bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparative analysis of fiber‐type composition in the iliofibularis muscle of phrynosomatid lizards (Squamata)
Authors: Bonine Kevin E. , Gleeson Todd T. , Garland Theodore 
Published: October 2004

AbstractThe lizard family Phrynosomatidae comprises three subclades: the closely related sand and horned lizards, and their relatives the Sceloporus group. This family exhibits great variation in ecology, behavior, and general body plan. Previous studies also show that this family exhibits great diversity in locomotor performance abilities; as measured on a high‐speed treadmill, sand lizards are exceptionally fast sprinters, members of the Sceloporus group are intermediate, and horned lizards are slowest. These differences are paralleled by differences in relative hindlimb span. To determine if muscle fiber‐type composition also varies among the three subclades, we examined the iliofibularis (IF), a hindlimb muscle used in lizard locomotion, in 11 species of phrynosomatid lizards. Using histochemical assays for myosin ATPase, an indicator of fast‐twitch capacity, and succinic dehydrogenase, denoting oxidative capacity, we classified fiber types into three categories based on existing nomenclature: fast‐twitch glycolytic (FG), fast‐twitch oxidative‐glycolytic (FOG), and slow‐twitch oxidative (SO). Sand lizards have a high proportion of FG fibers (64–70%) and a low proportion of FOG fibers (25–33%), horned lizards are the converse (FG fibers 25–31%, FOG fibers 56–66%), and members of the Sceloporus group are intermediate for both FG (41–48%) and FOG (42–45%) content. Hence, across all 11 species %FOG and %FG are strongly negatively correlated. Analysis with phylogenetically independent contrasts indicate that this negative relationship is entirely attributable to the divergence between sand and horned lizards. The %SO also varies among the three subclades. Results from conventional nested ANCOVA (with log body mass as a covariate) indicate that the log mean cross‐sectional area of individual muscle fibers differs among species and is positively correlated with body mass across species, but does not differ significantly among subclades. The log cross‐sectional area of the IF varies among species, but does not vary among subclades. Conversely, the total thigh muscle cross‐sectional area does not vary among species, but does vary among subclades; horned lizards have slimmer thighs. Muscle fiber‐type composition appears to form part of a coadapted suite of traits, along with relative limb and muscle sizes, that affect the locomotor abilities of phrynosomatid lizards. J. Morphol. 250:265–280, 2001. © 2001 Wiley‐Liss, Inc.
Refractive anomalies and visual activation in functional magnetic resonance imaging (fMRI): A versatile and low‐cost MR‐compatible device to correct a potential confound
Authors: Elbel Gregor‐K. , Kaufmann Christian , Schaefers Stefan , Buser Anne , Auer Dorothee P. 
Published: October 2004

AbstractPurposeTo develop a magnetic resonance (MR)‐compatible, versatile, easy‐to‐use, and low‐cost device for refractive correction.Materials and MethodsWe retrospectively evaluated the application and practicability of the refractive correction in 110 subjects who had participated in various functional MR imaging (fMRI) studies with complex visual stimulation paradigms since the introduction of the MR‐compatible lens frame at our site. The subjects consisted of 31 patients with Parkinson's disease (age range, 40–85; mean age, 63.2 years) and 79 healthy volunteers (age range, 18–79; mean age, 46.7 years).ResultsIn volunteers, experimentally induced myopia caused a substantial (>20%) reduction of the blood oxygenation level dependent (BOLD) response to a flickering dartboard.ConclusionRefractive errors (and the resulting optical blur) may play a nonnegligible role as a possible interfering factor in fMRI experiments with visual stimuli. The MR‐compatible frame (fitted with appropriate lenses) used in this study affords full refractive correction at reasonable cost and preparation time. J. Magn. Reson. Imaging 2002;15:101–107. © 2002 Wiley‐Liss, Inc.
Proton magnetic resonance spectroscopy of choroid plexus tumors in children
Authors: Horská Alena , Uluǧ Aziz M. , Melhem Elias R. , Filippi Christopher G. , Burger Peter C. , Edgar Mark A. , Souweidane Mark M. , Carson Benjamin S. , Barker Peter B. 
Published: October 2004

