bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hydrological connectivity of soil pipes determined by ground‐penetrating radar tracer detection
Authors: Holden Joseph 
Published: April 2004

AbstractSoil pipes are common and important features of many catchments, particularly in semi‐arid and humid areas, and can contribute a large proportion of runoff to river systems. They may also signiﬁcantly inﬂuence catchment sediment and solute yield. However, there are often problems in ﬁnding and deﬁning soil pipe networks which are located deep below the surface. Ground‐penetrating radar (GPR) has been used for non‐destructive identiﬁcation and mapping of soil pipes in blanket peat catchments. While GPR can identify subsurface cavities, it cannot alone determine hydrological connectivity between one cavity and another. This paper presents results from an experiment to test the ability of GPR to establish hydrological connectivity between pipes through use of a tracer solution. Sodium chloride was injected into pipe cavities previously detected by the radar. The GPR was placed downslope of the injection points and positioned on the ground directly above detected soil pipes. The resultant radargrams showed signiﬁcant changes in reﬂectance from some cavities and no change from others. Pipe waters were sampled in order to check the radar results. Changes in electrical conductivity of the pipe water could be detected by the GPR, without data post‐processing, when background levels were increased by more than approximately twofold. It was thus possible to rapidly determine hydrological connectivity of soil pipes within dense pipe networks across hillslopes without ground disturbance. It was also possible to remotely measure travel times through pipe systems; the passing of the salt wave below the GPR produced an easily detectable signal on the radargram which required no post‐processing. The technique should allow remote sensing of water sources and sinks for soil pipes below the surface. The improved understanding of ﬂowpath connectivity will be important for understanding water delivery, solutional and particulate denudation, and hydrological and geomorphological model development. Copyright © 2004 John Wiley & Sons, Ltd.
Tortoises and hares: dissolution, erosion and isostasy in landscape evolution
Authors: Simms Michael J. 
Published: April 2004

AbstractDenudation mechanisms differ fundamentally between limestone and silicate rock types, which are subject to very different rate thresholds and enhancers/inhibitors. Silicates are removed largely by erosion, the mechanical entrainment and transport of particles. This is a relatively high energy, and highly episodic, process which occurs only when a minimum threshold ﬂow velocity is exceeded; it is inhibited by vegetation cover and favoured by strongly seasonal runoff. Limestone is removed largely by chemical dissolution at a rate directly proportional to runoff. Dissolution is a relatively low energy process that can occur at any ﬂow velocity or in static water; in general it is enhanced by vegetation cover and non‐seasonality of runoff. These contrasting factors in the denudation of silicates versus limestone can produce strikingly uneven rates of surface lowering across a landscape, sometimes akin to the well known ‘tortoise and hare race’, where the slow and steady denudation of limestones may in the long term exceed the sometimes rapid, but often localized and episodic, erosion of silicates. Prolonged exposure of limestone to a humid temperate climate in a tectonically stable environment produces low‐relief corrosion plains in which limestone uplands are anomalous and, in most instances, due to recent unrooﬁng from beneath a siliciclastic cover. In a highly seasonal or semi‐arid climate almost the exact inverse may develop, with ‘ﬂashy’ runoff and sparse vegetation favouring erosion rather than dissolution. Even under a constant humid climate progressive unrooﬁng of a thick limestone unit within folded siliciclastics may lead to a topographic inversion over time, with the limestone outcrop always forming a topographic low ﬂanked by siliciclastic uplands. Valleys will be initiated on anticlinal crests, where the limestone is ﬁrst unroofed, but progressive lowering of the limestone causes these valleys to migrate to their ﬁnal position in the synclinal troughs. In humid climates isostatic compensation in response to slow, but continuous, denudation of extensive limestone outcrops may be a signiﬁcant factor in the development of relief on adjacent, more slowly eroding, silicate outcrops. Copyright © 2004 John Wiley & Sons, Ltd.
Vector smooth transition regression models for US GDP and the composite index of leading indicators
Authors: Camacho Maximo 
Published: April 2004

