bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypnotizability, dissociation and trauma in patients with a conversion disorder: an exploratory study
Authors: Moene Franny C. , Spinhoven Philip , Hoogduin Kees , Sandyck Pieter , Roelofs Karin 
Published: August 2002

AbstractLittle research has been conducted on the assumed high hypnotizability of conversion patients and on their dissociative experiences. Moreover, a relation is described between trauma, dissociation, somatization, psychopathology and conversion disorder. One hundred and two patients with motor conversion symptoms were tested for hypnotizability, dissociative experiences, trauma, somatization, general level of psychopathology and physical impairment. Our sample did not have higher levels of hypnotizability but they reported more dissociative experiences than normals. The trauma subgroup had higher levels of hypnotizability and dissociative experiences, psychopathology, somatization, and physical impairment than the non‐trauma subgroup. Uncorrected for general psychopathology, the trauma category ‘otherwise’ predicted 9.6% of the variance in the hypnotizability scores. After correction, only an additional 4.2%. The trauma category ‘emotional abuse’ contributed 18.9% to the prediction of the variance in the dissociation scores. After correction for general psychopathology, which explained 67.3% of the variance, only the sum score of the trauma categories contributed an additional 3.3%. Copyright © 2001 John Wiley & Sons, Ltd.
The network behind spatio‐temporal patterns: building low‐complexity retinal models in CNN based on morphology, pharmacology and physiology
Authors: Rekeczky Csaba , Roska Botond , Nemeth Erik , Werblin Frank S. 
Published: August 2002

AbstractIn this paper, a vertebrate retina model is described based on a cellular neural network (CNN) architecture. Though largely built on the experience of previous studies, the CNN computational framework is considerably simplified: first‐order RC cells are used with space‐invariant nearest‐neighbour interactions only. All non‐linear synaptic connections are monotonic continuous functions of the pre‐synaptic voltage. Time delays in the interactions are continuous represented by additional first‐order cells. The modelling approach is neuromorphic in its spirit relying on both morphological and pharmacological information. However, the primary motivation lies in fitting the spatio‐temporal output of the model to the data recorded from biological cells (tiger salamander). In order to meet a low‐complexity (VLSI) implementation framework some structural simplifications have been made. Large‐neighbourhood interaction (neurons with large processes), furthermore inter‐layer signal propagation are modelled through diffusion and wave phenomena. This work presents novel CNN models for the outer and some partial models for the inner (light adapted) retina. It describes an approach that focuses on efficient parameter tuning and also makes it possible to discuss adaptation, sensitivity and robustness issues on retinal ‘image processing’ from an engineering point of view. Copyright © 2001 John Wiley & Sons, Ltd.
Measurement of MAP kinase activation by flow cytometry using phospho‐specific antibodies to MEK and ERK: Potential for pharmacodynamic monitoring of signal transduction inhibitors
Authors: Chow Sue , Patel Harshna , Hedley David W. 
Published: August 2002

AbstractCancer cells frequently show abnormal signaling via the mitogen activated protein kinase (MAP kinase) pathway due to increased activity of surface receptors for growth factors, or as a result of ras mutations. The development of potent anti‐cancer agents that target this pathway prompts the need for analytical methods that allow pharmacodynamic monitoring of drug effects in patients during early phase clinical trial. We describe such a method, based on the activation of T‐lymphocytes in undiluted peripheral blood using phorbol myristate acetate (PMA). Following rapid hypotonic lysis and formaldehyde fixation, activation of the MAP kinase pathway can then be demonstrated using phospho‐specific antibodies that recognize the activated mediators MEK or ERK, followed by surface labeling with anti‐CD3 to identify T‐lymphocytes. This method was used to investigate the effects of a MEK inhibitor, U0126, and a new raf kinase inhibitor BAY 37‐9751 in blood samples from normal donors. Dose‐dependent inhibition of pERK activation was demonstrated for both agents. Furthermore, differential effects on pMEK activation allowed the molecular targets of the two inhibitors to be distinguished. In addition to monitoring drug effects in patients during treatment with inhibitors of the MAP kinase pathway, the general methodology described in this paper has the potential for wide application to the study of signal transduction at the single cell level using flow cytometry. Cytometry (Comm. Clin. Cytometry) 46:72–78, 2001. © 2001 Wiley‐Liss, Inc.
Performance analysis and interoperability issue of consolidation algorithms in point‐to‐multipoint ABR services
Authors: Rangsinoppamas Naris , Jaruvitayakovit Tanun , Prapinmongkolkarn Prasit 
Published: August 2002

