bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suppression of EGF‐induced cell proliferation by the blockade of Ca2+ mobilization and capacitative Ca2+ entry in mouse mammary epithelial cells
Authors: Ichikawa Jun , Kiyohara Toshikazu 
Published: September 2002

AbstractThe role of intracellular Ca2+ stores and capacitative Ca2+ entry on EGF‐induced cell proliferation was investigated in mouse mammary epithelial cells. We have previously demonstrated that EGF enhances Ca2+ mobilization (release of Ca2+ from intracellular Ca2+ stores) and capacitative Ca2+ entry correlated with cell proliferation in mouse mammary epithelial cells. To confirm their role on EGF‐induced cell cycle progression, we studied the effects of 2,5‐di‐tert‐butylhydroquinone (DBHQ), a reversible inhibitor of the Ca2+ pump of intracellular Ca2+ stores, and SK&38;F 96365, a blocker of capacitative Ca2+ entry, on mitotic activity induced by EGF. Mitotic activity was examined using an antibody to PCNA for immunocytochemistry. SK&38;F 96365 inhibited capacitative Ca2+ entry in a dose‐dependent manner (I50: 1–5μm). SK&38;F 96365 also inhibited EGF‐induced cell proliferation in the same range of concentration (I50: 1–5 μm). DBHQ suppressed [Ca2+]i response to UTP and thus depleted completely Ca2+ stores at 5 μm. DBHQ also inhibited EGF‐induced cell proliferation at an I50 value of ∼10 μm. The removal of these inhibitors from the culture medium increased the reduced mitotic activity reversibly. Using a fluorescent assay of DNA binding of ethidium bromide, no dead cells were detected in any of the cultures. These results indicate that the inhibitory effects of SK&38;F 96365 and DBHQ on cell proliferation were due to the inhibition of capacitative Ca2+ entry and Ca2+ mobilization suggesting the importance of capacitative Ca2+ entry and Ca2+ mobilization in the control of EGF‐induced cell cycle progression in mouse mammary epithelial cells. Copyright © 2001 John Wiley & Sons, Ltd.
Effects of citrinin on iron‐redox cycle
Authors: Da Lozzo Eneida Janiscki , Mangrich Antonio Salvio , Rocha Maria Eliane Merlin , de Oliveira Maria Benigna Martinelli , Carnieri Eva Gunilla Skare 
Published: September 2002

AbstractThe ability of the mycotoxin citrinin to act as an inhibitor of iron‐induced lipoperoxidation of biological membranes prompted us to determine whether it could act as an iron chelating agent, interfering with iron redox reactions or acting as a free radical scavenger. The addition of Fe3+ to citrinin rapidly produced a chromogen, indicating the formation of citrinin‐Fe3+ complexes. An EPR study confirms that citrinin acts as a ligand of Fe3+, the complexation depending on the [Fe3+]:[citrinin] ratios. Effects of citrinin on the iron redox cycle were evaluated by oxygen consumption or the o‐phenanthroline test. No effect on EDTA‐Fe2+→EDTA‐Fe3+ oxidation was observed in the presence of citrinin, but the mycotoxin inhibited, in a dose‐dependent manner, the oxidation of Fe2+ to Fe3+ by hydrogen peroxide. Reducing agents such as ascorbic acid and DTT reduced the Fe3+‐citrinin complex, but DTT did not cause reduction of Fe3+‐EDTA, indicating that the redox potentials of Fe3+‐citrinin and Fe3+‐EDTA are not the same. The Fe2+ formed from the reduction of Fe3+‐citrinin by reducing agents was not rapidly reoxidized to Fe3+ by atmospheric oxygen. Citrinin has no radical scavenger ability as demonstrated by the absence of DPPH reduction. However, a reaction between citrinin and hydrogen peroxide was observed by UV spectrum changes of citrinin after incubation with hydrogen peroxide. It was also observed that citrinin did not induce direct or reductive mobilization of iron from ferritin. These results indicate that the protective effect on iron‐induced lipid peroxidation by citrinin occurs due to the formation of a redox inactive Fe3+‐citrinin complex, as well as from the reaction of citrinin and hydrogen peroxide. Copyright © 2001 John Wiley & Sons, Ltd.
Abbreviations used:

DPPH

diphenylpicrylhydrazyl

DMPO

5,5‐dimenthyl‐1‐pyrroline‐N‐oxide

EDTA

ethylene diaminetetraacetic acid

DTT

dithiothreitol

EPR

electron paramagnetic resonance spectroscopy
Interference of MI‐D, a new mesoionic compound, on artificial and native membranes
Authors: Cadena Silvia M.S.C. , Carnieri Eva G.S. , Echevarria Aurea , de Oliveira Maria Benigna Martinelli 
Published: September 2002

AbstractMI‐D (4‐phenyl‐5‐(4‐nitrocinnamoyl)‐1,3,4‐thiadiazolium‐2‐phenylamine chloride), a new mesoionic compound, decreased the rate of swelling induced by valinomycin‐K+, as well as induced swelling in the presence of nigericin‐K+. Shrinkage was also affected, suggesting interference with the inner mitochondrial membrane, which would affect both fluidity and elasticity. Fluorescence polarization of DPH and DPH‐PA, probing the core and outer regions respectively, of the DMPC and native membranes, indicated that MI‐D shifts the midpoint of phase transition to higher values and orders of the fluid phase. These alterations in membrane fluidity are thus related to MI‐D effects on the energy‐linked functions of mitochondria. Copyright © 2001 John Wiley & Sons, Ltd.
Influence of vitamin E on the levels of fatty acids and MDA in some tissues of diabetic rats
Authors: Çelik Sait , Baydaş Gıyaseddin , Yılmaz Ökkeş 
Published: September 2002

AbstractThis study was performed to determine whether vitamin E supplementation in streptozotocin‐induced diabetic rats treated with insulin could affect the levels of fatty acid composition and malondialdehyde (MDA) of brain, liver and muscle tissues. Thirty Wistar albino rats were used during the experiments. They were randomly divided into three groups, each consisting of six individuals. The first group was diabetic, the second was control, and the third was diabetic but fed vitamin E. The level of stearic acid in brain tissues decreased (p<0.05) in the second and the third groups as compared to the first group. The percentage of arachidonic and polyunsaturated fatty acids slightly decreased (p<0.05) in the diabetic group in comparison to the second and third groups. The proportion of docosahexaenoic acid significantly increased (p<0.01) in the second and third groups in contrast to the first group. The level of docosatrienoic was slightly higher (p<0.05) in the third group than in other groups. In the liver tissues, the proportion of stearic, oleic and total monounsaturated fatty acids was slightly higher (p<0.05) in the first group than in the other groups. The level of arachidonic, docosahexaenoic, unsaturated and total polyunsaturated fatty acid slightly increased (p<0.05) in the second and third groups as compared to the first group. The level of myristic and stearic acids in muscle tissue slightly increased (p<0.05) in the first group as compared to the second and third groups. The proportion of arachidonic, docosahexaenoic and unsaturated fatty acids slightly increased (p<0.05) in the second and third groups relative to the first group. The amount of MDA was slightly higher in the diabetic group than in the other groups in all tissues. The results indicate that vitamin E supplementation, in experimental diabetes could play a role in controlling the oxidative status and altered fatty acid metabolism in tissues, thereby maintaining favourable fatty acid distribution in the tissues affected by diabetic complications. Copyright © 2001 John Wiley & Sons, Ltd.
Autocrine production of basic fibroblast growth factor translated from novel synthesized mRNA mediates thrombin‐induced mitogenesis in smooth muscle cells
Authors: Cucina Alessandra , Borrelli Valeria , Lucarelli Marco , Sterpetti Antonio V. , Cavallaro Antonino , Strom Roberto , Santoro‐D' Angelo Luciana , Scarpa Sigfrido 
Published: September 2002