AbstractIn this paper, I extend to a multiple‐equation context the linearity, model selection and model adequacy tests recently proposed for univariate smooth transition regression models. Using this result, I examine the nonlinear forecasting power of the Conference Board composite index of leading indicators to predict both output growth and the business‐cycle phases of the US economy in real time. Copyright © 2004 John Wiley & Sons, Ltd.
Müller cell response to laser‐induced increase in intraocular pressure in rats
Authors: Woldemussie Elizabeth , Wijono Mercy , Ruiz Guadalupe 
Published: April 2004

AbstractThe goal of this study was to investigate the reaction of the Müller cells to elevated intraocular pressure (IOP). Elevated IOP is one of the risk factors in glaucomatous retinal ganglion cell (RGC) degeneration. Müller cells play an important role in retinal homeostasis. The reaction of Müller cells was examined by evaluating temporal changes in glutamate aspartate transporter (GLAST), glutamine synthase (GS), glial fibrillary acidic protein (GFAP), and the B‐cell lymphoma (Bcl‐2) using immunoblotting and immunohistochemical techniques. After IOP was elevated for 4–60 days, there was a time‐related decrease in RGC ranging from 6% to 44%. There was also a time‐related increase in GLAST protein reaching maximum after 3 weeks of elevated IOP. On the other hand, there was very little change in the expression of GS during the first 2 weeks followed by some increase between 21 and 60 days. An increase in Bcl‐2 was biphasic with maximum increase after 4 days followed by decline after 15 and 21 days. GFAP, which is usually not expressed in normal Müller cells, was present at all time points. In all cases, the increase was most intense in the vicinity of the ganglion cells where the astrocytes and endfeet of the Müller cells are located. These results indicate that Müller cells react to the insult of elevated IOP by expressing GFAP and Bcl‐2, proteins that are expressed in reactive gliosis and other pathological conditions. The increase in GLAST along with minimum change in GS indicates a disturbance in glutamate homeostasis. © 2004 Wiley‐Liss, Inc.
In vitro myelination by oligodendrocyte precursor cells transfected with the neurotrophin‐3 gene
Authors: Rubio Nazario , Rodriguez Rodrigo , Arevalo Maria Angeles 
Published: April 2004

AbstractOligodendrocyte precursor cells require exogenous neurotrophin‐3 (NT‐3) for differentiation into oligodendrocytes. We transfected precursor cells with the gene for NT‐3 and looked for changes in their development into myelin‐forming cells. The expression of NT‐3 in transfected cells was demonstrated by reverse transcription followed by PCR as well as by Northern blots. Direct synthesis of the neurotrophin product and its release to the culture supernatants were also shown by specific ELISA. Transfection converts precursor cells into actively dividing cells that can incorporate 3H‐thymidine into DNA. In the absence of growth factors, a parallel increase in the survival of the transfected cultures was also demonstrated by the MTT test. The final demonstration of biological changes in transfected versus untreated cells was a 10‐fold increase in myelin basic protein production observed in Western blots and the direct observation by phase‐contrast and electron microscopy of myelin membranes in cocultures with hippocampal neurons. We discuss the future use of this transfected cells in regeneration and functional recovery in experimental models of multiple sclerosis. © 2004 Wiley‐Liss, Inc.
New method for the preparation of dibenzo[b, f][1,4]thiazepines
Authors: Fujii Takayoshi , Hao Wei , Yoshimura Toshiaki 
Published: April 2004

AbstractThe S‐amination of 9H‐thioxanthen‐9‐ol (2a) and 9‐substituted derivatives 2b–e (Me (b), Et (c), iPr (d), Ph (e)) with O‐mesitylenesulfonylhydroxylamine (MSH) was carried out. The expected product, 10‐amino‐9‐hydroxy‐9‐isopropyl‐9H‐thioxanthenium mesitylenesulfonate (3d), was obtained in 78(%) yield from the corresponding thioxanthen(9)‐ol 2d. However, in the case of 2a–c and 2e the reaction led instead to dibenzo[b,f][1,4]thiazepines 6a–c and 6e in moderate yields. © 2004 Wiley Periodicals, Inc. Heteroatom Chem 15:246–250, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/hc.20010
Medial temporal lobe activation during encoding and retrieval of novel face‐name pairs
Authors: Kirwan C. Brock , Stark Craig E.L. 
Published: April 2004

