bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reduction of telomerase activity in human liver cancer cells by a histone deacetylase inhibitor
Authors: Nakamura Mitsuyasu , Saito Hidetsugu , Ebinuma Hirotoshi , Wakabayashi Kanji , Saito Yoshimasa , Takagi Tamako , Nakamoto Nobuhiro , Ishii Hiromasa 
Published: August 2002

AbstractThe presence of telomerase has been demonstrated recently in many different malignancies. Several reports documented that in human hepatocellular carcinoma, the level of telomerase activity parallels its differentiation stage. In the present study, the effect of the differentiation‐inducing agent sodium butyrate on telomerase activity in four human liver cancer cell lines was investigated using the telomeric repeat amplification protocol. We assayed telomerase activity before and after butyrate treatment and in cell cycle synchronized non‐dividing quiescent cells. In addition, telomerase reverse transcriptase levels were measured at the mRNA level. All four cell lines possessed high but not identical levels of telomerase activity. Telomerase activity was significantly reduced by treatment with sodium butyrate as well as trichostatin A in a dose‐ and time‐dependent fashion, paralleling the reduction of cell proliferation. Although methotrexate, hydroxyurea, and colchicine synchronized the cell cycle at G1, S, and G2/M, respectively, and thereby also caused proliferating cells to cease dividing and become quiescent, in this case telomerase activity remained essentially unaltered compared to the control cultures. Moreover, levels of mRNA encoding telomerase reverse transcriptase were not always significantly altered by either sodium butyrate treatment or cell cycle synchronization. These results suggest that sodium butyrate, as a histone deacetylase inhibitor, effectively reduces telomerase activity without affecting transcription levels of the reverse transcriptase component. © 2001 Wiley‐Liss, Inc.
Reciprocal regulation of tissue‐type and urokinase‐type plasminogen activators in the differentiation of murine preadipocyte line 3T3‐L1 and the hormonal regulation of fibrinolytic factors in the mature adipocytes
Authors: Seki Taiichiro , Miyasu Tomoko , Noguchi Toshinori , Hamasaki Ayumi , Sasaki Rika , Ozawa Yukiko , Okukita Kaoru , Declerck Paul J. , Ariga Toyohiko 
Published: August 2002

AbstractAdipose tissue expresses a variety of genes including tumor necrosis factor α and type‐1 plasminogen activator inhibitor (PAI‐1); and these factors, produced by adipocytes, may be associated with the risk of coronary events in obesity. In this study, we characterized the production of fibrinolytic factors including tissue‐type plasminogen activator (tPA), urokinase‐type PA (uPA), and PAI‐1 in the differentiation of preadipocytes, and examined the hormonal regulation of these fibrinolytic factors in mature adipocytes. Mouse 3T3‐L1 preadipocytes were employed as a model of adipocytes. Adipocyte differentiation was induced by insulin, dexamethasone, and 3‐isobutyl‐1‐methyl xanthine (IBMX). α‐Glycerophosphate dehydrogenase (GPDH) activity and glucose transporter 4 (GLUT4) mRNA, indices for adipocyte maturation, were induced on Day 4, and gradually increased. GPDH activity reached its maximum level on Day 14. The level of tPA, a major PA in preadipocytes, dramatically decreased with differentiation. On the other hand, that of uPA reciprocally increased. PAI‐1 production was also dramatically induced concomitant with differentiation. In mature adipocytes, uPA production was dominant (25 μg/ml/24 h vs. 0.8 μg/ml/24 h for tPA). Total PA activity in the mature adipocytes was reduced by insulin or dexamethasone, but not by glucagon. Insulin, IBMX, and dexamethasone significantly decreased both uPA and tPA production, and increased PAI‐1 production. Glucagon had no effect on the production of these fibrinolytic factors. Our results reveal that uPA is one of the markers for the differentiation of 3T3‐L1 cells and that insulin, IBMX, and dexamethasone are potent regulators of the fibrinolytic activity in differentiated 3T3‐L1 cells, reciprocally affecting PA and PAI‐1 levels in them. © 2001 Wiley‐Liss, Inc.
Biosorption from aqueous solutions by eggshell membranes and Rhizopus oryzae: equilibrium and kinetic studies
Authors: Koumanova Bogdana , Peeva P , Allen Stephen J , Gallagher K A , Healy M G 
Published: August 2002