AbstractA variety of lesions may present as intraventricular masses in children. We report quantitative proton magnetic resonance spectroscopy (MRS) of two intraventricular tumors of the choroid plexus: choroid plexus carcinoma (CPC) and choroid plexus papilloma (CPP). Both lesions were characterized by high levels of choline‐containing compounds and a complete absence of creatine and the neuronal/axonal marker N‐acetyl aspartate. The CPC showed higher levels of choline compared to the CPP, and it also had elevated lactate. These preliminary results, if confirmed in a larger cohort of patients, indicate that proton MRS may have a role in the presurgical diagnosis of choroid plexus tumors in children, which may also have important implications for therapy and prognosis. J. Magn. Reson. Imaging 2001;14:78–82. © 2001 Wiley‐Liss, Inc.
Disturbance of hippocampal long‐term potentiation after transient ischemia in GFAP deficient mice
Authors: Tanaka Hidenobu , Katoh Akira , Oguro Keiji , Shimazaki Kuniko , Gomi Hiroshi , Itohara Shigeyoshi , Masuzawa Toshio , Kawai Nobufumi 
Published: October 2004

AbstractGFAP (glial fibrillary acidic protein) is an intermediate filament protein found exclusively in the astrocytes of the central nervous system. We studied the role of GFAP in the neuronal degeneration in the hippocampus after transient ischemia using knockout mice. Wild‐type C57 Black/6 (GFAP+/+) mice and mutant (GFAP−/−) mice were subjected to occlusion of both carotid arteries for 5–15 min. Hippocampal slices were prepared 3 days after reperfusion and the field excitatory postsynaptic potentials (fEPSP) in the CA1 were recorded. High frequency stimulation induced robust long‐term potentiation (LTP) in GFAP−/−, as in GFAP+/+ mice. After ischemia, however, the LTP in GFAP−/− was significantly depressed. Similarly, paired pulse facilitation (PPF) displayed little difference between GFAP+/+ and GFAP−/−, but after ischemia, the PPF in GFAP−/− showed a depression. Histological study revealed that loss of CA1 and CA3 pyramidal neurons after ischemia was marked in GFAP−/−. MAP2 (dendritic) immunostaining in the post‐ischemic hippocampus showed little difference but NF200 (axonal) immunoreactivity was reduced in GFAP−/−. S100β (glial) immunoreactivity was similar in the post‐ischemic hippocampus of the GFAP+/+ and GFAP−/−, indicating that reactive astrocytosis did not require GFAP. Our results suggest that GFAP has an important role in astrocyte‐neural interactions and that ischemic insult impairs LTP and accelerates neuronal death. © 2002 Wiley‐Liss, Inc.
Circadian profile of Per gene mRNA expression in the suprachiasmatic nucleus, paraventricular nucleus, and pineal body of aged rats
Authors: Asai Makoto , Yoshinobu Yuko , Kaneko Satoshi , Mori Akiko , Nikaido Takato , Moriya Takahiro , Akiyama Masashi , Shibata Shigenobu 
Published: October 2004

