bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrastructural analysis of the synaptic connectivity of TRPV1‐expressing primary afferent terminals in the rat trigeminal caudal nucleus
Authors: Yeo Eun Jin , Cho Yi Sul , Paik Sang Kyoo , Yoshida Atsushi , Park Mae Ja , Ahn Dong Kuk , Moon Cheil , Kim Yun Sook , Bae Yong Chul 
Published: March 2010

AbstractTrigeminal primary afferents that express the transient receptor potential vanilloid 1 (TRPV1) are important for the transmission of orofacial nociception. However, little is known about how the TRPV1‐mediated nociceptive information is processed at the first relay nucleus in the central nervous system (CNS). To address this issue, we studied the synaptic connectivity of TRPV1‐positive (+) terminals in the rat trigeminal caudal nucleus (Vc) by using electron microscopic immunohistochemistry and analysis of serial thin sections. Whereas the large majority of TRPV1+ terminals made synaptic contacts of an asymmetric type with one or two postsynaptic dendrites, a considerable fraction also participated in complex glomerular synaptic arrangements. A few TRPV1+ terminals received axoaxonic contacts from synaptic endings that contained pleomorphic synaptic vesicles and were immunolabeled for glutamic acid decarboxylase, the synthesizing enzyme for the inhibitory neurotransmitter γ‐aminobutyric acid (GABA). We classified the TRPV1+ terminals into an S‐type, containing less than five dense‐core vesicles (DCVs), and a DCV‐type, containing five or more DCVs. The number of postsynaptic dendrites was similar between the two types of terminals; however, whereas axoaxonic contacts were frequent on the S‐type, the DCV‐type did not receive axoaxonic contacts. In the sensory root of the trigeminal ganglion, TRPV1+ axons were mostly unmyelinated, and a small fraction was small myelinated. These results suggest that the TRPV1‐mediated nociceptive information from the orofacial region is processed in a specific manner by two distinct types of synaptic arrangements in the Vc, and that the central input of a few TRPV1+ afferents is presynaptically modulated via a GABA‐mediated mechanism. J. Comp. Neurol. 518:4134–4146, 2010. © 2010 Wiley‐Liss, Inc.
Mice deficient in brain‐derived neurotrophic factor have altered development of gastric vagal sensory innervation
Authors: Murphy Michelle C. , Fox Edward A. 
Published: March 2010

AbstractVagal sensory neurons are dependent on neurotrophins for survival during development. Here, the contribution of brain‐derived neurotrophic factor (BDNF) to survival and other aspects of gastric vagal afferent development was investigated. Post‐mortem anterograde tracing with 1,1′‐dioctadecyl‐3,3,3′,3′‐tetramethylindocarbo‐cyanine perchlorate (DiI) was used to label selectively vagal projections to the stomach on postnatal days (P) 0, 3, 4, and 6 in wild types and heterozygous or homozygous BDNF mutants. Sampling sites distributed throughout the ventral stomach wall were scanned with a confocal microscope, and vagal axon bundles, single axons, putative mechanoreceptor precursors (intraganglionic laminar endings, IGLEs; intramuscular arrays, IMAs), and efferent terminals were quantified. Also, myenteric neurons, which are innervated by IGLEs, were stained with cuprolinic blue and counted. Quantitative comparisons across wild‐type stomach compartments demonstrated that the adult distribution of IMAs was not present at P0 but began to form by P3–6. Among all the quantified elements, at P0, only IGLE density was significantly different in homozygous mutants compared with wild types, exhibiting a 50% reduction. Also, antrum innervation appeared disorganized, and some putative IMA precursors had truncated telodendria. At P3–6, the effect on IGLEs had recovered, the disorganization of antrum innervation had partially recovered, and some IMA telodendria were still truncated. The present results suggest that gastric IGLEs are among the vagal sensory neurons dependent on BDNF for survival or axon guidance. Alternatively, BDNF deficiency may delay gastric IGLE development. Also, BDNF may contribute to IMA differentiation and patterning of antral vagal innervation. J. Comp. Neurol. 518:2934–2951, 2010. © 2010 Wiley‐Liss, Inc.
Localized expression of urocortin genes in the developing zebrafish brain
Authors: Bräutigam Lars , Hillmer Janine M. , Söll Iris , Hauptmann Giselbert 
Published: March 2010

