bluuebunny/crossref_metadata_2025_split huggingface dataset:
Perceptions of insurance coverage for screening mammography among women in need of screening
Authors: McAlearney Ann Scheck , Reeves Katherine W. , Tatum Cathy , Paskett Electra D. 
Published: May 2005

AbstractBACKGROUNDBreast carcinoma remains a significant health problem in the U.S., especially among underserved populations. Although screening mammography is recommended for early detection, in 2002, approximately 25% of women age > 40 years had not had a mammogram within the past 2 years. The current study examined perceptions of insurance coverage and cost as barriers to screening mammography within an underserved, predominantly low‐income population of women in need of a mammogram.METHODSBetween 1998 and 2002, face‐to‐face interviews were conducted with 897 women age ≥ 40 years. All women were part of a randomized, controlled study evaluating a health education intervention designed to improve mammography screening. They were asked questions at baseline about cost and insurance coverage as barriers to mammography screening. Women's reports of their level of insurance coverage for mammography were compared with actual coverage by their insurance type to determine the accuracy of their perception of insurance coverage for mammography. The relation between perception of insurance coverage and the barrier of cost was investigated.RESULTSGreater than half of the women who needed a mammogram identified cost as a barrier to mammography; however, 40% of these women had an inappropriate perception of their insurance coverage. Underestimating or not knowing the level of mammography coverage was strongly associated with reporting cost‐related difficulty (odds ratio [OR] = 4.57, 95% confidence interval [95% CI], 1.95–10.70 for the underestimate category; OR = 4.42, 95% CI, 1.80–10.88 for the don't know category), regardless of true coverage levels.CONCLUSIONSProviding women with information regarding their actual coverage for mammograms may reduce the impact of cost as a barrier to screening mammography. Cancer 2005. © 2005 American Cancer Society.
Ltrk is differentially expressed in developing and adult neurons of the Lymnaea central nervous system
Authors: Bulloch Andrew G.M. , Diep Chi Q. , Logan Cairine C. , Bulloch Estrella S. , Robbins Stephen M. , Hislop Jonathan , Sossin Wayne S. 
Published: May 2005

AbstractThe Trk receptor family plays diverse roles in both development and plasticity of the vertebrate nervous system. Ltrk is a related receptor that is expressed in the CNS of the mollusk Lymnaea, although little is known of its cellular distribution. This study provides three independent lines of evidence (based on RT‐PCR, in situ hybridization, and immunohistochemistry) that Ltrk is universally expressed by neurons and dorsal body cells of both the juvenile and the adult Lymnaea CNS. The highest level of expression by neuronal somata occurs in the late juvenile stage, whereas axon collaterals express high levels throughout the animal's life span. Our data support multifunctional roles for Ltrk that parallel those of its mammalian counterparts. J. Comp. Neurol. 487:240–254, 2005. © 2005 Wiley‐Liss, Inc.
Breakpoints of variant 9;22 translocations in chronic myeloid leukemia locate preferentially in the CG‐richest regions of the genome
Authors: Fisher Andrew M. , Strike Paul , Scott Claire , Moorman Anthony V. 
Published: May 2005

AbstractFrom 5% to 10% of 9;22 translocations in chronic myeloid leukemia (CML) are reported to occur in variant form, that is, with the involvement of other regions of the genome in 3‐way or more rearrangements. The literature indicates that the alternative breakpoints are not distributed randomly in the genome but show hotspots. We present data on 289 unpublished cases of CML with variant 9;22 translocations having a total of 342 variant breakpoints, the largest independent series to date. We found that the distribution of breaks was in loose agreement with the literature but that some new hotspots were identified; furthermore, some published hotspots were not fully supported by our data. Moreover, when our 342 variant breakpoints were plotted against profiles of CG heterogeneity in the genome, a significant positive correlation between breakpoint locations and CG composition was observed. In an ancillary study, we compared the frequency of variant t(9;22) with that of variants of t(15;17) associated with acute promyelocytic leukemia (AML M3). We found that the frequency of the former, 9.3%, was significantly higher than that of the latter, 2.6%. © 2005 Wiley‐Liss, Inc.
Fusion of theEWSR1andATF1genes without expression of theMITF‐Mtranscript in angiomatoid fibrous histiocytoma
Authors: Hallor Karolin Hansén , Mertens Fredrik , Jin Yuesheng , Meis‐Kindblom Jeanne M. , Kindblom Lars‐Gunnar , Behrendtz Mikael , Kalén Anders , Mandahl Nils , Panagopoulos Ioannis 
Published: May 2005

