bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential effects of short‐term lindane administration on parameters related to oxidative stress in rat liver and erythrocytes
Authors: Bainy A. C. D. , Arisi A. C. M. , Azzalis L. A. , Simizu K. , Barros S. B. M. , Videla L. A. , Junqueira V. B. C. 
Published: October 2006

AbstractParameters related to oxidative stress in rat liver and erythrocytes were studied after short‐term administration (60 and 90 days) of 1000 ppm of lindane in the diet. Lindane induced an oxidative stress condition in the liver, which is related to an enhancement in microsomal NADPH‐cyto‐chrome c reductase and NADPH oxidase activities, superoxide radical formation and cytochrome P450 content, produced independently of the time of treatment. Also, decreased activities of glutathione peroxidase and catalase were concomitantly observed. Although these changes were paralleled by an increase in lipid peroxidation indices, such as production of thiobarbituric acid reactants and spontaneous chemiluminescence, no evidence of liver injury was obtained. Lindane treatment did not exert quantitatively important changes in the pro‐oxidant/anti‐oxidant status of the erythrocyte, with reduction in the red blood cell mass possibly reflecting actions of the insecticide on the eryth‐ropoietic process.
Development of pancellular toxicity in guinea pig lung by ingestion of oleylanilide
Authors: Das Salil K. , Mukherjee Shyamali , Desai Usha 
Published: October 2006

AbstractToxic oil syndrome (TOS), characterized by widespread thromboembolism, vasculotoxicity, and ARDS, develops in humans ingesting denatured edible oils. The mechanism(s) involved in targeted vasculocentric damage in this multisystem disorder is not known. Oleylanilide (OA) was synthesized and fed to male, young adult guinea pigs by gavage for 30 days at doses of 35, 50, and 100 mg/kg/day in groups of six animals each respective to weight. Controls were fed olive oil. Oleylanilide fed animals gained less weight than controls. At the end of experiment, right lungs were inflation fixed in appropriate fixative for histology and transmission electron microscopy (TEM) and left lungs were frozen at −70°C for biochemical analyses. The activity of glycerophosphate acyltransferase (GAT) and cholinephosphotransferase (CPT), two key enzymes involved in phospholipid biosynthesis, were decreased in lung due to OA ingestion. All doses of OA induced marked perivascular and peribronchoiolar monocytic infiltrates that often formed prominent nodules; segmental vascular smooth muscle cell proliferation and derangement of myocytic polarity, subendothelial foamy infiltrates, and edema; nuclear pyknosis and dropout in vascular and bronchial targetoid myocytes; and denudation of bronchiolar epithelial cells. Alveoli contained large numbers of monocytes, macrophages, red cells, edema, and debris. Transmission electron microscopy showed type I cell cytoplasmic ballooning and disintegration of type I cell; contracted and blebbed endothelial cells, fibrin thrombi in capillaries, intracellular megalamellar bodies in type II cells, and surfactant lamellae; and liposomes and fine granular precipitates within alveoli, and contraction and lift off of bronchiolar epithelial cells. Monocytes, mast cells, and eosinophils infiltrated bronchial walls. Furthermore, there was deposition of electron dense particles on the surface of the alveolar wall. Cytotoxicity of various cells is considered to be either directly caused by the anilides or a result of monocytes and free radicals. This is the first experimental model for “intractable” dysplastic vascular diseases in humans.
Cytosolic 5′‐nucleotidase/nucleoside phosphotransferase: A nucleoside analog activating enzyme?
Authors: Turriani Maura , Pesi Rossana , Nardone Antonella , Turchi Gino , Sgarrella Francesco , Ipata Pier Luigi , Tozzi Maria Grazia 
Published: October 2006