AbstractAging alters circadian components such as the free‐running period, the day‐to‐night activity ratio and photic entrainment in behavioral rhythms, and 2‐deoxyglucose uptakes and neuronal firing in the suprachiasmatic nucleus (SCN). A core clock mechanism in the mouse SCN appears to involve a transcriptional feedback loop in which Period (Per) and Cryptochrome (Cry) genes play a role in negative feedback. The circadian rhythm systems include photic entrainment, clock oscillation, and outputs of clock information such as melatonin production. In this experiment, we examined clock gene expression to determine whether circadian input, oscillation, and output are disrupted with aging. Circadian expression profiles of rPer1, rPer2, or rCry1 mRNA were very similar in the SCN, the paraventricular nucleus of the hypothalamus (PVN), and the pineal body of young and aged (22–26 months) rats. On the other hand, the photic stimulation‐induced rapid expression of Per1 and Per2 in the SCN was reduced with aging. The present results suggest that the molecular mechanism of clock oscillation in the SCN, PVN, and pineal body is preserved against aging, whereas the impairment of Per1 induction in the SCN after light stimulation may result in impaired behavioral photic entrainment in aged rats. J Neurosci. Res. 66:1133–1139, 2001. © 2001 Wiley‐Liss, Inc.
Neurogenesis of heterotopic gray matter in the brain of the microcephalic mouse
Authors: Sun Xue‐Zhi , Takahashi Sentaro , Fukui Yoshihiro , Hisano Setsuji , Kubota Yoshihisa , Sato Hiroshi , Inouye Minoru 
Published: October 2004

AbstractNeurogenesis of heterotopic gray matter in the brain of the microcephalic mouse prenatally exposed to X‐rays at embryonic day 13 (E13) was studied immunohistochemically. Bromodeoxyuridine (BrdU) as a marker to label the migrating position of neuroblasts generated at various embryonic stages showed that no “inside‐out” pattern of neuronal migration occurred in the heterotopic cell mass similar to that seen in the laminated cortex. Further results in which midkind (MK) immunoreactive radial glial fibers did not appear in the heterotopic cell mass demonstrated that heterotopia formed in the absence of radial glia system. Different types of cells (pyramidal and non‐pyramidal neurons) in the heterotopic cell mass were identified with immunoreactivity for anti‐parvalbumin and anti‐calbindin D‐28K antibodies in addition to current histological methods. Two major types of neurons were mixed together with random distribution in the heterotopic cell mass. This finding indicates that irradiation might have no selective effects on the precursors of pyramidal and non‐pyramidal neurons. Moreover, anti‐glial fibrillary acidic protein (GFAP) immunostaining showed that numerous astrocytes were present in the heterotopic cell mass. The fact that astrocytes appeared in the heterotopia without the transition from classic radial glial cells to astrocytes suggests that astrocytes might be generated directly from a separate astroglial precursor. J Neurosci. Res. 66:1083–1093, 2001. © 2001 Wiley‐Liss, Inc.
Myelin phagocytosis and remyelination of macrophage‐enriched central nervous system aggregate cultures
Authors: Copelman Cheryl A. , Diemel Lara T. , Gveric Djordje , Gregson Norman A. , Cuzner M. Louise 
Published: October 2004

AbstractAn increased level of myelin basic protein (MBP) degradation peptide 80–89, representative of myelin breakdown, is detected in myelinating foetal rat brain aggregate cultures supplemented with peritoneal macrophages at a time coinciding with the onset of myelination. During the period of myelination, the proportion of activated macrophages/microglia in the aggregates decreases, accompanied by a reduction in the content of MBP degradation products. During the recovery period following a demyelinating episode, the rate of MBP synthesis in antibody‐treated standard aggregates was greater than in their medium controls. However, the rate of MBP accumulation was not as efficient in macrophage‐enriched aggregates and was associated with persistently raised MBP peptide levels. Thus, as occurs in multiple sclerosis lesions, attempts at remyelination appear to be counterbalanced by macrophage‐mediated demyelination, with the continued presence of degraded myelin rendering a local environment that is not fully conducive to remyelination. J Neurosci. Res. 66:1173–1178, 2001. © 2001 Wiley‐Liss, Inc.
Glutamate decreases pyruvate carboxylase activity and spares glucose as energy substrate in cultured cerebellar astrocytes
Authors: Qu Hong , Eloqayli Haytham , Unsgård Geirmund , Sonnewald Ursula 
Published: October 2004

