bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lung cancer near an industrial site in Lithuania with major emissions of airway irritants
Authors: Petrauskaitė Rūta , Pershagen Göran , Gurevičius Romualdas 
Published: August 2002

AbstractTo assess the relation between air pollution with airway irritants, including sulfuric acid and lung cancer, a case‐control study was performed near an industry producing sulfuric acid and fertilizers in Kėdainiai county, central Lithuania. The county had the highest lung cancer rates of the country among men. Between 1967 and 1973, the levels of sulfuric acid exceeded 500 μg/m3 within 2 km of the industry and 100 μg/m3 more than 5 km away. A total of 277 men who were diagnosed as having lung cancer during 1981–1991 in Kėdainiai county were included as well as 1,108 population controls. Information on residential history since 1960, smoking habits, occupations and workplaces during lifetime was obtained from questionnaires mailed to next‐of‐kin. The relative risk of lung cancer associated with living within approximately 5 km from the plant was 1.02 (95% CI: 0.76–1.38) compared to those who had never lived in this area. No relation with distance or duration of residence was observed. Furthermore, workers at the plant did not have an increased lung cancer risk. The relative risk of lung cancer associated with smoking was 21.2 (95% CI: 7.51; 60.1) for current smokers and 14.0 (95% CI: 4.88; 40.3) for exsmokers. The duration of smoking, a low age at start and amount of cigarettes smoked daily were positively associated with lung cancer risk. Smoking levels appeared more pronounced among study controls than in the rest of the country. Our study could not confirm earlier evidence of an association between exposure to airway irritants, such as sulfuric acid and lung cancer. Smoking is the major determinant of the risk of lung cancer in men in Kėdainiai county. It is probable that higher smoking rates constitute the main reason for the increased lung cancer risk among men in this area. © 2002 Wiley‐Liss, Inc.
Signal processing in migrating T24 human bladder carcinoma cells: Role of the autocrine interleukin‐8 loop
Authors: Lang Kerstin , Niggemann Bernd , Zanker Kurt S. , Entschladen Frank 
Published: August 2002

AbstractT24 human bladder carcinoma cells reveal a high locomotor activity (70% locomoting cells) within a 3‐dimensional collagen matrix. This high migratory activity is induced by an autocrine engagement of the interleukin‐8 receptor A, as was shown by antibodies neutralizing the secreted interleukin‐8. Treatment of the cells with these specific antibodies reduced the locomotor activity by half. The intracellular signal transduction underlying the interleukin‐8‐induced T24 locomotion involves the activity of protein tyrosine kinases (PTKs), the phospholipase Cγ (PLCγ) and the protein kinase C (PKC), as proven by the use of specific enzyme inhibitors. These results suggest the following model for the regulatory signal transduction of interleukin‐8‐induced human T24 bladder carcinoma cell migration: The engagement of the interleukin‐8‐receptor, a receptor of the serpentine family, leads to the β‐arrestin‐mediated activation of PTKs. These kinases phosphorylate the PLCγ, which generates the second messengers diacylglycerol (DAG) and inositol‐1,4,5‐trisphosphate (IP3). DAG activates the PKC, whereas IP3 mediates the release of calcium from the endoplasmatic reticulum. By means of confocal laser microscopy, we observed an oscillation of the cytosolic calcium concentration in migrating T24 cells, which were loaded with the calcium‐dye fluo‐3/AM. Here, we report on a new autocrine function of secreted interleukin‐8 and the intracellular signal transduction leading to the regulation of cytosolic calcium and to a migratory tumor cell phenotype. © 2002 Wiley‐Liss, Inc.
Prolactin regulates antitumor immune response through induction of tumoricidal macrophages and release of IL‐12
Authors: Majumder Biswanath , Biswas Ratna , Chattopadhyay Utpala 
Published: August 2002

