bluuebunny/crossref_metadata_2025_split huggingface dataset:
B‐cell non‐Hodgkin's lymphoma and hepatitis C virus infection: A systematic review
Authors: Negri Eva , Little D'Anna , Boiocchi Mauro , La Vecchia Carlo , Franceschi Silvia 
Published: March 2004

AbstractA high prevalence of hepatitis C virus (HCV) infection in patients with B‐cell non‐Hodgkin's lymphoma (B‐NHL) has been reported in some, but not all, studies, and the association showed a strong regional variation. We conducted a systematic review of the prevalence of HCV infection in case series of B‐NHL and, when an appropriate control group was available, of the odds ratio of B‐NHL associated with HCV infection. A high HCV prevalence in B‐NHL was found in southern and eastern Europe, Japan and the southern United States, but not in central and northern Europe, Canada, northern United States, or a few Asian countries. Possible sources of heterogeneity and bias are discussed. The odds ratio of B‐NHL for HCV infection was relatively weak, ranging from 2 to 4 in most studies. Thus, even if the observed association were causal, the percentage of cases of B‐NHL attributable to HCV infection would be relatively low (10%) also in countries with a high prevalence of HCV infection in the general population, and extremely low in other countries. This may explain apparent inconsistencies between studies. Potential mechanisms of action are also discussed. © 2004 Wiley‐Liss, Inc.
Bone metastasis: Osteoblasts affect growth and adhesion regulons in prostate tumor cells and provoke osteomimicry
Authors: Knerr Kerstin , Ackermann Karin , Neidhart Tanja , Pyerin Walter 
Published: March 2004

AbstractBone metastasis is the primary cause of death in human prostate cancer. Disseminated from primary tumor and distributed via the bloodstream, a proportion of prostate carcinoma cells eventually reach the skeleton and develop into metastases, requiring adhesion to inner bone surfaces lined by osteoblasts. The crosstalk of tumor cells with osteoblasts is a critical but poorly characterized step in the metastatic process. Using an in vitro metastasis model system, we have been examining effects of osteoblast‐released factors on gene expression of prostate carcinoma cells. Here, we show by large‐scale transcript profiling and quantitative RT‐PCR that osteoblast‐released factors target in particular the proliferation and adhesion regulons of tumor cells. Genes encoding components of the cell‐cycle control machinery and connected pathways are predominantly repressed and cell proliferation is slowed down, resembling in vivo observations assumed to render commonly used chemotherapeutic measures ineffective. Genes encoding anchoring junction components are predominantly elevated, and the adhesion properties of tumor cells are altered. Moreover, prostate carcinoma cells are provoked to undergo osteomimicry, i.e., to express bone cell–related genes. The data indicate that the crosstalk with osteoblasts induces expressional changes in prostate carcinoma cells favoring the bone colonization process. © 2004 Wiley‐Liss, Inc.
Polygenic control of hepatocarcinogenesis in Copenhagen × F344 rats
Authors: De Miglio Maria R. , Pascale Rosa M. , Simile Maria M. , Muroni Maria R. , Virdis Patrizia , Kwong Kelvin M.‐T. , Wong Leslie K.L. , Bosinco Giovanni M. , Pulina Franca R. , Calvisi Diego F. , Frau Maddalena , Wood Geoffrey A. , Archer Michael C. , Feo Francesco 
Published: March 2004

