Recurrent facial taste neurons of sea catfish Plotosus japonicus : morphology and organization in the ganglion

This study investigated the morphology of the recurrent facial taste neurons and their organization in the recurrent ganglion of the sea catfish Plotosus japonicus. The recurrent ganglion is independent of the anterior ganglion, which consists of trigeminal, facial and anterior lateral line neurons that send peripheral fibres to the head region. The recurrent taste neurons are round or oval and bipolar, with thick peripheral and thin central fibres, and completely wrapped by membranous layers of satellite cells. Two peripheral nerve branches coursing to the trunk or pectoral fin originate from the recurrent ganglion. The results presented here show that the trunk and pectoral-fin neurons are independently distributed to form various sizes of groups, and the groups are intermingled throughout the ganglion. No distinct topographical relationship of the two nerve branches occurs in the ganglion. Centrally, the trunk and pectoral-fin branches project somatotopically in the anterolateral and intermediate medial regions of the trunk tail lobule of the facial lobe, respectively

Nonequilibrium Current in the One Dimensional Hubbard Model at Half-Filling

Nonlinear transport in the one dimensional Hubbard model at half-filling under a finite bias voltage is investigated by the adaptive time-dependent density matrix renormalization group method. For repulsive on-site interaction, dielectric breakdown of the Mott insulating ground state to a current-carrying nonequilibrium steady state is clearly observed when the voltage exceeds the charge gap. It is found that by increasing the voltage further the current-voltage characteristics are scaled only by the charge gap and the scaling curve exhibits almost linear dependence on the voltage whose slope is suppressed by the electron correlation. In the case of attractive interaction the linear conductance is the perfect one $2e^2/h$ which agrees with the prediction by the Luttinger liquid theory.Comment: 4 pages, 7 figure

The Encoding of Temporally Irregular and Regular Visual Patterns in the Human Brain

In the work reported here, we set out to study the neural systems that detect predictable temporal patterns and departures from them. We used functional magnetic resonance imaging (fMRI) to locate activity in the brains of subjects when they viewed temporally regular and irregular patterns produced by letters, numbers, colors and luminance. Activity induced by irregular sequences was located within dorsolateral prefrontal cortex, including an area that was responsive to irregular patterns regardless of the type of visual stimuli producing them. Conversely, temporally regular arrangements resulted in activity in the right frontal lobe (medial frontal gyrus), in the left orbito-frontal cortex and in the left pallidum. The results show that there is an abstractive system in the brain for detecting temporal irregularity, regardless of the source producing it

The cytokine tumor necrosis factor-like weak inducer of apoptosis and its receptor fibroblast growth factor-inducible 14 have a neuroprotective effect in the central nervous system

<p>Abstract</p> <p>Background</p> <p>Cerebral cortical neurons have a high vulnerability to the harmful effects of hypoxia. However, the brain has the ability to detect and accommodate to hypoxic conditions. This phenomenon, known as preconditioning, is a natural adaptive process highly preserved among species whereby exposure to sub-lethal hypoxia promotes the acquisition of tolerance to a subsequent lethal hypoxic injury. The cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are found in neurons and their expression is induced by exposure to sub-lethal hypoxia. Accordingly, in this work we tested the hypothesis that the interaction between TWEAK and Fn14 induces tolerance to lethal hypoxic and ischemic conditions.</p> <p>Methods</p> <p>Here we used <it>in vitro </it>and <it>in vivo </it>models of hypoxic and ischemic preconditioning, an animal model of transient middle cerebral artery occlusion and mice and neurons genetically deficient in TWEAK, Fn14, or tumor necrosis factor alpha (TNF-α) to investigate whether treatment with recombinant TWEAK or an increase in the expression of endogenous TWEAK renders neurons tolerant to lethal hypoxia. We used enzyme-linked immunosorbent assay to study the effect of TWEAK on the expression of neuronal TNF-α, Western blot analysis to investigate whether the effect of TWEAK was mediated by activation of mitogen-activated protein kinases and immunohistochemical techniques and quantitative real-time polymerase chain reaction analysis to study the effect of TWEAK on apoptotic cell death.</p> <p>Results</p> <p>We found that either treatment with recombinant TWEAK or an increase in the expression of TWEAK and Fn14 induce hypoxic and ischemic tolerance <it>in vivo </it>and <it>in vitro</it>. This protective effect is mediated by neuronal TNF-α and activation of the extracellular signal-regulated kinases 1 and 2 pathway via phosphorylation and inactivation of the B-cell lymphoma 2-associated death promoter protein.</p> <p>Conclusions</p> <p>Our work indicate that the interaction between TWEAK and Fn14 triggers the activation of a cell signaling pathway that results in the induction of tolerance to lethal hypoxia and ischemia. These data indicate that TWEAK may be a potential therapeutic strategy to protect the brain from the devastating effects of an ischemic injury.</p

