bluuebunny/crossref_metadata_2025_split huggingface dataset:
Controls on the transition from meandering to straight channels in the wetlands of the Okavango Delta, Botswana
Authors: Tooth S. , McCarthy T. S. 
Published: December 2004

AbstractPrevious studies of alluvial rivers have shown that channel patterns form a continuum controlled by interactions among factors such as gradient, discharge, sediment size, and bank strength. Data from channels in the permanent wetlands of the Okavango Delta add to these ﬁndings by focusing on pattern transitions in channels with banks formed by sedges and grasses that are rooted in peat and underlain by unconsolidated sediment. Channels are well deﬁned, and transport ﬁne–medium sand as bedload between the vertical, vegetation‐lined banks. Water depths, velocities, grain sizes, and bankline vegetation do not vary signiﬁcantly or systematically downstream, but the permeable banks allow water to leak from the channels, contributing to an overall downstream decrease in discharge and width. In addition, as the Okavango River ﬂows from the <12 km wide ‘Panhandle’ and splits into distributaries in the broader ‘Fan’, valley gradient steepens by c. 60 per cent.These downstream changes result in channel pattern adjustments. In the Panhandle, the Okavango River is a relatively wide (c. 30–100 m), actively meandering, sinuous channel (P > 2·0), but further downstream in the Fan, the narrower (<40 m) distributaries follow laterally stable, less sinuous (‘straight’) courses (P < 1·75). Some channel pattern discrimination diagrams based on simple indices of gradient, discharge, sediment size or stream power are inadequate for analysing the meandering–straight transition in the Okavango but Parker's (1976) approach, based on ratios of depth–width and slope–Froude number, accurately characterizes the transition. Our ﬁeld observations, combined with the results from previous experimental studies, suggest that in relatively wide channels (w/d > 10), thalweg meandering results in scour of the unconsolidated sediment at the bank base, leading to undermining and collapse of the vegetation, and to slow meander migration. However, as channels narrow downstream (w/d < 10) with discharge losses, proportionally increasing sidewall drag exerted by bankline vegetation suppresses thalweg meandering and bank scour, and channels follow stable, less sinuous courses. Copyright © 2004 John Wiley & Sons, Ltd.
Pattern robustness of diagnostic gene expression signatures in leukemia
Authors: Kohlmann Alexander , Schoch Claudia , Dugas Martin , Rauhut Sonja , Weninger Felix , Schnittger Susanne , Kern Wolfgang , Haferlach Torsten 
Published: December 2004

AbstractMicroarray technology has been proposed as an addition to the methods in current use for diagnosing leukemia. Before a new technology can be used in a diagnostic setting, the method has to be shown to produce robust results. It is known that, given the technical aspects of specimen sampling and target preparation, global gene expression patterns can change dramatically. Various parameters such as RNA degradation, shipment time, sample purity, and patient age can principally influence measured gene expression. However, thus far, no information has been available on the robustness of a diagnostic gene expression signature. We demonstrate here that for a subset of acute leukemia, expression profiling is applicable in a diagnostic setting, considering various influencing parameters. With the use of a set of differentially expressed genes, that is, a diagnostic gene expression signature, four genetically defined acute myeloid leukemia subtypes with recurrent chromosomal aberrations can clearly be identified. In addition, we show that preparation by different operators and using different sample‐handling procedures did not impair the robustness of diagnostic expression signatures. In conclusion, our results provide additional support for the applicability of microarrays in a diagnostic setting, and we have been encouraged to enroll patients in a prospective study in which microarrays will be tested as an additional routine diagnostic method in parallel with standard diagnostic procedures. © 2004 Wiley‐Liss, Inc.
A novel candidate region linked to development of both pheochromocytoma and head/neck paraganglioma
Authors: Cascón Alberto , Ruiz‐Llorente Sergio , Rodríguez‐Perales Sandra , Honrado Emiliano , Martínez‐Ramírez Ángel , Letón Rocío , Montero‐Conde Cristina , Benítez Javier , Dopazo Joaquín , Cigudosa Juan C. , Robledo Mercedes 
Published: December 2004