AbstractCop and CFF1 rats exhibit resistance to hepatocarcinogenesis, associated with high rates of remodeling of neoplastic lesions. We have mapped hepatocarcinogenesis susceptibility, resistance and remodeling loci affecting the number, volume and volume fraction of neoplastic nodules induced by the “resistant hepatocyte” model in male CFF2 rats. Three loci in significant linkage with the number or volume of nonremodeling lesions were identified on chromosomes 1, 4 and 18. Suggestive linkage with number or volume fraction of total, nonremodeling or remodeling lesions was found for 7 loci on chromosomes 1, 2, 13, 14 and 15. All of these loci showed significant allele‐specific effects on the phenotypic traits. We also detected by analysis of variance 19 2‐way interactions inducing phenotypic effects not predictable on the basis of the sum of separate effects. These novel epistatic loci were in significant linkage with the number and/or volume of total, nonremodeling or remodeling nodules. These data indicate that susceptibility to hepatocarcinogenesis in Cop rats is controlled by a complex array of genes with several gene–gene interactions and that different genetic mechanisms control remodeling and nonremodeling liver nodules. Frequent deregulation in human liver cancer of genes positioned in chromosomal segments syntenic to rat susceptibility/resistance loci suggests some similarities between the genetic mechanisms involved in hepatocarcinogenesis in rats and humans. © 2004 Wiley‐Liss, Inc.
Enhanced efficacy of DNA vaccination against Her‐2/neu tumor antigen by genetic adjuvants
Authors: Chang Sun Young , Lee Kyung‐Chul , Ko Sung‐Youl , Ko Hyun‐Jeong , Kang Chang‐Yuil 
Published: March 2004

AbstractCertain types of malignant tumors overexpress Her‐2/neu, a transmembrane glycoprotein of the class I receptor tyrosine kinase erbB family. To develop an effective Her‐2/neu vaccine for selective immunotherapy of these malignancies, we prepared Her‐2/neu DNA plasmid encoding the transmembrane and extracellular domain (pHM) and tested the ability of this construct to induce antitumor immunity in animal models. In addition, we investigated the effects of cytokine used as a genetic adjuvant. Modulation by factors that affect T‐cell function or hematopoiesis, including interleukin‐12, interleukin‐15, interleukin‐18, interleukin‐23, Eta‐1, Flt3L and GM‐CSF, was studied in the forms of monocistronic and bicistronic plasmid. Our results demonstrated that vaccination of pHM could induce successful antitumor immunity against Her‐2/neu‐expressing murine tumor cells in BALB/c mice. We also showed that the antitumor activity of pHM was augmented by coadministration and coexpression of different cytokines. Despite the similar levels of gene expression, the antitumor effects of bicistronic plasmids coexpressing Her‐2/neu antigen and cytokine were improved in comparison with coadministration of separate monocistronic plasmid. In particular, coexpression of interleukin‐18 or GM‐CSF with Her‐2/neu increased antitumor activity in both preventive and therapeutic experiments. These findings can help in the decision concerning which of the various cytokine adjuvants should be used for the development of a Her‐2/neu DNA vaccine. In addition, our results from a large panel of cytokine adjuvants in the various tumor models may provide an insight into the important immune components of antitumor immunity. © 2004 Wiley‐Liss, Inc.
Association of cigarette smoking with the risk of ovarian cancer
Authors: Pan Sai Yi , Ugnat Anne‐Marie , Mao Yang , Wen Shi Wu , Johnson Kenneth C. ,   The Canadian Cancer Registries Epidemiology Research Group
Published: March 2004

AbstractCigarette smoking may be associated with ovarian cancer risk. This association may differ by histological type. The authors conducted a population‐based case‐control study in Canada of 442 incident cases of ovarian cancer and 2,135 controls 20–76 years of age during 1994–1997 to examine this association, overall and by histological type. Compared to women who never smoked, those who smoked had higher odds (odds ratio [OR] = 1.22; 95% confidence interval [CI] = 0.98–1.53) of having ovarian cancer, and the OR was larger for ex‐smokers (1.30; 95% CI = 1.01–1.67) than for current smokers (1.10; 95% CI = 0.81–1.49). The association with cigarette smoking was stronger for mucinous tumors (OR = 1.77; 95% CI = 1.06–2.96) than for nonmucinous tumors (OR = 1.13; 95% CI = 0.89–1.44). In addition, the odds of smokers having mucinous tumors increased with years of smoking (OR = 1.36, 1.88, 1.19, 4.89 for <20, 21–30, 31–40 and >40 years, respectively; p for trend = 0.002), number of cigarettes smoked per day (OR = 1.55, 1.89, 2.28 for <10, 11–20 and >20 cigarettes/day, respectively; p for trend = 0.014) and smoking pack‐years (OR = 1.13, 2.65, 1.77 and 2.39 for <10, 11–20, 21–30 and >30 pack‐years, respectively; p for trend = 0.004). Our data suggest that cigarette smoking is associated with an increased risk of ovarian cancer, especially for mucinous types. © 2004 Wiley‐Liss, Inc.
Short‐term monitoring of fiscal policy discipline
Authors: Camba‐Mendez Gonzalo , Lamo Ana 
Published: April 2004

