bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of the CREB signaling cascade in the visual cortex by visual experience and neuronal activity
Authors: Suzuki Seigo , Al‐Noori Salwa , Butt Shehzad A. , Pham Tony A. 
Published: September 2004

AbstractThe cAMP‐responsive element (CRE) regulatory pathway has been studied as a model of signal‐regulated transcription and is critical for some forms of learning and adaptation. In cell culture systems, the extracellular‐regulated kinase (ERK) and ribosomal S6 kinase (RSK) couple synaptic signals to CRE‐mediated gene expression by modulating CRE‐binding protein (CREB) phosphorylation. However, it is not known whether sensory experience regulates gene expression in the brain by this mechanism. In this study, we ask: Are activated forms of ERK, RSK, and CREB colocalized in the cortex and are they coordinately regulated by synaptic signals? We find that these three signaling components are regulated in distinct ways. First, cells that show CRE‐lacZ reporter expression, primarily excitatory neurons, do not colocalize with cells containing phospho‐ERK. Second, while phosphorylation of ERK and RSK are modulated by visual experience, phosphorylation of CREB at serines 133, 142, or 143 is detected constitutively and is unaffected by experience. This finding suggests that neural activity might not regulate CREB phosphorylation in vivo. To test this hypothesis, we blocked action potentials by injection of tetrodotoxin and found no effect on CREB phosphorylation. These in vivo data show that, in contrast to cell culture systems, cortical synaptic activity controls CRE‐mediated gene expression without affecting CREB phosphorylation, possibly by modification of RSK and CREB‐associated coregulators. J. Comp. Neurol. 479:70–83, 2004. © 2004 Wiley‐Liss, Inc.
Calcium‐binding protein Caldendrin and CaMKII are localized in spinules of the carp retina
Authors: Schultz Konrad , Janssen‐Bienhold Ulrike , Gundelfinger Eckart D. , Kreutz Michael R. , Weiler Reto 
Published: September 2004

AbstractCalcium‐binding proteins translate the influx of Ca2+ at excitatory synapses into spatiotemporal signals that regulate a variety of processes underlying synaptic plasticity. In the fish retina, the synaptic connectivity between photoreceptors and horizontal cells undergoes a remarkable plasticity, triggered by the ambient light conditions. With increasing light, the synaptic dendrites of horizontal cells form numerous spinules that are dissolved during dark adaptation. The dynamic regulation of this process is calcium‐dependent and involves the Ca2+/calmodulin‐dependent protein kinase II (CaMKII), but astonishingly its principal regulator Calmodulin (CaM) could not be localized to spinules. Here, we show that antibodies directed against Caldendrin (CaBP1), a member of the EF‐hand calcium‐binding protein family, strongly label the terminal dendrites of horizontal cells invaginating cone pedicles. Double‐labeling experiments revealed that this label is closely associated with label for CaMKII. This association was confirmed at the ultrastructural level. Caldendrin immunoreactivity and CaMKII immunoreactivity are both present in horizontal cell dendrites flanking the synaptic ribbon within the cone pedicle and in particular in spinules formed by these terminals. Comparison of light‐ and dark‐adapted retinas revealed a shift of the membrane‐associated label for Caldendrin from the terminal dendrites into the spinules during light adaptation. These results suggest that Caldendrin is involved in the dynamic regulation of spinules and confirms the assumed potential of Caldendrin as a neural calcium sensor for synaptic plasticity. J. Comp. Neurol. 479:84–93, 2004. © 2004 Wiley‐Liss, Inc.
Expression of GDNF and GFRα1 in mouse taste bud cells
Authors: Takeda Masako , Suzuki Yuko , Obara Nobuko , Uchida Nobuhiko , Kawakoshi Kentaro 
Published: September 2004