Autoimmune and autoinflammatory mechanisms in uveitis

The eye, as currently viewed, is neither immunologically ignorant nor sequestered from the systemic environment. The eye utilises distinct immunoregulatory mechanisms to preserve tissue and cellular function in the face of immune-mediated insult; clinically, inflammation following such an insult is termed uveitis. The intra-ocular inflammation in uveitis may be clinically obvious as a result of infection (e.g. toxoplasma, herpes), but in the main infection, if any, remains covert. We now recognise that healthy tissues including the retina have regulatory mechanisms imparted by control of myeloid cells through receptors (e.g. CD200R) and soluble inhibitory factors (e.g. alpha-MSH), regulation of the blood retinal barrier, and active immune surveillance. Once homoeostasis has been disrupted and inflammation ensues, the mechanisms to regulate inflammation, including T cell apoptosis, generation of Treg cells, and myeloid cell suppression in situ, are less successful. Why inflammation becomes persistent remains unknown, but extrapolating from animal models, possibilities include differential trafficking of T cells from the retina, residency of CD8(+) T cells, and alterations of myeloid cell phenotype and function. Translating lessons learned from animal models to humans has been helped by system biology approaches and informatics, which suggest that diseased animals and people share similar changes in T cell phenotypes and monocyte function to date. Together the data infer a possible cryptic infectious drive in uveitis that unlocks and drives persistent autoimmune responses, or promotes further innate immune responses. Thus there may be many mechanisms in common with those observed in autoinflammatory disorders

Turnip yellow mosaic virus in Chinese cabbage in Spain: Commercial seed transmission and molecular characterization