AbstractAngiomatoid fibrous histiocytoma (AFH) is a rare soft tissue tumor that usually occurs in children and young adults. Only two cases of AFH with genetic rearrangements have been reported previously; both of these had aFUS–ATF1fusion gene. We have studied an AFH from a 9‐year‐old boy whose tumor displayed a t(12;22)(q13;q12) as the sole cytogenetic aberration. FISH,RT‐PCR, and sequence analyses revealed anEWSR1–ATF1fusion gene that has previously been reported in clear cell sarcoma (CCS), a soft tissue sarcoma that is morphologically and clinically distinct from AFH. This study thus has demonstrated that theEWSR1–ATF1chimera represents a fusion gene that can be associated with different tumor types. Simultaneous expression of theEWSR1–ATF1andMITF‐Mtranscripts in CCS has led to the proposal that theMITF‐Mpromoter is transactivated by EWSR1–ATF1. The AFH, however, did not express theMITF‐Mtranscript, supporting the theory thatMITF‐Mexpression in CCS is a reflection of its cellular origin, rather than a consequence of the presence of an EWSR1–ATF1 fusion protein. Activation of theEWSR1–ATF1oncogene is probably an early step in the transformation process, but the overall gene expression patterns are likely to vary considerably between AFH and CCS, in keeping with their clinicopathologic differences. © 2005 Wiley‐Liss, Inc.
Comparison of population‐ and family‐based methods for genetic association analysis in the presence of interacting loci
Authors: Howson Joanna M.M. , Barratt Bryan J. , Todd John A. , Cordell Heather J. 
Published: May 2005

AbstractWe compared different ascertainment schemes for genetic association analysis: affected sib‐pairs (ASPs), case‐parent trios, and unrelated cases and controls. We found, with empirical type 1 diabetes data at four known disease loci, that studies based on case‐parent trios and on unmatched cases and controls often gave higher odds ratio estimates and stronger significance test values than ASP designs. We used simulations and a simplified disease model involving two interacting loci, one of large effect and one smaller, to examine interaction models that could cause such an effect. The different ascertainment schemes were compared for power to detect an effect when only the locus of smaller effect was genotyped. ASPs showed the greatest power for association testing under most models of interaction except under additive and certain epistatic crossover models, for which case/controls and case‐parent trios did better. All ascertainment schemes gave an unbiased estimation of log genotype relative risks (GRRs) under a multiplicative model. Under nonmultiplicative interactions, GRRs at the minor locus as estimated from ASPs could be biased upwards or downwards, resulting in either an increase or decrease in power compared to the case/control or trio design. For the four known type 1 diabetes loci, we observed decreased risks with ASPs, which could be due to additive interactions with the remaining susceptibility loci. Thus, the optimal ascertainment strategy in genetic association studies depends on the unknown underlying multilocus genetic model, and on whether the goal of the study is to detect an effect or to accurately estimate the resulting disease risks. Genet. Epidemiol. © 2005 Wiley‐Liss, Inc.
Overexpression of human transferrin in two oligodendroglial cell lines enhances their differentiation
Authors: Paez Pablo M. , García Corina I. , Campagnoni Anthony T. , Soto Eduardo F. , Pasquini Juana M. 
Published: May 2005