AbstractThe effects of glutamate on [U‐13C]glucose metabolism were studied in cerebellar astrocytes using 13C magnetic resonance spectroscopy. Labeled glutamate, glutamine, aspartate, lactate, and alanine were observed both in the cell extracts and in media, and, additionally, labeled glycogen was detected in the cell extracts. However, only labeled lactate and alanine were quantifiable in the medium in addition to [U‐13C]glucose. In the presence of unlabeled glutamate, the amount of [U‐13C]glucose removed from the medium was decreased, indicating that glutamate might spare glucose as an energy substrate and thus decrease the uptake of glucose. Labeled glycogen, [4,5‐13C]glutamate, [3,4,5‐13C]glutamate, [3,4‐13C]aspartate, and [U‐13C]alanine were increased in the presence of glutamate. However, the increase in the amount of [3,4,5‐13C]glutamate from the second turn in the tricarboxylic acid (TCA) cycle was less pronounced than that of [4,5‐13C]glutamate from the first turn in the TCA cycle. This indicates the dilution of label, probably resulting from the synthesis of unlabeled oxaloacetate from glutamate in the TCA cycle. Furthermore, exogenous glutamate had an inhibiting effect on pyruvate carboxylation, presumably by formation of oxaloacetate from 2‐oxoglutarate derived from glutamate. It could be shown that glucose is a better substrate for energy production than glutamate; it is, however, less efficient in labeling amino acids than glutamate in cerebellar astrocytes. J Neurosci. Res. 66:1127–1132, 2001. © 2001 Wiley‐Liss, Inc.
Mutually exclusive apicobasolateral sorting of two oligodendroglial membrane proteins, proteolipid protein and myelin/oligodendrocyte glycoprotein, in Madin‐Darby canine kidney cells
Authors: Kroepfl John F. , Gardinier Minnetta V. 
Published: October 2004

AbstractOligodendrocytes elaborate an extensive membrane network that ensheathes CNS axons in multilamellar wrappings. A compaction process excludes much of the cytoplasm in mature myelin membranes, giving rise to distinct lipid/protein compositions in two membrane compartments (compact myelin and membranes of the cell body and processes). Insofar as oligodendrocytes arise from neuroepithelial progenitors, it seems likely that some elements are shared for protein targeting by these two cell types. We hypothesized that certain membrane proteins targeting different oligodendroglial membrane compartments would preferentially sort to opposite domains when transfected into Madin‐Darby canine kidney (MDCK) epithelial cells. Myelin/oligodendrocyte glycoprotein (MOG) is found in uncompacted membrane (cell body, processes), and it sorts exclusively to MDCK basolateral membrane. Proteolipid protein (PLP) is found in compact myelin, and it sorts exclusively to MDCK apical membrane. Myelin‐associated glycoprotein (MAG) is primarily in the periaxonal inner loop of myelin; however, it fails to target preferentially within MDCK cells. This inability of MAG to sort within MDCK cells suggests a lack of required oligodendroglial‐specific targeting components. In contrast, the sorting machinery in both oligodendrocytes and MDCK cells recognizes targeting signals for MOG and PLP, and we propose that these oligodendroglial membrane proteins delineate cognate basolateral and apical domains, respectively. J Neurosci. Res. 66:1140–1148, 2001. © 2001 Wiley‐Liss, Inc.
Serotonin 2C receptor knockout mice: Autoradiographic analysis of multiple serotonin receptors
Authors: López‐Giménez Juan F. , Tecott Laurence H. , Palacios José M. , Mengod Guadalupe , Vilaró M. Teresa 
Published: October 2004

