bluuebunny/crossref_metadata_2025_split huggingface dataset:
Different short‐term modulation of cortical motor output to distal and proximal upper‐limb muscles during painful sensory nerve stimulation
Authors: Urban P. P. , Solinski M. , Best C. , Rolke R. , Hopf H. C. , Dieterich M. 
Published: April 2004

AbstractThe pattern of upper‐limb muscle activation following painful stimulation has not been clarified in detail. We investigated the short‐term inhibitory and excitatory effects of painful electrical digital stimulation on the motoneuron pools of distal and proximal upper‐limb muscles. Transcranial magnetic stimulation (TMS) was used as test stimulus, and painful digital nerve stimulation as conditioning stimulus for motor evoked potential (MEP) recordings over the abductor digiti minimi (ADM), abductor pollicis brevis (APB), biceps brachii (BB), and deltoid muscles. Inhibition of the conditioned MEP response was most prominent in the distal muscles, whereas BB and deltoid muscles were only weakly inhibited. The mean MEP response over APB decreased with painful cutaneous stimuli, showing maximum inhibition (by 82%) at interstimulus intervals (ISIs) of 50 ms. Inhibition in the ADM was maximal (49%) but less pronounced at an ISI of 40 ms. The BB and deltoid muscles showed inhibition by 25% and 29%, respectively. Significant facilitation was present in BB and deltoid muscles by 43% and 41% at an ISI of 100 ms, but not in the smaller hand muscles. The observed pattern of upper‐limb muscle activation corresponds to the protective withdrawal reflex and the neuronal basis of the observed short‐term modulation of motor activity is compatible with a spinal or brainstem pathway. Muscle Nerve 29: 663–669, 2004
Continuous myofiber remodeling in uninjured extraocular myofibers: Myonuclear turnover and evidence for apoptosis
Authors: McLoon Linda K. , Rowe Jocelyn , Wirtschafter Jonathan , McCormick Kathleen M. 
Published: April 2004

AbstractUnlike normal mature limb skeletal muscles, in which satellite cells are quiescent unless the muscle is injured, satellite cells in mammalian adult extraocular muscles (EOM) are chronically activated. This is evidenced by hepatocyte growth factor, the myogenic regulatory factor, Pax‐7, and the cell‐cycle marker, Ki‐67, localized to the satellite cell position using serial sections and the positional markers laminin and dystrophin. Bromodeoxyuridine (brdU) labeling combined with dystrophin immunostaining showed brdU‐positive myonuclei, presumably the result of fusion of activated satellite cells into existing myofibers. One new myonucleus was added to every 1000 myofibers in cross‐section using a 12‐hour brdU‐labeling paradigm. The EOM thus appear to retain a stable nuclear population by an opposing process of apoptosis that results in myonuclear removal as visualized by terminal deoxynucleotidyltransferase‐mediated nick end labeling (TUNEL). Activated caspase‐3 was present in localized cytoplasmic domains extending from 10 to 210 μm within individual myofibers, suggesting segmental cytoplasmic reorganization. Understanding the cellular mechanisms that maintain this process of continuous myonuclear addition and removal in normal adult EOM may suggest new hypotheses to explain the preferential involvement or sparing of these muscles in skeletal muscle disease. © 2004 Wiley Periodicals, Inc. Muscle Nerve 29: 707–715, 2004
Syllable repertoire and the size of the song control system in captive canaries (Serinus canaria)
Authors: Leitner Stefan , Catchpole Clive K. 
Published: April 2004

AbstractIn songbirds, there is considerable interest in relationships between song structure and the size of the song control system in the forebrain. In male canaries, earlier studies have reported that repertoire size increased with age, and positive correlations were obtained between repertoire size and the volume of song control nuclei such as high vocal center (HVC). Here we investigate whether age has an effect upon both the song structure and the morphology of two song control nuclei [HVC and robustus archistriatalis (RA)] that are important in song production. We recorded songs from an aviary population of 1‐ and 2‐year‐old male domesticated canaries. We found that repertoire size, number of sexually attractive (sexy) syllables, and size of song nuclei did not differ between 1‐ and 2‐year‐old males. Neither did we find significant correlations between syllable repertoire size and the size of the song control nuclei. However, HVC size was positively correlated with the proportion of sexy syllables in the repertoires of 2‐year‐old males. Some older males may enhance vocal performance by modifying the control of syllables rather than by increasing repertoire size or neural space. © 2004 Wiley Periodicals, Inc. J Neurobiol 60: 21–27, 2004
Evidence for a secreted chemorepellent that directs glioma cell invasion
Authors: Werbowetski Tamra , Bjerkvig Rolf , Del Maestro Rolando F. 
Published: April 2004