AbstractIn this paper we propose a performance analysis of the consolidation algorithms in point‐to‐multipoint ABR services in ATM network. We also present a new efficient consolidation algorithm, which overcomes some drawbacks of the previous works. The performance of the previous works and our proposed consolidation algorithms are analysed mathematically. General equations for calculating the response time and allowed cell rate of the source are derived. The derived equations show relatively good agreement with simulation results and can be applied for using in various network topologies. In addition, the interoperability issue in multicast available bit rate (ABR) is investigated. It is found that the branch points implemented with different consolidation algorithms can work interoperably. It is concluded from the simulation results that the performance of the point‐to‐multipoint ABR services is dominated by the most upper stream branch point (the nearest one to the source), therefore, in order to avoid the consolidation noise and get a faster response in the network, the most upper stream branch point has to be implemented with a high accuracy consolidation algorithm while the lower stream branch point(s) should be implemented with a fast response consolidation algorithm with a less degree of complexity. Copyright © 2002 John Wiley & Sons, Ltd.
Immature teratoma of the ovary on fluid cytology
Authors: Selvaggi Suzanne M. , Guidos Barbara J. 
Published: August 2002

AbstractA case of an immature teratoma of the ovary in the peritoneal fluid of a 10‐yr‐old girl who presented with a pelvic mass is presented and discussed. The ThinPrep® preparation showed a few tight clusters of small tumor cells with a high nuclear/cytoplasmic ratio, round to oval nuclei with evenly distributed chromatin and one to two small distinct nucleoli, and scanty cytoplasm. The presence of immunohistochemical‐confirmed glial tissue on the cell block preparation confirmed the diagnosis of an immature ovarian teratoma. The differential diagnosis of fluid cytology is discussed. Diagn. Cytopathol. 25:411–414, 2001. © 2001 Wiley‐Liss, Inc.
Synthesis and biological studies of a new ginkgolide C derivative: Evidence that the cardioprotective effect of ginkgolides is unrelated to PAF inhibition
Authors: Pietri Sylvia , Liebgott Thibaut , Finet Jean‐Pierre , Culcasi Marcel , Billottet Ludovic , Bernard‐Henriet Christiane 
Published: August 2002

AbstractGinkgolides have been demonstrated to protect the myocardium in experimental ischemia‐reperfusion, but the extent to which this property is not related to platelet‐activating factor (PAF) inhibition remains debated. This study was undertaken to determine whether a ginkgolide devoid of any anti‐PAF activity could retain a cardioprotective activity. For this purpose, a new ginkgolide C (3) analogue, 7‐O‐(4‐methylphenyl) ginkgolide C (4), was obtained from 3 with retention of configuration, using, in the key step, a copper‐catalyzed arylation with tris‐(4‐methylphenyl) bismuth diacetate. No PAF inhibition on rabbit platelets in vitro was found for 4 up to 1.2.10–4 M. However, 4 was found a significantly better preserving agent than 3 or ginkgolide B, a potent PAF inhibitor (all drugs at 0.35 μM), on hemodynamic and metabolic (i.e., myocardial ATP contents and enzymatic activities) indices measured in rat isolated hearts undergoing ischemia‐reperfusion. The data provide additional support to a PAF‐unrelated pharmacological activity for ginkgolides. Because the water solubility of 4, estimated by high‐performance liquid chromatography analysis, was significantly lower than that of the parent molecule 3, a likely mechanism for the protective action of 4 involves its increased affinity for the myocardium, as compared to the relatively more hydrophilic 3. Drug Dev. Res. 54:191–201, 2001. © 2002 Wiley‐Liss, Inc.
Two distinct P2Y receptors are involved in purine‐ and pyrimidine‐evoked Ca2+ elevation in mammalian brain astrocytic cultures
Authors: Bolego Chiara , Centemeri Carlo , Abbracchio Maria P. , Ceruti Stefania , Cattabeni Flaminio , Jacobson Kenneth A. , Puglisi Lina , Rovati Gian Enrico , Burnstock Geoffrey , Nicosia Simonetta 
Published: August 2002

