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1. Blastic plasmacytoid dendritic cell neoplasm
2. 急性骨髄性白血病の分類 classification of acute myeloid leukemia

English Journal

Spatial memory extinction: A c-Fos protein mapping study.

Méndez-Couz M1, Conejo NM2, Vallejo G3, Arias JL1.Author information 1Laboratory of Neuroscience, Department of Psychology, Instituto de Neurociencias del Principado de Asturias (INEUROPA), University of Oviedo, Plaza Feijóo s/n, 33003 Oviedo, Spain.2Laboratory of Neuroscience, Department of Psychology, Instituto de Neurociencias del Principado de Asturias (INEUROPA), University of Oviedo, Plaza Feijóo s/n, 33003 Oviedo, Spain. Electronic address: conejonelida@uniovi.es.3Methodology Area, Department of Psychology, Instituto de Neurociencias del Principado de Asturias (INEUROPA), University of Oviedo, Plaza Feijóo s/n, 33003 Oviedo, Spain.AbstractWhile the neuronal basis of spatial memory consolidation has been thoroughly studied, the substrates mediating the process of extinction remain largely unknown. This study aimed to evaluate the functional contribution of selected brain regions during the extinction of a previously acquired spatial memory task in the Morris water maze. For that purpose, we used adult male Wistar rats trained in a spatial reference memory task. Learning-related changes in c-Fos inmunoreactive cells after training were evaluated in cortical and subcortical regions. Results show that removal of the hidden platform in the water maze induced extinction of the previously reinforced escape behavior after 16 trials, without spontaneous recovery 24h later. Extinction was related with significantly higher numbers of c-Fos positive nuclei in amygdala nuclei and prefrontal cortex. On the other hand, the lateral mammillary bodies showed higher number of c-Fos positive cells than the control group. Therefore, in contrast with the results obtained in studies of classical conditioning, we show the involvement of diencephalic structures mediating this kind of learning. In summary, our findings suggest that medial prefrontal cortex, the amygdala complex and diencephalic structures like the lateral mammillary nuclei are relevant for the extinction of spatial memory.
Behavioural brain research.Behav Brain Res.2014 Mar 1;260:101-10. doi: 10.1016/j.bbr.2013.11.032. Epub 2013 Dec 4.
While the neuronal basis of spatial memory consolidation has been thoroughly studied, the substrates mediating the process of extinction remain largely unknown. This study aimed to evaluate the functional contribution of selected brain regions during the extinction of a previously acquired spatial m
PMID 24315832

Repeated forced swim stress enhances CFA-evoked thermal hyperalgesia and affects the expressions of pCREB and c-Fos in the insular cortex.

Imbe H1, Kimura A2, Donishi T2, Kaneoke Y2.Author information 1Department of Physiology, Wakayama Medical University, Kimiidera 811-1, Wakayama City 641-8509, Japan. Electronic address: imbe@wakayama-med.ac.jp.2Department of Physiology, Wakayama Medical University, Kimiidera 811-1, Wakayama City 641-8509, Japan.AbstractStress affects brain activity and promotes long-term changes in multiple neural systems. Exposure to stressors causes substantial effects on the perception and response to pain. In several animal models, chronic stress produces lasting hyperalgesia. The insular (IC) and anterior cingulate cortices (ACC) are the regions exhibiting most reliable pain-related activity. And the IC and ACC play an important role in pain modulation via the descending pain modulatory system. In the present study we examined the expression of phospho-cAMP response element-binding protein (pCREB) and c-Fos in the IC and ACC after forced swim stress (FS) and complete Freund's adjuvant (CFA) injection to clarify changes in the cerebral cortices that affect the activity of the descending pain modulatory system in the rats with stress-induced hyperalgesia. FS (day 1, 10min; days 2-3, 20min) induced an increase in the expression of pCREB and c-Fos in the anterior IC (AIC). CFA injection into the hindpaw after the FS shows significantly enhanced thermal hyperalgesia and induced a decrease in the expression of c-Fos in the AIC and the posterior IC (PIC). Quantitative image analysis showed that the numbers of c-Fos-immunoreactive neurons in the left AIC and PIC were significantly lower in the FS+CFA group (L AIC, 95.9±6.8; L PIC, 181.9±23.1) than those in the naive group (L AIC, 151.1±19.3, p<0.05; L PIC, 274.2±37.3, p<0.05). These findings suggest a neuroplastic change in the IC after FS, which may be involved in the enhancement of CFA-induced thermal hyperalgesia through dysfunction of the descending pain modulatory system.
Neuroscience.Neuroscience.2014 Feb 14;259:1-11. doi: 10.1016/j.neuroscience.2013.11.045. Epub 2013 Nov 28.
Stress affects brain activity and promotes long-term changes in multiple neural systems. Exposure to stressors causes substantial effects on the perception and response to pain. In several animal models, chronic stress produces lasting hyperalgesia. The insular (IC) and anterior cingulate cortices (
PMID 24291670

