bluuebunny/crossref_metadata_2025_split huggingface dataset:
Patterns of grain‐size dependent sediment transport in low‐ordered, ephemeral channels
Authors: Yuill Brendan T. , Nichols Mary H. 
Published: June 2010

AbstractSediment data were analyzed to determine grain‐size dependant factors affecting sediment transport in a low‐ordered, ephemeral watershed. Sediment and flow samples were collected during 22 flow events at the outlet of a 4·53 ha sub‐watershed within the Walnut Gulch Experimental Watershed in south‐eastern Arizona. Measured concentrations ranged from 4191 to 115 045 mg l−1 and included grain sizes up to 8·0 mm in diameter. Two grain‐size dependent transport patterns were observed, that of the finer grain‐size fraction (approximately < 0·25 mm) and that of a coarser grain‐size fraction (approximately ≥ 0·25 mm). The concentration of the fine fraction decreased with flow duration, peaking near the beginning of a flow event and declining thereafter. The concentration of the fine fraction showed slight trends with season and recovery period. The concentration of the coarse fraction displayed a slight negative trend with instantaneous discharge and was not correlated with event duration. These patterns typically produced a condition where the majority of the fine fraction of the sediment yield was evacuated out of the watershed before the hydrograph peak while the majority of the coarser sediment was evacuated during the falling limb of the hydrograph. Each grain‐size dependent transport pattern was likely influenced by the source of the associated sediment. At the flow event time scale, the fines were primarily wash load, supplied from the hillslopes and the coarser grains were entrained from the channel bed. Because transport patterns differ based on grain size, attempts to define the total sediment concentration and sediment yield by the behavior of a single grain‐size fraction may lead to erroneous results, especially when a large range of sediment grain sizes are present. Copyright © 2010 John Wiley & Sons, Ltd.
Axonal integrity in the absence of functional peroxisomes from projection neurons and astrocytes
Authors: Bottelbergs Astrid , Verheijden Simon , Hulshagen Leen , Gutmann David H. , Goebbels Sandra , Nave Klaus‐Armin , Kassmann Celia , Baes Myriam 
Published: June 2010

AbstractAblation of functional peroxisomes from all neural cells in Nestin‐Pex5 knockout mice caused remarkable neurological abnormalities including motoric and cognitive malfunctioning accompanied by demyelination, axonal degeneration, and gliosis. An oligodendrocyte selective Cnp‐Pex5 knockout mouse model shows a similar pathology, but with later onset and slower progression. Until now, the link between these neurological anomalies and the known metabolic alterations, namely the accumulation of very long‐chain fatty acids (VLCFA) and reduction of plasmalogens, has not been established. We now focused on the role of peroxisomes in neurons and astrocytes. A neuron‐specific peroxisome knockout model, NEX‐Pex5, showed neither microscopic nor metabolic abnormalities indicating that the lack of functional peroxisomes within neurons does not cause axonal damage. Axonal integrity and normal behavior was also preserved when peroxisomes were deleted from astrocytes in GFAP‐Pex5−/− mice. Nevertheless, peroxisomal metabolites were dysregulated in brain including a marked accumulation of VLCFA and a slight reduction in plasmalogens. Interestingly, despite minor targeting of oligodendrocytes in GFAP‐Pex5−/− mice, these metabolic perturbations were also present in isolated myelin indicating that peroxisomal metabolites are shuttled between different brain cell types. We conclude that absence of peroxisomal metabolism in neurons and astrocytes does not provoke the neurodegenerative phenotype observed after deleting peroxisomes from oligodendrocytes. Lack of peroxisomal metabolism in astrocytes causes increased VLCFA levels in myelin, but this has no major impact on neurological functioning. © 2010 Wiley‐Liss, Inc.
Organization of glial cells in the adult sea cucumber central nervous system
Authors: Mashanov Vladimir S. , Zueva Olga R. , Garcia‐Arraras Jose E. 
Published: June 2010