AbstractAlthough the histologic distinction between pheochromocytomas and head and neck paragangliomas is clear, little is known about the genetic differences between them. To date, various sets of genes have been found to be involved in inherited susceptibility to developing both tumor types, but the genes involved in sporadic pathogenesis are still unknown. To define new candidate regions, we performed CGH analysis on 29 pheochromocytomas and on 24 paragangliomas mainly of head and neck origin (20 of 24), which allowed us to differentiate between the two tumor types. Loss of 3q was significantly more frequent in pheochromocytomas, and loss of 1q appeared only in paragangliomas. We also found gain of 11q13 to be a significantly frequent alteration in malignant cases of both types. In addition, recurrent loss of 8p22–23 was found in 62% of pheochromocytomas (including all malignant cases) versus in 33% of paragangliomas, suggesting that this region contains candidate genes involved in the pathogenesis of this abnormality. Using FISH analysis on tissue microarrays, we confirmed genomic deletion of this region in 55% of pheochromocytomas compared to 12% of paragangliomas. Loss of 8p22–23 appears to be an important event in the sporadic development of these tumors, and additional molecular studies are necessary to identify candidate genes in this chromosomal region. © 2004 Wiley‐Liss, Inc.
A deterministic method to characterize canopy radiative transfer properties
Authors: Link Timothy E. , Marks Danny , Hardy Janet P. 
Published: December 2004

AbstractInvestigations of snowcover dynamics beneath vegetation canopies require either measured or estimated solar and thermal radiation values at the snow surface. A deterministic method is presented that uses portable arrays of pyranometers and pyrgeometers to quantify the amount of incoming radiation at the snow surface. Example solar and thermal radiation datasets are presented from boreal deciduous, boreal coniferous and temperate coniferous forest stands. The data indicate that the canopies transmitted 33% (4–8 March), 15% (6–10 February), and 3% (22–24 September) of the above‐canopy radiation. In the boreal deciduous and temperate conifer stands, thermal radiation is increased by 25% and 34% respectively. Thermal gains partially offset solar reduction, such that incoming all‐wave radiation is decreased by 22% and 25% respectively for each of these stands. When recorded at a high temporal resolution, array data can estimate below‐canopy diffuse solar radiation values for estimation techniques that treat direct and diffuse transmission independently. We provide examples of how radiometer array data are used to derive simple canopy radiation transmissivity parameters for global, beam and diffuse radiation. Radiometer arrays also provide data for detailed investigations to assess within‐stand radiation variability, or to investigate radiation variations across land cover discontinuities, to advance our understanding of snowcover energetics in complex environments. Copyright © 2004 John Wiley & Sons, Ltd.
Trends in incidence and prognosis for head and neck cancer in the United States: A site‐specific analysis of the SEER database
Authors: Carvalho André Lopes , Nishimoto Inês Nobuko , Califano Joseph A. , Kowalski Luiz Paulo 
Published: December 2004

AbstractDespite recent advances in the diagnosis and treatment of head and neck cancer, there has been little evidence of improvement in 5‐year survival rates over the last few decades. To determine more accurate trends in site‐specific outcomes as opposed to a more general overview of head and neck cancer patients, we analyzed the site‐specific data collected in the Surveillance, Epidemiology, and End Results—SEER Public‐Use Database 1973–1999. Based on the selection criteria, 96,232 cases were evaluated for trend analysis in incidence, clinical stage, treatment and 5‐year survival. During the period 1973–1999, site‐specific incidence rates for head and neck cancer changed significantly. Site‐specific analysis of survival from 1974–1997 showed significant improvements in 5‐year survival rates for cancers of the nasopharynx, oropharynx and hypopharynx (38.1% to 56.7% for nasopharynx, p < 0.001; 36.3% to 49.1% for oropharynx, p = 0.001 and 28.3% to 33.3% for hypopharynx, p = 0.015). The prognosis for early‐stage salivary gland cancer during 1983–1997 and late‐stage larynx cancer during 1974–1997 also demonstrated improvement (82.7% to 88.5%, p = 0.012 and 22.2% to 38.3%, p = 0.013, respectively). On the other hand, the prognosis for regional stage oral cavity cancer as well as early‐stage larynx cancer patients declined during 1983–1997 (49.2% to 43.8%, p = 0.032 and 82.3% to 74.3%, p = 0.002, respectively). Site‐specific changes in treatment and staging were also noted. Site‐specific analysis allows for a more accurate description of incidence, staging, treatment, and prognostic trends for head and neck cancer. © 2004 Wiley‐Liss, Inc.
Identification of c‐Jun as a critical mediator for the intracrine 24 kDa FGF‐2 isoform‐induced cell proliferation
Authors: Hortala Marylis , Estival Agnes , Pradayrol Lucien , Susini Christiane , Clemente François 
Published: December 2004