AbstractUnder the Maastricht Treaty and the Stability and Growth Pact (SGP), European Union (EU) Member States commit themselves to avoid excessive deficits over 3% of GDP and to pursue the medium‐term objective of budgetary positions close to balance or in surplus. The SGP also provides regulation for the surveillance of budgetary positions. An analysis of tools for the surveillance of budgetary positions is the focus of this paper. In particular, it addresses two open issues in the empirical public finance literature which are crucial for monitoring fiscal policy discipline in the EU. First, the estimation of the structural component of the fiscal balance ratio. Second, the computation, when only annual fiscal data are available, of quarterly budget balance ratios, using relevant information from quarterly measured macroeconomic series. An econometric model that addresses both issues is presented and estimated. Additionally, this modelling framework allows us to answer questions such as: what is the safety margin that will prevent a particular country from reaching, with certain probability, a budget deficit that breaches the 3% upper bound? Copyright © 2004 John Wiley & Sons, Ltd.
Do dropouts suffer from dropping out? Estimation and prediction of outcome gains in generalized selection models
Authors: Li Mingliang , Poirier Dale J. , Tobias Justin L. 
Published: April 2004

AbstractIn this paper we describe methods for predicting distributions of outcome gains in the framework of a latent variable selection model. We describe such procedures for Student‐t selection models and a finite mixture of Gaussian selection models. Importantly, our algorithms for fitting these models are simple to implement in practice, and also permit learning to take place about the non‐identified cross‐regime correlation parameter. Using data from High School and Beyond, we apply our methods to determine the impact of dropping out of high school on a math test score taken at the senior year of high school. Our results show that selection bias is an important feature of this data, that our beliefs about this non‐identified correlation are updated from the data, and that generalized models of selectivity offer an improvement over the ‘textbook’ Gaussian model. Further, our results indicate that on average dropping out of high school has a large negative impact on senior‐year test scores. However, for those individuals who actually drop out of high school, the act of dropping out of high school does not have a significantly negative impact on test scores. This suggests that policies aimed at keeping students in school may not be as beneficial as first thought, since those individuals who must be induced to stay in school are not the ones who benefit significantly (in terms of test scores) from staying in school. Copyright © 2004 John Wiley & Sons, Ltd.
Bayesian geoadditive modelling of breastfeeding initiation in Nigeria
Authors: Adebayo Samson B. 
Published: April 2004

AbstractA study into the geographical variability of timing of initial child breastfeeding after birth was carried out with the data set from the 1999 Nigeria Demographic and Health Survey. The effect of the metrical covariate of the mother's age at birth was assumed to be nonlinear and estimated nonparametrically. Other categorical covariates are estimated in the usual parametric form. Within a Bayesian context, appropriate priors are assigned for the geographical location, vector of the unknown (nonlinear) smooth functions and a further vector of the fixed effect parameters. For instance, a Markov random field prior is assumed on the spatial effects. Inferences are based on Markov chain Monte Carlo techniques while Bayesian model diagnostics are based on the deviance information criteria. Copyright © 2004 John Wiley & Sons, Ltd.
Inhibition of apoptosis and caspase‐3 in vascular smooth muscle cells by plasminogen activator inhibitor type‐1
Authors: Chen Yabing , Kelm Robert J. , Budd Ralph C. , Sobel Burton E. , Schneider David J. 
Published: April 2004

