with 5‐aza‐2′‐deoxycytidine restored Reprimo expression. We then examined aberrant methylation of Reprimo in 645 tumors representing 16 tumor types. Promoter methylation of Reprimo was found in 79% of gastric cancers, 62% of gallbladder cancers, 57% of lymphomas, 56% of colorectal cancers, 40% of esophageal adenocarcinomas, 37% of breast cancers and 31% of leukemias. Methylation frequencies in ovarian cancers, bladder cancers, cervical cancers, brain tumors, malignant mesotheliomas and pediatric tumors were lower (0–20%). Reprimo methylation was rarely detected in nonmalignant tissues (0–11%) except for gastric epithelia. While colorectal polyps were also frequently methylated (27%), chronic cholecystitis samples were infrequently methylated (4%). Furthermore, we failed to identify Reprimo mutation in colorectal and gastric cancer cell lines and 50 primary colorectal cancers. Aberrant methylation of Reprimo with loss of expression is a common event and may contribute to the pathogenesis of some types of human malignancy. © 2005 Wiley‐Liss, Inc.
Diethylstilbestrol effects and lymphomagenesis in Mlh1‐deficient mice
Authors: Kabbarah Omar , Sotelo Andrea K. , Mallon Mary Ann , Winkeler Erin L. , Fan Ming‐Yu , Pfeifer John D. , Shibata Darryl , Gutmann David H. , Goodfellow Paul J. 
Published: February 2005

AbstractInherited defects in DNA mismatch repair (MMR) predispose to a variety of malignancies in humans and in mouse knockout models. In humans, hemizygosity for one of several DNA MMR genes greatly increases an individual's risk for colon and endometrial carcinoma. Hemizygous mice develop gastrointestinal tumors at a low to moderate frequency. Homozygous nulls have higher rates of gastrointestinal tumors and are particularly susceptible to lymphoma. In an effort to model endometrial carcinoma associated with mutation in MMR, we treated mice carrying knockout alleles for Mlh1 or Msh2 with the synthetic estrogen diethylstilbestrol (DES), a known promoter of uterine endometrial carcinoma. The C57BL/6 mice carrying DNA MMR mutations failed to develop endometrial carcinomas. However, the Mlh1‐deficient mice treated with DES tended to become moribund at an early age and had very early onset of lymphoma. Comparison of DES‐treated and untreated Mlh1−/− animals suggests the combination of Mlh1 deficiency and DES exposure accelerates lymphomagenesis. © 2005 Wiley‐Liss, Inc.
CCR10 is expressed in cutaneous T‐cell lymphoma
Authors: Notohamiprodjo Mike , Segerer Stephan , Huss Ralf , Hildebrandt Bernhard , Soler Dulce , Djafarzadeh Roghieh , Buck Wiebke , Nelson Peter J. , von Luettichau Irene 
Published: February 2005

AbstractCutaneous T‐cell lymphoma (CTCL) is characterized by recruitment of malignant T‐cell clones into the skin. The mechanisms involved in tumor homing are still not fully elucidated, though chemokines and chemokine receptors have been suggested to play a role in the pathogenesis. Here, we demonstrate extensive expression of CCR10 in skin biopsies of patients with Sézary syndrome (SS, n = 3), mycosis fungoides (MF, n = 2) and unspecified CTCL (n = 3). In addition, we expand prior findings of CXCR3 expression in MF to other entities of CTCL. Expression of CCR5 was detected in 2 of the examined skin biopsies. The functionality of CCR10 and CXCR3 in SS was demonstrated using the SS T‐cell line HUT78. Our data support a potential role of CXCR3 in CTCL and strongly suggest that CCR10 and its ligand CCL27 may contribute to the skin infiltration of malignant T‐cells in this group of lymphoproliferative disorders. © 2005 Wiley‐Liss, Inc.