bluuebunny/crossref_metadata_2025_split huggingface dataset:
Early steps in bilirubin‐mediated apoptosis in murine hepatoma (Hepa 1c1c7) cells are characterized by aryl hydrocarbon receptor‐independent oxidative stress and activation of the mitochondrial pathway
Authors: Oakes Garth H. , Bend John R. 
Published: September 2005

AbstractUnconjugated bilirubin (UCB), the end product of heme catabolism, causes apoptosis in cells of the central nervous system, endothelial cells, and hepatotoma cells. However, the molecular mechanisms that contribute to UCB cytotoxicity remain unclear. The purpose of this study was to characterize the sequence of early events leading to UCB‐mediated cytotoxicity in murine hepatoma Hepa 1c1c7 cells. In the present study, UCB (5–50 μM) was found to markedly increase the intracellular generation of reactive oxygen species (ROS) in a concentration‐dependent manner, which is significantly elevated by 30 min post‐treatment. This generation of ROS by UCB is not dependent on aryl hydrocarbon receptor (Ahr) signaling, as cells deficient in the Ahr (C12 cells) or the Ahr nuclear translocator protein (Arnt; C4 cells) were as efficient at generating ROS as wild type (WT) Hepa 1c1c7 cells. Mitochondrial membrane depolarization, evaluated with the lipophilic cationic dye, JC‐1, occurred at least by 2 h after treatment with 50 μM UCB. Analysis of the caspase cascade demonstrated that activation of caspase‐9 preceded activation of caspase‐3. No conversion of procaspase‐2 to active caspase‐2 was detected in this study. These results demonstrate that UCB‐mediated apoptosis in Hepa 1c1c7 cells is associated with increased oxidative stress and that caspase‐9, and definitely not caspase‐2, is the initiator caspase for apoptosis in UCB‐treated Hepa 1c1c7 cells. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:244–255, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20086
Probing the peripheral anionic site of acetylcholinesterase with quantitative structure activity relationships for inhibition by biphenyl‐4‐acyoxylate‐4′‐N‐Butylcarbamates
Authors: Lin Gialih , Chen Gan‐Hong , Yeh Shih‐Chieh , Lu Chun‐Ping 
Published: September 2005

AbstractBiphenyl‐4‐acyoxylate‐4′‐N‐butylcarbamates 1–8 are synthesized from 4,4′‐biphenol and are characterized as the pseudosubstrate inhibitors of acetylcholinesterase. In other words, the inhibitors bind to the enzyme and react with the enzyme to form the tetrahedral intermediates for the Ki steps, and then the tetrahedral intermediates exclude the leaving groups to form a common N‐butycarbamyl enzyme intermediate for the kc steps. Due to a linear character of the 4,4′‐biphenyl moiety, the 4′‐N‐butylcarbamate moieties of the inhibitors react with the Ser200 residue of the enzyme while the 4‐acyoxylate moieties of the inhibitors, on the other hand, should fit in the peripheral anionic site of the enzyme, which is located at the mouth of the deep active site gorge. Thus, carbamates with varied acyl substituents at the 4‐position of the biphenyl ring are good candidates for probing the quantitative structure activity relationships for the peripheral anionic site of the enzyme. The fact that the pKi, log kc, and log Ki values are correlated with neither the Taft substituent constant (σ*) nor the Taft steric constant (Es) indicates that the 4‐acyoxylate moieties of the inhibitors are too far away from the reaction center. However, the pKi, log kc, and log Ki values are linearly correlated with the Hansch hydrophobicity constant, π. The intensity constants (ψ) for these correlations are 0.16, −0.035, and 0.13, respectively. These results indicate that interactions between the 4‐acyoxylate groups of the inhibitors and the peripheral anionic site of the enzyme are mainly hydrophobic ones. The correlation results are slightly improved by using the two‐parameter correlations with the Taft substituent steric constant, Es, and π. For pKi, log kc, and log Ki–Es–π correlations, the ψ values are 0.21, −0.021, and 0.19, respectively; the intensity constants for steric effect (δ) are 0.08, 0.022, and 0.10, respectively. Besides hydrophobic interactions, the two‐parameter correlations also suggest that little steric hindrance occurs for the bulkier inhibitors to pass by the peripheral anionic site of the enzyme. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:234–243, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20087
Erythrocyte antioxidant defense response against cigarette smoking in humans—the glutathione S‐transferase vulnerability
Authors: Orhan Hilmi , Evelo Chris T. A. , Şahin Gönül 
Published: September 2005