AbstractQuantitative receptor autoradiography was used to study possible alterations of the densities of multiple serotonin (5‐HT) receptor subtypes and of serotonin transporter in the brain of 5‐HT2C receptor knockout mice. The radioligands employed were [3H]citalopram, [3H]WAY100,635, [3H]8‐OH‐DPAT, [3H]GR125743, [3H]sumatriptan, [3H]MDL100,907, [125I](±)DOI, [3H]mesulergine, [3H]5‐HT, [3H]GR113808, and [3H]5‐CT. As expected, radioligands that label 5‐HT2C receptors showed a complete absence of labeling in mutant mice choroid plexus and significantly reduced densities in other brain regions expressing 5‐HT2C receptors. With the rest of the radioligands, no significant alterations in the densities of labeled sites were found in any brain region. In situ hybridization showed no changes in 5‐HT2A receptor and serotonin transporter mRNA levels, whereas 5‐HT2C receptor mRNA levels were reduced in certain brain regions. The present results indicate that the mouse serotonergic system does not exhibit compensatory up‐ or down‐regulation of the majority of its components (serotonin transporter and most 5‐HT receptor subtypes) in response to the absence of 5‐HT2C receptors. © 2002 Wiley‐Liss, Inc.
Synergistic induction of HSP40 and HSC70 in the mouse hippocampal neurons after cerebral ischemia and ischemic tolerance in gerbil hippocampus
Authors: Tanaka Shigeru , Kitagawa Kazuo , Ohtsuki Toshiho , Yagita Yoshiki , Takasawa Kenichirou , Hori Masatsugu , Matsumoto Masayasu 
Published: October 2004

AbstractAn ischemia‐induced gene was screened using a differential display technique in mouse transient forebrain ischemia. One of the ischemia‐responsive clones was found to encode mouse hsp40. HSP40 has a critical regulatory function in the HSC70 ATPase activity. Expression of hsp40 mRNA was low in the nonischemic mouse hippocampus, but it was significantly upregulated 4 hr after ischemia by Northern blot analysis. In situ hybridization analysis revealed hsp40 mRNA induction in the neuron. HSP40 protein expression was also enhanced in the pyramidal and dentate granular neurons from 2 to 4 days after ischemia. The temporal expression and distribution profile of HSC70 protein was similar to that of HSP40, and both proteins were colocalized in ischemic hippocampal neurons. In the gerbil transient forebrain ischemia model, both HSP40 and HSC70 proteins were expressed strongly in ischemia‐resistant CA3 neurons and dentate granule cells 1 day after 5 min ischemia, but were not expressed in vulnerable CA1 neurons. However, both proteins were in parallel expressed in the tolerance‐acquired CA1 neurons. Based on the current observation that both HSP40 and HSC70 proteins were synergistically expressed in the ischemia‐resistant and tolerance‐acquired neurons, cochaperone HSP40 may play a significant role against postischemic neuronal response and lead to cell survival through interaction with simultaneously induced HSC70. © 2002 Wiley‐Liss, Inc.
Coexpression of thyroid hormone receptor isoforms in mouse oligodendrocytes
Authors: Bury Fabienne , Carré Jean‐Luc , Vega Sonia , Ghandour M. Said , Rodriguez‐Peña Angeles , Langley Keith , Sarliève Louis L. 
Published: October 2004

AbstractDouble and triple immunocytochemistry with stage‐specific markers and specific antireceptor antibodies was used to study expression of nuclear thyroid hormone receptor (TR) isoforms in cultured mouse oligodendrocytes. To evaluate the coexpression of each TR isoform, antibodies were raised in rabbits and mice against specific regions of α1‐TR and α2‐TR common to both α isoforms and β1‐TR. Their specificities were assessed by Western blotting and by immunocytochemistry on rat hepatocytes. Oligodendrocyte subpopulations were found to coexpress the α‐ and β1‐TR epitopes at defined developmental stages. Both α‐ and β1‐TR isoforms are colocalized in oligodendrocytes during an early stage identified by the marker OL‐1, before 2′,3′‐cyclic nucleotide 3′‐phosphohydrolase is expressed. Expression of β1‐TR varies during maturation, and that of α‐TR decreases during terminal maturation. © 2002 Wiley‐Liss, Inc.
Differential NF‐κB regulation of bcl‐x gene expression in hippocampus and basal forebrain in response to hypoxia
Authors: Qiu Jingxin , Grafe Marjorie R. , Schmura Shannon M. , Glasgow Joel N. , Kent Thomas A. , Rassin David K. , Perez‐Polo J. Regino 
Published: October 2004