[EN] Seed transmission of Turnip yellow mosaic virus (TYMV, genus Tymovirus) was evaluated in the whole seeds and seedlings that emerged from three commercial Chinese cabbage (Brassica pekinensis) seed batches. Seedlings in the cotyledon stage and adult plants were assayed for TYMV by DAS-ELISA and confirmed by RT-PCR. The proportion of whole seeds infected with TYMV was at least 0.15 %. The seeds of the three seed batches were grown in Petri dishes, and surveyed in the cotyledon stage in trays that contained a peat:sand mixture grown in greenhouses or growth chambers, which were analysed in the cotyledon and adult stages. The seed-to-seedling transmission rate ranged from 2.5 % to 2.9 % in two different seed batches (lot-08 and lot-09, respectively). Spanish isolates derived from turnip (Sp-03) and Chinese cabbage (Sp-09 and Sp-13), collected in 2003, 2009 and 2013 in two different Spanish regions, were molecularly characterised by analysing the partial nucleotide sequences of three TYMV genome regions: partial RNA-dependent RNA polymerase (RdRp), methyltransferase (MTR) and coat protein (CP) genes. Phylogenetic analyses showed that the CP gene represented two different groups: TYMV-1 and TYMV-2. The first was subdivided into three subclades: European, Australian and Japanese. Spanish isolate Sp-03 clustered together with European TYMV group, whereas Sp-09 and Sp-13 grouped with the Japanese TYMV group, and all differed from group TYMV-2. The sequences of the three different genomic regions examined clustered into the same groups. The results suggested that Spanish isolates grouped according to the original hosts from which they were isolated. The inoculation of the Spanish TYMV isolates to four crucifer plants species (turnip, broccoli, Brunswick cabbage and radish) revealed that all the isolates infected turnip with typical symptoms, although differences were observed in other hosts.Alfaro Fernández, AO.; Serrano, A.; Tornos, T.; Cebrian Mico, MC.; Córdoba-Sellés, MDC.; Jordá, C.; Font San Ambrosio, MI. (2016). Turnip yellow mosaic virus in Chinese cabbage in Spain: Commercial seed transmission and molecular characterization. EUROPEAN JOURNAL OF PLANT PATHOLOGY. 146(2):433-442. doi:10.1007/s10658-016-0929-3S4334421462Assis Filho, M., & Sherwood, J. L. (2000). Evaluation of seed transmission of Turnip yellow mosaic virus and Tobacco mosaic virus in Arabidopsis thaliana. Phytopathology, 90, 1233–1238.Benetti, M. P., & Kaswalder, F. (1983). Trasmisione per seme del virus del mosaico giallo rapa. Annali dell Istituto Sperimentale per la Patologia Vegetale, 8, 67–70.Blok, J., Mackenzie, A., Guy, P., & Gibbs, A. (1987). Nucleotide sequence comparisons of Turnip yellow mosaic virus isolates from Australia and Europe. Archives of Virology, 97, 283–295.Brunt, A., Crabtree, K., Dallwitz, M., Gibbs, A., Watson, L., & Zurcher, E.J. (1996). Plant Viruses Online: Descriptions and Lists from the VIDE Database. Version: 20th August 1996. URL http://biology.anu.edu.au/Groups/MES/vide/ .Campbell, R. N., Wipf-Scheibel, C., & Lecoq, H. (1996). Vector-assissted seed transmission of melon necrotic spot virus in melon. Phytopathology, 86, 1294–1298.Dreher, T. W., & Bransom, K. L. (1992). Genomic RNA sequence of Turnip yellow mosaic virus isolate TYMC, a cDNA-based clone with verified infectivity. Plant Molecular Biology, 18, 403–406.Fakhro, A., Von Bargen, S., Bandte, M., Büttner, C., Franken, P., & Schwarz, D. (2011). Susceptibility of different plant species and tomato cultivars to two isolates of Pepino mosaic virus. European Journal of Plant Pathology, 129, 579–590.Gibbs, A. J., & Gower, J. C. (1960). The use of a multiple-transfer method in plant virus transmission studies: some statistical points arising in the analysis of results. Annals of Applied Biology, 48, 75–83.Hayden, C. M., Mackenzie, A. M., & Gibbs, A. J. (1998a). Virion protein sequence variation among Australian isolates of turnip yellow mosaic tymovirus. Archives of Virology, 143, 191–201.Hayden, C. M., Mackenzie, A. M., Skotnicki, M. L., & Gibbs, A. (1998b). Turnip yellow mosaic virus isolates with experimentally produced recombinant virion proteins. Journal of General Virology, 79, 395–403.Hein, A. (1984). Transmission of Turnip yellow mosaic virus through seed of Camelina sativa gold of pleasure. Journal of Plant Diseases and Protection, 91, 549–551.Herrera-Vásquez, J. A., Córdoba-Sellés, M. C., Cebrián, M. C., Alfaro-Fernández, A., & Jordá, C. (2009). Seed transmission of Melon necrotic spot virus and efficacy of seed-disinfection treatments. Plant Pathology, 58, 436–452.Hull, R. (2002). Matthews’ plant virology (4a ed.1001 pp). San Diego: Academic Press.Johansen, E., Edwards, M. C., & Hampton, R. O. (1994). Seed transmission of viruses: current perspectives. Annual Review of Phytopathology, 32, 363–386.Kirino, N., Inoue, K., Tanina, K., Yamazaki, Y., & Ohki, S. T. (2008). Turnip yellow mosaic virus isolated from Chinese cabbage in Japan. Journal of General Plant Pathology, 74, 331–334.Markham, R., & Smith, K. S. (1949). Studies on the virus of turnip yellow mosaic. Parasitology, 39, 330–342.Mathews, R. E. F. (1980). Turnip yellow mosaic virus, CMI/AAB Descriptions of plant virus No. 230 (No. 2 revised). Kew: Commonwealth Mycology Institute/Association of Applied Biologists.Mitchell, E. J., & Bond, J. M. (2005). Variation in the coat protein sequence of British isolates of Turnip yellow mosaic virus and comparison with previously published isolates. Archives of Virology, 150, 2347–2355.Pagán, I., Fraile, A., Fernández-Fueyo, E., Montes, N., Alonso-Blanco, C., & García-Arenal, F. (2010). Arabidopsis thaliana as a model for the study of plant-virus co-evolution. Philosophical Transations of the Royal Society Biological Sciences, 365, 1983–1995.Paul, H. L., Gibbs, A., & Wittman-Liebold, B. (1980). The relationships of certain Tymoviruses assessed from the amino acid composition of their coat proteins. Intervirology, 13, 99–109.Pelikanova, J. (1990). Garlic mustard a spontaneous host of TYMV. Ochrana Rostlin, 26, 17–22.Procházková, Z. (1980). Host range and symptom differences between isolates of Turnip mosaic virus obtained from Sisymbrium loeselii. Biologia Plantarum, 22, 341–347.Rimmer, S. R., Shtattuck, V. I., & Buchwaldt, L. (2007). Compendium of brassica diseases (1ª Edición ed.p. 117). USA: APS press.Rot, M. E., & Jelkman, W. (2001). Characterization and detection of several filamentous viruses of cherry: Adaptation of an alternative cloning method (DOP-PCR), and modification of an RNA extraction protocol. European Journal of Plant Pathology, 107, 411–420.Sabanadzovic, S., Abou-Ghanem, N., Castellano, M. A., Digiaero, M., & Martelli, G. P. (2000). Grapevine fleck virus-like in Vitis. Archives of Virology, 145, 553–565.Špack, J., & Kubelková, D. (2000). Serological variability among European isolates of Radish mosaic virus. Plant Pathology, 49, 295–301.Špack, J., Kubelková, D., & Hnilicka, E. (1993). Seed transmission of Turnip yellow mosaic virus in winter turnip and winter oilseed rapes. Annals of Applied Biology, 123, 33–35.Stobbs, L. W., Cerkauskas, R. F., Lowery, T., & VanDriel, L. (1998). Occurrence of Turnip yellow mosaic virus on oriental cruciferours vegetables in Southern Ontario, Canada. Plant Disease, 82, 351.Tamura, K., Peterson, D., Peterson, N., Stecher, G., Nei, M., & Kumar, S. (2011). 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Aurintricarboxylic acid prevents GLUR2 mRNA down-regulation and delayed neurodegeneration in hippocampal CA1 neurons of gerbil after global ischemia

