bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analytical velocity potentials in cells with a rigid spherical wall
Authors: Barnyak M. , Gavrilyuk I. , Hermann M. , Timokha A. 
Published: July 2010

AbstractBy using Kelvin's inversion, we construct analytical harmonic functions satisfying the zero‐Neumann condition on the inner spherical wall everywhere except a single point where the velocity is infinite. This set of functions can be used to construct approximate velocity potentials associated with liquid sloshing in a spherical tank, and in other hydrodynamic problems.
CabaretistasandIndias Bonitas: Gender and Representations of Mexico in the Americas during the Cárdenas Era
Authors: KIDDLE AMELIA M. 
Published: July 2010

AbstractThis article examines the promotion of Mexico's national image in the Americas during the Cárdenas period, using as a starting point a scandal arising from a 1940 performance of Mexican dancers at a cabaret in Panama. Mexican diplomats found the show objectionable because it clashed with the image of women that they used in their efforts to raise the country's reputation abroad. By investigating these efforts, as well as the career of Eva Pérez Caro, the dance troupe's leader, the article contributes to our understanding of the relationship between gender, cultural performance and nationalism, and the role that they played in Mexico's foreign relations.
Segmented Party–Voter Linkages in Latin America: The Case of the UDI
Authors: LUNA JUAN PABLO 
Published: July 2010

AbstractBy analysing the socially segmented party–voter linkages deployed by the Unión Demócrata Independiente (Independent Democratic Union, UDI), a Chilean conservative party, this article demonstrates the usefulness of combining Kitschelt's party–voter linkage framework with Gibson's conceptual approach to conservative party electoral coalition-making. In Latin America, parties take advantage of social fragmentation and the availability of non-state campaign financing to combine multiple linkage types and thus attract socially diverse constituencies. Although it is an opposition party, UDI's historical trajectory and organisation have enabled it to receive private funds from its traditional and party-identified core constituency (business and conservative sectors), whose programmatic preferences and interests it represents, and then use these resources in a ‘charismatic’ mobilisation approach and particularistic exchanges with a non-core constituency (low-income, non-traditional voters of the radical right), in a segmented, but nationally integrated, electoral strategy.
How Can Female Germline Stem Cells Contribute to the Physiological Neo-Oogenesis in Mammals and Why Menopause Occurs?
Authors: Bukovsky Antonin 
Published: July 2010

AbstractAt the beginning of the last century, reproductive biologists have discussed whether in mammalian species the fetal oocytes persist or are replaced by neo-oogenesis during adulthood. Currently the prevailing view is that neo-oogenesis is functional in lower vertebrates but not in mammalian species. However, contrary to the evolutionary rules, this suggests that females of lower vertebrates have a better opportunity to provide healthy offspring compared to mammals with oocytes subjected to environmental threats for up to several decades. During the last 15 years, a new effort has been made to determine whether the oocyte pool in adult mammals is renewed as well. Most recently, Ji Wu and colleagues reported a production of offspring from female germline stem cells derived from neonatal and adult mouse ovaries. This indicates that both neonatal and adult mouse ovaries carry stem cells capable of producing functional oocytes. However, it is unclear whether neo-oogenesis from ovarian somatic stem cells is physiologically involved in follicular renewal and why menopause occurs. Here we review observations that indicate an involvement of immunoregulation in physiological neo-oogenesis and follicular renewal from ovarian stem cells during the prime reproductive period and propose why menopause occurs in spite of persisting ovarian stem cells.
Terazosin for treating symptomatic benign prostatic obstruction: a systematic review of efficacy and adverse effects
Authors: Wilt T.J. , Howe W. , MacDonald R. 
Published: July 2010