AbstractNucleoside phosphotransferase acting on inosine and deoxyinosine has been partially purified from cultured Chinese hamster lung fibroblasts (V79). The activity is associated with a cytosolic 5′‐nucleotidase acting on IMP and deoxyIMP. The transfer of the phosphate group from IMP to inosine catalyzed by this enzyme was activated by ATP and 2,3‐bisphosphoglycerate. Inosine, deoxyinosine, guanosine, deoxyguanosine, and the nucleoside analogs 2′,3′‐dideoxyinosine and 8‐azaguanosine are substrates, while adenosine and deoxyadenosine are not. IMP, deoxyIMP, GMP, and deoxyGMP are the best phosphate donors.The cytosolic 5′‐nucleotidase/phosphotransferase substrate, 8‐azaguanosine, was found to be very toxic for cultured fibroblasts (LD50 = 0.32 μM). Mutants resistant to either 8‐azaguanosine and the correspondent base 8‐azaguanine were isolated and characterized. Our results indicated that the 8‐azaguanosine‐resistant cells were lacking both cytosolic 5′‐nucleotidase and hypoxanthine‐guanine phosphoribosyltransferase, while 8‐azaguanine resistant cells were lacking only the latter enzyme. Despite this observation, both mutants displayed 8‐azaguanosine resistance, thus indicating that cytosolic 5′‐nucleotidase is not essential for the activation of this nucleoside analog.
Significance of TCDD‐induced changes in protein phosphorylation in the adipocyte of male guinea pigs
Authors: Enan Essam , Matsumura Fumio 
Published: October 2006

AbstractThe chemical TCDD (2,3,7,8‐tetrachlorodibenzo‐p‐dioxin) at very low concentrations has been found to cause a rapid rise in protein phosphorylation activities in the extranuclear fraction (i.e., cytosol and cellular membranes) of the adipose tissue from male guinea pigs. The effect occurred both in vivo and when TCDD was added to adipose in tissue culture (in situ). To study the cause for such a TCDD‐induced biochemical change, isolated adipose tissues were treated with TCDD in conjunction with various diagnostic agents known to affect protein synthesis (actinomycin D and cycloheximide) and protein phosphorylation activities (genistein). The stimulatory effect of TCDD on protein phosphorylation was not totally abolished by actinomycin D; however, cycloheximide and genistein partially suppressed the effect of TCDD. Such an action of TCDD was accompanied by a quick rise in ras GTP binding activity as well as a rise in phosphorylation of nuclear c‐myc protein product within 10 minutes after TCDD addition, indicating that TCDD is likely to activate the signal transduction pathway for growth factors. In view of the absence of an inhibitory action of actinomycin D and the short time required for TCDD to induce these changes, we have formulated a working hypothesis that stimulation of protein phosphorylation activities by TCDD may not be mediated by a transcriptional process. To test this possibility, an extranuclear fraction was obtained from the homogenate of adipose tissue, and the effect of TCDD was studied in vitro cell‐and nucleus‐free conditions. It was found that TCDD was capable of activating protein phosphorylation activity under cell free conditions even in the absence of nuclei. Such an action of TCDD is dependent on the action of the Ah receptor.
Multiple activation of chloroform in kidney microsomes from male and female DBA/2J mice
Authors: Ade Paola , Guastadisegni Cecilia , Testai Emanuela , Vittozzi Luciano 
Published: October 2006

AbstractMicrosomes from the renal cortex of DBA/2J mice can metabolize chloroform through oxidative and reductive pathways, similar to hepatic microsomes.The oxidative or reductive nature of CHCl3 activation is strictly dependent on the oxygenation of the incubation mixture, as indicated by the formation of qualitatively different adducts to phos‐pholipids (PLs).The protein and lipid binding levels measured in kidney microsomes from control females differed significantly from the binding levels observed with kidney microsomes from male and testosterone‐treated female DBA/2J mice in aerobic conditions only. Therefore, the sex‐dependent CHCl3‐induced acute nephrotoxicity seems related only with the oxidative CHCl3activation.The levels of adducts to PL polar heads and to protein showed a strict correlation with each other. Therefore, the assay of adducts to PL polar heads may be used as a substitute for the assay of adducts to protein. This might be especially convenient when studying the effects of both phosgene and the trichloromethyl radicals.
A comparative study of inhibition of acetylcholinesterase, trypsin, neuropathy target esterase, and spleen cell activation by structurally related organophosphorus compounds
Authors: Pruett Stephen B. , Chambers Howard W. , Chambers Janice E. 
Published: October 2006