AbstractThrombin is known to stimulate smooth muscle cell (SMC) growth in culture but the mechanisms underlying growth stimulation remain unclear. Previous works have observed a significant increase in platelet‐derived growth factor AA and basic fibroblast growth factor (bFGF) release by bovine aortic SMC after addition of thrombin. The aim of this study was to clarify the link between thrombin, bFGF and SMC proliferation by examining the kinetics of autocrine production of bFGF by thrombin‐stimulated SMC and its contribution to thrombin‐induced mitogenesis. Experiments were performed to assess the dynamics of thrombin‐induced bFGF mRNA transcription and to distinguish, following thrombin stimulus, between the activation of ‘old’ bFGF protein and/or bFGF mRNA, or novel mRNA synthesis and subsequent translation. Bovine aortic SMCs were stimulated with thrombin in serum‐free culture. bFGF mRNA expression was determined by RT‐PCR. Mitogenic activity of thrombin was determined by 3H‐thymidine uptake. Our results demonstrate that the peak of bFGF mRNA expression occurred 24 h after thrombin stimulation. Experiments performed with cycloheximide, a translation inhibitor, revealed a translation peak later than 24 h after thrombin stimulation. Thrombin‐induced mitogenic activity in SMCs was partially inhibited by the addition of anti‐bFGF antibody (p< 0.001) and of hirudin (p< 0.001). When hirudin was added 24 h after stimulation, thrombin‐induced mitogenic activity was not inhibited. In conclusion, thrombin‐induced mitogenesis was partially mediated by the autocrine production of bFGF, mainly due to protein synthesis by novel mRNA with a transcription peak at 24 h and a later translation peak. Copyright © 2001 John Wiley & Sons, Ltd.
A 45‐kDa midgut glycoprotein from Anopheles albimanus mosquito mediates the killing of trypanosomes
Authors: Nok Andrew J. , Njoku G. C. , Balogun E. 
Published: September 2002

AbstractTrypanosomes do not inhabit or grow in anopheles mosquitoes, the vector for the transmission of Plasmodium parasites the causative agent for malaria. The possession of lytic factors by the anopheline mosquito was thus considered. Head and midgut sections prepared in phosphate buffered saline were tested for trypanocidal action against T. congolense. While the head section was inactive towards the trypanosomes, the midgut extract at 0.2 mg ml−1 diminished the motility of the parasites within 2 min of incubation; killing 50% of the population after 5 min. At 0.5 mg ml−1 of the extract, about 90% of the parasites were killed within 2 min of incubation. The midgut fraction was subjected to a purification protocol involving successive chromatography on: octyl‐sepharose, reactive brown agarose and fetuin‐agarose columns. A final trypanocidal active fraction (gp45), which moved homogeneously during electrophoresis as a 45‐kDa protein, was recovered from the fetuin‐agarose column. The protein reacted positively with thiobarbituric acid, which suggests it is a sialoglycoprotein. Desialylation of the glycoprotein nullified its trypanocidal activity on T. congolense. Similarly, when the saccharides, lactose, methyl‐β‐galactoside, lactulose, methyl‐umbelliferyl‐β‐galactoside (MU‐Gal), were included in the culture medium, they inhibited the gp45 trypanocidal activity. Asialo‐fetuin and asialo‐RBC also inhibited the gp45‐induced killing of T. congolense cells. The potential use of anopheline 45 kDa protein in the production of transgenic tsetse flies (Glossina spp.) in the control of trypanosomiasis is discussed. Copyright © 2002 John Wiley & Sons, Ltd.
Aspirin alone antiplatelet regimen after intracoronary placement of the Carbostent™: The Antares study
Authors: Bartorelli Antonio L. , Trabattoni Daniela , Montorsi Piero , Fabbiocchi Franco , Galli Stefano , Ravagnani Paolo , Grancini Luca , Cozzi Sergio , Loaldi Alessandro 
Published: September 2002

AbstractThe effect of stent coatings in preventing early thrombotic occlusion remains to be proved. The purpose of this study was to evaluate the safety and efficacy of the Carbostent™, a new coronary stent with a nonthrombogenic coating (Carbofilm™), in 110 consecutive patients (73.6% men, mean age 61 ± 9 years) who met prespecified clinical and angiographic inclusion criteria and were treated with aspirin monotherapy after stenting. Stable angina (75.5%), unstable angina (18.2%), and silent ischemia (6.3%) were clinical indications for coronary revascularization. Patients received 10,000 U of heparin and no IIb/IIIa inhibitors or postprocedural heparin. Complex lesion characteristics (B2, C) were present in 39 out of 129 (30.2%) lesions. Mean lesion length was 15.6 ± 7.4 mm, and 32% of the lesions were >15 mm (range 16–52 mm). Small coronary vessels (<3.0 mm) were treated in 28% of the cases. A total of 165 Carbostent™ were used in 129 coronary lesions of the 110 patients. Single‐vessel stenting was performed in 97 (88%) patients and multivessel stent placement in 13 (12%) patients. The mean length of the stented segment was 21 ± 13 mm (range 9–95 mm). Procedural and clinical success was achieved in all patients. At 1‐month follow‐up, there were no stent thrombosis or other major adverse cardiac events. We observed 2 (1.8%) non‐Q‐wave myocardial infarctions and 2 (1.8%) vascular complications. This study indicates that the Carbostent™ may prevent stent thrombosis in selected patients treated with aspirin only. A randomized study comparing aspirin alone versus combined ticlopidine and aspirin after Carbostent™ implantation will be needed to confirm these results. Cathet Cardiovasc Intervent 2002;55:150–156. © 2002 Wiley‐Liss, Inc.
Extraction of large intracoronary thrombus in acute myocardial infarction by percutaneous fogarty maneuver: Intentional abuse of a novel interventional device
Authors: Eggebrecht Holger , Baumgart Dietrich , Naber Christoph , Dirsch Olaf , Haude Michael , Erbel Raimund 
Published: September 2002