AbstractWe have previously demonstrated that the addition of apotransferrin (aTf) to oligodendroglial cell (OLGc) primary cultures accelerates their maturation. Cells treated with aTf developed a multipolar morphology and displayed increased expression of mature OLGc markers. In this work, we studied the effect of Tf overexpression in two OLGc lines, N19 and N20.1. The former cells exhibit characteristics of OLGc precursors (O2A), while N20.1 cells express markers of more mature OLGcs. Using the complete cDNA of the human Tf gene, we obtained clones overexpressing Tf in both cell lines. These clones were evaluated for the expression of OLGc differentiation markers. In agreement with our previous results, we found that in the cells overexpressing Tf, there was an increased O4, GC, and MBP immunoreactivity. To study the myelinogenic potential of these cells, we co‐cultured N19 and N20.1 Tf‐transfected cells together with cortical neurons. There was a dramatic increase in the morphological differentiation of the OLGcs accompanied by enhanced GC and MBP expression. The OLGcs appeared to establish contact with neurites and extend their processes along them. Only two MBP isoforms were detected in Tf‐overexpressing clones, while all the isoforms were present in the co‐cultures, suggesting that there was a modulation of MBP expression by neurons. Concomitantly, we found an increase in several proteins involved in axon–glia interaction, such as MAG, N‐CAM, and F3/Contactin. This co‐culture system represents a potentially powerful tool to study neuron–glia interactions that occur during myelinogenesis and the role of Tf in this process. © 2005 Wiley‐Liss, Inc.
Tracing transplanted oligodendrocytes during migration and maturation in the shiverer mouse brain
Authors: Gansmuller A. , Clerin E. , Krüger F. , Gumpel M. , Lachapelle F. 
Published: May 2005

AbstractFragments of neural tissue from normal newborn mouse were stained with Hoechst 33342 dye before transplantation into the newborn shiverer mouse brain. Combination of this technique with immunohistochemistry demonstrated that, after transplantation, these cells are able to survive as long as unstained cells and to myelinate in the shiverer mouse host brain. Stained cells express the normal sequence of differentiation in terms of chronology of differentiation marker expression [04, galactocerebroside (GalC), myelin basic protein (MBP)], as normal cell do in situ. It has thus been possible by this technique to show the migration pathways of transplanted cells and to correlate them with the expression of specific markers: long distance migration along white matter axonal pathways occurs when cells are o4‐positive, GalC‐negative. By contrast, only GalC‐positive cells are able to migrate across the grey matter in the absence of radial glia. Finally, it has been possible to propose a migration and differentiation sequence of these cells, suggesting that MBP‐positive oligodendrocytes divide after migration in the target zone.
Soluble factor(s) produced in injured fish optic nerve regulate the postinjury number of oligodendrocytes: Possible role of macrophages
Authors: Sivron T. , Cohen A. , Hirschberg D. L. , Jeserich G. , Schwartz M. 
Published: May 2005

AbstractMammalian central nervous system (CNS) axons are virtually incapable of regenerating after injury. However, CNS neurons of lower vertebrates, such as fish and amphibians, are endowed with a high regenerative capacity. Lately, the glial cells have been credited with the regenerative ability of any specific CNS. We have previously demonstrated that many oligodendrocytes are recovered in cultures of injured rat optic nerve, while only a few oligodendrocytes are recovered from injured fish optic nerve in culture. We further demonstrated that medium conditioned by regenerating fish optic nerves (CM), which has been shown to cause axonal elongation in injured rabbit optic nerves, causes a decrease in the number of oligodendrocytes in rat glial cultures. In the present study, we demonstrate that soluble factors in the CM are capable of reducing the number of fish oligodendrocytes in fish optic nerve cultures. In addition, an inverse relationship was found between the number of macrophages and the number of oligodendrocytes. These results thus suggest that macrophages and/or activated resident microglial cells are directly or indirectly responsible for the presence of these soluble factor(s) that regulate the postinjury number of oligodendrocytes in the fish optic nerves.
Determination of the membrane potential of cultured mammalian schwann cells and its sensitivity to potassium using a thiocarbocyanine fluorescent dye
Authors: Hargittai P. T. , Youmans S. J. , Lieberman E. M. 
Published: May 2005

AbstractThe membrane potential of cultured rat sciatic nerve Schwann cells was determined with conventional microelectrode and voltage‐sensitive fluorescent dye, Di‐S‐C3(5), optical techniques. The value for membrane potential obtained with microelectrodes was −42.1 ± 4.7 mV (n = 8). Using optically determined fluorescent intensity changes caused by changes in external potassium ion concentration, in the presence or absence of valinomycin (null point method), the membrane potential was estimated at −45.7 ± 6.2 mV (n = 7); with a gramicidin and valinomycin double ionophore method it was −52.2 ± 9.1 (n = 4). The membrane potential of Schwann cells was found to be potassium sensitive at and above the physiological range of [K+] at 27.5 mV/10 × Δ[K+], which is approximately half the Nernstian value. This result suggests that other ion permeabilities strongly influence the resting membrane potential of cultured Schwann cells. Since Na+ had little effect on the membrane potential, it is concluded that Cl− is a likely candidate for the other permeant ionic species. The optical method has been shown to be a useful tool for the systematic study of the membrane potential of Schwann cells in culture and for the characterization of its ionic basis and regulation.
Ca2+ influx into leech neuropile glial cells mediated by nicotinic acetylcholine receptors
Authors: Hochstrate Peter , Schlue Wolf‐Rüdiger 
Published: May 2005