AbstractSecreted chemotropic cues guide the migration of neuronal and glial cell precursors during neural development. It is not known if chemotropism contributes to directing the invasion of brain tissue by glioma cells. A model system has been developed that allows quantification of invasive behavior using gliomas spheroids embedded in collagen gels. Here we provide evidence that glioma spheroids secrete a chemorepellent factor(s) that directs cells away from the spheroid and into the collagen matrix. The relationship between total invasion, cell number, and implantation distance suggests that glioma cells respond to a gradient of the chemorepellent cue(s) that is well established at 48 h. C6 astrocytoma cells normally invade the collagen at an angle perpendicular to the spheroid edge. In contrast, an adjacent spheroid causes cells to turn away from their normal trajectory and slow their rate of invasion. Astrocytoma cells are repelled by an adjacent glioma spheroid but rapidly infiltrate astrocyte aggregates, indicating that astrocytes do not express the repellent cue. Uniform concentrations of repellent factor(s) in spheroid conditioned medium overwhelm endogenous gradients and render glioma cells less able to exhibit this chemotropic response. Concentration gradients of spheroid conditioned medium in cell migration assays also demonstrate the chemorepellent cue(s)'s tropic effect. Our findings indicate that glioma spheroids produce a secreted diffusible cue(s) that promotes glioma cell invasion. Identification of this factor(s) may advance current therapies that aim to limit tumor cell invasion. © 2004 Wiley Periodicals, Inc. J Neurobiol 60: 71–88, 2004
Overexpression of Bcl‐2 prevents neomycin‐induced hair cell death and caspase‐9 activation in the adult mouse utricle in vitro
Authors: Cunningham Lisa L. , Matsui Jonathan I. , Warchol Mark E. , Rubel Edwin W. 
Published: April 2004

AbstractMechanosensory hair cells of the inner ear are especially sensitive to death induced by exposure to aminoglycoside antibiotics. This aminoglycoside‐induced hair cell death involves activation of an intrinsic program of cellular suicide. Aminoglycoside‐induced hair cell death can be prevented by broad‐spectrum inhibition of caspases, a family of proteases that mediate apoptotic and programmed cell death in a wide variety of systems. More specifically, aminoglycoside‐induced hair cell death requires activation of caspase‐9. Caspase‐9 activation requires release of mitochondrial cytochrome c into the cytoplasm, indicating that aminoglycoside‐induced hair cell death is mediated by the mitochondrial (or “intrinsic”) cell death pathway. The Bcl‐2 family of pro‐apoptotic and anti‐apoptotic proteins are important upstream regulators of the mitochondrial apoptotic pathway. Bcl‐2 is an anti‐apoptotic protein that localizes to the mitochondria and promotes cell survival by preventing cytochrome c release. Here we have utilized transgenic mice that overexpress Bcl‐2 to examine the role of Bcl‐2 in neomycin‐induced hair cell death. Overexpression of Bcl‐2 significantly increased hair cell survival following neomycin exposure in organotypic cultures of the adult mouse utricle. Furthermore, Bcl‐2 overexpression prevented neomycin‐induced activation of caspase‐9 in hair cells. These results suggest that the expression level of Bcl‐2 has important effects on the pathway(s) important for the regulation of aminoglycoside‐induced hair cell death. © 2004 Wiley Periodicals, Inc. J Neurobiol 60: 89–100, 2004
Correlation of Pax‐2 expression with cell proliferation in the developing chicken inner ear
Authors: Li Huawei , Liu Hong , Corrales C. Eduardo , Mutai Hideki , Heller Stefan 
Published: April 2004