AbstractThis study assesses the use of eggshell membranes and Rhizopus oryzae as media for the biosorption of p‐chlorophenol (p‐CP), 2,4‐dichlorophenol (2,4‐DCP), 3,5‐dichlorophenol (3,5‐DCP), reactive dye and cadmium from aqueous solutions. The performance of the adsorbents was quantified by measuring the equilibrium uptake and the batch rate kinetics from solutions. The constants in the Freundlich, Langmuir and Redlich–Peterson isotherm models were calculated through the linearization of the equations and linear regression. The kinetics of the adsorption systems for cadmium and a reactive dye have been assessed in a batch stirred adsorber. The effect of the process parameters such as pH, adsorbate concentration, adsorbent dosage, adsorbent particle size, temperature and agitation speed are reported. The external mass transfer coefficients are reported for some different system conditions. Both materials are determined to be effective adsorbents and could find application in the treatment of contaminated wastestreams.© 2002 Society of Chemical Industry
Structural effects of ion‐exchange membrane on the separation of L‐phenylalanine (L‐Phe) from fermentation broth using electrodialysis
Authors: Choi Jae‐Hwan , Oh Suk‐Jung , Moon Seung‐Hyeon 
Published: August 2002

AbstractThe effects of membrane structure on the separation of L‐phenylalanine (L‐Phe) by electrodialysis from a fermentation broth and on the fouling tendency were investigated in this study. Two anion‐exchange membranes (Neosepta AFX and AM‐1, Tokuyama, Japan) were selected and characterized using the chronopotentiometry method. For a fresh membrane, AFX showed a lower electrical resistance and a lower permselectivity than AM‐1. After being fouled with humic acid, however, the electrical resistance of AFX was higher than that of AM‐1. The L‐Phe selectivities for both membranes were lower than those of the fresh membranes. The result may be attributed to the structural difference between AFX and AM‐1 membranes. AFX has a lower repulsion force against the co‐ion and could be more strongly affected by the foulants than AM‐1 because AFX has a more porous structure than AM‐1. Experiments on the separation of L‐Phe from the fermentation broth were carried out using two different stack configurations, ie desalting electrodialysis and water‐splitting electrodialysis. It was observed that the recovery efficiency of L‐Phe through electrodialysis for 100 min reached 95% for AFX and 85% for AM‐1. In the desalting configuration of electrodialysis, the solution pH must be adjusted to alkaline conditions to recover the L‐Phe through the anion‐exchange membrane. On the contrary, it was possible to recover the L‐Phe without adjustment of the solution pH in the water‐splitting electrodialysis because OH− generated from the bipolar membrane converted neutral L‐Phe into an anion.© 2002 Society of Chemical Industry
Removal of aqueous phenol catalysed by a low purity soybean peroxidase
Authors: Wilberg Katia , Assenhaimer Cristhiane , Rubio Jorge 
Published: August 2002

AbstractThe application of a low purity soybean peroxidase (LP‐SBP), obtained from wasted seed hulls, as catalyst for phenol polymerisation in aqueous solution in the presence of hydrogen peroxide is described. The polymers formed precipitate out from solution and may be readily separated by physico‐chemical techniques. LP‐SBP offers the advantage of reduced cost compared with horseradish peroxidase (HRP). The SBP activity in fresh hulls was greater than in aged hulls and was preserved at −10 °C. There was a linear correlation between initial phenol concentration (1, 2, 5 and 10 mmol dm−3) and the minimum dosage of LP‐SBP required to precipitate 95% of the phenolic polymers. Polyethylene glycol (molecular weight, 6000) at 1000 mg dm−3 did not extend LP‐SBP lifetime. At all phenol concentrations tested, a retention time of about 100 min was sufficient to achieve yields of 95%.© 2002 Society of Chemical Industry
Quantitative sensory testing in gulf war veterans with chronic fatigue syndrome
Authors: Peckerman Arnold , Natelson Benjamin H. , Kipen Howard , Smith Sharon L. , Dahl Kristina , Pollet Chclaudia , Ottenweller John E. 
Published: August 2002