AbstractThe involvement of PRL in regulating monocyte/macrophage functions is suggested by the presence of PRL‐Rs in these cells. Here, we show that PRL, though it failed to activate mouse peritoneal resident macrophages (RMs), acted as a second signal and activated mouse peritoneal inflammatory macrophages (EMs) to a tumoricidal state. The cytotoxicity of mouse tumor‐associated macrophages (TAMs) isolated at day 1 of tumor (Ehrlich ascites carcinoma, EAC) growth was enhanced by PRL. However, with progression of tumor growth, TAMs became nonresponsive to the hormone. PRL‐induced killing of P815 target cells by EMs and TAMs was independent of TNF but correlated with the hormone‐induced augmentation of NO2− and O2− release in these macrophages. Administration of PRL in vivo inhibited EAC growth and augmented NO2− release by TAMs. PRL synergized with the TH1 cytokine IFN‐γ, a known activator of macrophages, in inducing tumor killing and release of NO2− from EMs and TAMs. The hormone might activate macrophages at least partially, through the release of IFN‐γ as anti‐IFN‐γ blocked IFN‐γ– as well as PRL‐induced cytotoxicity in EMs. The TH2 cytokine IL‐4 suppressed PRL‐induced activation of macrophages. PRL induced release of IL‐12 from EMs also, which suggested that the hormone might drive the TH1 response through IL‐12. Our observations further suggest that PRL alone and in synergy with IFN‐γ, released through induction of IL‐12, may generate tumoricidal macrophages and thus regulate the antitumor immune response of tumor hosts. © 2001 Wiley‐Liss, Inc.
Economy in water and fertilizer use in trickle fertigated potato1
Authors: Chawla J.K. , Narda N.K. 
Published: August 2002

AbstractFertilizer and water use in trickle fertigated potato using different fertilizer application rates, frequencies of application and wetted soil volumes were compared with a furrow irrigated and conventionally fertilized crop. Results indicate that water and fertilizer savings to the extent of 30 and 70% respectively with comparable yield levels were possible under the trickle fertigated crop as compared to the furrow irrigated crop of potatoes. Highest yield of 36.29 t ha−1 of fresh tubers was obtained under trickle irrigation as compared to 21.5 t ha−1 for the furrow irrigated crop. Copyright © 2001 John Wiley & Sons, Ltd.
Investigating the TNP‐OVA and direct popliteal lymph node assays for the detection of immunostimulation by drugs associated with anaphylaxis in humans
Authors: Gutting Bradford W. , Updyke Lawrence W. , Amacher David E. 
Published: August 2002

AbstractUsing current animal models, it is not possible to identify low‐molecular‐weight compounds (LMWCs) that are likely to be associated with anaphylaxis. It is generally accepted that the ultimate effector mechanism involves drug‐induced IgE antibody. The objective of the present study was to determine if diclofenac, zomepirac and glafenine, which are associated with anaphylaxis in humans, have immunostimulating potential in the murine TNP‐OVA (trinitrophenyl‐ovalbumin) popliteal lymph node assay (PLNA), and more specifically to determine if the immunostimulation caused by these LMWCs results in IgE antibody production. These LMWCs were chosen because both zomepirac and glafenine were removed from the market due to high association with anaphylaxis, and diclofenac, which remains on the market, is frequently associated with anaphylaxis. In addition to conducting a TNP‐OVA PLNA, the immunostimulating potential of these compounds was examined in the direct PLNA. When co‐administered with TNP‐OVA, all three LMWCs caused dose‐dependent (0.25, 0.50, 1.00 and 1.25 mg) increases in popliteal lymph node (PLN) weight and cellularity that were observed beginning with the 0.25‐mg dose. In addition, beginning with the 0.25‐mg dose, all three compounds caused dose‐dependent increases in TNP‐OVA specific IgM and IgG1 antibody‐forming cells (AFCs). Diclofenac induced an isotype switch and caused a dose‐dependent increase in the number of IgE AFCs with no detectable IgG2a AFCs and minimal high‐dose‐only IgG2b AFCs. Zomepirac induced IgE, IgG2a and IgG2b AFCs following the injection of 0.50 mg only, and glafenine induced IgE, IgG2a and IgG2b AFCs following the injection of 0.50–1.00 mg. In the direct PLNA, diclofenac caused dose‐dependent increases in PLN weight and cellularity that were observed beginning with dose of 0.50 mg, whereas zomepirac failed to increase any PLN parameter and glafenine only increased the PLN weight. These results suggest that diclofenac, zomepirac and glafenine are immunostimulating LMWCs in the TNP‐OVA PLNA with the potential to induce IgE antibody against a co‐administered hapten‐conjugate. Furthermore, these results suggest that the TNP‐OVA PLNA offered significant advantages over the direct PLNA. Although it is not realistic to suggest that a single assay, based on a low number of test compounds, can identify all LMWCs with the potential to cause anaphylaxis in humans, these observations do demonstrate the potential utility of the PLNAs in examining LMWC‐induced immunomodulation and support further development and investigation of the assays. Copyright © 2002 John Wiley & Sons, Ltd.
Airway reactivity response to aged carbon–graphite/epoxy composite material smoke
Authors: Kimmel Edgar C. , Reboulet James E. , Courson David L. , Still Kenneth R. 
Published: August 2002