AbstractGDNF (glial cell line‐derived neurotrophic factor) affects the survival and maintenance of central and peripheral neurons. Using an immunocytochemical method, we examined whether the taste bud cells in the circumvallate papillae of normal mice expressed GDNF and its GFRα1 receptor. Using double immunostaining for either of them and NCAM, PGP 9.5, or α‐gustducin, we additionally sought to determine what type of taste bud cells expressed GDNF or GFRα1, because NCAM is reported to be expressed in type‐III cells, PGP 9.5, in type‐III and some type‐II cells, and α‐gustducin, in some type‐II cells. Normal taste bud cells expressed both GDNF and GFRα1. The percentage of GDNF‐immunoreactive cells among all taste bud cells was 31.63%, and that of GFRα1‐immunoreactive cells, 83.21%. Confocal laser scanning microscopic observations after double immunostaining showed that almost none of the GDNF‐immunoreactive cells in the taste buds were reactive with anti‐NCAM or anti‐PGP 9.5 antibody, but could be stained with anti‐α‐gustducin antibody. On the other hand, almost all anti‐PGP 9.5‐ or anti‐α‐gustducin‐immunoreactive cells were positive for GFRα1. Thus, GDNF‐immunoreactive cells did not include type‐III cells, but type‐II cells, which are α‐gustducin‐immunoreactive; on the other hand, GFRα1‐immunoreactive cells included type‐II and ‐III cells, and perhaps type‐I cells. We conclude that GDNF in the type‐II cells may exert trophic actions on type‐I, ‐II, and ‐III taste bud cells by binding to their GFRα1 receptors. J. Comp. Neurol. 479:94–102, 2004. © 2004 Wiley‐Liss, Inc.
Apical‐to‐basal gradients in age‐related cochlear degeneration and their relationship to “primary” loss of cochlear neurons
Authors: Ohlemiller Kevin K. , Gagnon Patricia M. 
Published: September 2004

AbstractThe predominant conceptual framework for understanding human age‐related hearing loss (ARHL, or presbycusis) holds that three different cochlear elements (organ of Corti, afferent neurons, and stria vascularis) can degenerate independently, and exert independent influences on hearing. Within this framework, temporal bones from subjects with ARHL may be classified as exemplifying sensory (referring to organ of Corti), “primary” neural (loss of afferent neurons without loss of their hair cell targets), strial, or mixed ARHL. While there is general agreement as to the types of cochlear cells most affected by aging, there is less agreement about how to classify ARHL, and whether contributions of particular structures to hearing loss can be isolated. The cochlear apex of humans and animals is particularly prone to apparent primary loss of neurons that may represent an aspect of neural ARHL. We recently reported that in 129S6/SvEv mice apical neuronal loss is often accompanied by abnormalities of spiral limbus, pillar cells, and Reissner's membrane (Ohlemiller and Gagnon [2004] J Comp Neurol 469:377–390). We proposed that the initial pathology occurs within limbus, leading to disruption of perilymphatic ion homeostasis, and eventual loss of neurons as one consequence. We have now examined this issue quantitatively in young and old mice of four different strains (129S6/SvEv, CBA/J, C57BL/6, and BALB/c). Abnormalities of apical spiral limbus were found to correlate only weakly with neuronal loss. Strong correlations were found between neuronal loss and abnormalities of both pillar cells and Reissner's membrane, however. Apical neuronal loss and apical‐to‐basal progression of pathology of limbus, pillar cells, and Reissner's membrane run counter to most reported age‐related cochlear trends. Our findings suggest that these changes share a common triggering influence. J. Comp. Neurol. 479:103–116, 2004. © 2004 Wiley‐Liss, Inc.
Unsymmetrically Substituted Dimethyldiaminosilanes as Ligands towards Zirconium(IV)
Authors: Passarelli Vincenzo , Zanella Pierino 
Published: September 2004