AbstractThe study assessed peripheral sensory function and its relation to self‐reported wartime exposures to potentially neurotoxic substances in Gulf War veterans with chronic fatigue syndrome (CFS). Male Gulf veterans fulfilling the 1994 CDC diagnostic criteria for CFS were compared with matched controls. Quantitative sensory testing was performed to establish thresholds of perception for the sense of light touch and radiant heat. The Devens survey was used to collect data on self‐reported exposures to by‐products of combustion and organophosphate compounds. Gulf veterans with CFS had elevated tactile but normal thermal thresholds compared with their controls. Sick veterans had greater rates of self‐reported exposures and/or noxious side effects for all assessed toxicants. Interestingly, both Gulf veteran groups, including those reporting no symptoms, had impaired perception of light touch when compared with age‐matched samples of non‐Gulf war veteran men. The results of this study are consistent with a hypothesis that Gulf veterans with CFS have a subtle neurological deficit that might reflect underlying peripheral neuropathy. The association between this deficit and self‐report of multiple potentially neurotoxic exposures suggests that war zone pollutants may be possible contributing factors. Copyright © 1999 John Wiley & Sons, Ltd.
Adrenomedullin in the central nervous system
Authors: Serrano J. , Alonso D. , Fernández A.P. , Encinas J.M. , López J.C. , Castro‐Blanco S. , Fernández‐Vizarra P. , Richart A. , Santacana M. , Uttenthal L.O. , Bentura M.L. , Martínez‐Murillo R. , Martínez A. , Cuttitta F. , Rodrigo J. 
Published: August 2002

AbstractAdrenomedullin (AM) is a novel vasodilator peptide first purified from human pheochromocytoma by tracing its capacity to stimulate cAMP production in platelets. AM immunoreactivity is widely distributed in the central nervous system (CNS) and in the rat has been demonstrated by immunohistochemical techniques to be present in many neurons throughout the brain and spinal cord, as well as in some vascular endothelial cells and perivascular glial cells. Electron microscopy shows that the immunoreactivity is located mainly in the neuronal cytoplasm, but also occurs in the cell nucleus in some cells of the caudate putamen and olfactory tubercle. Biochemical analyses suggest that higher molecular forms, presumably precursor forms, may predominate over fully processed AM in some brain areas. The expression of AM immunoreactivity is increased in cortical neurons, endothelial cells, and perivascular processes after a simulation of ischemia by oxygen and glucose deprivation. Immunohistochemical, electrophysiological, and pharmacological studies suggest that AM in the CNS can act as a neurotransmitter, neuromodulator, or neurohormone, or as a cytoprotective factor in ischemic/hypoxic conditions, in addition to its vasodilator role. Microsc. Res. Tech. 57:76–90, 2002. © 2002 Wiley‐Liss, Inc.
Adrenomedullin has multiple roles in disease stress: Development and remission of the inflammatory response
Authors: Elsasser Ted H. , Kahl Stas 
Published: August 2002

AbstractThe upregulation of adrenomedullin (AM) gene expression and increases in systemic circulatory as well as localized tissue AM concentrations is well coordinated with the onset and progression of trauma, infection, and sepsis. As such, the coordinated change in AM suggests a key role for this peptide in the inflammatory response. By clinical definition, the process of inflammation constitutes an orchestrated cascade of localized tissue and systemic responses to immunological challenges. Classical responses to the onset of disease stresses are manifested in the timely elaboration of humoral, blood‐borne signal effectors (such as adrenocortical and locally produced tissue hormones, immune cytokines, and inorganic signals such as nitric oxide) as well as patterned migration and infiltration of circulating bone marrow‐derived cells (mononuclear cells such as monocyte‐macrophages and polymorphonuclear cells like neutrophils) largely associated with or delivered through the vascular system. The body's attempts to combat acute infection to restore homeostatic equilibrium are further compromised by underlying disease situations. Atherosclerosis, diabetes, and cardiovascular disease, as well as nutritional metabolic derangements and persistent subclinical infection perturb the regulatory feedback loops necessary for proper control of response effectors like hormones and cytokines. When imbalances occur, tissue necrosis can ensue as driven by free radical damage to cell components. A true appreciation of the inflammatory response can only be grasped through an integrative approach in which the relationship between the different physiological systems is viewed in terms of a changing, dynamic interaction. In essence, the inflammatory response can be thought of in three phases: a period of severity assessment, a period of remediation, and a period of homeostatic restoration. Indeed, AM has differential effects on cellular metabolism, immune function, endocrine function, and cardiovascular function. This peptide appears to play a pivotal role in both reprioritizing the biological needs of tissues and organs during the three phases of inflammatory response as well as a role in restoring homeostatic equilibrium to the body. Microsc. Res. Tech. 57:120–129, 2002. Published 2002 Wiley‐Liss, Inc.
Origin and co‐localization of nitric oxide synthase, CGRP, PACAP, and VIP in the cerebral circulation of the rat
Authors: Edvinsson Lars , Elsås Tor , Suzuki Norihiro , Shimizu Toshihiko , Jer‐Fu Lee Tony 
Published: August 2002