AbstractTumor cells frequently synthesize an N‐terminally extended the FGF‐2 isoform of 24 kDa devoid of signal peptide but that contains a functional nuclear localization sequence (NLS). Although the signaling pathways elicited by secreted FGF‐2 are well described, the molecular mechanisms involved in the growth promoting action of nuclearized 24 kDa FGF‐2 remain unknown. The cancer cell line AR4‐2J was engineered to stably express only the 24 kDa FGF‐2 isoform and cDNA microarrays were used to identify targets implicated in the intracrine‐induced cell proliferation. Levels of 27 transcripts were found either upregulated or downregulated compared to control cells. Among the 18 upregulated genes was c‐jun, which is often involved in cell proliferation. Real‐time PCR and Western blot analyses confirmed c‐jun induction at both mRNA and protein levels. The c‐jun antisense oligonucleotide strategy pointed out the involvement of c‐Jun in the 24 kDa FGF‐2‐induced cell proliferation. The mitogenic effect was found to depend on ERK pathway and not on phosphoinositide 3‐kinase, p38 MAPK, c‐Jun NH2‐terminal kinase signal transducers. In addition, the MEK inhibitor PD98059 reduced the 24 kDa FGF‐2‐dependent c‐Jun level. These data show that intracrine FGF‐2‐mediated regulation of cell growth involves ERK activation and consequent c‐Jun expression. Thus, despite its incapacity to be secreted, the intracellular‐localized 24 kDa FGF‐2 can activate a growth‐related signaling pathway normally elicited by cell surface receptors. © 2004 Wiley‐Liss, Inc.
Exosomes: A new delivery system for tumor antigens in cancer immunotherapy
Authors: Cho Jung‐Ah , Yeo Dong‐jun , Son Hye‐Youn , Kim Hyun‐Wha , Jung Dae‐Sun , Ko Jae‐Kyun , Koh Jason Soonju , Kim Yong‐Nyun , Kim Chul‐Woo 
Published: December 2004

AbstractExosomes are small membrane vesicles that are released into the extracellular environment during fusion of multivesicular bodies with plasma membrane. Exosomes are secreted by various cell types including hematopoietic cells, normal epithelial cells and even some tumor cells. They are known to carry MHC class I, various costimulatory molecules and some tetraspanins. Recent studies have shown the potential of using native exosomes as immunologic stimulants. Here, we demonstrate a novel means of using exosomes engineered to express a specific tumor antigen to generate an immune response against tumors. We expressed a target tumor antigen, human MUC1 (hMUC1), in 2 MHC type‐distinct mouse cell lines, CT26 and TA3HA. Analysis of exosomes purified from these cells revealed that exosomes contained the target MUC1 antigen on their surfaces as well as other well‐described exosomal proteins, including Hsc70 and MHC class I molecules. In addition, both autologous and allogenic exosomes were able to stimulate the activation of immune cells and suppress hMUC1‐expressing tumor growth in a MUC1‐specific and dose‐related manner. Therefore, these data suggest that exosomes can be engineered from tumor cell lines to deliver a target immunogen capable of inducing an effective immune response and that they may represent a new cell‐free tumor vaccine. © 2004 Wiley‐Liss, Inc.
Reproductive and hormonal factors and risk of brain tumors in adult females
Authors: Hatch Elizabeth E. , Linet Martha S. , Zhang Jianying , Fine Howard A. , Shapiro William R. , Selker Robert G. , Black Peter M. , Inskip Peter D. 
Published: December 2004

AbstractCauses of brain tumors are largely unknown, and there is an urgent need to identify possible risk factors. Several observations point to a possible role of reproductive hormones, but few epidemiologic studies have examined whether reproductive factors, such as age at menarche and parity, are associated with brain tumor risk. We conducted a multi‐center case‐control study of newly diagnosed glioma (n = 212) and meningioma (n = 151) and frequency‐matched controls (n = 436) in women from hospitals in Phoenix, Arizona; Boston, Massachusetts; and Pittsburgh, Pennsylvania between 1994 and 1998. Research nurses interviewed patients regarding potential risk factors for brain tumors, including reproductive factors and hormone use. Unconditional logistic regression analyses were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Risk of glioma increased with older age at menarche [OR = 1.90 (95% CI = 1.09–3.32) for age at menarche ≥14 vs. <12 years]. Early age at first birth was associated with reduced risk of glioma [OR = 0.43 (95% CI = 0.23–0.83) for a first birth before age 20 vs. nulliparity], but there was little effect of number of births. Exogenous hormone use was also associated with a lower risk of glioma, but risks did not vary systematically according to duration of use or age at first use. Possibly owing to low statistical power, there were few noteworthy associations between meningioma and reproductive factors, other than a nonsignificant (p = 0.09) trend of increasing risk with increasing age at menopause. The findings suggest that hormonal exposures early in life may be associated with risk of glioma, but the evidence is inconsistent and does not point clearly to a specific causal or protective hypothesis. © 2004 Wiley‐Liss, Inc.
Mammaglobin a in breast cancer: Existence of multiple molecular forms
Authors: O'Brien Neil A. , O'Donovan Norma , Ryan Bríd , Hill Arnold D.K. , McDermott Enda , O'Higgins Niall , Duffy Michael J. 
Published: December 2004