AbstractExposure of na&&inodot;uml;ve guinea pigs for a total of 30 min to aged smoke from pyrolysis of 5, 10 and 100 g of carbon–graphite/epoxy‐advanced composite material (cgeCM) elicited changes in the ventilation and breathing pattern reminiscent of an acute, asthmatic episode. The severity of these responses was dose related. Although breathing pattern changes were not definitive of stimulation by a single type of respiratory irritant, non‐dimensional indices derived from breath structure appeared to be characteristic of bronchoconstriction possibly complicated by CO2‐stimulated ventilation. The highest exposure concentration also elicited convulsions in the animals, which may or may not be related to the airway reactivity (AR) response. Upon treatment with fresh air, breathing returned to normal. However, this recovery was transient with some respiratory parameters returning to abnormal levels, possibly indicating a rebound or delayed component of the response. Filtration of particulate material from the smoke moderated but did not eliminate the AR response. Animals exposed to diluted smoke from the pyrolysis of 2 g of cgeCM showed no remarkable changes in breathing or ventilation, suggesting that there may be a threshold for aged cgeCM smoke‐elicited AR response. Published in 2002 by John Wiley & Sons, Ltd.
Effect of zinc on hepatic lipid peroxidation and antioxidative enzymes in ethanol‐fed rats
Authors: Pathak A. , Mahmood A. , Pathak R. , Dhawan D. 
Published: August 2002

AbstractA 3‐ml aliquot of 30% ethanol was fed daily to normal as well as zinc‐treated (227 mg l−1) rats for periods of 2, 4 and 8 weeks. A highly significant increase in the levels of hepatic lipid peroxidation was observed in ethanol‐fed rats after 4 and 8 weeks of treatment. On the other hand, the levels of lipid peroxidation came down significantly following ethanol feeding to zinc‐treated rats. The activities of glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD) in liver were elevated significantly after ethanol administration to rats for durations of 2, 4 and 8 weeks. Interestingly, zinc treatment to rats given ethanol was able to bring down the elevated levels of SOD, catalase and GPx to within normal limits, However, zinc administration alone did not cause any significant alteration in the activities of these antioxidative enzymes. Copyright © 2002 John Wiley & Sons, Ltd.
Cement–cement interface strength: Influence of time to apposition
Authors: Park Sang‐Hyun , Silva Mauricio , Park Jong‐Seok , Ebramzadeh Edward , Schmalzried Thomas P. 
Published: August 2002

AbstractCement–cement interfaces were created under simulated operating‐room conditions. In order to analyze the effect of time to apposition on interface strength, two cement surfaces were brought together 1, 2, 4, and 6 min after 1 min of mixing and 45 s of waiting. Cement–cement interface strength was evaluated with the use of a three‐point bending to failure test. Scanning electron microscopy (SEM) images of the failed interface were obtained. The mean interface strength decreased when the cement–cement interface was time delayed. Compared to bulk cement, interface strength in time‐delayed groups decreased 8% after 1‐min delay (p=.037), 18% after 2‐min delay (p=.0004), 20% after 4‐min delay (p=.0005), and 42% after 6‐min delay (p<.0001). No statistically significant differences in interface strength were found between the 2‐ and 4‐min delayed groups (p=.73). SEM images revealed that after 6‐min delay, up to 50% of the cement surface can remain unbonded, explaining the decrease in strength of the cement–cement interface as a function of time to apposition. This laboratory study indicates that time to apposition plays a critical role in cement–cement interface strength. If any cementing technique involves the joining of two cement surfaces, it is recommended that the two cement surfaces be mated together within 5 min and 45 s after the start of mixing (1 min mixing; 45 s waiting; 4 min delay), in order to obtain a strong cement–cement interface bond. Delay beyond this can result in substantial reduction in the strength of the cement–cement interface bond. © 2001 John Wiley & Sons, Inc. J Biomed Mater Res (Appl Biomater) 58: 741–746, 2001
The relationship between stress, porosity, and nonlinear damage accumulation in acrylic bone cement
Authors: Murphy B. P. , Prendergast P. J. 
Published: August 2002