AbstractThe origin of perivascular nerve fibres storing nitric oxide synthase (NOS) and co‐localisation with perivascular neuropeptides were examined in the rat middle cerebral artery (MCA) by retrograde tracing with True Blue (TB) in combination with immunocytochemistry. Application of TB to the proximal part of the middle cerebral artery labelled nerve cell bodies ipsilaterally in the trigeminal, sphenopalatine, otic, and superior cervical ganglia. A few labelled cell bodies were seen contralaterally, suggesting bilateral innervation. In the parasympathetic sphenopalatine and otic ganglia, numerous TB‐labelled cell bodies contained neuronal NOS (C‐ and N‐terminal), vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase activating peptide (PACAP). In the trigeminal ganglion, almost all TB‐labelled cell bodies contained calcitonin gene‐related peptide (CGRP) but only a few cells contained NOS. In the superior cervical ganglion, the majority of the TB‐labelled nerve cells contained neuropeptide Y (NPY) but none of them contained NOS. Removal of the ipsilateral sphenopalatine ganglion caused a slight reduction in the number of perivascular VIP‐, PACAP‐, and NOS‐containing fibres after 3 days in the MCA while there was no difference at 2 and 4 weeks after the denervation as compared to control. This indicates that the parasympathetic VIP‐, PACAP‐, and NOS‐immunoreactive nerve fibres in the rat MCA originate from several sources. Microsc. Res. Tech. 53:221–228, 2001. © 2001 Wiley‐Liss, Inc.
Microglia in neuroregeneration
Authors: Aldskogius Håkan 
Published: August 2002

AbstractMicroglia has the potential to produce and release a range of factors that directly and/or indirectly promote regeneration in the injured nervous system. The overwhelming evidence indicates, however, that this potential is generally not expressed in vivo. Activated microglia may enhance neuronal degeneration following axotomy, thereby counteracting functional recovery. Microglia does not seem to contribute significantly to axonal outgrowth after peripheral nerve injury, since this process proceeds uneventful even if perineuronal microglia is eliminated. The phagocytic phenotype of microglia is highly suppressed during Wallerian degeneration in the central nervous system. Therefore, microglia is incapable of rapid and efficient removal of myelin debris and its putative growth inhibitory components. In this way, microglia may contribute to regeneration failure in the central nervous system. Structural and temporal correlations are compatible with participation by perineuronal microglia in axotomy‐induced shedding of presynaptic terminals, but direct evidence for such participation is lacking. Currently, the most promising case for a promoting effect on neural repair by activated microglia appears to be as a mediator of collateral sprouting, at least in certain brain areas. However, final proof for a critical role of microglia in these instances is still lacking. Results from in vitro studies demonstrate that microglia can develop a regeneration supportive phenotype. Altering the microglial involvement following neural injury from a typically passive or even counterproductive state and into a condition where these cells are actively supporting regeneration and plasticity is, therefore, an exciting challenge and probably a realistic goal. Microsc. Res. Tech. 54:40–46, 2001. © 2001 Wiley‐Liss, Inc.
Pituitary adenylate cyclase‐activating polypeptide and its receptors in amphibians
Authors: Yon Laurent , Alexandre David , Montéro Maité , Chartrel Nicolas , Jeandel Lydie , Vallarino Mauro , Conlon J. Michael , Kikuyama Sakae , Fournier Alain , Gracia‐Navarro Francisco , Roubos Eric , Chow Billy , Arimura Akira , Anouar Youssef , Vaudry Hubert 
Published: August 2002

AbstractPituitary adenylate cyclase‐activating polypeptide (PACAP), a novel peptide of the secretin/glucagon/vasoactive intestinal polypeptide superfamily, has been initially characterized in mammals in 1989 and, only 2 years later, its counterpart has been isolated in amphibians. A number of studies conducted in the frog Rana ridibunda have demonstrated that PACAP is widely distributed in the central nervous system (particularly in the hypothalamus and the median eminence) and in peripheral organs including the adrenal gland. The cDNAs encoding the PACAP precursor and 3 types of PACAP receptors have been cloned in amphibians and their distribution has been determined by in situ hybridization histochemistry. Ontogenetic studies have revealed that PACAP is expresssed early in the brain of tadpoles, soon after hatching. In the frog Rana ridibunda, PACAP exerts a large array of biological effects in the brain, pituitary, adrenal gland, and ovary, suggesting that, in amphibians as in mammals, PACAP may act as neurotrophic factor, a neurotransmitter and a neurohormone. Microsc. Res. Tech. 54:137–157, 2001. © 2001 Wiley‐Liss, Inc.
Changes in central steroid receptor expression, steroid synthesis, and dopaminergic activity related to the reproductive cycle of the ring dove
Authors: Lea Robert W. , Clark Judith A. , Tsutsui Kazuyoshi 
Published: August 2002