AbstractATP and 2‐methyl‐thio‐ATP (2‐Me‐SATP) increase cytosolic calcium concentrations ([Ca2+]i) in rat striatal astrocytes (Centemeri et al. [1997] Br J Pharmacol 121:1700–1706). The aim of the present study was to: (1) characterize pyrimidine‐induced [Ca2+]i increases in the same experimental system, and (2) try to identify the multiple P2Y receptor subtypes mediating Ca2+ mobilization. UDP and UTP triggered a concentration‐dependent [Ca2+]i elevation (EC50s = 0.58 μM ± 0.4 and 31 μM ± 6, respectively). Pyrimidine‐evoked [Ca2+]i elevation was solely due to mobilization from intracellular stores, because: (1) removing calcium from extracellular medium or (2) blocking its influx with Ni2+ did not modify UTP responses; (3) the store‐depleting agent thapsigargin completely abolished UTP‐evoked [Ca2+]i increments. Guanosine‐5′‐O‐(2‐thiodiphosphate) partially inhibited the UTP response, whereas pertussis toxin (PTx) had no effect. The phospholipase C inhibitor U‐73122 significantly reduced the UTP‐evoked [Ca2+]i rise. Computer‐assisted analysis indicated that the UTP and UDP responses are mediated by a single receptor, while ATP and 2‐Me‐SATP interact with two distinct receptors. The selective P2Y1 receptor antagonist MRS2179 abolished the ATP higher potency component. Sequential challenges with the same nucleotides resulted in almost complete homologous desensitization. Pre‐exposure to UTP lowered the subsequent responses to either ATP or 2‐Me‐SATP. Maximally active concentrations of UTP and ATP were not additive. In conclusion, [Ca2+]i elevation in astrocytes by purines and pyrimidines is mediated by two distinct P2Y receptors, likely the P2Y1 and P2Y6 subtypes. Drug Dev. Res. 52:122–132, 2001. © 2001 Wiley‐Liss, Inc.
Extracellular ATP activates transcription factor NFAT in mouse microglial cells
Authors: Ferrari Davide , Stroh Christopher , Wesselborg Sebastian , Di Virgilio Francesco , Schulze‐Osthoff Klaus 
Published: August 2002

AbstractThe effect of extracellular ATP on the activation of NFAT, an important transcription factor involved in cytokine expression, was investigated in the mouse microglial cell line N9. Incubation with ATP resulted in the potent and rapid activation of NFAT. Both NFAT1 and NFAT2 were activated by a calcineurin‐dependent pathway that required the influx of extracellular Ca2+. Inhibition of calcineurin by immunosuppressive drugs or Ca2+ chelation prevented ATP‐induced activation and nuclear translocation of NFAT. Activation of NFAT by ATP involved a P2X7 purinoreceptor‐mediated pathway. 2′,3′ ‐(4‐benzoyl)‐benzoyl‐ATP, an ATP analog with high affinity to the P2X7 receptor, was a strong agonist of NFAT activation. In addition, microglial N9 clones selected for the absence of P2X7, but still expressing the P2Y subtype, revealed no NFAT activation in response to ATP, although NFAT could be still triggered by agents increasing intracellular Ca2+. Our data therefore suggest that triggering of the P2X7 receptor by extracellular ATP is a potent mediator of transcription factor NFAT activation, and thus could be involved in early proinflammatory processes in the immune and nervous system. Drug Dev. Res. 52:213–219, 2001. © 2001 Wiley‐Liss, Inc.
Fetal handedness and head position preference: A developmental study
Authors: de Vries J.I.P. , Wimmers R.H. , Ververs I.A.P. , Hopkins B. , Savelsbergh G.J.P. , van Geijn H.P. 
Published: August 2002

AbstractHand–head contacts were observed by means of serial ultrasound recordings in 10 healthy fetuses from 12 to 38 weeks of gestational age. Contacts were distinguished as being unimanual or bimanual, and if unimanual, whether they were made with the right or left hand. Both types of contact and ones made unimanually with the right or left hand were identified at each age as to whether they were associated with a preferential head position. A strong unimanual bias was evident at each age except for Week 36. At this age, there was a bimanual bias. Unimanual contacts did not develop a lateralized preference, and neither type of contact established a stable relationship with head position. Furthermore, there was no evidence to support the suggestion that hand contact and head position codevelop to form a preferred ipsilateral synergy. Findings are discussed relative to contradictory evidence from other fetal and neonatal studies. © 2001 John Wiley & Sons, Inc. Dev Psychobiol 39: 171–178, 2001
Diabetic foot ulcers: a quality of life issue
Authors: Vileikyte Loretta 
Published: August 2002