AbstractOrganophosphorus (OP) compounds can bind to and inactivate several target molecules other than acetylcholinesterase (AChE). In the present study, five sets of structurally related organophosphorus compounds were used to evaluate the relationships between organophosphorus binding sites of AChE, neuropathy target esterase (NTE), trypsin, and the target molecule(s) involved in inhibition of splenocyte activation by OP compounds. The concentration of each OP compound required to inhibit enzyme activity or splenocyte activation by concanavalin A by 50% was determined. The pattern of IC50 values indicated that AChE, trypsin, NTE, and the molecule(s) involved in inhibition of splenocyte activation are distinct with regard to patterns of inhibition by OP compounds. However, there was a striking similarity in the patterns of inhibition for trypsin and NTE with substantial differences for only 2 of 20 compounds. This pattern suggests similarity in the active sites of these molecules. There were also similarities in the IC50 patterns for lymphocyte activation and trypsin or NTE activity. However, the correlation was not as strong as between NTE and trypsin, and the data suggested the possibility of multiple target molecules for inhibition of splenocyte activation by OP compounds. More importantly, there was essentially no correlation between the pattern of IC50 values for AChE and splenocyte activation. This strongly suggests that acetylcholine and AChE of the type found in the brain are not important in the regulation of splenocyte activation by concanavalin A.
2,3,7,8‐tetrachlorodibenzo‐p‐dioxin induced alterations of pyruvate carboxylase levels and lactate dehydrogenase isozyme shifts in C57BL/6J male mice
Authors: Sparrow Barney R. , Thompson Cynthia S. , Ryu Byung‐Woo , Selevonchick Daniel P. , Schaup Henry W. 
Published: October 2006

AbstractA dose‐dependent reduction of hepatic pyruvate carboxylase levels and activity occurs in C57BL/6J male mice given 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) i.p. in a corn oil carrier. The dose range was from 1 to 75 μg/kg body weight and the analysis was done 8 days postinjection. At the maximum TCDD level investigated, we found a 10‐fold reduction in pyruvate carboxylase activity. Furthermore, TCDD at a dose of 1 μg/kg body weight blocks corn oil induction of an increase in the amount of pyruvate carboxylase in liver protein extracts. At doses beyond those required to initiate a reduction in pyruvate carboxylase, lactate dehydrogenase isozyme patterns shift. This is accompanied by an increase in blood lactic acid levels. We propose that TCDD‐mediated reduction in pyruvate carboxylase and lactate dehydrogenase isozyme shifts may represent a major component in TCDD toxicity.
Age‐related differences in TGF‐α and proto‐oncogenes expression in rat liver after a low dose of carbon tetrachloride
Authors: Dalu Abraham , Cronin Gerald M. , Lyn‐Cook Beverly D. , Mehendale Harihara M. 
Published: October 2006

AbstractThe resiliency of rats during early postnatal development to CCl4 or to an interactive hepatotoxicity of chlordecone (CD) + CCl4 has been shown to be due to an efficient stimulation of tissue repair. The objective of the current study was to investigate if this is due to efficient expression of transforming growth factor‐α (TGF‐α) and proto‐oncogenes. Postnatally developing (20 day old) and adult (60 day old) male Sprague–Dawley rats were challenged with a single low dose of CCl4 (100 μL/kg, ip) or corn oil. Liver samples were collected during a time course (0–96 h) after the administration of CCl4 and used to examine TGF‐α and early (c‐fos) and late (H‐ras and K‐ras) proto‐oncogenes mRNA expressions. Significant increases in TGF‐α, H‐ras, and K‐ras gene expressions were evident as early as 12 hours after CCl4 and peaked between 24 and 48 hours in an age‐dependent manner as detected by slot‐blot analysis. Results of the study revealed three‐ and twofold increases in TGF‐α gene expression in 20 and 60 day old rats, respectively, after CCl4. There were 3.5‐ and 2.5‐fold increases in H‐ras and 4.4‐ and 3.4‐fold increases in K‐ras in 20 and 60 day old rats, respectively. In contrast, a 10‐fold increase in c‐fos mRNA expression was evident in 20 day old rats 1 hour after CCl4 treatment, returning to the baseline value by 3 hours, whereas in 60 day old rats, this increase was less than twofold. The overall findings of this study indicate that TGF‐α and the early and late proto‐oncogene mRNA expressions were enhanced in an age‐ and time‐dependent manner in response to a low dose of CCl4. These results further strengthen the view that the remarkable resiliency of rats to hepatotoxicants during early postnatal development is due to substantial increases in stimulation of hepatocellular regeneration and tissue repair mechanisms, leading to regression of liver injury and recovery. © 1996 John Wiley & Sons, Inc.
Mechanism of toxicity of precocene II in rat hepatocyte cultures
Authors: Hammond Alison H. , Garle Michael J. , Fry Jeffrey R. 
Published: October 2006