AbstractThe corticotropin‐releasing hormone (CRH) family consists of four paralogous genes, CRH and urocortins (UCNs) 1, 2, and 3. In a previous study, we analyzed CRH in the teleost model organism zebrafish and its transcript distribution in the embryonic brain. Here, we describe full‐length cDNAs encoding urotensin 1 (UTS1), the teleost UCN1 ortholog, and UCN3 of zebrafish. Major expression sites ofuts1in adult zebrafish are the caudal neurosecretory system and brain. By using RT‐PCR analysis, we show thatuts1mRNA is also present in ovary, maternally contributed to the embryo, and expressed throughout embryonic development. Expression ofucn3mRNA was detected in a range of adult tissues and during developmental stages from 24 hours post fertilization onward. Analysis of spatial transcript distributions by whole‐mount in situ hybridization revealed limited forebrain expression ofuts1anducn3during early development. Small numbers ofuts1‐synthesizing neurons were found in subpallium, hypothalamus, and posterior diencephalon, whereasucn3‐positive cells were restricted to telencephalon and retina. The brainstem was the main site ofuts1anducn3synthesis in the embryonic brain.uts1Expression was confined to the midbrain tegmentum; distinct hindbrain cell groups, including locus coeruleus and Mauthner neurons; and the spinal cord.ucn3Expression was localized to the optic tectum, serotonergic raphe, and distinct rhombomeric cell clusters. The prominent expression ofuts1anducn3in brainstem is consistent with proposed roles of CRH‐related peptides in stress‐induced modulation of locomotor activity through monoaminergic brainstem neuromodulatory systems. J. Comp. Neurol. 518:2978–2995, 2010. © 2010 Wiley‐Liss, Inc.
Age changes in myelinated nerve fibers of the cingulate bundle and corpus callosum in the rhesus monkey
Authors: Bowley Michael P. , Cabral Howard , Rosene Douglas L. , Peters Alan 
Published: March 2010

AbstractAging is accompanied by deficits in cognitive function, which may be related to the vulnerability of myelinated nerve fibers to the normal process of aging. Loss of nerve fibers, together with age‐related alterations in myelin sheath structure, may result in the inefficient and poorly coordinated conduction of neuronal signals. Until now, the ultrastructural analysis of cerebral white matter fiber tracts associated with frontal lobe areas critical in cognitive processing has been limited. In this study we analyzed the morphology and area number density of myelinated nerve fibers in the cingulate bundle and genu of the corpus callosum in behaviorally assessed young, middle aged, and old rhesus monkeys (Macaca mulatta). In both structures, normal aging results in a 20% decrease in the number of myelinated nerve fibers per unit area, while remaining nerve fibers exhibit an increasing frequency of degenerative changes in their myelin sheaths throughout middle and old age. Concomitantly, myelination continues in older monkeys, suggesting ongoing, albeit inadequate, reparative processes. Despite similar patterns of degeneration in both fiber tracts, only the age‐related changes in the cingulate bundle correlate with declining cognitive function, underscoring its role as a critical corticocortical pathway linking the medial prefrontal, cingulate, and parahippocampal cortices in processes of working memory, recognition memory, and other higher cognitive faculties. These results further demonstrate the important role myelinated nerve fiber degeneration plays in the pathogenesis of age‐related cognitive decline. J. Comp. Neurol. 518:3046–3064, 2010. © 2010 Wiley‐Liss, Inc.
Endocannabinoid system in the adult rat circumventricular areas: An immunohistochemical study
Authors: Suárez Juan , Romero‐Zerbo Silvana Y. , Rivera Patricia , Bermúdez‐Silva Francisco Javier , Pérez Juan , De Fonseca Fernando Rodríguez , Fernández‐Llebrez P. 
Published: March 2010