AbstractThe nervous system of echinoderms has long been considered too unique to be directly comparable to the nervous system of other Deuterostomia. Using two novel monoclonal antibodies in combination with epifluorescence, confocal, and electron microscopy, we demonstrate here that the central nervous system of the sea cucumber Holothuria glaberrima possesses a major non‐neuronal cell type, which shares striking similarities with the radial glia of chordates. The basic features in common include (a) an elongated shape, (b) long radial processes, (c) short lateral protrusions branching off the main processes and penetrating into the surrounding neuropile, (d) prominent orderly oriented bundles of intermediate filaments, and (e) ability to produce Reissner's substance. Radial glia account for the majority of glia cells in echinoderms and constitutes more than half of the total cell population in the radial nerve cord and about 45% in the circumoral nerve ring. The difference in glia cell number between those regions is significant, suggesting structural specialization within the seemingly simple echinoderm nervous system. Both cell death and proliferation are seen under normal physiological conditions. Although both glia and neurons undergo apoptosis, most of the mitotic cells are identified as radial glia, indicating a key role of this cell type in cell turnover in the nervous system. A hypothesis is proposed that the radial glia could be an ancestral feature of the deuterostome nervous system, and the origin of this cell type might have predated the diversification of the Chordata and Ambulacraria lineages. © 2010 Wiley‐Liss, Inc.
Dynamic expression of Cx47 in mouse brain development and in the cuprizone model of myelin plasticity
Authors: Parenti Rosalba , Cicirata Federico , Zappalà Agata , Catania Angela , La Delia Francesco , Cicirata Valentina , Tress Oliver , Willecke Klaus 
Published: June 2010

AbstractThe study shows the dynamic expression of connexin47 (Cx47) in oligodendrocytes and myelin of mice, either in myelinogenesis occurring in early development or in an experimental model of new‐myelinogenesis of adult mice. Cx47 first appeared in the embryonic mouse brain at E10.5 successively the expression increased, principally in regions populated by developing oligodendrocytes. The expression declined postnatally toward adulthood and immunoreactivity was restricted to a few specific areas, such as the corpus callosum, the striatum, the cerebellum, and the spinal cord. Since the expression of Cx47 in developing oligodendrocytes preceded those of Cx32 and Cx29, a role of Cx47 in myelinogenesis was postulated. This hypothesis was tested in a model of re‐myelination, which principally involved the corpus callosum, occurring in adult mice by treatment with cuprizone. Cx47 was upregulated during demyelination and recovered during the remyelination phase. During demyelination, Cx47 was first over‐expressed in the corpus callosum and later, when the myelin virtually disappeared in the injured areas, Cx47 was expressed in astrocytes located inside and closely around the demyelinated areas. The remyelination of injured areas occurred after stopping the administration of cuprizone and continued to complete recovery. In this period the expression of Cx47 shifted from astrocytes to newly‐formed myelin. Thus, Cx47 exhibits in this model a transient and de novo expression in astrocytes with a topographic segregation in the injured areas, only when oligodendrocytes and the myelin were most severely affected. Taken as a whole the evidence suggests that Cx47 play a key role in myelination. © 2010 Wiley‐Liss, Inc.
Toll‐like receptor expression in the peripheral nerve
Authors: Goethals Sofie , Ydens Elke , Timmerman Vincent , Janssens Sophie 
Published: June 2010

AbstractToll‐like receptors comprise a family of evolutionary conserved pattern recognition receptors that act as a first defense line in the innate immune system. Upon stimulation with microbial ligands, they orchestrate the induction of a host defense response by activating different signaling cascades. Interestingly, they appear to detect the presence of endogenous signals of danger as well and as such, neurodegeneration is thought to trigger an immune response through ligation of TLRs. Though recent data report the expression of various TLRs in the central nervous system, TLR expression patterns in the peripheral nervous system have not been determined yet. We observed that Schwann cells express relatively high levels of TLRs, with especially TLR3 and TLR4 being prominent. Sensory and motor neurons hardly express TLRs at all. Through the use of NF‐κB signaling as read‐out, we could show that all TLRs are functional in Schwann cells and that bacterial lipoprotein, a ligand for TLR1/TLR2 receptors yields the strongest response. In sciatic nerve, basal levels of TLRs closely reflect the expression patterns as determined in Schwann cells. TLR3, TLR4, and TLR7 are majorly expressed, pointing to their possible role in immune surveillance. Upon axotomy, TLR1 becomes strongly induced, while most other TLR expression levels remain unaffected. Altogether, our data suggest that similar to microglia in the brain, Schwann cells might act as sentinel cells in the PNS. Furthermore, acute neurodegeneration induces a shift in TLR expression pattern, most likely illustrating specialized functions of TLRs in basal versus activated conditions of the peripheral nerve. © 2010 Wiley‐Liss, Inc.
GSK3β overexpression induces neuronal death and a depletion of the neurogenic niches in the dentate gyrus
Authors: Sirerol‐Piquer MaSalomé , Gomez‐Ramos Pilar , Hernández Félix , Perez Mar , Morán María A. , Fuster‐Matanzo Almudena , Lucas José J. , Avila Jesús , García‐Verdugo Jose Manuel 
Published: June 2010