AbstractThe human medial temporal lobe (MTL) is known to be involved in declarative memory, yet the exact contributions of the various MTL structures are not well understood. In particular, the data as to whether the hippocampal region is preferentially involved in the encoding and/or retrieval of associative memory have not allowed for a consensus concerning its specific role. To investigate the role of the hippocampal region and the nearby MTL cortical areas in encoding and retrieval of associative versus non‐associative memories, we used functional magnetic resonance imaging (fMRI) to measure brain activity during learning and later recognition testing of novel face‐name pairs. We show that there is greater activity for successful encoding of associative information than for non‐associative information in the right hippocampal region, as well as in the left amygdala and right parahippocampal cortex. Activity for retrieval of associative information was greater than for non‐associative information in the right hippocampal region also, as well as in the left perirhinal cortex, right entorhinal cortex, and right parahippocampal cortex. The implications of these data for a clear functional distinction between the hippocampal region and the MTL cortical structures are discussed. © 2004 Wiley‐Liss, Inc.
Targeting an extracellular epitope of the human multidrug resistance protein 1 (MRP1) in malignant cells with a novel recombinant single chain Fv antibody
Authors: Binyamin Liat , Assaraf Yehuda G. , Haus‐Cohen Maya , Stark Michal , Reiter Yoram 
Published: April 2004

AbstractInherent and acquired multidrug resistance (MDR) is characterized by a simultaneous resistance to diverse anticancer drugs and is a major impediment towards curative chemotherapy of cancer. Hence one important goal is to develop strategies aimed at specific targeting of major anticancer drug efflux transporters of the ATP‐binding cassette (ABC) superfamily including multidrug resistance protein 1 ‐MRP1 (ABCC1). To date, no monoclonal antibody has been isolated that can target an extracellular MRP1 epitope. Using a phage display approach, we have isolated a recombinant single‐chain Fv (scFv) antibody that specifically reacts with the extracellular N‐terminus of the human MRP1. Flow cytometric analysis revealed that this scFv fragment binds specifically to various viable human tumor cells that display variable MRP1 expression levels but not to MRP1 null cells. Furthermore, this scFv antibody failed to react with tumor cells that overexpress other members of the MRP family that have an extracellular N‐terminus (MRP2 and MRP3) as well as with MRP4, MRP5, and breast cancer resistance protein. Flow cytometric analysis also showed a good correlation between the fluorescence intensity of the anti‐MRP1 scFv antibody and MRP1 levels in viable tumor cells. These findings constitute the first successful isolation of a small recombinant scFv antibody directed to an extracellular epitope of the MRP1 in viable malignant cells. These novel small Fv‐based recombinant antibodies that possess superior tumor penetration capabilities may possibly be used to selectively target drugs or tumor cells that express MRP‐1. © 2004 Wiley‐Liss, Inc.
Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane‐induced rat colon carcinogenesis through elevation of colonic PPARγ expression and alteration of lipid composition
Authors: Kohno Hiroyuki , Yasui Yumiko , Suzuki Rikako , Hosokawa Masashi , Miyashita Kazuo , Tanaka Takuji 
Published: April 2004

AbstractOur previous short‐term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in cis(c)9, trans(t)11, t13‐conjugated linolenic acid (CLN), inhibited the development of azoxymethane (AOM)‐induced colonic aberrant crypt foci (ACF). In our study, the possible inhibitory effect of dietary administration of BMO on the development of colonic neoplasms was investigated using an animal colon carcinogenesis model initiated with a colon carcinogen AOM. Male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks to induce colon neoplasms. They also received diets containing 0.01%, 0.1% or 1% BMO for 32 weeks, starting 1 week before the first dosing of AOM. At the termination of the study (32 weeks), AOM induced 83% incidence (15/18 rats) of colonic adenocarcinoma. Dietary supplementation with 0.01% and 0.1% BMO caused significant reduction in the incidence (47% inhibition by 0.01% BMO, p<0.02; 40% inhibition by 0.1% BMO, p<0.05; and 17% inhibition by 1% BMO) and the multiplicity (64% inhibition by 0.01% BMO, p<0.005; 58% inhibition by 0.1% BMO, p<0.02; and 48% inhibition by 1% BMO, p<0.05) of colonic adenocarcinoma, though a clear dose response was not observed. Such inhibition was associated with the increased content of CLA (c9,t11‐18:2) in the lipid composition in colonic mucosa and liver. Also, BMO administration in diet enhanced expression of peroxisome proliferator‐activated receptor (PPAR) γ protein in the nonlesional colonic mucosa. These findings suggest that BMO rich in CLN can suppress AOM‐induced colon carcinogenesis and the inhibition might be caused, in part, by modification of lipid composition in the colon and liver and/or increased expression of PPARγ protein level in the colon mucosa. © 2004 Wiley‐Liss, Inc.
Pathways of urothelial cancer progression suggested by Bayesian network analysis of allelotyping data
Authors: Bulashevska Svetlana , Szakacs Orsolya , Brors Benedikt , Eils Roland , Kovacs Gyula 
Published: April 2004