AbstractIntracoronary thrombus in the infarct‐related artery remains a challenge for interventional catheter‐based techniques in acute myocardial infarction and may result in severe complications due to distal embolization. We describe a patient with acute myocardial infarction in whom a large intracoronary thrombus of the left anterior descending coronary artery was successfully removed by percutaneous Fogarty maneuver using an expanded filter protection device. Cathet Cardiovasc Intervent 2002;55:228–232. © 2002 Wiley‐Liss, Inc.
Intracoronary retrieval of the dehisced radiopaque ring of a guiding catheter: An unusual complication of coronary angioplasty
Authors: Chen Yi , Fang Ching‐Chang , Yu Ching‐Lung , Jao Yeun Tarl Fresner Ng , Wang Shih‐Pu 
Published: September 2002

AbstractThe guiding catheter used in coronary intervention may be damaged or some parts could be dehisced during the procedure, producing adverse effects in the vascular tree. So much so that immediate surgery is usually indicated. We report a case with a dehisced radiopaque ring of the catheter during the procedure. It was retrieved percutaneously without thoracotomy. Cathet Cardiovasc Intervent 2002;55:262–264. © 2002 Wiley‐Liss, Inc.
Prognostic value of cardiac troponin I elevation after percutaneous coronary intervention in patients with chronic renal insufficiency: A 12‐month outcome analysis
Authors: Gruberg Luis , Fuchs Shmuel , Waksman Ron , Pichard Augusto D. , Kent Kenneth M. , Laird John R. , Wu Hongsheng , Elsayyad Sayed , Allen Craig M. , Satler Lowell F. 
Published: September 2002

AbstractSerum cardiac troponin I (cTnI) is a highly specific marker for myocardial damage in patients with chronic renal insufficiency (CRI), unlike creatine kinase myocardial band fraction (CK‐MB), which may be elevated in the absence of myocardial injury in patients with CRI. We studied 116 consecutive CRI patients (serum creatinine ≥ 1.8 mg/dL, not on dialysis) with normal baseline cTnI levels who underwent successful percutaneous coronary intervention (PCI). Patients were divided into two groups: group 1, elevated postprocedural cTnI (n = 50), and group 2, normal cTnI (n = 66). Patients with elevated cTnI were older and had a higher incidence of postinfarction angina and lower creatinine clearance compared to patients who did not have cTnI elevation. Atheroablative devices (rotational and directional atherectomy and excimer laser coronary angioplasty) were more frequently used in group 1 patients (27.1% vs. 18.5%; P = 0.04). In‐hospital mortality, cardiac mortality, and Q‐wave myocardial infarction rates did not differ between the two groups. At 12‐month follow‐up, total mortality rates were significantly higher in group 1 (28.0% vs. 9.9%; P = 0.002). Multivariate analysis showed that cTnI was an independent predictor of late mortality (OR = 2.26; CI = 1.07–4.77; P = 0.03). Thus, in patients with CRI, elevated cTnI levels after successful PCI is an important predictor of poor long‐term outcome. Our data suggest that patients with cTnI elevation > 3 times above normal values are particularly at higher risk. Cathet Cardiovasc Intervent 2002;55:174–179. © 2002 Wiley‐Liss, Inc.
High‐throughput SNP genotyping
Authors: Jenkins Suzanne , Gibson Neil 
Published: September 2002