Objective To systematically review and evaluate the effectiveness and adverse effects of the α‐antagonist, terazosin, for treating urinary symptoms associated with benign prostatic obstruction (BPO). Methods Studies were sought and included in the review if they were randomized trials of at least 1 month duration, involved men with symptomatic BPO and compared terazosin with placebo or active controls. The study, patient characteristics and outcome data were extracted in duplicate onto standardized forms using a prospectively developed protocol. Results Seventeen studies involving 5151 men met the inclusion criteria, i.e. placebo‐controlled (10), α‐blockers (seven), finasteride alone or combined with terazosin and placebo (one), and microwave therapy (one). The study duration was 4–52 weeks; the mean age of the men was 65 years and 82% were white. Baseline urological symptom scale scores and flow rates showed that men had moderate BPO. Efficacy outcomes were rarely reported in a way that allowed for data pooling, but indicated that terazosin improved symptom scores and flow rates more than did placebo or finasteride, and similarly to other α‐antagonists. The pooled mean percentage improvement for the Boyarsky symptom score was 37% for terazosin and 15% for placebo (four studies). The mean percentage improvement for the American Urological Association symptom score was 38%, compared with 17% and 20% for placebo and finasteride, respectively (two studies). The pooled mean improvement in the International Prostate Symptom Score of 40% was similar to that with tamsulosin (43%). Peak urinary flow rates improved more with terazosin (22%) than with placebo (11%) and finasteride (15%), but did not differ significantly from the other α‐antagonists. The percentage of men discontinuing terazosin was comparable with those receiving placebo and finasteride, but greater than with other α‐antagonists. Adverse effects were greater than with placebo and included dizziness, asthenia, headache and postural hypotension. Conclusions The available evidence indicates that terazosin improves the symptoms and flow rates associated with BPO; it was more effective than placebo or finasteride and similar to other α‐antagonists. Adverse effects were generally mild but more frequent than with other α‐antagonists and associated with a two‐ to four‐fold increase in treatment discontinuation.
Regulation of human UDP‐galactose: ceramide β‐galactosyltransferase (CGT) gene expression
Authors: Yu R. K. , Tencomnao T. 
Published: July 2010

Myelination is a highly coordinated event during nervous system development, which involves the synthesis of many myelin specific components. The most abundant glycolipid in myelin is galactocerebroside (GC), whose synthesis is catalysed by CGT. To elucidate the transcriptional control of the hCGT gene, we sequenced 2.3 kb of the 5′‐flanking region of this gene. Transient transfection of the human oligodendroglioma (HOG; GC+) and neuroblastoma (LAN‐5; GC–) cell lines using a series of luciferase reporter plasmids containing deletion fragments of the hCGT 5′‐flanking region showed that this promoter functions in a cell‐specific manner. Three positive regulatory regions were identified: a region at −292/−256 containing an Sp1 site, a region at −747/−688 containing sites for TGGCA‐BP, CRE, and ER half‐site, a distal region at −1325/−1279 containing a nitrogen regulatory site. A negative regulatory domain (−1594/−1326) was also identified. Using mutation analyses and cotransfection experiments in HOG cells, we confirmed that the Sp1 motif (−267/−259) and the CRE motif (−697/−690) were critical for hCGT expression. Gel shift assays showed that these motifs are bound by nuclear extracts from both cell lines and mouse brains. Using antibodies to Sp1, Sp3, and CREB, these proteins were shown to be components of the complexes. However, the CRE complexes were the only notable differences between HOG and LAN‐5 cells, which may be responsible for the differential transcription of this gene. Thus, the hCGT promoter contains both positive and negative regulatory regions for the cell‐specific expression, and these regions function cooperatively.Acknowledgements:  Supported by NIH NS11853‐27.
Compartmentalized neurotransmitter and amino acid synthesis in vivo studied by high field MRS
Authors: Gruetter R. , Henry P. G. , Lei H. , Choi I.‐Y. 
Published: July 2010

Glutamatergic action occurs by the glial uptake of extracellular glutamate and conversion into glutamine, which is exported to neurons. Recently, a 1 : 1 stoichiometry between total oxidative brain glucose consumption, CMRglc(ox), and glutamatergic action was reported. This relationship required, that all of the glucose phosphorylated in glia was exported to neurons in the form of lactate. We recently reaffirmed in the awake human brain that the majority of ATP produced in glia is oxidative (Gruetter et al. 2001). In that study we also observed that the exchange rate between TCA cycle intermediates and amino acids, Vx, is on the order of the flux through pyruvate dehydrogenase, VPDH, which implied that this exchange rate is influenced by the malate–aspartate shuttle (MAS). Recently we have extended this line of investigation to the intact rat brain. TCA cycle flux and glutamate/glutamine metabolism was assessed in vivo at two different anesthetic levels (pentobarbital and α‐chloralose anesthesia) using 13C NMR in conjunction with 13C glucose infusions. Several metabolic rates were extracted from the rate of label incorporation using a mathematical model (Gruetter et al. 2001). The apparent rate of glutamatergic neurotransmission, VNT, was low, even though glucose metabolism was still substantial, suggesting that the stoichiometry between glucose metabolism and glutamatergic neurotransmission is far from 1 : 1. The rate of pyruvate carboxylation was ∼25% of glutamine synthase flux. Vx was found to be equal to VPDH, indicating that Vx is coupled to CMRglc(ox), consistent with MAS being the major mechanism that facilitates label exchange across the inner mitochondrial membrane.Reference Gruetter et al. (2001) Am. J. Physiol.281, 100E.
The role of NAAG and NAALADase in axon‐to‐glia signalling
Authors: Grossfeld R. M. , Urazaev A. K. , Lieberman E. M. 
Published: July 2010