AbstractIncreased expression of plasminogen activator inhibitor type 1 (PAI‐1) is associated with decreased apoptosis of neoplastic cells. We sought to determine whether PAI‐1 alters apoptosis in vascular smooth muscle cells (VSMC) and, if so, by what mechanisms. A twofold increase in the expression of PAI‐1 was induced in VSMC from transgenic mice with the use of the SM‐22α gene promoter (SM22‐PAI+). Cultured VSMC from SM22‐PAI+ mice were more resistant to apoptosis induced by tumor necrosis factor plus phorbol myristate acetate or palmitic acid compared with VSMC from negative control littermates. Both wild type (WT) and a stable active mutant form of PAI‐1 (Active) inhibited caspase‐3 amidolytic activity in cell lysates while a serpin‐defective mutant (Mut) PAI‐1 did not. Similarly, both WT and Active PAI‐1 decreased amidolytic activity of purified caspase‐3, whereas Mut PAI‐1 did not. WT but not Mut PAI‐1 decreased the cleavage of poly‐[ADP‐ribose]‐polymerase (PARP), the physiological substrate of caspase‐3. Noncovalent physical interaction between caspase‐3 and PAI‐1 was demonstrable with the use of both qualitative and quantitative in vitro binding assays. High affinity binding was eliminated by mutations that block PAI‐1 serpin activity. Accordingly, attenuated apoptosis resulting from elevated expression of PAI‐1 by VSMC may be attributable, at least in part, to reversible inhibition of caspase‐3 by active PAI‐1.
Even‐tempered slater‐type orbitals revisited: From hydrogen to krypton
Authors: Chong Delano P. , Van Lenthe Erik , Van Gisbergen Stan , Baerends Evert Jan 
Published: March 2004

AbstractEven‐tempered Slater‐type orbital basis sets were developed in 1973, based on total atomic energy optimization. Here, we revisit ET STOs and propose new sets based on past experience and recent computational studies. From preliminary atomic and molecular tests, these sets are shown to be very well balanced and to perform, at lower cost, almost as well as a very large (close to complete) basis set. © 2004 Wiley Periodicals, Inc. J Comput Chem 25: 1030–1036, 2004
Conformational energies for 2‐substituted butanes
Authors: Wiberg Kenneth B. , Wang Yi‐Gui 
Published: March 2004

AbstractThe conformational free energies for some 2‐substituted butanes where X = F, Cl, CN, and CCH were calculated using G3‐B3, CBS‐QB3, and CCSD(T)/6‐311++G(2d,p) as well as other theoretical levels. The above methods gave consistent results with free energies relative to the trans conformers as follows: X = CCH, g+ = 0.77 ± 0.05 kcal/mol. g− = 0.88 ± 0.05 kcal/mol; X = CN, g+ = 0.85 ± 0.05 kcal/mol, g− = 0.75 ± 0.05 kcal/mol; X = Cl, g+ = 0.70 ± 0.05 kcal/ml, g− = 0.80 ± 0.05 kcal/mol; and X = F, g+ = 0.53 ± 0.05 kcal/mol, g− = 0.83 ± 0.05 kcal/mol. The conformational free energies also were estimated using the observed liquid phase IR spectra and intensities calculated using B3LYP/6‐311++G** and MP2/6‐311++G**. The rotational free energy profiles for all of the compounds were estimated at the G3‐B3 level. © 2004 Wiley Periodicals, Inc. J Comput Chem 25: 1127–1132, 2004
Cyclic k‐cycle systems of order 2kn + k: A solution of the last open cases
Authors: Vietri Andrea 
Published: April 2004