AbstractThe effect of cholinergic agonists and antagonists on the intracellular free Ca2+ concentration ([Ca2+]i) of leech neuropile glial cells was investigated by use of iontophoretically injected fura‐2. In neuropile glial cells, cholinergic agonists induced a marked increase in [Ca2+]i that was inhibited by d‐tubocurarine, α‐bungarotoxin, strychnine, and atropine. The efficacy of the various agonists and antagonists indicates that the [Ca2+]i increase is mediated by the nicotinic acetylcholine (ACh) receptors that have been characterized previously in these cells by using electrophysiological methods. In the presence of high agonist concentrations, [Ca2+]i partly recovered, suggesting that the ACh receptors desensitize.The [Ca2+]i increase induced by cholinergic agonists was abolished in Ca2+‐free solution, which indicates that it is caused by Ca2+ influx from the external medium. The agonist‐induced [Ca2+]i increase was partly preserved in Na+‐free solution, whereas the agonist‐induced membrane depolarization was strongly suppressed. The agonist‐induced [Ca2+]i increase was also partly preserved in the presence of 5 mM Ni2+, which almost abolished the K+‐induced [Ca2+]i increase mediated by voltage‐dependent Ca2+ channels. It is concluded that at low agonist concentrations the [Ca2+]i increase in leech neuropile glial cells is mediated exclusively by the ion channels associated with the nicotinic ACh receptors. At high agonist concentrations, voltage‐dependent Ca2+ channels activated by the concomitant membrane depolarization also contribute to the agonist‐induced Ca2+ influx. © 1995 Wiley‐Liss, Inc.
Potassium currents in endfeet of isolated Müller cells from the frog retina
Authors: Skatchkov Serguei N. , Vyklicky Ladislav , Orkand Richard K. 
Published: May 2005

AbstractVoltage dependent potassium currents were recorded using the whole‐cell mode of the patch‐clamp technique for the first time from endfeet of Müller cells dissociated from the frog retina. Recordings from intact cells and isolated endfeet indicate that the inward rectifier potassium channel is the dominant ion channel in these cells and that the density of these channels is highest in the endfoot as has been previously reported for several other species. The present study uses rapid changes in [K+]o to understand the behavior of these channels in buffering [K+]o in the retina. With rapid changes in [K+]o, it was found that, at a membrane potential of −90 mV, which is close to EK, increasing [K+]o from 3 to 10 mM produced an inward K+ current 5.48 ± 0.89 SD (n = 9) times larger than outward current induced by decreasing [K+]o from 3 to 1 mM. The outward current was maximal at a holding potential of about −80 mV and exhibited inactivation at more positive potentials. At −40 mV both the inward and outward currents are markedly reduced. The current voltage curve for the inward current was linear at holding potentials from −50 mV to −140 mV. Using 20 mV voltage steps, it was found that the voltage dependent K+ currents were unaffected by the addition of 2 mM Cd2+, a blocker of Ca2+‐activated potassium currents, decreasing [Cl−]o from 120 mM to 5 mM or the substitution of 30 mM Na+ by TEA. The addition of 5 mM [Cs+]o blocked only the inward current. Both the outward and inward currents disappeared in the absence of intracellular and extracellular K+; 0.3 mM [Ba2+]o blocked the inward current completely and strongly inhibited the outward current in a time and voltage dependent manner. We conclude that at physiological [K+]o and membrane potential, the K+ channels in the Müller cell endfoot are well suited to carry K+ both inward and outward across the membrane as required for spatial buffering. © 1995 Wiley‐Liss, Inc.
Neural correlates of the misattribution of self‐generated speech
Authors: Allen Paul P. , Amaro Edson , Fu Cynthia H.Y. , Williams Steven C.R. , Brammer Michael , Johns Louise C. , McGuire Philip K. 
Published: May 2005