Recent investigations from our laboratories have identified N‐acetylaspartylglutamate (NAAG) as the probable primary axon‐to‐glia signalling agent and source of signalling glutamate (GLU) at nonsynaptic regions of crayfish nerve fibers. NAAG is released from giant axons and mimics the action of the natural signalling agent in hyperpolarizing the glia. GLU formed extracellularly during inactivation of NAAG by NAALADase has a similar, but smaller, effect on the glia. A consequence of these actions of NAAG and GLU appears to be an activation of a signal transduction cascade leading to modulation of water and K+ homeostasis of the neuronal microenvironment. GLU or a related substance also appears to be a neuron‐glia signalling agent at nonsynaptic and synaptic regions of vertebrate nervous system. Therefore, conserved mechanisms of neuron‐glia signalling, mediated at least in part by NAAG and/or GLU, may regulate signal transmission and processing at axons and synapses under physiological and pathological conditions in invertebrates and vertebrates.Acknowledgements:  Supported by NIH grant NS34799 and Guilford Pharmaceuticals (Baltimore, MD).
Redefining chemical anatomy of glutamatergic neurotransmission
Authors: Schafer M. K. , Weihe E. 
Published: July 2010

With the recent identification of the two isoforms of vesicular glutamate transporters VGLUT1 and VGLUT2 and of the presumed neuronal glutamine transporter SAT1 novel tools have been made available to unequivocally define the anatomy of glutamatergic pathways on the cellular and synaptic level. Using highly specific antisera and cRNA probes two distinct glutamatergic pathways expressing either VGLUT1 or VGLUT2 could be detected throughout the central nervous system. Areas where VGLUT1 predominated included the cerebral and cerebellar cortex and the hippocampus. VGLUT2 was mainly expressed in the thalamus, hypothalamus and brain stem. VGLUT1 and VGLUT2 synapses exhibited distinct region‐ and pathway‐specific relationships with each other and with other classical transmitter and peptidergic systems. The glutamine transporter SAT1 was expressed in CNS neurons and in ependymal cells. Neuronal SAT1 expression comprised virtually all glutamatergic neurons but also specific subsets of cholinergic, GABAergic and aminergic neurons in the CNS. In addition to widespread expression of VGLUT1 and VGLUT2 in the CNS, peripheral tissues such as sensory neurons and pancreatic islet cells differentially expressed VGLUT isoforms and SAT1.Our results suggest pathway‐specific functional duality in the regulation of vesicular glutamate release at excitatory synapses and provide evidence for glutamine transport and metabolism in excitatory glutamatergic and diverse nonglutamatergic neurons as well.
Iron (III) induces aggregation of hyperphosphorylated τ and its reduction to iron (II) reverses the aggregation: implications in the formation of neurofibrillary tangles of Alzheimer's disease
Authors: Yamamoto Akira , Shin Ryong‐Woon , Hasegawa Kazuhiro , Naiki Hironobu , Sato Hiroyuki , Yoshimasu Fumio , Kitamoto Tetsuyuki 
Published: July 2010

AbstractIron as well as aluminum is reported to accumulate in neurons with neurofibrillary tangles (NFTs) of Alzheimer's disease (AD) brain. Previously we demonstrated that aluminum (III) shows phosphate‐dependent binding with hyperphosphorylated τ (PHFτ), the major constituent of NFTs, thereby inducing aggregation of PHFτ. Herein we report that iron (III) can also induce aggregation of soluble PHFτ. Importantly, for the aggregation of PHFτ to occur, iron in the oxidized state (III) is essential since iron in the reduced state (II) lacks such ability. Furthermore, iron (III)‐induced aggregation is reversed by reducing iron (III) to iron (II). Thus the iron‐participating aggregation is mediated not only by τ phosphorylation but also by the transition of iron between reduced (II) and oxidized (III) states. Further incubation of insoluble PHFτ aggregates isolated from AD brain with reducing agents produced liberation of solubilized PHFτ and iron (II), indicating that PHFτ in association with iron (III) constitutes the insoluble pool of PHFτ. These results indicate that iron might play a role in the aggregation of PHFτ leading to the formation of NFTs in AD brain.
Proteasome inhibition by paired helical filament‐tau in brains of patients with Alzheimer's disease
Authors: Keck Susi , Nitsch Robert , Grune Tilman , Ullrich Oliver 
Published: July 2010