AbstractThe long‐term survival of cemented hip replacements depends on the ability of the cemented fixation to resist fatigue damage. Damage has been assumed to accumulate linearly (Miner's law) even though it is unlikely to be the case in such a porous brittle material. This study addresses the nonlinear stress‐dependent nature of fatigue damage accumulation in acrylic bone cement. Specimens were subjected to a zero‐to‐tension fatigue load in water at 37°C. A total of 15 specimens were tested, i.e., five specimens at each of three stress levels. The specimens were cyclically loaded to a certain fraction of their fatigue lives and the amount of microcracking present at that time was quantified by counting each crack and measuring its length. This procedure was repeated until the specimen failed. A total of 801 cracks formed in the 15 specimens. All cracks were found to initiate at pores. Crack propagation directions were distributed normally about the direction perpendicular to the applied load at the lower stress levels, but at higher stress, the distribution tended to be broader. At higher stresses, more cracks were produced per pore. The damage accumulation process in acrylic bone cement was found to be nonlinear with the degree of nonlinearity increasing with stress. Furthermore, great variability was found which was attributed to the differences in porosity between specimens. A power law equation is given which describes the predicted relationship between damage accumulation and number of loading cycles as a function of the stress level. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 646–654, 2002
von Hippel‐Lindau tumor suppressor protein represses platelet‐derived growth factor B‐chain gene expression via the Sp1 binding element in the proximal PDGF‐B promoter
Authors: Rafty Louise A. , Khachigian Levon M. 
Published: August 2002

AbstractVHL is the causative gene for von Hippel‐Lindau disease and sporadic clear cell renal cancer. It has been shown that pVHL can suppress the expression of certain genes that are overexpressed in renal carcinomas. One such gene is that encoding the potent mitogen and chemoattractant, platelet‐derived growth factor B‐chain (PDGF‐B). The regulatory mechanisms underlying pVHL suppression of PDGF‐B expression, however, are completely unknown. This understanding would shed vital light on the control of growth factor gene expression by this tumor suppressor. Here we report that pVHL can repress both endogenous steady‐state PDGF‐B mRNA expression and PDGF‐B promoter‐dependent transcription in WKY12‐22 cells. Transient transfection analysis utilizing PDGF‐B promoter‐chloramphenicol acetyl transferase (CAT) reporter constructs revealed that pVHL inhibition of PDGF‐B expression is mediated via the Sp1‐binding element in the proximal region of the PDGF‐B promoter. Recent studies have demonstrated a physical interaction between pVHL and Sp1, which activates the PDGF‐B promoter. We show that Sp1 can rescue PDGF‐B promoter activity and endogenous PDGF‐B mRNA expression from pVHL repression. These findings thus demonstrate a pivotal role for Sp1 in pVHL inhibition of PDGF‐B transcription. J. Cell. Biochem. 85: 490–495, 2002. © 2002 Wiley‐Liss, Inc.
Extracellular matrix regulates alpha s1‐casein gene expression in rabbit primary mammary cells and CCAAT enhancer binding protein (C/EBP) binding activity
Authors: Jolivet Geneviève , Meusnier Chantal , Chaumaz Gilles , Houdebine Louis‐Marie 
Published: August 2002

AbstractPrevious studies have shown that both the signal transducer and activator of transcription 5 (STAT5) and the CCAAT enhancer binding proteins (C/EBPs) are involved in the regulation of casein gene expression by mammary epithelial cells. Prolactin (Prl) activation of STAT5 is necessary for casein gene expression. The extracellular matrix (ECM) regulates also casein gene expression. Here, we have investigated whether ECM regulates C/EBPs activity in primary rabbit mammary epithelial cells. Isolated primary mammary cells were cultured on plastic or on floating collagen I gel. Prolactin induced αs 1‐casein gene expression when cells were cultured on collagen but not on plastic. It is noteworthy that activated STAT5 was detected in both culture conditions. Several STAT5 isoforms (STAT5a, STAT5b, and other STAT5 related isoforms, some with lower molecular weight than the full‐length STAT5a and STAT5b) were detected under the different culture conditions. However, their presence was not related to the expression of αs 1‐casein gene. The binding of nuclear factors to a C/EBP specific binding site and the protein level of C/EBPβ differed in cells cultured on plastic or on collagen but these parameters were not modified by Prl. This suggests that C/EBP binding activity was regulated by ECM and not by Prl. Interestingly, these modifications were correlated to the expression of the αs 1‐casein gene. Hence, the activation of the αs 1‐casein gene expression depends on two independent signals, one delivered by Prl via the activation of STAT5, the other delivered by ECM via C/EBP. J. Cell. Biochem. 82:371–386, 2001. © 2001 Wiley‐Liss, Inc.
Inhibitory effect of regucalcin on protein phosphatase activity in the nuclei of rat kidney cortex
Authors: Morooka Yoshiko , Yamaguchi Masayoshi 
Published: August 2002