AbstractOverexpression of GSK3β in transgenic mice induces learning deficits and some features associated with Alzheimer's disease (AD), including dentate gyrus (DG) atrophy. Here, we assessed whether these mice also recapitulate DG atrophy as well as impaired neurogenesis reported in AD. Ultrastructural analysis revealed that there were fewer and more disorganized neurogenic niches in these animals, coupled with an increase in the proportion of immature neurons. Indeed, the maturation of granule cells is delayed as witnessed by the alterations to the length and patterning of their dendritic trees and to the mossy fiber terminals. Together with an increase in neuronal death, these phenomena lead to a marked decrease in the number and disorganization of granule cells of the DG. Our results suggest that GSK3β overexpression perturbs proliferation and maturation, resulting in the loss of immature neurons. In turn, the activation of microglia is stimulated in conjunction with a decrease in the birth of new functional neurons, leading to the deterioration of this structure. These data support the idea that by inducing degeneration of the DG, GSK3β could be involved in the pathogenesis of AD. © 2010 Wiley‐Liss, Inc.
Projections to the anterodorsal thalamus and lateral mammillary nuclei arise from different cell populations within the postsubiculum: Implications for the control of head direction cells
Authors: Yoder Ryan M. , Taube Jeffrey S. 
Published: June 2010

AbstractThe neural representation of directional heading is encoded by a population of cells located in a circuit that includes the postsubiculum (PoS), anterodorsal thalamus (ADN), and lateral mammillary nuclei (LMN). Throughout this circuit, many cells rely on both movement‐ and landmark‐related information to discharge as a function of the animal's directional heading. The PoS projects to both the ADN and LMN, and these connections may convey critical spatial information about landmarks, because lesions of the PoS disrupt landmark control in head direction (HD) cells and hippocampal place cells [Goodridge and Taube (1997) J Neurosci 17:9315–9330; Calton et al. (2003) J Neurosci 23:9719–9731]. The PoS → ADN projection originates in the deep layers of PoS, but no studies have determined whether the PoS → LMN projection originates from the same cells that project to ADN. To address this issue, two distinct cholera toxin‐subunit B (CTB) fluorophore conjugates (Alexa Fluor 488 and Alexa Fluor 594) were injected into the LMN and ADN of the same rats, and PoS sections were examined for cell bodies containing either or both CTB conjugates. Results indicated that the PoS → LMN projection originates exclusively from a thin layer of cells located superficial to the layer(s) of PoS → ADN projection cells, with no overlap. To verify the laminar distribution and morphological characteristics of PoS → LMN and PoS → ADN cells, biotinylated dextran amine was injected into LMN or ADN of different rats, and tissue sections were counterstained with thionin. Results indicated that the PoS → LMN projection arises from large pyramidal cells in layer IV, whereas the PoS → ADN projection arises from a heterogeneous cell population in layers V/VI. This study provides the first evidence that the PoS → ADN and PoS → LMN projections arise from distinct, nonoverlapping cell layers in PoS. Functionally, the PoS may provide landmark information to HD cells in LMN. © 2010 Wiley‐Liss, Inc.
Behavior abnormality following intravenous immunoglobulin treatment in patients with primary antibody deficiencies
Authors: Saroukhani Sepide , Aghamohammadi Asghar , Mahmoudi‐Gharaei Javad , Abolhassani Hassan , Cheraghi Taher , Imanzadeh Amir , Moazzami Kasra , Parvaneh Nima , Rezaei Nima 
Published: June 2010