AbstractUnsymmetrically substituted dimethyldiaminosilanes of the general formula SiMe2(NR2)(NR′2) have been prepared by treating LiNR2 with SiMe2Cl(NR′2) (NR2, NR′2 = NMe2, NC4H8, NHiPr, NHtBu, NHCH2CH2NMe2 or NHCH2CH2OMe). Their ligating properties towards zirconium(IV) have been investigated as a function of the nitrogen substituents and the syntheses of the binary compound Zr[SiMe2(NiPr)(NtBu)]2 and of the zirconium derivatives ZrX3(L) [X = Cl, NMe2; L = SiMe(NR)(NR′2), NR = NiPr, NtBu, NCH2CH2NMe2, NCH2CH2OMe; NR′2 = NMe2, NC4H8, NHiPr, NHtBu] are also reported. The solution structures and dynamics of the compounds have been elucidated by 1D/2D multinuclear NMR spectroscopy. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
Formation of Sulfur−Sulfur Bonds in Copper Complexes
Authors: Aullón Gabriel , Alvarez Santiago 
Published: September 2004

AbstractThe recently reported dinuclear complexes [Cu2(μ‐S2)(diketiminato)2] that have short S−S distances across their Cu2S2 rings are theoretically studied with the help of density functional calculations and a topological analysis of the electron density. The possibility of obtaining the isomeric form without a S−S bond is explored by comparing the structure and bonding with its oxo analogue. A study of the influence of several terminal‐chelating ligands on the relative stability of the sulfido‐ and the disulfido‐bridged forms is also presented. The only way to stabilize a sulfido‐bridged isomer is found to be via two‐electron reduction, whereas chemical substitutions are not able to produce the cleavage of the S−S bond. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
The Immobilized Porphyrin‐Mediator System Mn(TMePyP)/clay/HBT (clay‐PMS): A Lignin Peroxidase Biomimetic Catalyst in the Oxidation of Lignin and Lignin Model Compounds
Authors: Crestini Claudia , Pastorini Alessandra , Tagliatesta Pietro 
Published: September 2004

AbstractA biomimetic system for lignin peroxidase (LiP) was designed by using a cationic porphyrin, [Mn(TMePyP)OAc5], supported on the smectitic clay montmorillonite [Mn(TMePyP)/clay]. The natural role of the polypeptidic pocket of LiP was mimicked by the clay. The possibility to use low‐molecular‐weight redox mediators as active readily diffusible oxidizing species has been investigated. This assembly — a sort of “synthetic enzyme” — can be defined as an immobilized porphyrin‐mediator system (clay‐PMS). The clay‐PMS was found to be a stable, recyclable, and efficient catalyst for the environmentally friendly H2O2‐catalyzed oxidation of different lignins and representative lignin model compounds. The clay‐PMS showed a higher reactivity than Mn(TMePyP)/clay alone due to an effective role of the redox mediator on the oxidation. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
Sources of sulphur in gypsiferous sediments and crusts and pathways of gypsum redistribution in southern Tunisia
Authors: Drake Nick A. , Eckardt Frank D. , White Kevin, H. 
Published: September 2004

AbstractSouthern Tunisia contains one of the most extensive gypsum accumulations in Africa comprising Triassic, Cretaceous, Eocene and Mio‐Pliocene marine evaporites, spring deposits, playa sediments, aeolian sands and gypsum crusts. Sulphur isotope analysis (δ34S) of bedrock samples, groundwater, playa brines, playa sediments, and gypsiferous crusts provides insight into the sources of gypsum in the region and sheds light on the processes that lead to gypsum crust formation. Results suggest that recycling of marine gypsum is the most likely source of the sulphate in the groundwater, playa sediments and crusts. The low δ34S values found in Eocene and Mio‐Pliocene samples suggest that this recycling has been going on for millions of years. Though bedrock appears to be the ultimate source of the gypsum in the crusts, transport of this sulphate to playas, concentration therein, and subsequent dispersal across the landscape by aeolian processes provides the most likely pathway for surﬁcial gypsum crust formation. Comparison of these results with those from Australia, Chile and Namibia suggests that, although the source of the sulphur varies from region to region, the processes of surﬁcial crust formation appear to be similar. Copyright © 2004 John Wiley & Sons, Ltd.
Petrology, geochemistry and environmental significance of silcrete‐calcrete intergrade duricrusts at Kang Pan and Tswaane, central Kalahari, Botswana
Authors: Nash David J. , Mclaren Sue J. , Webb John A. 
Published: September 2004