Restoration of quinine-stimulated Fos-immunoreactive neurons in the central nucleus of the amygdala and gustatory cortex following reinnervation or cross-reinnervation of the lingual taste nerves in rats.

King CT, Garcea M, Spector AC.Author information Department of Psychology, Stetson University, DeLand, Florida, 32723.AbstractRemarkably, when lingual gustatory nerves are surgically re-routed to inappropriate taste fields in the tongue, some taste functions recover. We previously demonstrated that quinine-stimulated oromotor rejection reflexes and neural activity (assessed by Fos-immunoreactivity) in subregions of hindbrain gustatory nuclei were restored if the posterior tongue, which contains receptor cells that respond strongly to bitter compounds, was cross-reinnervated by the chorda tympani nerve. Such functional recovery was not seen if instead, the anterior tongue, where receptor cells are less responsive to bitter compounds, was cross-reinnervated by the glossopharyngeal nerve, despite that this nerve typically responds robustly to bitter substances. Thus, recovery depended more on the taste field being reinnervated than on the nerve itself. Here, the distribution of quinine-stimulated Fos-immunoreactive neurons in two taste-associated forebrain areas was examined in these same rats. In the central nucleus of the amygdala (CeA), a rostrocaudal gradient characterized the normal quinine-stimulated Fos response, with the greatest number of labeled cells rostrally situated. Quinine-stimulated neurons were found throughout the gustatory cortex but a 'hot spot' was observed in its anterior-posterior center in subregions approximating the dysgranular/agranular layers. Fos neurons here and in the rostral CeA were highly correlated with quinine-elicited gapes. Denervation of the posterior tongue eliminated, and its reinnervation by either nerve restored, numbers of quinine-stimulated labeled cells in the rostral-most CeA and in the subregion approximating dysgranular gustatory cortex. These results underscore the remarkable plasticity of the gustatory system and also help clarify the functional anatomy of neural circuits activated by bitter taste stimulation. J. Comp. Neurol., 2014. © 2014 Wiley Periodicals, Inc.
The Journal of comparative neurology.J Comp Neurol.2014 Jan 29. doi: 10.1002/cne.23546. [Epub ahead of print]
Remarkably, when lingual gustatory nerves are surgically re-routed to inappropriate taste fields in the tongue, some taste functions recover. We previously demonstrated that quinine-stimulated oromotor rejection reflexes and neural activity (assessed by Fos-immunoreactivity) in subregions of hindbra
PMID 24477770

Japanese Journal

Morphology and Nanostructure of Granular Materials Built from Nanoparticles

Castillo Jose L.,Martin Santiago,Rodriguez-Perez Daniel [他],Perea Alvaro,Garcia-Ybarra Pedro L.
KONA Powder and Particle Journal 31(0), 214-233, 2014
… Monte Carlo simulations have shownthat the morphological properties (bulk porosity and surface roughness) of agranular deposit can be tailored by properly adjusting the velocity of theparticles approaching the deposit. …
NAID 130003398569