AbstractAlzheimer's disease (AD) is characterized neuropathologically by intracellular neurofibrillary tangles (NFTs) formed of tau‐based paired helical filaments (PHFs) and extracellular β‐amyloid plaques. The degree of Alzheimer dementia correlates with the severity of PHFs and NFTs. As an intraneuronal accumulation of oxidatively damaged proteins has been found in the brains of patients with AD, a dysfunction of the proteasomal system, which degrades damaged proteins, has been assumed to cause protein aggregation and therefore neurodegeneration in AD. In this study, we revealed that such proteasome dysfunction in AD brain results from the inhibitory binding of PHF‐tau to proteasomes. We analysed the proteasome activity in brains from patients with AD and age‐matched controls, and observed a significant decrease to 56% of the control level in the straight gyrus of patients with AD. This loss of activity was not associated with a decrease in the proteasome protein. PHF‐tau co‐precipitated during proteasome immunoprecipitation and proteasome subunits could be co‐isolated during isolation of PHFs from AD brain. Furthermore, the proteasome activity in human brains strongly correlated with the amount of co‐precipitated PHF‐tau during immunoprecipitation of proteasome. Incubation of isolated proteasomes with PHF‐tau isolated from AD brain, and with PHFs after in vitro assembly from human recombinant tau protein, resulted in a distinct inhibition of proteasome activity by PHF‐tau. As this inhibition of proteasome activity was sufficient to induce neuronal degeneration and death, we suggest that PHF‐tau is able directly to induce neuronal damage in the AD brain.
The adhesion protein TAG‐1 has a ganglioside environment in the sphingolipid‐enriched membrane domains of neuronal cells in culture
Authors: Loberto Nicoletta , Prioni Simona , Prinetti Alessandro , Ottico Elena , Chigorno Vanna , Karagogeos Domna , Sonnino Sandro 
Published: July 2010

AbstractWe studied the interactions between gangliosides and proteins at the exoplasmic surface of the sphingolipid‐enriched membrane domains by ganglioside photolabeling combined with cell surface biotin labeling. After cell photolabeling with radioactive photoactivable derivatives of GM3, GM1 and GD1b gangliosides, followed by cell surface biotin labeling, sphingolipid‐enriched domains were prepared and immunoprecipitated with streptavidin‐coupled beads, under experimental conditions preserving the integrity of the lipid domain. About 50% of the total radioactivity linked to proteins was associated with acylated tubulin, about 10% with a 135‐kDa protein present as a series of species with pI ranging from 6.5 to 8.0, about 5% with a protein of about 70 kDa and with pI near to 6.5. By immunoprecipitation with streptavidin‐coupled beads under conditions disrupting the integrity of the lipid domain, the 135 kDa protein was recovered in the immunoprecipitate, that did not contain tubulin. Thus, the 135 kDa protein has an exoplasmic domain, and it was then identified as the GPI‐anchored neural cell adhesion molecule TAG‐1. Remarkably, TAG‐1 was cross‐linked in a similar extent by the photoactivated ganglioside GM3, GM1 and GD1b. The three gangliosides bear different oligosaccharide chains, suggesting that the ganglioside/TAG−1 interaction is not specifically associated with the ganglioside oligosaccharide structure.
Intranigral infusion of interleukin‐1β activates astrocytes and protects from subsequent 6‐hydroxydopamine neurotoxicity
Authors: Saura Josep , Parés Mireia , Bové Jordi , Pezzi Susana , Alberch Jordi , Marin Concepció , Tolosa Eduardo , Martí María José 
Published: July 2010