AbstractCalcrete–silcrete intergrade duricrusts are an important component of the Kalahari Group sediments of central southern Africa and yet have neither been analysed systematically nor in any detail. In this study, the petrological and geochemical characteristics of suites of calcrete, silcrete and intergrade duricrusts from two fresh, relatively deep exposures at Kang Pan and Tswaane (adjacent to the Okwa Valley) in the central Kalahari, Botswana, are described. The duricrust proﬁle at Kang Pan consists of a highly indurated crystalline non‐pedogenic calcrete which has been extensively siliciﬁed by chalcedony, and, rarely, cryptocrystalline silica or microquartz. Siliciﬁcation is most extensive in lower parts of the proﬁle, where replacement is related to groundwater ﬂuctuations, and in upper sections due to periodic ﬂooding by ephemeral surface water. The exposure at Tswaane consists of a sequence of pale green glauconitic non‐pedogenic silcrete and cal‐silcrete overlain by non‐pedogenic calcrete, all of which have formed within sediments situated upon granitoid‐gneiss bedrock. The siliceous duricrusts are dominated by cryptocrystalline silica cements and appear to have developed through the replacement of a pre‐existing non‐pedogenic calcrete. These siliceous duricrusts have also been calciﬁed at a later date during the formation of the overlying calcrete to produce a complex range of silica–carbonate cements. At both sites, the style and type of siliciﬁcation present appears to be determined by the duration of wetting and the permeability of the precursor calcrete. Geochemical evidence indicates a lack of chemical weathering proﬁle development within the granitoid–gneiss bedrock and considerable differences between the chemical signature of the bedrock and combined duricrusts from Kang and Tswaane. This suggests that bedrock made a minimal contribution in terms of silica and carbonate species to duricrust formation, and that the majority of cementing agents were non‐local. It would therefore appear likely that the geomorphological context of each site had a major inﬂuence upon the development of calcrete, silcrete and intergrade duricrust cements. Copyright © 2004 John Wiley & Sons, Ltd.
Telomere‐mediated mitotic disturbances in immortalized ovarian epithelial cells reproduce chromosomal losses and breakpoints from ovarian carcinoma
Authors: Gisselsson David , Lv Mei , Tsao Sai‐Wha , Man Cornelia , Jin Charlotte , Höglund Mattias , Kwong Yok Lam , Jin Yuesheng 
Published: September 2004

AbstractOvarian carcinomas (OCs) often exhibit highly complex cytogenetic changes. Abnormal chromosome segregation at mitosis is one potential mechanism for genomic rearrangements in tumors. In this study, OCs were demonstrated to have dysfunctional short telomeres, anaphase bridging, and multipolar mitoses with supernumerary centrosomes. When normal human ovarian surface epithelial (HOSE) cells were transfected with human papilloma virus 16 e6/e7 genes and subsequently driven into telomere crisis, the same set of mitotic disturbances occurred in a distinct sequence, initiated by telomere dysfunction, followed by anaphase bridging, and then supernumerary centrosomes and multipolar mitoses. The anaphase bridges resolved either by kinetochore‐spindle detachment, corresponding to whole‐chromosome losses in the HOSE karyotypes, or by extensive fragmentation of intercentromeric DNA sequences, corresponding to a high frequency of pericentromeric rearrangements. At later passages, the high degree of instability at telomere crisis was moderated by telomerase expression and centrosome coalescence, ultimately leading to a level of mitotic instability that was highly similar to that in OC cell lines and to complex karyotypes that were similar to those observed in high‐grade OCs. This suggests that a significant proportion of the structural chromosome changes and genomic losses in OC are caused by a specific sequence of mitotic disturbances triggered by telomere crisis. That the model did not produce any of the whole‐chromosome gains observed in OC indicates that these changes develop through a different mechanism. © 2004 Wiley‐Liss, Inc.
Duplication of chromosome arms 9q and 11q: Evidence for a novel, 14q32 translocation–independent pathogenetic pathway in multiple myeloma
Authors: Liebisch Peter , Scheck Daniel , Erné Seiichi Alvise , Wellmann Alexander , Wendl Christiane , Janczik Sibylle , Kolmus Sonja , Kröber Alexander , Einsele Hermann , Straka Christian , Goldschmidt Hartmut , Benner Axel , Stilgenbauer Stephan , Döhner Hartmut 
Published: September 2004