AbstractEndocannabinoids (ECs) are important neuromodulators involved in a plethora of physiological processes such as modulation of synaptic transmission, neuroprotection, immune function, and neurodevelopment, among others. However, still lacking is a detailed study on the presence of this system in the circumventricular areas, brain structures controlling the interaction between cerebrospinal fluid and brain parenchyma. The aim of this work was to provide the anatomical basis supporting a functional role of ECs in the activity of circumventricular areas. To this end, an immunohistochemical study of the EC system in rat brain was performed. Receptors and synthesizing and degrading enzymes for ECs were widely distributed in rat ependyma and subependyma, marginal glia, and circumventricular organs (CVOs) such as the choroid plexus, subfornical organ, subcommissural organ, median eminence, and area postrema. These zones constitute barrier systems between the brain parenchyma and the ventricular or subarachnoid cerebrospinal fluid (CSF) and between the extracellular hemal milieu of CVOs and the brain parenchyma or the CSF. By immunohistochemistry and real‐time polymerase chain reaction we found DAGLα, DAGLβ, NAPE‐PLD, MAGL, and FAAH in the ependyma. These finding suggest that the ependyma can release and clear ECs from the ventricular CSF. Subependymal astrocytes and tanycytes displayed DAGLα immunoreactivity but parenchymal astrocytes did not express EC‐synthesizing enzymes, thus establishing a sharp distinction between these two astrocyte populations. CB1 was located in fibers innervating discrete subventricular zones such as the neurogenic striatal subventricular zone and the fourth ventricle. CB1 fibers also innervated some CVOs. J. Comp. Neurol. 518:3065–3085, 2010. © 2010 Wiley‐Liss, Inc.
β‐Endorphin expression in the mouse retina
Authors: Gallagher Shannon K. , Witkovsky Paul , Roux Michel J. , Low Malcolm J. , Otero‐Corchon Veronica , Hentges Shane T. , Vigh Jozsef 
Published: March 2010

AbstractEvidence showing expression of endogenous opioids in the mammalian retina is sparse. In the present study we examined a transgenic mouse line expressing an obligate dimerized form of Discosoma red fluorescent protein (DsRed) under the control of the pro‐opiomelanocortin promoter and distal upstream regulatory elements to assess whether pro‐opiomelanocortin peptide (POMC), and its opioid cleavage product, β‐endorphin, are expressed in the mouse retina. Using double label immunohistochemistry we found that DsRed fluorescence was restricted to a subset of GAD‐67‐positive cholinergic amacrine cells of both orthotopic and displaced subtypes. About 50% of cholinergic amacrine cells colocalized DsRed and a large fraction of DsRed‐expressing amacrine cells was positive for β‐endorphin immunostaining, whereas β‐endorphin‐immunoreactive neurons were absent in retinas of POMC null mice. Our findings contribute to a growing body of evidence demonstrating that opioid peptides are an integral component of vertebrate retinas, including those of mammals. J. Comp. Neurol. 518:3130–3148, 2010. © 2010 Wiley‐Liss, Inc.
Listeria monocytogenes is sensed by the NLRP3 and AIM2 inflammasome
Authors: Kim Sarah , Bauernfeind Franz , Ablasser Andrea , Hartmann Gunther , Fitzgerald Katherine A. , Latz Eicke , Hornung Veit 
Published: March 2010