AbstractActivation of glial cells is a prevalent response to neuronal damage in brain disease and ageing, with potential neuroprotective and neurotoxic consequences. We were interested in studying the role of glial activation on dopaminergic neurons of the substantia nigra in an animal model of Parkinson's disease. Thus, we evaluated the effect of a pre‐existing glial activation on the dopaminergic neuronal death induced by striatal infusion of 6‐hydroxydopamine. We established a model of local glial activation by stereotaxic infusion of interleukin‐1β in the substantia nigra of adult rats. Interleukin‐1β (20 ng) induced a marked activation of astrocytes at days 2, 5 and 10, revealed by heat‐shock protein 27 and glial fibrillary acid protein immunohistochemistry, but did not affect the microglial markers OX‐42 and heat‐shock proteins 32 or 47. Intranigral infusion of interleukin‐1β 5 days before a striatal injection of 6‐hydroxydopamine significantly protected nigral dopaminergic cell bodies, but not striatal terminals from the 6‐hydroxydopamine lesion. Also, in the animals pre‐treated with interleukin‐1β, a significant prevention of 6‐hydroxydopamine‐induced reduction of adjusting steps, but not of 6‐hydroxydopamine‐induced amphetamine rotations, were observed. These data show the characterization of a novel model of local astroglial activation in the substantia nigra and support the hypothesis of a neuroprotective role of activated astrocytes in Parkinson's disease.
Mice transgenic for exon 1 of Huntington's disease: properties of cholinergic and dopaminergic pre‐synaptic function in the striatum
Authors: Vetter J. M. , Jehle T. , Heinemeyer J. , Franz P. , Behrens P. F. , Jackisch R. , Landwehrmeyer G. B. , Feuerstein T. J. 
Published: July 2010

AbstractIn Huntington's disease (HD), neuronal loss is most prominent in the striatum leading to emotional, cognitive and progressive motor dysfunction. The R6/2 mice, transgenic for exon 1 of the HD gene, develop a neurological phenotype with similarities to these features of HD. In striatal tissue, electrically evoked release of tritiated acetylcholine (ACh) and dopamine (DA) were compared in wild‐type (WT) and R6/2 mice. In R6/2 mice, the evoked release of ACh, its M2 autoreceptor‐mediated maximum inhibition and its dopamine D2 heteroreceptor‐mediated maximum inhibition was diminished to 51%, 74% and 87% of controls, respectively. Also, the activities of choline acetyltransferase and of synaptosomal high‐affinity choline uptake decreased progressively with age in these mice. In the DA release model, however, electrical stimulation elicited equal amounts of [3H]‐DA both in WT and R6/2 mice. Moreover, high‐affinity DA uptake into striatal slices was similar in WT and R6/2 mice. In order to confirm these findings in vivo, intrastriatal levels of extracellular DA were measured by intracerebral microdialysis in freely moving mice: striatal DA levels were found to be equal in WT and R6/2 mice. In conclusion, in the transgenic R6/2 mice changes occur mainly in striatal cholinergic neurones and their pre‐synaptic modulation, but not in the dopaminergic afferent terminals. Whether similar events also contribute to the pathogenesis of HD in humans has to be established.
Temporal–spatial characterization of chicken clock genes: circadian expression in retina, pineal gland, and peripheral tissues
Authors: Chong Nelson W. , Chaurasia Shyam S. , Haque Rashidul , Klein David C. , Iuvone P. Michael 
Published: July 2010

AbstractThe molecular core of the vertebrate circadian clock is a set of clock genes, whose products interact to control circadian changes in physiology. These clock genes are expressed in all tissues known to possess an endogenous self‐sustaining clock, and many are also found in peripheral tissues. In the present study, the expression patterns of two clock genes, cBmal1 and cMOP4, were examined in the chicken, a useful model for analysis of the avian circadian system. In two tissues which contain endogenous clocks – the pineal gland and retina – circadian fluctuations of both cBmal1 and cMOP4 mRNAs were observed to be synchronous; highest levels occurred at Zeitgeber time 12. Expression of these genes is also rhythmic in several peripheral tissues; however, the phases of these rhythms differ from those in the pineal gland and retina: in the liver the peaks of cMOP4 and cBmal1 mRNAs are delayed 4–8 h and in the heart they are advanced by 4 h, relative to those in the pineal gland and retina. These results provide the first temporal characterization of cBmal1 and cMOP4 mRNAs in avian tissues: their presence in avian peripheral tissues indicates they may influence temporal features of daily rhythms in biochemical, physiological, and behavioral functions at these sites.