AbstractWhole genome approaches using single nucleotide polymorphism (SNP) markers
have the potential to transform complex disease genetics and expedite pharmacogenetics
research. This has led to a requirement for high‐throughput SNP genotyping
platforms. Development of a successful high‐throughput genotyping platform
depends on coupling reliable assay chemistry with an appropriate detection
system to maximise efficiency with respect to accuracy, speed and cost. Current
technology platforms are able to deliver throughputs in excess of 100 000 genotypes
per day, with an accuracy of >99%, at a cost of 20–30 cents per genotype.
In order to meet the demands of the coming years, however, genotyping platforms
need to deliver throughputs in the order of one million genotypes per day
at a cost of only a few cents per genotype. In addition, DNA template requirements
must be minimised such that hundreds of thousands of SNPs can be interrogated
using a relatively small amount of genomic DNA. As such, it is predicted that
the next generation of high‐throughput genotyping platforms will exploit large‐scale
multiplex reactions and solid phase assay detection systems. Copyright ©
2001 John Wiley & Sons, Ltd.
Integrating genotypic data with transcriptomic and proteomic data
Authors: Shields Denis C , O'Halloran Aisling M 
Published: September 2002

AbstractHistorically genotypic variation has been detected at the phenotypic level,
at the metabolic level, and at the protein chemistry level. Advances in technology
have allowed its direct visualisation at the level of DNA variation. Nevertheless,
there is still an enormous interest in phenotypic, metabolic and protein property
variability, since such variation gives insights into potential functionally
important differences conferred by genetic variation. High‐throughput transcriptomics
and proteomics applied to different individuals drawn from a population has
the potential to identify the functional consequences of genetic variability,
in terms of either differences in expression of mRNA or in terms of differences
in the quantities, pI(s) or molecular weight(s) of an expressed protein. Family
studies can define the genetic component of such variation (segregation analysis)
and with the genotyping of well‐spaced markers can map the causative factors
to broad chromosomal regions (linkage analysis). Association studies in the
variant proteins have the greatest power to confirm the presence of cis‐acting
genetic variants. The most powerful study designs may combine elements of
both family and association studies applied to proteomic and transcriptomic
analyses. Such studies may provide appreciable advances in our understanding
of the genetic aetiology of complex disorders. Copyright © 2002 John
Wiley & Sons, Ltd.
REALIS: Postgenomic analysis of Listeria monocytogenes
Authors: Kärst Uwe ,   The REALIS Consortium
Published: September 2002

AbstractListeria monocytogenes is a remarkably successful food‐borne pathogen.
It is capable a) of surviving and proliferating under conditions that exist
within the food chain, such as at low temperatures, high salt and low pH and
b) of colonizing animal host tissues after ingestion of contaminated food,
causing opportunistic infections mainly, but not exclusively, in immunocompromised
hosts.The ultimate goals of REALIS are two fold: Firstly, it aims to completely
decipher all genes required for survival in and adaptation of Listeria
monocytogenes to two very different environments, ie., the infected host
and the external environment. Secondly, using genomics and postgenomic tools,
REALIS seeks to precisely address fundamental questions regarding evolutionary
relationships between pathogenic and non‐pathogenic Listeria and to define
qualities of particularly successful clonal pathovariants in causing disease.This project will provide both industry and health care managers with rational
approaches to curbing food‐borne contamination, minimising risks of infection
and providing novel pharma­cological approaches for halting the fulminant
course of infection. Copyright © 2001 John Wiley & Sons, Ltd.
GEF at work: Vav in protruding filopodia
Authors: Kranewitter Wolfgang J. , Danninger Claudia , Gimona Mario 
Published: September 2002

AbstractThe Dbl family proto‐oncogene vav is a nucleotide exchange factor for Rho family GTPases and is involved in triggering cytoskeletal changes contributing to the alterations of cell shape and motility, as well as in the induction of gene expression. In vitro and in vivo Vav is regulated by multiple tyrosine phosphorylation and binding to phosphatidylinositol phosphates. Although recruitment of Vav to the plasma membrane appears important for the activation of Vav function, there is little information on the precise subcellular localization of Vav in living cells. Employing live video fluorescence and immunoelectron microscopy, we show that GFP‐tagged full‐length Vav, and several mutants in which the N‐terminal regulatory calponin homology (CH) domain has been deleted, specifically localize to the tips of filopodia. This localization was congruent with a high content of tyrosine phosphorylation in these regions. Consistent with earlier observations, mutants lacking the C‐terminal SH domain region were unable to translocate to the filopodia tips. The enrichment in filopodial tips persisted despite their lateral movement but was dependent on forward growth. Upon retraction, the signal was rapidly lost, indicating that Vav undergoes a specific and transient translocation in response to actin‐based, protrusive events in filopodia. Cell Motil. Cytoskeleton 49:154–160, 2001. © 2001 Wiley‐Liss, Inc.