AbstractThe inflammasome pathway functions to regulate caspase‐1 activation in response to a broad range of stimuli. Caspase‐1 activation is required for the maturation of the pivotal pro‐inflammatory cytokines of the pro‐IL‐1β family. In addition, caspase‐1 activation leads to a certain type of cell death known as pyroptosis. Activation of the inflammasome has been shown to play a critical role in the recognition and containment of various microbial pathogens, including the intracellularly replicating Listeria monocytogenes; however, the inflammasome pathways activated during L. monocytogenes infection are only poorly defined. Here, we demonstrate that L. monocytogenes activates both the NLRP3 and the AIM2 inflammasome, with a predominant involvement of the AIM2 inflammasome. In addition, L. monocytogenes‐triggered cell death was diminished in the absence of both AIM2 and NLRP3, and is concomitant with increased intracellular replication of L. monocytogenes. Altogether, these data establish a role for DNA sensing through the AIM2 inflammasome in the detection of intracellularly replicating bacteria.
Calix[6]arene‐Picolinamide Extractants for Radioactive Waste Treatment: Effect of Additional Carboxy Binding Sites in the Pyridine 6‐Positions on Complexation, Extraction Efficiency and An/Ln Separation
Authors: Macerata Elena , Sansone Francesco , Baldini Laura , Ugozzoli Franco , Brisach Frederic , Haddaoui Jaouad , Hubscher‐Bruder Véronique , Arnaud‐Neu Françoise , Mariani Mario , Ungaro Rocco , Casnati Alessandro 
Published: March 2010

AbstractThe effect of the presence of an additional ester or amide carboxy group in the 6‐position of the pyridine nuclei of calixarene‐based picolinamide ligands on the extraction and complexation properties of lanthanide(III) and actinide(III) metal ions was studied. For this purpose, six new ligands 1–6 were synthesized; their conformational properties were studied both in solution and in the solid state, and their binding properties towards lanthanide (LnIII) and actinide (AnIII) metal ions were determined under extracting conditions simulating those present in radioactive waste. In the presence of BrCosan as synergizer, a rather high efficiency in the extraction of trivalent metal ions by these ligands was observed even at [HNO3] > 2–3 M. Complexation of LnIII metal ions was also studied under homogeneous conditions (methanol solution), both in chloride and nitrate media, by using spectrophotometry and calorimetry. A comparison with the data obtained with ligands L1–L3, lacking the additional binding sites in the 6‐position of the pyridine nuclei, is reported and the effects of the structure of the ligands on the stoichiometry of the complexes, coordination of the metal ions, basicity of the pyridine binding groups and efficiency and selectivity in the extractions are also discussed.
Phosphiranes as Ligands: Tungsten(0) and Palladium(0) Complexes of Phosphirano[1,2‐c][1,2,3]diazaphospholes
Authors: Maurer Stefan , Burkhart Christian , Maas Gerhard 
Published: March 2010

AbstractPhosphirano[1,2‐c][1,2,3]diazaphospholes 5, which feature a strongly pyramidalized phosphorus atom at a ring fusion position, were identified as a new type of phosphane ligands for transition metals. The derivatives 5a–c smoothly form W(CO)5 complexes, which are thermally quite stable – in contrast to the known lability of various carbonylmetal complexes of simple phosphiranes. In the temperature range 120–150 °C, they undergo a clean decomplexation in toluene solution. Bicyclic phosphiranes 5a and 5b, but not the acceptor‐substituted derivative 5c, readily react with the [(E,E)‐dibenzylideneacetone]palladium(0) complex Pd2(dba)3·CHCl3 to form the corresponding isolable complexes [(5a)2(dba)Pd] and [(5b)2(dba)Pd]. In agreement with the formation of these complexes, it was found that 5a,b as ligands effectively promote the Suzuki cross‐coupling of 4‐bromotoluene with benzeneboronic acid. The solid‐state structure of bicyclic phosphirane 5b and of the complexes [(5a)(CO)5W], [(5b)2(dba)Pd] (pentane solvate) and [(5b)2(dba)Pd] (benzene solvate) were determined by X‐ray diffraction analysis.
Microfluidic cell arrays for metabolic monitoring of stimulated cardiomyocytes
Authors: Cheng Wei , Klauke Norbert , Smith Godfrey , Cooper Jonathan M. 
Published: March 2010