Abstract14q32 translocations [t(14q)] represent critical but not universal events in multiple myeloma (MM). Gains of chromosome arms 1q, 9q, and 11q (+1q, +9q, and +11q) have recently been identified as frequent aberrations in this disease, but their pathogenetic significance remains unclear. We studied a series of 108 MM patients using fluorescence in situ hybridization and DNA probes mapping to chromosome bands 1q21, 9q34, 11q25, 13q14, and 14q32. Three subsets of tumors were defined: (1) MM+/+ (detection of +9q and +11q; 43.5% of cases), (2) MM+/− (+9q or +11q; 21.3%), and (3) MM−/− (neither +9q nor +11q; 35.2%). The incidence of t(14q) was significantly different in these subgroups: 23% in MM+/+, 56% in MM+/−, and 89% in MM−/−. Deletion of 13q (13q−) also was significantly less frequent in MM+/+ (23%) than in MM+/− and MM−/− (36% and 63%, respectively). The nonrandom distribution of chromosomal aberrations in the present series of MM tumors points to a novel, 14q32 translocation–independent pathogenetic pathway in plasma cell neoplasms. © 2005 Wiley‐Liss, Inc.
Acute lymphoblastic leukemia in a patient with Greig cephalopolysyndactyly and interstitial deletion of chromosome 7 del(7)(p11.2 p14) involving the GLI3 and ZNFN1A1 genes
Authors: Mendoza‐Londono Roberto , Kashork Catherine D. , Shaffer Lisa G. , Krance Robert , Plon Sharon E. 
Published: September 2004

AbstractGreig cephalopolysyndactyly (GCPS; OMIM 175700) is an autosomal dominant condition caused by mutations of the gene GLI3, located on 7p13. To date, several cases of deletions and/or translocations involving this locus have been reported in patients with GCPS. GLI3 is a transcription factor from the GLI‐Kruppel gene family that has been implicated in three distinct entities: GCPS, Pallister–Hall syndrome, and postaxial polydactyly type A. The zinc finger protein, subfamily 1, member 1 gene (ZNFN1A1; OMIM 603023), on 7p12, codes for a lymphoid‐restricted zinc finger transcription factor, ZNFN1A1, also called IKAROS, that regulates lymphocyte differentiation and has been associated with the development of childhood leukemia. We present the case of a 9‐year‐old Latin‐American boy who was referred for stem cell transplantation because of recurrent acute lymphoblastic leukemia (ALL). On evaluation, he was found to have dysmorphic features consistent with GCPS, including a prominent forehead, down‐slanting palpebral fissures, 1‐2‐3 toe syndactyly, broad thumbs and first toes, and mild developmental delay. He had developed ALL at 5 years of age. Chromosome analysis of bone marrow and fibroblastic cells showed an interstitial deletion of chromosome arm 7p, del(7)(p11.2p14), in 74% and 44% of the cells, respectively. We performed FISH analysis with a BAC clone containing the ZNFN1A1 gene and demonstrated that it is contained in the deleted segment. To our knowledge, this is the first report of a patient with GCPS and leukemia. We hypothesize that constitutional deletion of the ZNFN1A1 gene in this patient may have resulted in an increased risk of lymphoid malignancy. © 2005 Wiley‐Liss, Inc.
Cancer risk according to type and location of ATM mutation in ataxia‐telangiectasia families
Authors: Cavaciuti E. , Laugé A. , Janin N. , Ossian K. , Hall J. , Stoppa‐Lyonnet D. , Andrieu N. 
Published: September 2004