AbstractIn vertebrates, the paired‐box transcription factor Pax‐2 is one of the earliest markers of the developing inner ear and is robustly expressed in the otic placode and the otic vesicle. Mutations in the Pax‐2 gene result in developmental defects of the vestibular and auditory apparatus. We set out to investigate whether regions of Pax‐2 expression in the developing otic vesicle correlate with areas of cell proliferation or cell death, which would indicate a possible role of Pax‐2 in these processes. Regionalized proliferation and local apoptosis are the principal mechanisms that lead to the complex morphogenesis of the highly compartmentalized inner ear starting from a simple vesicle. We found a high correlation of Pax‐2 expression with proliferating cells in the walls of the early otic vesicle. Apoptotic cells were mostly localized outside of the Pax‐2‐expressing regions. At later stages, we found the highest intensity of proliferating and Pax‐2‐positive cells in areas of the developing sensory epithelia. When hair cells begin to differentiate, they maintain a lower level of Pax‐2 expression than neighboring cells for a brief period, before they completely down‐regulate expression of this transcription factor. We conclude that a significant proportion of proliferating cells in the developing otocyst express Pax‐2, in particular in regions that include developing sensory patches. This implicates Pax‐2 as a marker for proliferating hair and supporting cell progenitors. Furthermore, the likelihood that Pax‐2‐expressing cells in the otocyst die by apoptosis is much lower when compared with cells residing in Pax‐2‐negative regions. © 2004 Wiley Periodicals, Inc. J Neurobiol 60: 61–70, 2004
Expression of BAFF (BLyS) in T cells infiltrating labial salivary glands from patients with Sjögren's syndrome
Authors: Lavie Frédéric , Miceli‐Richard Corinne , Quillard Jeanine , Roux Sophie , Leclerc Philippe , Mariette Xavier 
Published: April 2004

AbstractPrimary Sjögren's syndrome (pSS) is an autoimmune disorder characterized by lymphocytic infiltration of the salivary glands. Most of the infiltrating cells are T cells, but other features of the disease include polyclonal B‐cell activation, systemic production of autoantibodies, and increased risk of developing B‐cell non‐Hodgkin's lymphoma. Recently, a new tumour necrosis factor, the B‐cell activating factor (BAFF; also known as BLyS), has been implicated in the polyclonal activation of B cells. Using immunohistochemistry, this study evaluated BAFF expression in labial salivary gland biopsies from 14 patients with pSS, 14 normal controls, and two patients with sarcoidosis. Labial salivary gland samples from seven patients with pSS, seven controls, and one patient with sarcoidosis were double‐stained using indirect immunofluorescence. RT‐PCR analysis was also performed on lip biopsy samples from two patients and two controls. In all 14 pSS specimens, infiltrating inflammatory cells strongly expressed BAFF protein, as did some ductal epithelial cells, but acinar cells were negative. Some B cells were present in the vicinity of the BAFF‐positive cells. In the 14 normal labial salivary glands, some ductal cells were moderately positive, but acinar cells were negative. In the labial salivary glands from the two patients with sarcoidosis, infiltrating lymphocytes were not stained. BAFF mRNA expression was confirmed by RT‐PCR in salivary glands from pSS patients. Double immunofluorescence revealed T cells and macrophages to be the main cell types expressing BAFF in salivary glands from pSS patients. In conclusion, BAFF may be expressed by T cells at the site of autoimmune damage and could play a role in the pathogenesis of pSS, particularly by triggering the activation of self‐antigen‐driven autoimmune B cells. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Gene expression profiles from hypertrophic scar fibroblasts before and after IL‐6 stimulation
Authors: Dasu Mohan RK , Hawkins Hal K , Barrow Robert E , Xue Hui , Herndon David N 
Published: April 2004