AbstractAn array of PDMS microchambers was aligned to an array of sensor electrodes and stimulating microelectrodes, which was used for the electrochemical monitoring of the metabolic activity of single isolated adult ventricular myocytes inside the chamber array, stimulated within a transient electric field. The effect of the accumulation of metabolic byproducts in the limited extracellular volume of the picolitre chambers was demonstrated by measuring single muscle cell contraction optically, while concomitant changes in intracellular calcium transients and pH were recorded independently using fluorescent indicator dyes. Both the amplitude of the cell shortening and the magnitude of the intracellular calcium transients decreased over time and both nearly ceased after 20 min of continuous stimulation in the limited extracellullar volume. The intracellular pH decreased gradually during 20 min of continuous stimulation after which a dramatic pH drop was observed, indicating the breakdown of the intracellular buffering capacity. After continuous stimulation, intracellular lactate was released into the microchamber through cell electroporation and was detected electrochemically at a lactate microbiosensor, within the chamber. A mitochondrial uncoupler was used to mimic ischaemia and thus to enhance the cellular content of lactate. Under these circumstances, intracellular lactate concentrations were found to have risen to ∼15 mM. This array system has the potential of simultaneous electrochemical and optical monitoring of extracellular and intracellular metabolites from single beating heart cells at a controlled metabolic state.
The potential of methane‐oxidizing bacteria for applications in environmental biotechnology
Authors: Wendlandt Karin‐Dagmar , Stottmeister Ulrich , Helm Jana , Soltmann Bettina , Jechorek Mirko , Beck Matthias 
Published: March 2010

AbstractMethanotrophic bacteria possess a unique set of enzymes enabling them to oxidize, degrade and transform organic molecules and synthesize new compounds. Therefore, they have great potential in environmental biotechnology. The application of these unique properties was demonstrated in three case studies: (i) Methane escaping from leaky gas pipes may lead to massive mortality of trees in urban areas. Lack of oxygen within the soil surrounding tree roots caused by methanotrophic activity was identified as one of the reasons for this phenomenon. The similarity between metabolic reactions performed by the key enzymes of methanotrophs (methane monooxygenase) and ammonium oxidizers (ammonium monooxygenase) might offer a solution to this problem by applying commercially available nitrification and urease inhibitors. (ii) Methanotrophs are able to co‐metabolically degrade contaminants such as low‐molecular‐weight‐chlorinated hydrocarbons in soil and water in the presence of methane. Batch and continuous trichloroethylene degradation experiments in laboratory‐scale reactors using Methylocystis sp. GB 14 were performed, partly with cells entrapped in a polymer matrix. (iii) Using a short, two‐stage pilot‐scale process, the intracellular polymer accumulation of poly‐β‐hydroxybutyrate (PHB) in methanotrophs reached a maximum of 52%. Interestingly, an ultra‐high‐molecular‐weight PHB of 3.1 MDa was accumulated under potassium deficiency. Under strictly controlled conditions (temperature, pH and methane supply) this process can be nonsterile because of the establishment of a stable microbial community (dominant species Methylocystis sp. GB 25 ≥86% by biomass). The possibility to substitute methane with biogas from renewable sources facilitates the development of a methane‐based PHB production process that yields a high‐quality biopolymer at competitive costs.
Analytical approach to Boussinesq equation with space‐ and time‐fractional derivatives
Authors: Yıldırım Ahmet , Sezer Sefa Anıl , Kaplan Yasemin 
Published: March 2010