AbstractCigarette smoking leads to uptake of a multitude of reactive chemicals including many electrophiles and may also give rise to oxidative stress. Human red blood cells are important targets for electrophilic and oxidant foreign compounds. We investigated the oxidative stress in erythrocytes upon cigarette smoking, and the response of antioxidant defense system against it. With this aim, simultaneous determination of erythrocyte superoxide dismutase (SOD), selenium dependent glutathione peroxidase (Se‐GPx), catalase (CAT), glutathione S‐transferase (GST) activities and plasma levels of thiobarbituric acid reactive substances (TBARS), and the degree of erythrocyte membrane lipid peroxidation (EMLP) were carried out in blood samples of smokers and their controls. Plasma TBARS levels and EMLP in smokers were significantly higher than the control levels (p < 0.01 and p < 0.005, respectively). SOD activity was diminished in smokers compared to nonsmoker controls (p < 0.005). Erythrocyte Se‐GPx activity was also found significantly diminished in smokers (p < 0.005), while plasma Se‐GPx activity was not changed. We observed that erythrocyte CAT activity was not different in smokers compared to nonsmoker controls. We found that the erythrocyte GST activity is significantly lower in young adult smokers (3.03 ± 0.18 U/mg protein; mean ± SEM; n = 46) than in nonsmoking contemporaries (3.98 ± 0.26 U/mg protein; mean ± SEM; n = 41). Together with previously reported data, it can be concluded that the decrease in GST activity leads to extra GST synthesis during erythrocyte proliferation. The same data were also analyzed for the sex differences. The statistically significant differences remained the same between nonsmoker and smoker females. Only EMLP degree and SOD activity were significantly different between nonsmoker and smoker males; however, when compared the parameters between male and female nonsmokers, GST activity was found to be significantly higher in females than that of males. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:226–233, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20088
Modulation of sulfur mustard induced cell death in human epidermal keratinocytes using IL‐10 and TNF‐α
Authors: Qabar Aziz , Nelson Marian , Guzman Juanita , Corun Charlene , Hwang Bor‐Jang , Steinberg Mark 
Published: September 2005

AbstractWe compared the effects of overexpressing a tightly regulated anti‐inflammatory cytokine, interleukin 10 (IL‐10), and the pro‐inflammatory cytokine tumor necrosis factor‐alpha (TNF‐α) on sulfur mustard induced cytotoxicity in human epidermal keratinocytes. Both cytokines were overexpressed when compared with the cells transfected with the empty vector as determined by quantitative ELISA. Cells overexpressing interleukin 10 suppressed the pro‐inflammatory cytokines interleukin 8 and interleukin 6 following exposure to 50–300 μM sulfur mustard. These cells exhibited delayed onset of sulfur mustard induced cell death. On the other hand, cells overexpressing tumor necrosis factor alpha induced a sustained elevation in both interleukin 6 and 8 expression following exposure to 50–300 μM sulfur mustard. These cells were sensitized to the effects of sulfur mustard that resulted in an increased sulfur mustard induced cell death. Normal human epidermal keartinocytes treated with sulfur mustard exhibited elevated levels of tumor necrosis factor alpha expression and increased activity of nuclear factor kappa B. Gene array data indicated that cells overexpressing interleukin 10 induced several genes that are involved in growth promotion and cell‐fate determination. We, therefore, identify IL‐10 and TNF‐α signal transduction pathways and their components as possible candidates for early therapeutic intervention against sulfur mustard induced cell injury. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:213–225, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20089
Gene and protein expressions in human cord blood cells after exposure to acrylonitrile
Authors: Diodovich Cristina , Malerba Ilaria , Ferrario Daniele , Bowe Gerard , Bianchi Marco Giorgio , Acquati Francesco , Taramelli Roberto , Parent‐Massin Dominique , Gribaldo Laura 
Published: September 2005