Aurintricarboxylic acid (ATA), an inhibitor of endonuclease activity and other protein–nucleic acid interactions, blocks apoptosis in several cell types and prevents delayed death of hippocampal pyramidal CA1 neurons induced by transient global ischemia. Global ischemia in rats and gerbils induces down-regulation of GluR2 mRNA and increased α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-induced Ca(2+) influx in CA1 before neurodegeneration. This result and neuroprotection by antagonists of AMPA receptors suggests that formation of AMPA receptors lacking GluR2, and therefore Ca(2+) permeable, leads to excessive Ca(2+) influx in response to endogenous glutamate; the resulting delayed neuronal death in CA1 exhibits many characteristics of apoptosis. In this study, we examined the effects of ATA on expression of mRNAs encoding glutamate receptor subunits in gerbil hippocampus after global ischemia. Administration of ATA by injection into the right cerebral ventricle 1 h before (but not 6 h after) bilateral carotid occlusion prevented the ischemia-induced decrease in GluR2 mRNA expression and the delayed neurodegeneration. These findings suggest that ATA is neuroprotective in ischemia by blocking the transcriptional changes leading to down-regulation of GluR2, rather than by simply blocking endonucleases, which presumably act later after Ca(2+) influx initiates apoptosis. Maintaining formation of Ca(2+) impermeable, GluR2 containing AMPA receptors could prevent delayed death of CA1 neurons after transient global ischemia, and block of GluR2 down-regulation may provide a further strategy for neuroprotection

3D finite compartment modeling of formation and healing of bruises may identify methods for age determination of bruises

Simulating the spatial and temporal behavior of bruises may identify methods that allow accurate age determination of bruises to assess child abuse. We developed a numerical 3D model to simulate the spatial kinetics of hemoglobin and bilirubin during the formation and healing of bruises. Using this model, we studied how skin thickness, bruise diameter and diffusivities affect the formation and healing of circular symmetric bruises and compared a simulated bruise with a natural inhomogeneous bruise. Healing is faster for smaller bruises in thinner and less dense skin. The simulated and natural bruises showed similar spatial and temporal dynamics. The different spatio-temporal dynamics of hemoglobin and bilirubin allows age determination of model bruises. Combining our model predictions with individual natural bruises may allow optimizing our model parameters. It may particularly identify methods for more accurate age determination than currently possible to aid the assessment of child abuse