AbstractExisting serum‐based markers for breast cancer all lack organ specificity. Mammaglobin A (MGA) is a 93 amino acid protein expressed almost exclusively in breast tissue. The aim of our study was to investigate the different forms of MGA protein in fibroadenomas and breast carcinomas. MGA protein was measured by Western blotting in 132 breast cancers, 29 fibroadenomas and 14 nonbreast tissues. MGA protein in breast tissue was found to exist in 2 main forms. These forms migrated with approximate molecular masses of 18 and 25 kDa. Both forms of MGA were detected more frequently in breast carcinomas compared to fibroadenomas. The high molecular weight form of MGA but not the low molecular weight form was found more frequently in hormone receptor‐positive than in receptor‐negative cancers. Furthermore, an inverse relationship was found between the high molecular weight form of MGA and both tumour grade and proliferation index. No significant correlation was found between the MGA proteins and either tumor size or nodal status. Our results show that MGA protein exists in 2 main forms in breast tissue. As the high molecular weight form correlated positively with hormone receptors and negatively with tumor grade and proliferation rate, its presence is likely to be associated with a favourable prognosis for breast cancer. As expression of MGA is almost breast specific, it is a promising marker for breast cancer. Its most immediate use is likely to be in detecting micrometastases from breast cancer. © 2004 Wiley‐Liss, Inc.
Anti‐proliferative and proapoptotic effects of (−)‐epigallocatechin‐3‐gallate on human melanoma: Possible implications for the chemoprevention of melanoma
Authors: Nihal Minakshi , Ahmad Nihal , Mukhtar Hasan , Wood Gary S. 
Published: December 2004

AbstractMelanoma accounts for only about 4% of all skin cancer cases but most of skin cancer‐related deaths. Standard systemic therapies such as interferon (IFN) have not been adequately effective in the management of melanoma. Therefore, novel approaches are needed for prevention and treatment of this disease. Chemoprevention by naturally occurring agents present in food and beverages has shown benefits in certain cancers including nonmelanoma skin cancers. Here, employing 2 human melanoma cell lines (A‐375 amelanotic malignant melanoma and Hs‐294T metastatic melanoma) and normal human epidermal melanocytes (NHEM), we studied the antiproliferative effects of epigallocatechin‐3‐gallate (EGCG), the major polyphenolic antioxidant present in green tea. EGCG treatment was found to result in a dose‐dependent decrease in the viability and growth of both melanoma cell lines. Interestingly, at similar EGCG concentrations, the normal melanocytes were not affected. EGCG treatment of the melanoma cell lines resulted in decreased cell proliferation (as assessed by Ki‐67 and PCNA protein levels) and induction of apoptosis (as assessed cleavage of PARP, TUNEL assay and JC‐1 assay). EGCG also significantly inhibited the colony formation ability of the melanoma cells studied. EGCG treatment of melanoma cells resulted in a downmodulation of anti‐apoptotic protein Bcl2, upregulation of proapoptotic Bax and activation of caspases ‐3, ‐7 and ‐9. Furthermore, our data demonstrated that EGCG treatment resulted in a significant, dose‐dependent decrease in cyclin D1 and cdk2 protein levels and induction of cyclin kinase inhibitors (ckis) p16INK4a, p21WAF1/CIP1 and p27KIP1. Our data suggest that EGCG causes significant induction of cell cycle arrest and apoptosis of melanoma cells that is mediated via modulations in the cki‐cyclin‐cdk network and Bcl2 family proteins. Thus, EGCG, alone or in conjunction with current therapies, could be useful for the management of melanoma. © 2004 Wiley‐Liss, Inc.
Prescription drug use and risk of acute myeloid leukemia by French‐American‐British subtype: Results from a Los Angeles County case‐control study
Authors: Pogoda Janice M. , Katz Jonathan , McKean‐Cowdin Roberta , Nichols Peter W. , Ross Ronald K. , Preston‐Martin Susan 
Published: December 2004