AbstractAcrylonitrile is a very high volume industrial chemical used primarily in the manufacture of plastics and rubber, which displays a pronounced acute toxicity and may be carcinogenic. The damage to the hematopoietic function by acrylonitrile may result from interference with cytokine production and cytokine receptor binding. Our present data show that acrylonitrile modulates the expression of some genes implicated in cell differentiation, cell‐cycle progression, and clonogenic potential of human cord blood cells. A macroarray hybridization analysis showed that expression of the CXCR4, MCP‐1, and MRP8 genes was modified by acrylonitrile exposure. Moreover, the acrylonitrile cell target seems to be the myeloid compartment, as assessed by a CFU‐GM assay. In particular, the downregulation of CXCR4, MCP1, and MRP8 can be responsible for the observed reduction of cell proliferation and clonogenic capability of CFU‐GM precursors. A Western blot assay showed an acrylonitrile‐dependent induction of Bax, while Bcl‐2 expression changed only after 48 h of chemical exposure. Bax was overexpressed in respect to Bcl‐2, and this fact can be responsible for the induction in cell death after 24 h of treatment. C‐fos and c‐jun were also downregulated after 24 h and 6 h of treatment, respectively. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:204–212, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20090
Methods for monitoring oxidative stress response in yeasts
Authors: Jamnik Polona , Raspor Peter 
Published: September 2005

AbstractChanges in the chemical or physical conditions of the cell that impose a negative effect on growth demand rapid cellular responses, which are essential for survival. Molecular mechanisms induced upon exposure of cells to such adverse conditions are commonly designated as stress responses. Herein, different methods which can be used to monitor oxidative stress response in yeasts are presented including monitoring of oxygen partial pressure during yeast cultivation, cell viability determination, measuring activity of enzymatic and level of nonenzymatic primary antioxidant defense systems, and examination of transcriptome and proteome changes. Additionally, some studies are given as examples of particular method's application for studying oxidative stress response in yeasts. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:195–203, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20091
Histone modifying enzymes and cancer: Going beyond histones
Authors: Zhang Ke , Dent Sharon Y.R. 
Published: September 2005

AbstractMutations in the molecular pathways that regulate cell proliferation, differentiation, and cell death all contribute to cancer formation. Enzymes that covalently modify histones affect these pathways by controlling the dynamic remodeling of chromatin structure. This article reviews several connections between histone modifying enzymes and cancer that are likely mediated via both histone and non‐histone substrates. We propose that multiple protein modifications, including phosphorylation, methylation, and acetylation, cross regulate one another to coordinate intermolecular signaling, and that miscues in this regulation can lead to oncogenesis. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.
Differential effect of insulin and elevated glucose level on adenosine handling in rat T lymphocytes
Authors: Pawelczyk Tadeusz , Sakowicz‐Burkiewicz Monika , Kocbuch Katarzyna , Szutowicz Andrzej 
Published: September 2005

AbstractReduced proliferation potential is among other T cell functional defects long known feature of diabetes. However, the mechanism responsible for this impairment is still unknown. Our study was undertaken to investigate the effect of changes in glucose and insulin concentrations on adenosine metabolism, transport and receptor‐mediated action in rat T lymphocytes. Presented results indicate that vulnerability of T cells to metabolic stress is determined by insulin but not by glucose concentration. However, glucose and insulin differentially affected the activities of adenosine metabolizing enzymes in resting and proliferating T cells. The Con A‐induced proliferation of cultured T lymphocytes did not depended on expression level and functional state of nucleoside transporters. Inhibition of adenosine kinase (AK) with 5‐iodotubercidin lowers the proliferation potential of T cells to the level observed for insulin‐deprived cells. Moreover, insulin‐deprived T lymphocytes but not cells cultured in the presence of insulin released significant quantities of adenosine. Under resting conditions, the cAMP level was fivefold higher in cells deprived of insulin comparing to cells cultured in the presence of insulin. Exposition of insulin‐deprived T lymphocytes to specific antagonist (ZM241385) of A2a receptor but not to specific antagonist (Alloxazine) of A2b receptor suppressed cAMP elevation and completely restored the proliferation potential of T cells. Concluding, adenosine released by insulin‐deprived T cells due to suppressed AK activity by acting on A2a receptors leads to increases in cAMP level and suppression of T cell proliferation. We assume that this mechanism may significantly contribute to immune impairment observed in diabetes. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.
Neural expression ofα‐internexinpromoter in vitro and in vivo
Authors: Wang Pei , Wang Seu‐Mei , Hsieh Chia‐Ju , Chien Chung‐Liang 
Published: September 2005