AbstractObjectiveTreatment with intravenous immunoglobulin (IVIG) is considered a safe therapy for patients with primary antibody deficiencies (PADs), whilst adverse effects have been frequently reported. Meantime behavioral disorders reactions have not been reported yet. In this study, we describe for the first time a group of patients with PADs, who were under IVIG therapy and experienced some behavioral disorders.MethodsFive patients, including two hyper IgM syndromes, one X‐linked agammaglobulinemia, one common variable immunodeficiency, and one hypo IgM disease, were surveyed. Analysis of Conner's Parents Rating Scales‐Revised Short (CPRS‐R:S) and child behavior checklist (CBCL) was performed for the patients, suspected to hyperactivity.ResultsAnalysis of CPRS‐R:S showed an evidence of mild hyperactivity before IVIG administration in four patients, whereas another patient had evidence of severe hyperactivity. After IVIG administration, hyperactivity scores of three patients were changed from mild hyperactive behavior to markedly hyperactive behavior or attention deficit hyperactivity disorder range of hyperactivity. In the CBCL scores, there were abnormal externalization scores for three patients; while two remaining patients had abnormal internalization scores.ConclusionsAlthough predisposition to behavioral disorders can be due to a genetic background, further investigations are necessary to test the hypotheses about responsibility of either IVIG or underling disease in progression of behavioral abnormalities. Copyright © 2010 John Wiley & Sons, Ltd.
Suicide inactivation of the diphenolase and monophenolase activities of tyrosinase
Authors: Muñoz‐Muñoz Jose Luis , Garcia‐Molina Francisco , Varon Ramon , Garcia‐Ruíz Pedro A. , Tudela Jose , Garcia‐Cánovas Francisco , Rodríguez‐López Jose Neptuno 
Published: June 2010

AbstractThe suicide inactivation mechanism of tyrosinase acting on its phenolic substrates has been studied. Kinetic analysis of the proposed mechanism during the transition phase provides explicit analytical expressions for the concentrations of o‐quinone versus time. The electronic, steric, and hydrophobic effects of the phenolic substrates influence the enzymatic reaction, increasing the catalytic speed by three orders of magnitude and the inactivation by one order of magnitude. To explain this suicide inactivation, we propose a mechanism in which the enzymatic form oxy‐tyrosinase is responsible for the inactivation. In this mechanism, the rate constant of the reaction would be directly related with the strength of the nucleophilic attack of the C‐1 hydroxyl group, which depends on the chemical shift of the carbon C‐1 (δ1) obtained by 13C‐NMR. The suicide inactivation would occur if the C‐2 hydroxyl group transferred the proton to the protonated peroxide, which would again act as a general base. In this case, the coplanarity between the copper atom, the oxygen of the C‐1 and the ring would only permit the oxidation/reduction of one copper atom, giving rise to copper (0), hydrogen peroxide, and an o‐quinone, which would be released, thus inactivating the enzyme. One possible application of this property could be the use of these suicide substrates as skin depigmenting agents. © 2010 IUBMB IUBMB Life 62(7): 539–547, 2010
The mitochondrial bioenergetic capacity of carcinomas
Authors: Formentini Laura , Martínez‐Reyes Inmaculada , Cuezva José M. 
Published: June 2010

AbstractMetabolic reprogramming of cancer cells is a phenotypic trait necessary to promote proliferation and survival. Despite past controversies, recent transcriptomic, proteomic, functional and structural studies of mitochondria of the cancer cell indicate that an impaired biogenesis and activity of the organelle is required for the development of some tumors. Cancer aggressiveness can be estimated by its bioenergetic signature, a protein ratio that correlates the expression of β‐F1‐ATPase of oxidative phosphorylation relative to the glycolytic GAPDH. The bioenergetic signature also provides a gauge that informs of the metabolic activity of tumors and cancer cells as well as of the response to chemotherapy. The convergence of different epithelial tumors on the same bioenergetic signature supports that it provides an important tool and common target for cancer therapy. We stress that targeting the energetic metabolism of tumors affords a valuable strategy to combat the disease. © 2010 IUBMB IUBMB Life 62(7): 554–560, 2010
The polarity of the amino acid residue 118 of calcineurin B is closely linked to calcineurin enzyme activity
Authors: Chen Qing , Wu Wu , Li Jing , Wei Qun 
Published: June 2010

AbstractCalcineurin(Cn), a multifunctional regulator expressed in several tissues and organs, consists of CnA (catalytic subunit) and CnB (regulatory subunit). The crystal structure shows that the hydrophobic groove formed by 118–123 residues of CnB is necessary for its interactions with two different immunosuppressant‐immunophilin complexes and with CnA. In this report, we focus on Met118 of CnB to study the association between conformational states of CnB and the phosphatase activity of Cn. We found that hydrophobicity in the region around site118 of CnB is essential for the Cn activity. Polar mutants significantly weakened the enzymatic activity compared with the nonpolar ones. The data showed that some modest alterations in the vicinity of site118 impaired the integrality and compactness of hydrophobic microenvironment, and this might explain why CnB mutants defective in hydrophobicity failed in activating Cn. This requirement of hydrophobic microenvironment around site118 in CnB suggests that, besides the mutations in the catalytic subunit CnA, which impairs Cn phosphatase activity, and had been identified to be associated with diseases such as Alzheimer's disease (AD), the mutations in CnB might also affect Cn enzymatic activityin vivo, and this might be helpful for our further research on mechanisms of diseases associated with Cn. © 2010 IUBMB IUBMB Life 62(7): 561–567, 2010
FT‐IR spectroscopy in diagnosis of diabetes in rat animal model
Authors: Severcan Feride , Bozkurt Ozlem , Gurbanov Rafig , Gorgulu Guvenc 
Published: June 2010