AbstractIn this paper, the homotopy perturbation method (HPM) is developed to obtain approximate analytical solutions of a fractional Boussinesq equation with initial condition. The fractional derivatives are described in the Caputo sense. Some examples are given and comparisons are made, the comparisons show that the HPM is very effective and convenient and overcomes the difficulty of traditional methods. The numerical results show that the approaches are easy to implement and accurate when applied to space‐ and time‐fractional equations. Copyright © 2010 John Wiley & Sons, Ltd.
Deafferentation enhances neurogenesis in the young and middle aged hippocampus but not in the aged hippocampus
Authors: Shetty Ashok K. , Hattiangady Bharathi , Rao Muddanna S. , Shuai Bing 
Published: March 2010

AbstractIncreased neurogenesis in the dentate gyrus (DG) after brain insults such as excitotoxic lesions, seizures, or stroke is a well known phenomenon in the young hippocampus. This plasticity reflects an innate compensatory response of neural stem cells (NSCs) in the young hippocampus to preserve function or minimize damage after injury. However, injuries to the middle‐aged and aged hippocampi elicit either no or dampened neurogenesis response, which could be due to an altered plasticity of NSCs and/or the hippocampus with age. We examined whether the plasticity of NSCs to increase neurogenesis in response to a milder injury such as partial deafferentation is preserved during aging. We quantified DG neurogenesis in the hippocampus of young, middle‐aged, and aged F344 rats after partial deafferentation. A partial deafferentation of the left hippocampus without any apparent cell loss was induced via administration of Kainic acid (0.5 μg in 1.0 μl) into the right lateral ventricle of the brain. In this model, degeneration of CA3 pyramidal neurons and dentate hilar neurons in the right hippocampus results in loss of commissural axons which leads to partial deafferentation of the dendrites of dentate granule cells and CA1‐CA3 pyramidal neurons in the left hippocampus. Quantification of newly born cells that are added to the dentate granule cell layer at postdeafferentation days 4–15 using 5′‐bromodeoxyuridine (BrdU) labeling revealed greatly increased addition of newly born cells (∼three fold increase) in the deafferented young and middle‐aged hippocampi but not in the deafferented aged hippocampus. Measurement of newly born neurons using doublecortin (DCX) immunostaining also revealed similar findings. Analyses using BrdU‐DCX dual immunofluorescence demonstrated no changes in neuronal fate‐choice decision of newly born cells after deafferentation, in comparison to the age‐matched naive hippocampus in all age groups. Thus, the plasticity of hippocampal NSCs to increase DG neurogenesis in response to a milder injury such as partial hippocampal deafferentation is preserved until middle age but lost at old age. © 2010 Wiley‐Liss, Inc.
Overexpression of LSD1 contributes to human carcinogenesis through chromatin regulation in various cancers
Authors: Hayami Shinya , Kelly John D. , Cho Hyun‐Soo , Yoshimatsu Masanori , Unoki Motoko , Tsunoda Tatsuhiko , Field Helen I. , Neal David E. , Yamaue Hiroki , Ponder Bruce A.J. , Nakamura Yusuke , Hamamoto Ryuji 
Published: March 2010

AbstractA number of histone demethylases have been identified and biochemically characterized, but the pathological roles of their dysfunction in human disease like cancer have not been well understood. Here, we demonstrate important roles of lysine‐specific demethylase 1 (LSD1) in human carcinogenesis. Expression levels of LSD1 are significantly elevated in human bladder carcinomas compared with nonneoplastic bladder tissues (p < 0.0001). cDNA microarray analysis also revealed its transactivation in lung and colorectal carcinomas. LSD1‐specific small interfering RNAs significantly knocked down its expression and resulted in suppression of proliferation of various bladder and lung cancer cell lines. Concordantly, introduction of exogenous LSD1 expression promoted cell cycle progression of human embryonic kidney fibroblast cells. Expression profile analysis showed that LSD1 could affect the expression of genes involved in various chromatin‐modifying pathways such as chromatin remodeling at centromere, centromeric heterochromatin formation and chromatin assembly, indicating its essential roles in carcinogenesis through chromatin modification.