Abstractα‐Internexin is a 66 kDa neuronal intermediate filament protein found most abundantly in the neurons of the nervous systems during early development. To characterize the function of mouseα‐internexinpromoter, we designed two different expression constructs driven by 0.7 kb or 1.3 kb of mouseα‐internexin5′‐flanking sequences; one was the enhanced green fluorescent protein (EGFP) reporter for monitoring specific expression in vitro, and the other was thecrefor studying the functional DNA recombinase in transgenic mice. After introducing DNA constructs into non‐neuronal 3T3 fibroblasts and a neuronal Neuro2A cell line by lipofectamine transfection, we observed that the expression of EGFP with 1.3 kb mouseα‐internexinpromoter was in a neuron‐dominant manner. To establish a tissue‐specific pattern in the nervous system, we generated a transgenic mouse line expressing Cre DNA recombinase under the control of 1.3 kbα‐Internexinpromoter. The activity of the Cre recombinase at postnatal day 1 was examined by mating thecretransgenic mice to ROSA26 reporter (R26R) mice with knock‐in Cre‐mediated recombination. Analyses of postnatal day 1 (P1) newborns showed that β‐galactosidase activity was detected in the peripheral nervous system (PNS), such as cranial nerves innervating the tongue and the skin as well as spinal nerves to the body trunk. Furthermore, X‐gal‐labeled dorsal root ganglionic (DRG) neurons showed positive for α‐Internexin in cell bodies but negative in their spinal nerves. The motor neurons in the spinal cord did not exhibit any β‐galactosidase activity. Therefore, thecretransgene driven by mouseα‐internexinpromoter, described here, provides a useful animal model to specifically manipulate genes in the developing nervous system. J. Cell. Biochem. 97: 275–287, 2006. © 2005 Wiley‐Liss, Inc.
Roles of osteonectin in the migration of breast cancer cells into bone
Authors: Campo McKnight Dianalee A. , Sosnoski Donna M. , Koblinski Jennifer E. , Gay Carol V. 
Published: September 2005

AbstractThe focus of this study was to gain insight into the role(s) of osteonectin in the preferential metastasis of breast cancer cells to bone. Osteonectin was isolated from conditioned media of several cell lines including breast cancer (MDA‐MB‐435, MDA‐MB‐468), osteoblasts (hFOB1.19), non‐neoplastic breast epithelial (hTERT‐HME1), and vascular endothelial cells isolated from a bone biopsy (HBME‐1). Chemical/physical properties of osteonectin from these five sources was analyzed to determine if unique configurations of osteonectin exist and therefore identify a chemotactic isoform. Osteonectin from all sources had a molecular weight of ∼46 kDa, N‐linked glycosylation, and undetectable phosphorylated serines, sialic acids and O‐linked oligosaccharides. The cDNA for osteonectin from the breast cancer, osteoblast, and breast epithelial cell lines was identical, while the vascular endothelial cell cDNA contained point mutations that resulted in eight amino acid substitutions. Bone‐derived osteonectin was then analyzed to assess its influence on breast cancer cell motility and migration. Although osteonectin increased undirected MDA‐MB‐231 cell motility, it did not chemoattract the same breast cancer cell line. However, the breast cancer cells did migrate toward the known chemoattractant vitronectin and to bone extracts derived from wild‐type and osteonectin‐null mice. Migration to vitronectin was enhanced when osteonectin was also present. We concluded that osteonectin was not a chemotactic factor. However, through its anti‐adhesive properties, osteonectin induced undirected breast cancer cell motility, and may have enhanced chemoattraction to vitronectin. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.
Gender acts as a context for interpreting diagnostic criteria
Authors: Flanagan Elizabeth H. , Blashfield Roger K. 
Published: September 2005

AbstractThis study used a unique methodology to determine the aspects of case vignettes that elicited an effect of case gender on diagnosis. A total of 99 psychiatrists and psychologists were shown cases representing a man or a woman that contained varying numbers of histrionic and antisocial criteria. The cases were presented by computer a few sentences at a time. Clinicians were asked to offer a diagnosis for the case after each group of sentences was presented. Results indicated that case gender tended to affect clinicians' diagnostic decisions when criteria related to that diagnosis were shown, suggesting that case gender was acting as a context in which diagnostic criteria were interpreted. © 2005 Wiley Periodicals, Inc. J Clin Psychol 61: 1485–1498, 2005.
What's an integrationist? A study of self‐identified integrative and (occasionally) eclectic psychologists
Authors: Norcross John C. , Karpiak Christie P. , Lister Kelly M. 
Published: September 2005