AbstractThis review examines possible neural mechanisms involved in the expression of parental behavior in the ring dove, Streptopelia risoria. This avian species has proved an excellent animal model for studies concerning endocrine‐behavior interactions for many years. Studies were performed to localize the expression of central androgen and progesterone receptor in both sexes. Expression of androgen receptor (androgen receptor immunoreactivity, AR‐ir) was widespread but increased, similarly in both sexes, with increasing day‐length. Progesterone receptor‐immunoreactivity (PR‐ir) was more localized in several discrete areas of the hypothalamus. Similarly, no sex differences were observed in PR‐ir, and expression increased in birds maintained on long days. AR‐ir demonstrated dramatic changes over the breeding cycle, being greatest in courting birds and almost undetectable in parenting birds of both sexes brooding their young. PR‐ir showed a differential expression over the breeding cycle relative to its hypothalamic localization. PR‐ir decreased in the tuberal hypothalamic area in brooding birds of both sexes; whereas in the preoptic area, PR‐ir was maintained. Significant increases in dopaminergic activity during the parenting phase of the breeding cycle occurred in specific neural regions including the PVM and DMA. Studies demonstrated the ability of the diencephalon of both sexes of the ring dove brain to synthesize progesterone, with indications that in the male brooding dove, synthesis is increased. Finally, a model is presented that proposes a mechanism whereby these central systems may interact to result in the expression of full parental behavior in both sexes of the ring dove. Microsc. Res. Tech. 55:12–26, 2001. © 2001 Wiley‐Liss, Inc.
Just in time and place: NOS/NO system assembly in neuromuscular junction formation
Authors: Blottner Dieter , Lück Gabriele 
Published: August 2002

AbstractRecent advances in the molecular, biochemical, and anatomical aspects of postsynaptic membrane components at the neuromuscular junction (NMJ) are briefly reviewed focussing on assembly, architecture, and function of the multi‐subunit dystrophin‐protein complex (DPC) and its associated nitric oxide (NO)‐signaling complex. Elucidation of unique structural binding motifs of NO‐synthases (NOS), and microscopical codistribution of neuronal NOS (nNOS), the major isoform of NOS expressed at the NMJ, with known synaptic proteins, i.e., family members of the DPC, nicotinic acetylcholine receptor (AChR), NMDA‐receptor, type‐1 sodium andShakerK+‐channel proteins, and linker proteins (e.g., PSD‐95, 43K‐rapsyn), suggests targeting and assembly of the NO‐signaling pathway at postsynaptic membrane components. NO mediates agrin‐induced AChR‐aggregation and downstream signal transduction in C2 skeletal myotubes while administration of L‐arginine, the limiting substrate for NO‐biosynthesis, enhances aggregation of synapse‐specific components such as utrophin. At the NMJ, NO appears to be a mediator of (1) early synaptic protein clustering, (2) synaptic receptor activity and transmitter release, or (3) downstream signaling for transcriptional control. Multidisciplinary data obtained from cellular and molecular studies and from immunolocalization investigations have led us to propose a working model for step‐by‐step binding of nNOS, e.g., to subunit domains of targeted and/or preexisting membrane components. Formation of NOS‐membrane complexes appears to be governed by agrin‐signaling as well as by NO‐signaling, supporting the idea that parallel signaling pathways may account for the spatiotemporally defined postsynaptic assembly thereby linking the NOS/NO‐signaling cascade to early membrane aggregations and at the right places nearby preexisting targets (e.g., juxtaposition of NO source and target) in synapse formation. Microsc. Res. Tech. 55:171–180, 2001. © 2001 Wiley‐Liss, Inc.
Regeneration in echinoderm larvae
Authors: Vickery Michael C.L. , Vickery Minako S. , Amsler Charles D. , McClintock James B. 
Published: August 2002

AbstractThe ability of echinoderms to regenerate missing body parts has been a subject of interest to scientists for many years. Asexual reproduction (by fission or budding) is a phenomenon that involves regeneration of missing structures. Although asexual reproduction and regeneration have been the focus of many studies in adult echinoderms, there have been comparatively fewer studies examining these phenomena in echinoderm larvae, and most of these have been conducted in the last few years. In this article we review regeneration in larval echinoderms. We also discuss larval asexual reproduction. Microsc. Res. Tech. 55:464–473, 2001. © 2001 Wiley‐Liss, Inc.