AbstractCell death often occurs after hypoxic/ischemic injury to the central nervous system. Changes in levels of the anti‐apoptotic Bcl‐XL protein may be a determining factor in hypoxia‐induced neuronal apoptosis. The transcription factor NF‐κB regulates bcl‐x gene expression. In this study, we examined the role of NF‐κB in the regulation of bcl‐x in hypoxia‐induced cell death. Rat hippocampus and basal forebrain tissues were collected at different time points after hypoxia (7%O2, 93% N2 for 10 or 20 min). We found that 1) hypoxia induced apoptosis in the hippocampus and basal forebrain; 2) the NF‐κB dimers c‐Rel/p50 and p50/p50 bound to the bcl‐x promoter NF‐κB sequence (CS4) in the hippocampus, but only p50/p50 bound to the CS4 sequence in the basal forebrain and hypoxia‐induced differential binding patterns of c‐Rel/p50 and p50/p50 correlated with the bcl‐x expression pattern in the hippocampus; 3) the hypoxia‐induced patterns of binding of c‐Rel/p50 to the bcl‐x promoter CS4 sequence were different from those to the IgG‐κB enhancer sequence, whereas those of p50/p50 were similar to both sequences; 4) nuclear protein levels of c‐Rel, but not p50, correlated with the c‐Rel/p50 DNA binding patterns to the bcl‐x CS4 site; and 5) there were differential responses to hypoxia among the different NF‐κB protein subunits. These results suggest that there is a tissue‐specific regulation of bcl‐x gene expression by NF‐κB in hypoxia‐induced cell death in the hippocampus. The absence of these regulating features in the basal forebrain may account for the early appearance of apoptosis in response to hypoxia as compared with that in hippocampus. J. Neurosci. Res. 64:223–234, 2001. © 2001 Wiley‐Liss, Inc.
Serotonin regulation of nerve growth factor synthesis in neonatal and adult astrocytes: Comparison to the β‐adrenergic agonist isoproterenol
Authors: Krzan Mojca , Wu Vivian W. , Schwartz Joan P. 
Published: October 2004

AbstractAlthough serotonin regulates synthesis of the neurotrophic factor S‐100β by astrocytes, its ability to affect nerve growth factor (NGF) synthesis has never been examined. We report here that there is a correlation between the effect of serotonin on cyclic adenosine monophosphate (cAMP) content and on NGF content in neonatal astrocytes but not in adult astrocytes. In neonatal striatal astrocytes, serotonin increases both cAMP and NGF, whereas, in neonatal cerebellar astrocytes, serotonin decreases both. The increase in neonatal cortical astrocyte cAMP appeared to be too small (45%) to increase NGF significantly. The β‐adrenergic agonist isoproterenol increased cAMP and NGF in both cortical and striatal astrocytes derived from neonatal rats. In contrast, there was a dissociation between cAMP changes and NGF changes in astrocytes derived from adult rats. Both serotonin and isoproterenol increased cAMP in adult cortical astrocytes, without any effect on NGF content. However, adult striatal astrocytes responded to serotonin with an elevation of both cAMP and NGF, whereas isoproterenol could only enhance cAMP, without affecting NGF. Thus, in neonatal astrocytes, a change of sufficient magnitude in cAMP was correlated with a comparable change in NGF, in response to activation of either serotonergic or β‐adrenergic receptors; in cerebellar astrocytes, the decrease in cAMP was accompanied by a decrease in NGF. In contrast, adult astrocytes were not responsive: Although cAMP changes were large, NGF synthesis was increased only in striatal astrocytes and only in response to serotonin. J. Neurosci. Res. 64:261–267, 2001. Published 2001 Wiley‐Liss, Inc.