AbstractWe exhibit cyclic (Kv, Ck)‐designs with v > k, v ≡ k (mod 2k), for k an odd prime power but not a prime, and for k = 15. Such values were the only ones not to be analyzed yet, under the hypothesis v ≡ k (mod 2k). Our construction avails of Rosa sequences and approximates the Hamiltonian case (v = k), which is known to admit no cyclic design with the same values of k. As a particular consequence, we settle the existence question for cyclic (Kv, Ck)‐designs with k a prime power. © 2004 Wiley Periodicals, Inc. J Combin Designs 12: 299–310, 2004.
Synthetic retinoids as inducers of apoptosis in ovarian carcinoma cell lines
Authors: Holmes William F. , Soprano Dianne Robert , Soprano Kenneth J. 
Published: April 2004

AbstractApoptosis is also known as programmed cell death. Apoptosis plays an essential role in maintaining normal tissue and cell physiology in multicellular organisms. Clearance of aberrant or pre‐cancerous cells occurs through the induction of apoptosis. It has been reported that many tumors and tumor cell lines have dysfunctional apoptosis signaling, causing these tumors to escape immune monitoring and internal cellular control mechanisms. One potential cause of this dysfunctional apoptosis is the tumor suppressor p53, an important regulator of growth arrest and apoptosis that is mutated in over 50% of all cancers. Retinoids have great potential in the areas of cancer therapy and chemoprevention. While some tumor cells are sensitive to the growth inhibitory effects of natural retinoids such as all‐trans‐retinoic acid (ATRA), many ovarian tumor cells are not. 6‐[3‐(1‐Admantyl)]‐4‐hydroxyphenyl]‐2‐naphthalene carboxylic acid (CD437) and fenretinide N‐[4‐hydroxyphenyl] retinamide (4‐HPR) are conformationally restricted synthetic retinoids that induce growth arrest and apoptosis in both ATRA‐sensitive and ATRA‐resistant ovarian tumor cell lines. Recently, we have identified the molecular pathways of apoptosis induced by treatment of ovarian carcinoma cells with mutated p53 by CD437 and 4‐HPR. © 2004 Wiley‐Liss, Inc.
Fibroblast growth factor‐2 over‐rides insulin‐like growth factor‐I induced proliferation and cell survival in human neuroblastoma cells
Authors: Russo Vincenzo C. , Andaloro E. , Fornaro S.A. , Najdovska S. , Newgreen D.F. , Bach L.A. , Werther G.A. 
Published: April 2004

AbstractThe insulin‐like growth factor (IGF) system is a key regulator of cell growth, survival and differentiation, and these functions are co‐modulated by other growth factors including fibroblast growth factor‐2 (FGF‐2). To investigate IGF/FGF interactions in neuronal cells, we employed neuroblastoma cells (SK‐N‐MC). In serum free conditions proliferation of the SK‐N‐MC cells was promoted by IGF‐I (25 ng/ml), but blunted by FGF‐2 (50 ng/ml). IGF‐I‐induced proliferation was abolished in the presence of FGF‐2 even when IGF‐I was used at 100 ng/ml. In addition to our previously described FGF‐2 induced proteolytic cleavage of IGFBP‐2, we found that FGF‐2 increased IGFBP‐6 levels in conditioned medium (CM) without affecting IGFBP‐6 mRNA abundance. Modulation of IGFBP‐2 and ‐6 levels were not significant mechanisms involved in the blockade of IGF‐I action since the potent IGF‐I analogues [QAYL]IGF‐I and des(1–3)IGF‐I (minimal IGFBP affinity) were unable to overcome FGF‐2 inhibition of cell proliferation. FGF‐2 treated cells showed morphological differentiation expressing the TUJ1 neuronal marker while cells treated with IGF‐I alone showed no morphological change. When IGF‐I was combined with FGF‐2, however, cell morphology was indistinguishable from that seen with FGF‐2 alone. FGF‐2 inhibited proliferation and enhanced differentiation was also associated with a 70% increase in cell death. Although IGF‐I alone was potently anti‐apoptotic (60% decreased), IGF‐I was unable to prevent apoptosis when administrated in combination with FGF‐2. Gene‐array analysis confirmed FGF‐2 activation of the intrinsic and extrinsic apoptotic pathways and blockade of IGF anti‐apoptotic signaling. FGF‐2, directly and indirectly, overcomes the proliferative and anti‐apoptotic activity of IGF‐I by complex mechanisms, including enhancement of differentiation and apoptotic pathways, and inhibition of IGF‐I induced anti‐apoptotic signalling. Modulation of IGF binding protein abundance by FGF‐2 does not play a significant role in inhibition of IGF‐I induced mitogenesis. © 2003 Wiley‐Liss, Inc.
Control of human articular chondrocyte differentiation by reduced oxygen tension
Authors: Murphy Christopher L. , Polak Julia M. 
Published: April 2004