AbstractThe structural rearrangement of collagen fibres in hypertrophic scar causes abnormal contracture, low tensile strength, and raised scars, which cause functional impairment and disfigurement. It is hypothesized that changes in the genes of cytokines, extracellular matrix proteins, and proteins regulating programmed cell death are related to hypertrophic scar formation. To test this hypothesis, fibroblasts were cultured from hypertrophic scars and their response to interleukin‐6 (IL‐6) stimulation was studied by defining their gene expression profiles. Affymetrix gene chip analysis was used to identify up‐ or down‐regulation in the 12 625 genes present in the affymetrix array. RT‐PCR and ELISA assays were used to validate microarray expression profiles further. Comparison of gene profiles showed an increase of 12 genes in hypertrophic scar fibroblasts compared with normal skin fibroblasts, while the expression of 14 genes decreased. Thirty‐three genes were affected by IL‐6 treatment in the hypertrophic scar fibroblasts, while 57 genes were affected in normal skin fibroblasts. Messenger RNA to β‐actin ratios for matrix metalloproteinase‐1 (MMP‐1) and MMP‐3 were increased with IL‐6 in normal skin fibroblasts from 2.43 ± 0.06 to 5.50 ± 0.45 and from 0.75 ± 0.09 to 1.98 ± 0.01, respectively. No change in these matrix metalloproteinases could be shown with IL‐6 stimulation in hypertrophic scar fibroblasts. Secreted protein levels of pro‐MMP‐1 and MMP‐3 were elevated in the supernatants from normal skin fibroblasts from 2.00 ± 0.09 and 1.72 ± 0.10 ng/ml to 4.60 ± 0.12 and 3.41 ± 0.20 ng/ml, respectively, after treatment with IL‐6 (p < 0.05). No changes were observed in hypertrophic scar fibroblasts treated with IL‐6. Values are means ± SEM. The absence of any up‐regulation of MMP‐1 and MMP‐3 in hypertrophic scar fibroblasts, in response to IL‐6, suggests that suppression of matrix metalloproteinases may play a role in the excessive accumulation of collagen formed in hypertrophic scars. While the pathogenesis of abnormal hypertrophic scars remains poorly understood, the use of gene expression arrays may prove helpful in identifying the mechanisms responsible for this type of abnormal scar formation and in formulating an effective therapeutic protocol. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
TIMP‐3 and endocrine therapy of breast cancer: an apoptosis connection emerges
Authors: Edwards Dylan R 
Published: April 2004

AbstractThe tissue inhibitors of metalloproteinases (TIMPs) control the activities of matrix metalloproteinases (MMPs) and as such, they have been recognized as potential suppressors of angiogenesis and tumour invasion and metastasis. However, TIMP‐3 has several unique properties that set it apart from other TIMPs, including its ability to bind to extracellular matrix, inhibit related adamalysin metalloproteinases (ADAMs), and induce apoptosis. New data suggest that high levels of TIMP‐3 mRNAs in human breast tumours are associated with success of adjuvant endocrine therapy, but not chemotherapy. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Under‐reporting of serious adverse drug reactions in Sweden
Authors: Bäckström M , Mjörndal T , Dahlqvist R 
Published: April 2004

AbstractIntroductionAdverse drug reactions (ADR) constitute a major problem, both from a medical point of view and as an economical burden. Spontaneous reporting of ADRs is one of the methods for post marketing surveillance of drug safety. Under‐reporting can also provide an important obstacle to rapid and relevant signal detection.AimTo investigate the rate of under‐reporting serious ADRs of selected ICD 10 diagnoses.MethodIn order to investigate the under‐reporting rate we investigated at five hospitals within the county of Norrbotten in Sweden the total number of diagnosed cases during a period of 5 years (1996–2000) with the following diagnoses: cerebral haemorrhage (I 61.0–I 61.9), pulmonary embolism (I 26.0 and I 26.9), embolism or thrombosis (I 74.0–I 74.9), phlebititis, thrombophlebitits or venous thrombosis (I 80.0–I 80.3, I 80.8 and I 80.9) and portal vein thrombosis and other thrombosis or emboli (I 82.0–I 82.3, I 82.8 and I 82.9). The identity of these patients was obtained through a database search. The patients' case records were then scrutinized by a specially trained nurse and the drugs used at the time of the event were noted. An assessment of the possibility of an ADR was performed using standard WHO causality criteria. Later, database search in the Swedish ADR registry was performed in order to investigate whether these suspected ADRs had been reported to the national authority in Sweden or not.ResultsIn total 1349 case records were found and scrutinized. Of these, 107 patients had received drugs that could have been a probable or possible cause to the diagnoses. Of these 92 cases had not been reported and only 15 patients were found in the database, giving an overall under‐reporting rate of all ADRs of 86%.The most commonly occurring diagnoses were cerebral haemorrhage followed by venous thrombosis, 545 and 468 respectively. Among those cases that should have been reported according to the existing rules for spontaneous reporting of suspected ADRs the most frequently occurring diagnosis was cerebral haemorrhage (I 61.0) in connection to treatment with anticoagulants.ConclusionThe rate of spontaneous ADR reporting is very low, also for serious and fatal reactions. Copyright © 2004 John Wiley & Sons, Ltd.
The thickness profile of ultra‐high molecular weight polyethylene films during sequential biaxial drawing
Authors: Moens M. T. R. , Govaert L. E. , Peters G. W. M. , Meijer H. E. H. 
Published: April 2004