AbstractUrothelial cancers of the bladder (UC) comprise biologically heterogeneous group of tumors and display complex genetic alterations. Several genetic changes have been analyzed in detail and some of them are associated with the development and progression of UCs. Only a few studies, however, are focused on identifying the order in which the aberrations may appear during UC tumorigenesis. We have analyzed 123 papillary UCs of the bladder by microsatellites for each of the chromosomal regions that have been suggested to be specifically involved in this type of tumor. We used Bayesian network modeling that enables to uncover multivariate probabilistic dependencies between variables. This methodology applied to LOH data allowed us to discover patterns of losses in UCs. Exploiting the mechanism of probabilistic reasoning in Bayesian networks we suggest primary and secondary events in tumor pathogenesis and reconstruct the possible flow of progression of allelic changes. Losses of chromosome 9p and 9q were found to be the primary events. Losses of 8p and 17p are important events leading to progression of tumor cell clones. The loss of 17p occurs when both abnormalities of chromosome 9 and 8p are already present. There are chromosomal losses related to 8p (1q, 18q, 10q) and some losses like 5q/5p were associated with 17p, leading to the hypothesis of different genetic pathways of UC progression. The abnormalities of chromosome regions 13q, 16q, 6q, 14q, 3p are suggested to be late events being accumulated during the progression of cancer. Although some genetic changes were associated only with the 8p pathway, most secondary genetic changes appear in both pathways. Supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020‐7136/suppmat/index.html. © 2004 Wiley‐Liss, Inc.
HPV‐18 E6*I modulates HPV‐18 full‐length E6 functions in a cell cycle dependent manner
Authors: Guccione Ernesto , Pim David , Banks Lawrence 
Published: April 2004

AbstractThe E6 ORFs of the high‐risk Human Papillomavirus (HPV) Types 16 and 18 have been shown to encode (besides the full‐length product) several truncated forms, termed E6*. We have reported previously that the HPV‐18 E6*I protein interacts with the full‐length E6 protein as well as with the ubiquitin ligase E6‐AP and, as a result of this, E6* can inhibit E6‐mediated degradation of p53. Moreover, ectopic expression of the HPV‐18 E6*I protein has an antiproliferative effect in cervical cancer‐derived cell lines. These results led us to investigate further the modulatory functions of E6*I on E6. Using epitope tagged versions of the 2 proteins we have analyzed the sub‐cellular distribution of the full‐length HPV18 E6 and HPV18 E6*I, as well as their respective cellular abundance during the cell cycle, and show specific upregulation of E6*I during G2/M. We also investigated the effect of E6*I overexpression in cell lines derived from cervical tumors, with respect to the expression levels of E6 target proteins, such as p53, hDlg and Scribble and find a corresponding increase in p53 expression also during G2/M. In addition we show that the overexpression of E6*I reduces the amount of E6 in the insoluble nuclear and membrane fractions of the cell. E6 levels can, however, be restored by the addition of a specific proteasome inhibitor, suggesting that the interaction between E6 and E6*I leads to the destabilization of a subset of the E6 protein. These results suggest that the E6*I protein can function as a fine regulator of the full‐length E6 protein by direct interaction that leads both to changes in its cellular abundance as well as its distribution during particular phases of the cell cycle. © 2004 Wiley‐Liss, Inc.
Progression to androgen‐independent LNCaP human prostate tumors: Cellular and molecular alterations
Authors: Zhou Jin‐Rong , Yu Lunyin , Zerbini Luiz F. , Libermann Towia A. , Blackburn George L. 
Published: April 2004