AbstractThe role of regucalcin, which is a regulatory protein of calcium signaling, in the regulation of protein phosphatase activity in the nuclei of rat kidney cortex was investigated. Protein phosphatase activity towards phosphotyrosine, phosphoserine, and phosphothreonine was found in the nuclei. The enzyme activity towards three phosphoamino acids was significantly increased by the addition of calcium chloride (10–50 μM) in the enzyme reaction mixture. This increase was significantly inhibited by trifluoperazine (25 or 50 μM), an antagonist of calmodulin. The presence of regucalcin (50 or 100 nM) in the enzyme reaction mixture caused a significant decrease in protein phosphatase activity towards three phosphoamino acids. This effect was also seen in the presence of calcium (25 μM) and/or calmodulin (5 μg/ml). Protein phosphatase activity towards three phosphoamino acids was significantly increased in the presence of anti‐regucalcin monoclonal antibody (25 or 50 ng/ml) in the enzyme reaction mixture. This effect was completely blocked by the addition of regucalcin (100 nM). The effect of antibody (25 ng/ml) in increasing protein phosphatase activity towards phosphotyrosine was significantly inhibited by vanadate (10−4 M). Also, the antibody's effect towards phosphoserine and phosphothreonine was significantly inhibited by cyclosporin A (10−5 M). Endogenous regucalcin was found in the nuclei of rat kidney cortex using Western blot analysis. Nuclear regucalcin level was significantly reduced by the administration of saline (0.9% NaCl) for seven days in rats. Protein phosphatase activity towards three phosphoamino acids was significantly decreased by saline administration. The effect of anti‐regucalcin monoclonal antibody (25 ng/ml) in increasing protein phosphatase activity towards three phosphoamino acids was weakened in the renal cortex nuclei of saline‐administrated rats. The present study demonstrates that endogenous regucalcin plays a suppressive role in the regulation of protein phosphatase activity in the nuclei of rat kidney cortex cells. © 2001 Wiley‐Liss, Inc.
Semiautomatic sequence‐specific assignment of proteins based on the tertiary structure—The program st2nmr
Authors: Pristovšek Primož , Rüterjans Heinz , Jerala Roman 
Published: August 2002

AbstractThe sequence‐specific assignment of resonances is still the most time‐consuming procedure that is necessary as the first step in high‐resolution NMR studies of proteins. In many cases a reliable three‐dimensional (3D) structure of the protein is available, for example, from X‐ray spectroscopy or homology modeling. Here we introduce the st2nmr program that uses the 3D structure and Nuclear Overhauser Effect spectroscopy (NOESY) peak list(s) to evaluate and optimize trial sequence‐specific assignments of spin systems derived from correlation spectra to residues of the protein. A distance‐dependent target function that scores trial assignments based on the presence of expected NOESY crosspeaks is optimized in a Monte Carlo fashion. The performance of the program st2nmr is tested on real NMR data of an α‐helical (cytochrome c) and β‐sheet (lipocalin) protein using homology models and/or X‐ray structures; it succeeded in completely reproducing the correct sequence‐specific assignments in most cases using 2D and/or 15N/13C Nuclear Overhauser Effect (NOE) data. Additionally to amino acid residues the program can also handle ligands that are bound to the protein, such as heme, and can be used as a complementary tool to fully automated assignment procedures. © 2002 Wiley Periodicals, Inc. J Comput Chem 23: 335–340, 2002
Use of exchange maximization to generate starting vectors for self‐consistent field calculations on metal cluster/adsorbate systems
Authors: Buenker R. J. , Whitten J. L. , Izgorodina E. I. , Liebermann H.‐P. , Kokh D. B. 
Published: August 2002

AbstractLocalized molecular orbitals (LMOs) derived from exchange maximization with respect to all atom‐centered basis functions in the basis set are shown to generate a good starting electronic field for self‐consistent field calculations on extended systems such as metal clusters, for which well‐defined chemical bonds are not present. Examples studied are a cluster of 20 Ni atoms and the Pt97CO, Ag43/H3CNON, Ag91/H2CO, and vinylidene/Ni metal cluster plus adsorbate systems. It is also shown that improved starting vectors can be obtained by remixing a subset of the LMOs with the largest exchange eigenvalues through diagonalization of the Fock matrix computed with a null electronic field. Employing only a subset of the exchange‐maximized LMOs in the first iterations, and then gradually expanding the space in which the diagonalizations are carried out in succeeding cycles, is shown to be an effective means of guiding the SCF procedure to the converged full‐basis solution. © 2002 Wiley Periodicals, Inc. J Comput Chem 23: 943–949, 2002