AbstractIn recent years, Fourier Transform Infrared (FT‐IR) spectroscopy has had an increasingly important role in the field of pathology and diagnosis of disease states. In the current study, FT‐IR spectroscopy together with cluster analysis were used as a diagnostic tool in the discrimination of diabetic samples from control ones in rat kidney plasma membrane apical sides (brush‐border membranes), liver microsomal membranes and Extensor digitorum longus (EDL) and Soleus (SOL) skeletal muscle tissues.A variety of alterations in the spectral parameters, such as frequency and signal intensity/area was observed in diabetic tissues and membranes compared to the control samples. Based on these spectral variations, using cluster analysis successful differentiation between diabetic and control groups was obtained in different spectral regions. The results of this current study further revealed the power and sensitivity of FT‐IR spectroscopy in precise and automated diagnosis of diabetes. (© 2010 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Image enhancement in ultramicroscopy by improved laser light sheets
Authors: Saghafi Saiedeh , Becker Klaus , Jährling Nina , Richter Melanie , Kramer Edgar R. , Dodt Hans‐Ulrich 
Published: June 2010

AbstractIn the majority of implementations of light sheet microscopy, such as ultramicroscopy, the laser beam illuminating the specimen is truncated by a slit aperture before it is focused to a light sheet by a single cylindrical lens. A light sheet generated in this way can be made very thin near to the focal point, but unfortunately its Rayleigh range is severely limited. This problem can be partially solved by using a smaller slit aperture. However, this also causes a major loss in power, a severe broadening of the beam waist, and thus a significant loss of resolution along the detection axis. We developed improved light‐sheet‐generation optics, which provide longer Raleigh ranges, whilst retaining beam waists comparable to our standard system with one cylindrical lens. Using the modified system we achieved a marked improvement in the resolution of ultramicroscopy reconstructions of representative biological specimens. (© 2010 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Fish consumption, bone mineral density, and risk of hip fracture among older adults: The cardiovascular health study
Authors: Virtanen Jyrki K , Mozaffarian Dariush , Cauley Jane A , Mukamal Kenneth J , Robbins John , Siscovick David S 
Published: June 2010

Abstract
Marine n-3 polyunsaturated fatty acids (PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) may be beneficial for bone health, but few studies have investigated the association with fish consumption. Our aim was to study associations of fish and EPA + DHA consumption with bone mineral density (BMD) and hip fracture risk and determine whether high linoleic acid (LA) intake, the major dietary n-6 PUFA, modifies the associations. The study population consisted of 5045 participants aged 65 years and older from the Cardiovascular Health Study. Data on BMD were available for 1305 participants. Food-frequency questionnaire was used to assess dietary intake, and hip fracture incidence was assessed prospectively by review of hospitalization records. After multivariable adjustment, femoral neck BMD was 0.01 g/cm2 lower in the highest versus lowest tuna/other-fish intake category (p = .05 for trend). EPA + DHA intake (higher versus lower median of 0.32 g/day) was associated with lower femoral neck BMD (0.66 versus 0.71 g/cm2, p &lt; .001) among those with LA intake greater than the median 12.1 g/day (p = .03 for interaction). No significant associations were found with total-hip BMD. During mean follow-up of 11.1 years, 505 hip fractures occurred. Fish or EPA + DHA consumption was not significantly associated with fracture incidence [hazard ratio (HR) for extreme categories: HR = 1.23, 95% confidence interval (CI) 0.83–1.84 for tuna/other fish; HR = 1.16, 95% CI 0.91–1.49 for fried fish; and HR = 0.98, 95% CI 0.71–1.36 for EPA + DHA]. High LA intake did not modify these associations. In this large prospective cohort of older adults, fish consumption was associated with very small differences in BMD and had no association with hip fracture risk. © 2010 American Society for Bone and Mineral Research.