AbstractIn this study, the evolution of the thickness profile of UHMW‐polyethylene films during sequential biaxial drawing is studied. The basic assumption is that a nonuniform thickness distribution of the drawn film is the result of the amplification of initial imperfections. Finite element simulations of the drawing process have been performed in which the drawing of a piece of film with a geometric imperfection is considered. For these numerical simulations, a viscoelastic model is adopted. Although the model does not describe the behavior of UHMW‐PE films in full detail, it is able to capture typical features of inhomogeneous deformation. The most striking observation is that severe localization occurs at the beginning of the second drawing step (i.e. in the direction transverse to the first step). In this stage of the drawing process, a localization band develops. These phenomena are also observed in validation experiments. A discrepancy between the simulations and the validation experiments is observed at the end of the drawing process. In the simulations, the deformation is stabilized again, and the resulting thickness profile is practically uniform. In the experiments however, the bad thickness profile at the beginning of the second drawing step is conserved up to the end of the drawing process. The simulations have been performed for different process parameters. Hence, it is possible to access the influence of these parameters on the evolution of the thickness profile. Furthermore, a suggestion is done to explain the deformation phenomena. The stability of the deformation can be determined from stress‐strain curves during the biaxial drawing process. It is concluded that, although no absolute values are acquired, trends are predicted correctly and they can serve as quidelines for process control.
An alternative model for predicting the cure kinetics of a high temperature cure epoxy adhesive
Authors: Rogers Angela D. , Lee‐Sullivan Pearl 
Published: April 2004

AbstractThe purpose of this work was to develop a cure kinetics model for a commercially available high temperature cure epoxy adhesive commonly used in the aerospace industry. While there are several phenomenological cure kinetic models commonly used in the literature for describing the rate of conversion of thermosetting epoxy adhesives as a function of degree of conversion, none of these models adequately depicts the adhesive used in this work over the entire range of conversion. Hence, by curve fitting empirical data collected using differential scanning calorimetry and refinement of existing models, an alternative model is proposed. The form of the present model suggests that chemical curing is the result of the combination of two autocatalytic reactions. The model is able to account for both the chemically controlled and diffusion controlled regimes of the cure. This paper also describes a novel iterative approach for predicting kinetics parameters as a function of isothermal cure temperature. Excellent agreement between experimental measurements and model predictions has been demonstrated over the entire range of conversion.
Analysis of closed‐discharge single‐screw extrusion of power‐law fluids
Authors: Guzmán Job D. , Schieber Jay D. 
Published: April 2004

AbstractFor rheometry and polymer processing applications, it is important to correlate fluid material properties with extrusion parameters like pressure buildup and revolutions per minute. Previous attempts to obtain such correlations have resorted to numerical techniques or approximate relationships. Here we show that upon a suitable rotation of coordinate axes, analysis of the metering zone in closed‐discharge single‐screw extrusion is simplified. Taking advantage of such simplification, we have derived an analytic, self‐consistent relation between fluid properties and extrusion parameters, where the power‐law model is used throughout the analysis.
Residual birefringence in modified polycarbonates
Authors: Wimberger‐Friedl R. , de Bruin J. G. , Schoo H. F. M. 
Published: April 2004

AbstractThe residual birefringence in quenched and injection‐molded specimens of bisphenol‐A polycarbonate (BAPC) homopolymer and its copolymers with substituted bisphenol‐A is investigated. The chemical modifications lead to a different stressoptical behavior in the melt and glass state, which generates differences in the residual birefringence of molded specimens. In this way the origins of the residual birefringence can be interpreted in a better way. In quenched samples it is found that the level of birefringence depends on the stress‐optical coefficient in the glassy state, but the unbalance of the birefringence distributions scales with the stress‐optical coefficient in the melt state. This supports the idea that transient thermal stresses present during vitrification induce molecular orientation, which is responsible for the unbalance of the distributions. The residual birefringence distributions in injection‐molded specimens all display a broad plateau in the core, as is usually observed in BAPC. The level of the plateau is found to scale with the stress‐optical coefficient of the melt state. This is a proof for the interpretation of this plateau being induced by transient thermal stresses during vitrification and not by residual stresses. It cannot be eliminated by optimizing molding conditions but only by drastically reducing the stress‐optical coefficient in the melt state.