AbstractEpidemiological studies have indicated that ataxia‐telangiectasia (AT) heterozygotes in AT families have an increased risk of cancer, particularly of breast cancer (BC). However, in BC case–control studies, no significant differences were found in the frequency of ATM mutations between patients and controls. In such studies missense mutations were found more frequently than truncating mutations, suggesting that the cancer risk depends on mutation type. To investigate this possibility, we assessed the risk of BC according to the type and position of the ATM truncating mutation in extended AT families. DNA or RNA that had been isolated from blood or buccal cells of AT children and their relatives was screened for ATM germ‐line mutations using restriction endonuclease fingerprinting, the protein truncation test, fluorescence‐assisted mismatch analysis, and direct sequencing. The standardized incidence ratio of cancer associated with ATM heterozygosity status and type of mutation was estimated. We tested for genotype–phenotype correlations by simulations, permuting mutations among parental branches. No significant difference was found in the relative risk of breast cancer or any other type of cancer based on mutation type. However, the occurrence of BC may be associated with truncating mutations in certain binding domains of the ATM protein (e.g., P53/BRCA1, β‐adaptin, and FAT domains; P = 0.006). In this limited sample set, the presence of missense or truncating ATM mutations was not associated with different cancer risks. The risk of BC appeared to be associated with the alteration of binding domains rather than with the length of the predicted ATM protein. © 2004 Wiley‐Liss, Inc.
Glutamate transport by retinal Müller cells in glutamate/aspartate transporter‐knockout mice
Authors: Sarthy Vijay P. , Pignataro Leonardo , Pannicke Thomas , Weick Michael , Reichenbach Andreas , Harada Takayuki , Tanaka Kohichi , Marc Robert 
Published: September 2004

AbstractGlutamate transporters are involved in maintaining extracellular glutamate at a low level to ensure a high signal‐to‐noise ratio for glutamatergic neurotransmission and to protect neurons from excitotoxic damage. The mammalian retina is known to express the excitatory amino acid transporters, EAAT1–5; however, their specific role in glutamate homeostasis is poorly understood. To examine the role of the glial glutamate/aspartate transporter (GLAST) in the retina, we have studied glutamate transport by Müller cells in GLAST−/− mice, using biochemical, electrophysiological, and immunocytochemical techniques. Glutamate uptake assays indicated that the Km value for glutamate uptake was similar in wild‐type and GLAST−/− mouse retinas, but the Vmax was ∼50% lower in the mutant. In Na+‐free medium, the Vmax was further reduced by 40%. In patch‐clamp recordings of dissociated Müller cells from GLAST−/− mice, application of 0.1 mM glutamate evoked no current showing that the cells lacked functional electrogenic glutamate transporters. The result also indicated that there was no compensatory upregulation of EAATs in Müller cells. [3H]D‐Aspartate uptake autoradiography, however, showed that Na+‐dependent, high‐affinity transporters account for most of the glutamate uptake by Müller cells, and that Na+‐independent glutamate transport is negligible. Additional experiments showed that the residual glutamate uptake in Müller cells in the GLAST−/− mouse retina is not due to known glutamate transporters—cystine‐glutamate exchanger, ASCT‐1, AGT‐1, or other heteroexchangers. The present study shows that while several known glutamate transporters are expressed by mammalian Müller cells, new Na+‐dependent, high‐affinity glutamate transporters remain to be identified. © 2004 Wiley‐Liss, Inc.