AbstractWe examined the views and practices of self‐identified eclectic and integrative psychologists, particularly in the context of historical changes since 1977 and 1988. Results from 187 eclectic clinical psychologists indicated that 50% previously adhered to another theoretical orientation, the majority preferred the term integrative to eclectic, and 85% conceptualized eclecticism/integration as the endorsement of a broader orientation. The most common paths toward integration were theoretical integration, common factors, and assimilative integration, as opposed to technical eclecticism. The most frequent theoretical contributor to integrative practice was cognitive therapy. © 2005 Wiley Periodicals, Inc. J Clin Psychol 61: 1587–1594, 2005.
Brief scheduled phone support from a clinician to enhance computer‐aided self‐help for obsessive‐compulsive disorder: Randomized controlled trial
Authors: Kenwright Mark , Marks Isaac , Graham Candida , Franses Abigail , Mataix‐Cols David 
Published: September 2005

AbstractTreatment‐resistant obsessive‐compulsive disorder (OCD) patients from around the United Kingdom who employed computer‐guided self‐help by using BTSteps over 17 weeks were randomized to have brief live phone support from a clinician either (1) in nine Scheduled clinician‐initiated calls or (2) only in calls Requested by the patient (n = 22 per condition). Call content and mean duration were similar across conditions. Scheduled‐support patients dropped out significantly less often, did more homework of self‐exposure and self‐imposed ritual prevention (95% vs. 57%), and showed more improvement in OCD symptoms and disability. Mean total support time per patient over 17 weeks was 76 minutes for Scheduled and 16 minutes for Requested patients. Giving brief support proactively by phone enhanced OCD patients' completion of and improvement with computer‐aided self‐help. © 2005 Wiley Periodicals, Inc. J Clin Psychol 61: 1499–1508, 2005.
Reevaluating the distinction between Axis I and Axis II disorders: The case of borderline personality disorder
Authors: Ruocco Anthony C. 
Published: September 2005

AbstractThe division between Axis I clinical syndromes and Axis II personality disorders is a long‐standing distinction based primarily on three guiding principles: phenomenology, cause, and course. Clinical syndromes were generally thought to be characterized by transient symptoms with biological causes and an unstable course; personality disorders were supposed by many to be characterized by long‐standing personality traits, whose roots were primarily psychological, and a stable and unremitting course. Borderline personality disorder (BPD), however, is a condition characterized by distinct clinical symptoms, varied causes, and a relatively unstable course. Past theorizing about the distinction between Axis I and Axis II disorders is presented in light of recent empirical evidence refuting the rationalization for the separation of personality disorders and clinical syndromes using BPD as a means for comparison. © 2005 Wiley Periodicals, Inc. J Clin Psychol 61: 1509–1523, 2005.
Downstream processing of 1,3‐propanediol fermentation broth
Authors: Hao Jian , Xu Feng , Liu Hongjuan , Liu Dehua 
Published: September 2005

AbstractThe downstream processing of 1,3‐propanediol fermentation broth using flocculation, reactive extraction, and reactive distillation was studied. Cellular debris and soluble protein in the broth were flocculated by combined use of chitosan and polyacrylamide at optimal concentrations of 150 ppm and 70 ppm, respectively; the soluble protein in the broth decreased to 0.06 g L−1, and the recovery ratio of the supernatant liquor to broth was greater than 99%. 1,3‐Propanediol and other alcohols were extracted from the supernatant liquor by reacting with butyraldehyde. In a four‐stage countercurrent extraction with the volume ratio of the extraction solvent to the aqueous phase being 20:100, more than 99% 1,3‐propanediol acetal (2‐propyl‐1,3‐dioxane) and 2,3‐butanediol acetal (2‐propyl‐4,5‐dimethyl‐1,3‐dioxolane) were recovered from the aqueous phase; 35% of the glycerol acetals were recovered. The acetals produced were hydrolyzed in a reactive distillation column using the strongly acidic cation‐exchange resin as catalyst, the bottom product obtained was a mixture of 1,3‐propanediol (407 g L−1), 2,3‐butanediol (252 g L−1), glycerol (277 g L−1), and glycerol acetals (146 g L−1). Copyright © 2005 Society of Chemical Industry