AbstractAuditory hallucinations are thought to arise through the misidentification of self‐generated verbal material as alien. The neural mechanisms that normally mediate the differentiation of self‐generated from nonself speech are unclear. We investigated this in healthy volunteers using functional MRI. Eleven healthy volunteers were scanned whilst listening to a series of prerecorded words. The source (self/nonself) and acoustic quality (undistorted/distorted) of the speech was varied across trials. Participants indicated whether the words were spoken in their own or another person's voice via a button press. Listening to self‐generated words was associated with more activation in the left inferior frontal and right anterior cingulate cortex than words in another person's voice, which was associated with greater engagement of the lateral temporal cortex bilaterally. Listening to distorted speech was associated with activation in the inferior frontal and anterior cingulate cortex. There was an interaction between the effects of source of speech and distortion on activation in the left temporal cortex. In the presence of distortion participants were more likely to misidentify their voice as that of another. This misattribution of self‐generated speech was associated with reduced engagement of the cingulate and prefrontal cortices. The evaluation of auditory speech involves a network including the inferior frontal, anterior cingulate, and lateral temporal cortex. The degree to which different areas within this network are engaged varies with the source and acoustic quality of the speech. Accurate identification of one's own speech appears to depend on cingulate and prefrontal activity. Hum Brain Mapp, 2005. © 2005 Wiley‐Liss, Inc.
Functional interactions between oculomotor regions during prosaccades and antisaccades
Authors: Miller Lee M. , Sun Felice T. , Curtis Clayton E. , D'Esposito Mark 
Published: May 2005

AbstractHuman behavior reflects a continual negotiation of automatic and directed actions. The oculomotor network is a well‐characterized neural system in which to study this balance of behavioral control. For instance, saccades made toward and away from a flashed visual stimulus (prosaccades and antisaccades, respectively) are known to engage different cognitive processes. Brain regions important for such controlled execution include the presupplementary motor area (pre‐SMA), frontal eye fields (FEF), and intraparietal sulcus (IPS). Recent work has emphasized various elements of this network but has not explored the functional interactions among regions. We used event‐related fMRI to image human brain activity during performance of an interleaved pro/antisaccade task. Since traditional univariate statistics cannot address issues of functional connectivity, a multivariate technique is necessary. Coherence between fMRI time series of the pre‐SMA with the FEF and IPS was used to measure functional interactions. The FEF, but not IPS, showed significant differential coherence between pro‐ and antisaccade trials with pre‐SMA. These results suggest that the pre‐SMA coordinates with FEF to maintain a controlled, preparatory set for task‐appropriate oculomotor execution. Hum Brain Mapp, 2005. © 2005 Wiley‐Liss, Inc.
Hippocampal theta activity and behavioral sequences in a reward‐directed approach locomotor task
Authors: Sinnamon H.M. 
Published: May 2005

AbstractHippocampal rhythmic slow wave activity (theta) has been implicated in the processing of stimuli associated with movement. This study determined whether the theta rhythm showed phase relationships or changes in amplitude and frequency with the onset of stimuli and behavioral sequences in a skilled locomotor approach task. Rats with bipolar electrodes spanning CA1 approached a stall, turned to enter it, approached and depressed a treadle, waited 1.35 s, and approached a milk reward located forward either to the right or to the left. Auditory cues indicated the location of the reward during the waiting period and at the reward onset. A video capture system (20‐ms sampling) was synchronized to the hippocampal recording system (10‐ms sampling). Behavioral events identified by motion analysis were used to generate averages of hippocampal slow wave activity, theta peak amplitudes, and intervals between peaks. Theta activity at 8–10 Hz was almost continuous during the behavioral sequences. Phase relations with stimuli or movement onsets occurred infrequently and were not consistent across the four subjects. Theta peak amplitude and frequency decreased as the rat slowed locomotion in the stall and reached the treadle. Onset of locomotion directed to a reward location occurred on a positive peak of averaged theta activity. When locomotion had short latencies, increases in theta frequency appeared after the onset but, when it had longer latencies, frequency increases appeared 200 ms before onset. The results indicate that the execution of instrumental movement modulates both theta amplitude and frequency, and that the preparation for locomotion modulates theta frequency. © 2005 Wiley‐Liss, Inc.