AbstractChemotherapy is a well‐established risk factor for acute myeloid leukemia (AML) but little is known about other prescription drugs and AML risk. We report data from a population‐based Los Angeles County study in which 299 matched case‐control pairs had complete data on prescription drug use and 88% of cases were subtyped according to the French‐American‐British (FAB) criteria. Cases were diagnosed between 1987 and 1994. Prescription nonsteroidal anti‐inflammatory drug (NSAID) use for at least 4 weeks in the 2 to 10 years before diagnosis was associated with decreased risk (odds ratio = 0.5, 95% confidence interval = 0.3, 1.0; p = 0.04) with dose‐response most evident for FAB subtype M2 (OR = 0.6, CI: 0.1, 2.9 for duration ≤6 months; OR = 0.2, CI: 0.0, 1.6 for >6 months). For subtype M4, ORs increased with increasing duration of benzodiazepine use in the 2 to 10 years before diagnosis (OR = 1.5, CI: 0.3, 9.0 for ≤6 months vs. OR = 5.0, CI: 0.6, 42.8 for >6 months). These results suggest that prescription drugs other than chemotherapy may have FAB subtype‐specific effects on AML risk. © 2004 Wiley‐Liss, Inc.
Bortezomib is an efficient agent in plasma cell leukemias
Authors: Esparís‐Ogando Azucena , Alegre Adrián , Aguado Beatriz , Mateo Gema , Gutiérrez Norma , Bladé Joan , Schenkein David , Pandiella Atanasio , San Miguel Jesús F. 
Published: December 2004

AbstractPlasma cell leukemia (PCL) represents the most aggressive form of monoclonal gammopathy for which new treatment approaches are needed. Here we report the effect of Bortezomib on cells from 4 patients with PCL, as well as the in vivo efficacy on a patient with secondary PCL. Bortezomib reduced PCL numbers and was more efficient in cell growth inhibition than dexamethasone or doxorubicin. Treatment with Bortezomib induced procaspase‐3 and poly(ADP‐ribose) polymerase cleavage and decreased the amount of extracellular signal regulated kinase (Erk1/2) and phospho‐Erk1/2. However, Bortezomib did not substantially affect the levels of the Erk1/2 upstream activating kinase (MEK1), p27 or p21. Finally, we had the opportunity to use Bortezomib in a heavily pretreated patient with overt secondary PCL and severe anemia and thrombocytopenia. Following Bortezomib treatment, circulating plasma cells disappeared; what is more striking, the peripheral blood counts returned to normal, becoming transfusion‐independent. These data support the inclusion of Bortezomib in the therapeutic armamentarium of PCL. © 2005 Wiley‐Liss, Inc.
c‐myc‐induced hepatocarcinogenesis in the absence of IGF‐I receptor
Authors: Cadoret Axelle , Desbois‐Mouthon Christèle , Wendum Dominique , Leneuve Patricia , Perret Christine , Tronche François , Housset Chantal , Holzenberger Martin 
Published: December 2004

AbstractNumerous tumours, including hepatocarcinomas, produce IGFs, and some depend on these growth factors in a paracrine or autocrine fashion. We have shown that c‐myc‐induced experimental hepatocarcinogenesis is associated with enhanced production of IGF‐II. To assess the role of the IGF‐I receptor (IGF‐IR) in hepatocarcinogenesis, we generated conditional mutant mice that overexpressed c‐myc and were knocked out for IGF‐IR specifically in the liver. We compared these mice with littermate controls that also overexpressed c‐myc but had wild‐type IGF‐IR alleles. We found that the pretumoral phase, induced by early c‐myc expression and characterised by increased cell proliferation, was largely unaffected by the lack of IGF‐IR. To our further surprise, hepatocellular carcinomas (HCCs) lacking IGF‐IR readily developed and progressed at the same rate as control HCCs. At 9 months, all c‐myc transgenic mice displayed well‐differentiated multifocal tumours, regardless of whether their livers—and their tumours—were able to produce IGF‐IR. Levels of IRS‐1 and IRS‐2 were elevated in all tumours in the presence or absence of IGF‐IR, suggesting that the signalling pathway downstream of IGF‐IR is activated via IGF‐IR‐independent mechanisms in HCC. In conclusion, the deregulation of IGF signalling pathways, which often occurs during liver tumorigenesis, does not necessarily require IGF‐IRs, and hepatic IGF‐IR alone may not play a determinant role in c‐myc‐induced hepatocarcinogenesis. © 2004 Wiley‐Liss, Inc.