AbstractFoot ulcers are a serious complication of diabetes mellitus that are associated with adverse sequelae and high costs. In addition, such foot ulcers have a significant impact on quality of life (QoL). For example, the loss of mobility associated with foot ulcers affects patients' ability to perform simple, everyday tasks and to participate in leisure activities. These and other consequences of foot ulcers often lead to depression and poor QoL. Notably, several studies have shown that patients with diabetes mellitus and foot ulcers were more depressed and had poorer QoL than those who had no diabetic complications. Given the detrimental effect foot ulcers have on patients, it is essential that these foot ulcers are prevented or treated more effectively than at present. Evidence suggests that many foot ulcers can be prevented by using intensive interventions and adopting a multidisciplinary approach to treatment. In addition, preventative strategies may become more effective if new research into how patients with diabetes experience and interpret their health threats (e.g. diagnosis ‘loss of sensation’ or a foot ulcer episode) is taken into account. With regard to treatment, new options should enable ulcers to heal more quickly than with standard therapies. One area of interest is the use of growth factors. For example, recombinant platelet‐derived growth factor, in addition to good ulcer care, has been shown to improve the number of ulcers that heal and healing times significantly compared with good ulcer care alone. Other potential new treatments include the use of skin substitutes. In summary, improved preventative measures and wound treatment should reduce the potential for patients with diabetes mellitus to experience impaired QoL caused by foot ulcers. Copyright © 2001 John Wiley & Sons, Ltd.
The AGE‐receptor in the pathogenesis of diabetic complications
Authors: Vlassara Helen 
Published: August 2002

AbstractNative glucose‐derived glycation derivatives (advanced glycation end products, AGE) in vascular, renal and neuronal tissues contribute to organ damage. Glycation derivatives include a number of chemically and cell‐reactive substances, also termed glycoxidation products or glycotoxins (GT). Cell‐associated AGE‐specific receptors (AGE‐Rs), AGE‐R1‐3, RAGE, as well as the scavenger receptors ScR‐II and CD‐36 that are present on vascular, renal, hemopoietic, and neuronal/glial cells, serve in the regulation of AGE uptake and removal. AGE‐Rs also modulate cell activation, growth‐related mediators, and cell proliferation, consequently influencing organ structure/function. This occurs via oxidant stress triggered via receptor‐dependent or ‐independent pathways, and leads to signal activation pathways, resulting in pro‐inflammatory responses. In susceptible individuals, the AGE‐R expression/function may be subject to environmental or gene‐related modulation, which in turn may influence tissue‐specific gene functions. In this context, altered expression and activity of AGE‐R components has recently been found in both mouse diabetes models and humans with diabetic complications. Although several gene polymorphisms are detected in most AGE‐R components, no significant correlation to diabetic complications has as yet been found. Further investigation is underway to define whether primary or secondary genetic links of pathogenic significance exist in this system. Various AGE‐binding peptides or soluble receptors have emerged as potential sequestering agents for toxic AGEs as potential therapies for diabetic complications. Copyright © 2001 John Wiley & Sons, Ltd.
Thiazolidinediones for the prevention of diabetes in the non‐obese diabetic (NOD) mouse: implications for human type 1 diabetes
Authors: Beales Philip E. , Pozzilli Paolo 
Published: August 2002

AbstractBackgroundThiazolidinediones (TZDs) are a recently introduced generation of drugs acting as receptor agonists to reduce insulin resistance and used currently in combination with other hypoglycaemic agents for the treatment of type 2 diabetes. In addition, TZDs possess anti‐inflammatory properties that make them of interest for reducing the T‐cell inflammation occurring in the islets in type 1 diabetes.MethodsThe action of TZD treatment on diabetes incidence in the non‐obese diabetic (NOD) mouse was studied by investigating the effect of rosiglitazone (RGL) (400 mg/kg body weight by gavage) from 3 weeks of age (soon after weaning) onwards and comparing its effect to that of troglitazone (TGL) given by the same route.ResultsWe found that RGL and TGL both significantly reduced diabetes incidence by >50% in the NOD mouse compared to litter‐matched control NOD mice (p<0.05 and p<0.01, respectively). However, the withdrawal of TGL from the market due to hepatotoxicity led us to re‐analyse our data for toxic liver effects. We found that TGL was more toxic to mice than RGL (causing ten deaths as compared with one death).ConclusionRGL reduces diabetes incidence in the NOD mouse model of type 1 diabetes. This may be an effect resulting from its action as on inhibitor of pro‐inflammatory genes such as cytokines and metabolic proteases. Its use may be considered for trials designed to protect beta‐cell function in humans, especially in patients with latent autoimmune diabetes of adults (LADA) and also for disease prevention. Copyright © 2002 John Wiley & Sons, Ltd.
Towards a cellular and molecular understanding of neurulation
Authors: Colas Jean‐François , Schoenwolf Gary C. 
Published: August 2002