AbstractCell number is often a limiting factor in studies of chondrocyte physiology, particularly for human investigations. Chondrocytes can be readily proliferated in monolayer culture, however, differentiated phenotype is soon lost. We therefore endeavored to restore normal phenotype to human chondrocytes after serial passage in monolayer culture by manipulating cell morphology and oxygen tension towards the in vivo state. Third passage cells were encapsulated in alginate and exposed to either 20% or more physiologic 5% oxygen tensions. To assess cell phenotype, gene expression was measured using TaqMan real‐time PCR. Encapsulated, primary chondrocytes cultured in 20% oxygen were used as a positive reference. Passaged human chondrocytes were fibroblastic in appearance and had lost normal phenotype as evidenced by a decrease in expression of collagen II, aggrecan, and sox9 genes of 66, 6, and 14 fold, respectively; with concomitant high expression of type I collagen (22 fold increase). A partial regaining of the differentiated phenotype was observed by encapsulation in 20% oxygen; however, even after 4 weeks, collagen II gene expression was not fully restored. Collagen II and aggrecan expression were increased, on average, 3 fold, in 5% oxygen tension compared to 20% cultures. Furthermore, matrix glycosaminoglycan (GAG) levels were significantly increased in reduced oxygen. In fact, after 4 weeks in 5% oxygen, encapsulated third passage cells had collagen II expression fully regained and aggrecan and sox9 levels actually exceeding primary cell levels in 20% oxygen. Our results show that the phenotype of serially passaged human articular chondrocytes is more fully restored by combining encapsulation with culture in more physiological levels of oxygen. Sox9, an essential transcription factor for chondrocyte differentiation is strongly implicated in this process since its expression was upregulated almost 27 fold. These findings have implications for the optimal conditions for the in vitro culture of chondrocytes. © 2004 Wiley‐Liss, Inc.
Initial interactions in electromagnetic field‐induced biosynthesis
Authors: Blank Martin , Goodman Reba 
Published: April 2004

AbstractLow frequency electromagnetic (EM) fields induce gene expression, and recent insights into physical interactions of EM fields with model systems suggest a mechanism that could initiate this process. The consistently low thresholds at which EM fields stimulate biological processes indicate that they require little energy. Since it has been shown that such weak fields accelerate electron transfer reactions, they could stimulate transcription by interacting with electrons in DNA to destabilize the H‐bonds holding the two DNA strands together. Such a mechanism is consistent with the low electron affinity of the bases in previously identified electromagnetic response elements (EMREs) needed for EM field interaction with DNA. It is also in line with both endogenous and in vitro stimulation of biosynthesis by electric fields. The frequency response of several EM sensitive biological systems suggests that EM fields require repetition and are most effective at frequencies that coincide with natural rhythms of the processes affected. © 2004 Wiley‐Liss, Inc.