AbstractPrecocene II was more toxic in 24 hour cultures than in 72 hour cultures of rat hepatocytes. In 24 hour cultures, there was no observable toxicity at 75 μM precocene II after exposure for 6 hours, but after 24 hours, 65% of the cells were dead. In contrast, although 794 μM killed 50% of the cells in the 72 hour cultures after a 24 hour exposure, 1 mM killed 96% of the cells within 6 hours. In both 24 and 72 hour cultures, cell death was preceded by a rapid, early loss of mitochondrial membrane potential, followed by decreases in glutathione, reduced pyridine nucleotide status, and plasma membrane Na+/K+‐ATPase activity. There was also a rapid loss of ATP in the 72 hour cultures but not in the 24 hour cultures; therefore, onset of cell death may be closely linked to loss of ATP. Inhibition of cytochrome P‐450 prevented the toxicity, and partially protected against the loss of membrane potential and glutathione, in 24 hour cultures but was ineffective in 72 hour cultures. Therefore, in addition to depletion of glutathione, precocene II appears to damage mitochondria and plasma membrane functions and can do so by more than one pathway. © 1996 John Wiley & Sons, Inc.
Differential regulation of cytochrome P450 3A1 and P450 3A2 in rat liver following dexamethasone treatment
Authors: Choudhuri Supratim , Zhang Xu Jie , Waskiewicz Mark J. , Thomas Paul E. 
Published: October 2006

AbstractInduction of P450 3A1 and P450 3A2 was studied in adult rat liver following treatment with a single high dose of dexamethasone (DEX). The increase of both P450 3A1 and 3A2 occurred at the level of mRNA as well as protein. P450 3A isozymes thus induced were catalytically active. No constitutive expression of P450 3A1 mRNA or protein was observed in males or females. Constitutive expression of P450 3A2 mRNA and protein was observed in males but not in females. Additionally, in females, P450 3A2 was almost nondetectable compared to that in males, at any dose of DEX. A time course study following DEX treatment showed that P450 3A1 mRNA and protein were detectable in both sexes at 12 hours, increased until 48 hours, and then declined. The decline was more rapid in males. P450 3A2 mRNA and protein increased as early as 3 hours, increased further up to 48 hours, and slowly declined thereafter. A dose‐response study indicated that P450 3A1 mRNA and protein progressively increased in both sexes from a dose of 30 mg/kg. In contrast, P450 3A2 mRNA and protein in males did not increase up to a dose of 30 mg/kg but increased at higher doses. Total P450 content and P450 3A catalytic activity were also found to increase with time and dose. © 1996 John Wiley & Sons, Inc.
Ricin disturbs calcium homeostasis in the rabbit heart
Authors: Ma Lianmin , Hsu Chia‐Hsuh , Fugate Robert , Patterson Eugene , Thadani Udho , Robinson Casey P. 
Published: October 2006

AbstractRicin, a toxic lectin from the castor bean, affects the cardiovascular system. Because calcium is very important in cardiotoxicity and cell intoxication, we studied the effects of ricin pretreatment to rabbits on basal intracellular calcium levels and calcium uptake and release from isolated papillary muscle, microsomes, and mitochondria. An increase in basal intracellular calcium levels was observed. Ricin pretreatment nearly doubled the intracellular‐free Ca2+ concentration as measured by fura‐2 fluorescence microscopy in isolated myocytes (p = 0.002). Ricin did not alter basal calcium efflux in isolated papillary muscles. However, ricin inhibited the NE‐induced calcium efflux (expressed as fractional efflux ratios) in papillary muscles from rabbits receiving the minimum lethal dose of ricin at 25–35 minutes (p = 0.002 and 0.003, respectively). Ricin depressed basal calcium uptake into isolated papillary muscles at 5 minutes (mean ± SEM, μmol/g wet weight) (control: 3.68 ± 0.57; ricin: 2.31 ± 0.28, p = 0.045, n = 6). Ricin pretreatment significantly depressed calcium uptake into microsomes (mean ± SEM, μmol/g protein) (control: 9.9 ± 1.9; ricin: 3.1 ± 1.9, p = 0.025, n = 6). Calcium uptake into mitochondria was increased at the beginning (2 minutes, p = 0.048), but not thereafter. Thus, administration of ricin disturbed calcium homeostasis in the rabbit heart, which may be at least partially responsible for altering cardiac function and myocardial cell death. © 1996 John Wiley & Sons, Inc.
Functional expression of voltage‐gated sodium channels in primary cultures of human cervical cancer
Authors: Diaz Daniel , Delgadillo Dulce Maria , Hernández‐Gallegos Elizabeth , Ramírez‐Domínguez Martha Eugenia , Hinojosa Luz María , Ortiz Cindy Sharon , Berumen Jaime , Camacho Javier , Gomora Juan Carlos 
Published: October 2006