AbstractNeurulation occurs during the early embryogenesis of chordates, and it results in the formation of the neural tube, a dorsal hollow nerve cord that constitutes the rudiment of the entire adult central nervous system. The goal of studies on neurulation is to understand its tissue, cellular and molecular basis, as well as how neurulation is perturbed during the formation of neural tube defects. The tissue basis of neurulation consists of a series of coordinated morphogenetic movements within the primitive streak (e.g., regression of Hensen's node) and nascent primary germ layers formed during gastrulation. Signaling occurs between Hensen's node and the nascent ectoderm, initiating neurulation by inducing the neural plate (i.e., actually, by suppressing development of the epidermal ectoderm). Tissue movements subsequently result in shaping and bending of the neural plate and closure of the neural groove. The cellular basis of the tissue movements of neurulation consists of changes in the behavior of the constituent cells; namely, changes in cell number, position, shape, size and adhesion. Neurulation, like any morphogenetic event, occurs within the milieu of generic biophysical determinants of form present in all living tissues. Such forces govern and to some degree control morphogenesis in a tissue‐autonomous manner. The molecular basis of neurulation remains largely unknown, but we suggest that neurulation genes have evolved to work in concert with such determinants, so that appropriate changes occur in the behaviors of the correct populations of cells at the correct time, maximizing the efficiency of neurulation and leading to heritable species‐ and axial‐differences in this process. In this article, we review the tissue and cellular basis of neurulation and provide strategies to determine its molecular basis. We expect that such strategies will lead to the identification in the near future of critical neurulation genes, genes that when mutated perturb neurulation in a highly specific and predictable fashion and cause neurulation defects, thereby contributing to the formation of neural tube defects. © 2001 Wiley‐Liss, Inc.
Insulin‐like growth factor I stimulates myoblast expansion and myofiber development in the limb
Authors: Mitchell Pamela J. , Johnson Sally E. , Hannon Kevin 
Published: August 2002

AbstractInsulin‐like growth factor I (IGF‐I) is expressed in the anterior and posterior mesodermal cells of the developing limb. However, a definite role for IGF‐I during early limb organogenesis is unknown. To determine the inherent participation of IGF‐I during limb organ development, a retroviral delivery system (RCAS) was used to overexpress IGF‐I throughout the developing hind limb of stage 24 chicken embryos. The area of the belly of the external gastrocnemius muscle in the IGF‐I infected limb was an average of 160, 90, 70, and 80% larger than the contralateral control muscle belly, 4, 5, 6, and 7 days postinjection, respectively (all differences P < 0.01). In comparison to the contralateral control muscles, there were a significantly greater number of muscle fibers in the IGF‐I infected muscles (P < 0.05), confirming that the majority of IGF‐I–mediated muscle enlargement was due to an increase in total fiber numbers (hyperplasia). Four days postinjection, there was a 32% increase in myoblast to myofiber ratio in the muscle of injected limbs compared with the muscle in the contralateral noninjected control limbs (P < 0.05). This result demonstrates that IGF‐I acts to expand the undifferentiated myoblast population, and as a result, more myofibers subsequently develop, and the muscles expressing ectopic IGF‐I are enlarged by means of hyperplasia. There was no difference in tibiotarsus and fibula length or diameter between the IGF‐I injected and control limb, suggesting that ectopic IGF‐I expression within the mesoderm was not a nonspecific growth stimulant of all tissues of the developing limb, but specifically enhanced skeletal muscle development and growth. Ectopic IGF‐I expression had no significant effect on myostatin mRNA concentrations. Our results support a model where mesodermally expressed IGF‐I acts to regulate the number of primary myofibers, and, therefore, size of skeletal muscles, which form during the initial events of limb myogenesis. © 2001 Wiley‐Liss, Inc.