AbstractLethal phenotypes of human prostate cancer are characterized by progression to androgen‐independence and metastasis. For want of a clinically relevant animal model, mechanisms behind this progression remain unclear. Our study used an in vivo model of androgen‐sensitive LNCaP human prostate cancer cell xenografts in male SCID mice to study the cellular and molecular biology of tumor progression. Primary tumors were established orthotopically, and the mice were then surgically castrated to withdraw androgens. Five generations of androgen‐independent tumors were developed using castrated host mice. Tumor samples were used to determine expressions of cellular and molecular markers. Androgen‐independent tumors had increased proliferation and decreased apoptosis compared to androgen‐sensitive tumors, outcomes associated with elevated expression of p53, p21/waf1, bcl‐2, bax and the bcl‐2/bax ratio. Blood vessel growth in androgen‐independent tumor was associated with increased expression of vascular endothelial growth factor. Overexpression of androgen receptor mRNA and reduced expression of androgen receptor protein in androgen‐independent tumors suggest that the androgen receptor signaling pathway may play an important role in the progression of human prostate cancer to androgen‐independence. The in vivo orthotopic LNCaP tumor model described in our study mimics the clinical course of human prostate cancer progression. As such, it can be used as a model for defining the molecular mechanisms of prostate cancer progression to androgen‐independence and for evaluating the effect of preventive or therapeutic regimens for androgen‐independent human prostate cancer. © 2004 Wiley‐Liss, Inc.
Prevalence of familial pancreatic cancer in Germany
Authors: Bartsch Detlef K. , Kress Ralf , Sina‐Frey Mercedes , Grützmann Robert , Gerdes Berthold , Pilarsky Christian , Heise Joachim W. , Schulte Klaus‐Martin , Colombo‐Benkmann Mario , Schleicher Cristina , Witzigmann Helmut , Pridöhl Olaf , Ghadimi Michael B. , Horstmann Olaf , von Bernstorff Wolfgang , Jochimsen Lisa , Schmidt Jan , Eisold Sven , Estévéz‐Schwarz Lope , Hahn Stephan A. , Schulmann Karsten , Böck Wolfgang , Gress Thomas M. , Zügel Nikolaus , Breitschaft Karl , Prenzel Klaus , Messmann Helmut , Endlicher Esther , Schneider Margarete , Ziegler Andreas , Schmiegel Wolff , Schäfer Helmut , Rothmund Matthias , Rieder Harald 
Published: April 2004

AbstractBased on several case‐control studies, it has been estimated that familial aggregation and genetic susceptibility play a role in up to 10% of patients with pancreatic cancer, although conclusive epidemiologic data are still lacking. Therefore, we evaluated the prevalence of familial pancreatic cancer and differences to its sporadic form in a prospective multicenter trial. A total of 479 consecutive patients with newly diagnosed, histologically confirmed adenocarcinoma of the pancreas were prospectively evaluated regarding medical and family history, treatment and pathology of the tumour. A family history for pancreatic cancer was confirmed whenever possible by reviewing the tumour specimens and medical reports. Statistical analysis was performed by calculating odds ratios, regression analysis with a logit‐model and the Kaplan‐Meier method. Twenty‐three of 479 (prevalence 4.8%, 95% CI 3.1–7.1) patients reported at least 1 first‐degree relative with pancreatic cancer. The familial aggregation could be confirmed by histology in 5 of 23 patients (1.1%, 95% CI 0.3–2.4), by medical records in 9 of 23 patients (1.9%, 95% CI 0.9–3.5) and by standardized interviews of first‐degree relatives in 17 of 23 patients (3.5%, 95% CI 2.1–5.6), respectively. There were no statistical significant differences between familial and sporadic pancreatic cancer cases regarding sex ratio, age of onset, presence of diabetes mellitus and pancreatitis, tumour histology and stage, prognosis after palliative or curative treatment as well as associated tumours in index patients and families, respectively. The prevalence of familial pancreatic cancer in Germany is at most 3.5% (range 1.1–3.5%) depending on the mode of confirmation of the pancreatic carcinoma in relatives. This prevalence is lower than so far postulated in the literature. There were no significant clinical differences between the familial and sporadic form of pancreatic cancer. © 2004 Wiley‐Liss, Inc.