AbstractCervical cancer (CaC) is the third most frequent cause of death from cancer among women in the world and the first in females of developing countries. Several ion channels are upregulated in cancer, actually potassium channels have been suggested as tumor markers and therapeutic targets for CaC. Voltage‐gated sodium channels (VGSC) activity is involved in proliferation, motility, and invasion of prostate and breast cancer cells; however, the participation of this type of channels in CaC has not been explored. In the present study, we identified both at the molecular and electrophysiological level VGSC in primary cultures from human cervical carcinoma biopsies. With the whole cell patch clamp technique, we isolated and identified a voltage‐gated Na+ current as the main component of the inward current in all investigated cells. Sodium current was characterized by its kinetics, voltage dependence, sensitivity to tetrodotoxin (TTX) block and dependence to [Na+]o. By analyzing the expression of mRNAs encoding TTX‐sensitive Na+ channel α subunits with standard RT‐PCR and specific primers, we detected Nav1.2, Nav1.4, Nav1.6, and Nav1.7 transcripts in total RNA obtained from primary cultures and biopsies of CaC. Restriction enzyme analysis of PCR products was consistent with the molecular nature of the corresponding genes. Notably, only transcripts for Nav1.4 sodium channels were detected in biopsies from normal cervix. The results show for the first time the functional expression of VGSC in primary cultures from human CaC, and suggest that these channels might be considered as potential molecular markers for this type of cancer. J. Cell. Physiol. 210: 469–478, 2007. © 2006 Wiley‐Liss, Inc.
Using lessons from health care to protect the privacy of library users: Guidelines for the de‐identification of library data based on HIPAA
Authors: Nicholson Scott , Smith Catherine Arnott 
Published: October 2006

AbstractWhile libraries have employed policies to protect the data about use of their services, these policies are rarely specific or standardized. Since 1996 the U.S. healthcare system has been grappling with the Health Insurance Portability and Accountability Act (HIPAA), which is designed to provide those handling personal health information with standardized, definitive instructions as to the protection of data. In this work, the authors briefly discuss the present situation of privacy policies about library use data, outline the HIPAA guidelines to understand parallels between the two, and finally propose methods to create a de‐identified library data warehouse based on HIPAA for the protection of user privacy.
Navigational characteristics of e‐document readers
Authors: Qayyum Asim , Bilykh Igor 
Published: October 2006

AbstractThe purpose of this study was to examine the navigational patterns of graduate students' text markings when they interact with electronic documents during an active reading process, thus taking on the role of authors. The readings took place in two settings, private and document sharing, where in the latter environment each document was shared among a group of students. The resulting interaction was monitored and electronically logged for each of these environments, which then provided us with user‐navigational patterns taxonomy. Descriptive and statistical tests were carried out on the activities observed within this taxonomy to develop a framework for comparing the reading patterns for readers working in individual and document sharing environments. This framework was then used to obtain user feedback during the interview sessions that were held with the participants of this study. Because of our investigation, we were able to create a set of specific recommendation that system designers can use in order to create better, more intuitive, and userfriendly electronic reading and marking systems.
How neutral can technology be?
Authors: Caidi Nadia , Shankar Kalpana , Dalbello Marija , Froehlich Thomas J. 
Published: October 2006

AbstractIs technology amoral? Is design value‐laden but code neutral? While philosophers, technologists, science and technology studies (STS) scholars, and social critics continue to debate whether or not information technologies are neutral and an autonomous force acting independently of other social processes, these discussions are only marginally addressed in Information studies. Yet, discussing these issues is of compelling importance for the training of the next generation of information professionals. The differing assumptions and values about the social nature of technology have implications for research and practice, and are of compelling importance from an ethics, design, policymaking and globalization perspective. This panel will address the varying approaches (e.g., instrumental theory of technology versus more interpretive approaches) and discuss the implications of technological (non) neutrality in a variety of settings, including ubiquitous computing, health care technologies, digital library development, and others.
Sparking synergies between research and practice: The contribution of social informatics
Authors: Rosenbaum Howard , Sawyer Steve , Davenport Elisabeth , Day Ronald 
Published: October 2006

AbstractThe purpose of this panel is to address the relationships among research and practice in the domain of information systems in organizations. Using the perspective of social informatics, we highlight issues with current work, areas of particular interest, and problems vexing both professional and scholarly interests