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171.
A magnitude code common to numerosities and number symbols in human intraparietal cortex 总被引:8,自引:0,他引:8
Activation of the horizontal segment of the intraparietal sulcus (hIPS) has been observed in various number-processing tasks, whether numbers were conveyed by symbolic numerals (digits, number words) or by nonsymbolic displays (dot patterns). This suggests an abstract coding of numerical magnitude. Here, we critically tested this hypothesis using fMRI adaptation to demonstrate notation-independent coding of numerical quantity in the hIPS. Once subjects were adapted either to dot patterns or to Arabic digits, activation in the hIPS and in frontal regions recovered in a distance-dependent fashion whenever a new number was presented, irrespective of notation changes. This remained unchanged when analyzing the hIPS peaks from an independent localizer scan of mental calculation. These results suggest an abstract coding of approximate number common to dots, digits, and number words. They support the idea that symbols acquire meaning by linking neural populations coding symbol shapes to those holding nonsymbolic representations of quantities. 相似文献
172.
Invasive pneumococcal disease in Portugal prior to and after the introduction of pneumococcal heptavalent conjugate vaccine 总被引:1,自引:0,他引:1
The rates of invasive pneumococcal disease (IPD), serotype distribution and antimicrobial susceptibility prior to and after the introduction of the heptavalent pneumococcal conjugate vaccine in Portuguese children were evaluated. The changes in incidence of IPD in children under 1 year old between the two periods of the study was not significant (P=0.53), despite the 21% decline. In children under 18 years old there was a 27.7% decrease in vaccine serotypes. All nonvaccine serotypes increased 71.4%. The decrease in vaccine serotypes was more impressive during the first year of life (-54.8%) than for children between 1 and 5 years of age (-19.1%). Among children under 1 year old, penicillin nonsusceptible isolates declined between the two periods of the study (47.2% vs. 25.0%) (P=0.03), as did those of cefotaxime and ceftriaxone nonsusceptible isolates. No changes were observed for isolates nonsusceptible to tetracycline and macrolides. The serotypes of these nonsusceptible isolates differed after the introduction of vaccine (P=0.01). Multiresistance increased 57.1% after the introduction of vaccine. Multiresistant isolates with vaccine serotype declined 42.9% (P<0.001), and nonvaccine serotypes appeared during the vaccination period (P<0.001). These findings suggest a replacement of vaccine serotypes by nonvaccine serotypes, mainly among nonsusceptible isolates. 相似文献
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175.
Gagliardi MC Lemassu A Teloni R Mariotti S Sargentini V Pardini M Daffé M Nisini R 《Cellular microbiology》2007,9(8):2081-2092
We previously described an escape mechanism exploited by Mycobacterium tuberculosis (Mtb) to prevent the generation of fully competent dendritic cells (DC). We have now tested the effect of isolated mycobacterial components on human monocyte differentiation into DC and demonstrated that cell wall (CW)-associated alpha-glucan induces monocytes to differentiate into DC (Glu-MoDC) with the same altered phenotype and functional behaviour of DC derived from Mtb-infected monocytes (Mt-MoDC). In fact, Glu-MoDC lack CD1 molecule expression, fail to upregulate CD80 and produce IL-10 but not IL-12. We also showed that Glu-MoDC are not able to prime effector T cells or present lipid antigens to CD1-restricted T-cell clones. Thus, we propose a mechanism of Mtb-monocyte interaction mediated by CW-associated alpha-glucan, which allows the bacterium to evade both innate and acquired immune responses. 相似文献
176.
Manuela Sironi Giorgia Menozzi Giacomo P Comi Matteo Cereda Rachele Cagliani Nereo Bresolin Uberto Pozzoli 《Genome biology》2007,7(12):R120
Background
Transposable elements (TEs) represent more than 45% of the human and mouse genomes. Both parasitic and mutualistic features have been shown to apply to the host-TE relationship but a comprehensive scenario of the forces driving TE fixation within mammalian genes is still missing. 相似文献177.
178.
The antibody-mediated targeted delivery of cytokines to sites of disease is a promising avenue for cancer therapy, but it
is largely unexplored for the treatment of chronic inflammatory conditions. Using both radioactive and fluorescent techniques,
the human monoclonal antibodies L19 and G11 (specific to two markers of angiogenesis that are virtually undetectable in normal
adult tissues) were found to selectively localize at arthritic sites in the murine collagen-induced model of rheumatoid arthritis
following intravenous (i.v.) administration. The same animal model was used to study the therapeutic action of the L19 antibody
fused to the cytokines IL-2, tumour necrosis factor (TNF) and IL-10. Whereas L19–IL-2 and L19–TNF treatment led to increased
arthritic scores and paw swellings, the fusion protein L19–IL-10 displayed a therapeutic activity, which was superior to the
activity of IL-10 fused to an antibody of irrelevant specificity in the mouse. The anti-inflammatory cytokine IL-10 has been
investigated for the treatment of patients with rheumatoid arthritis, but clinical development plans have been discontinued
because of a lack of efficacy. Because the antigen recognised by L19 is strongly expressed at sites of arthritis in humans
and identical in both mice and humans, it suggests that the fusion protein L19–IL-10 might help overcome some of the clinical
limitations of IL-10 and provide a therapeutic benefit to patients with chronic inflammatory disorders, including arthritis. 相似文献
179.
The redox enzyme phospholipid hydroperoxide glutathione peroxidase (PHGPx) has emerged as one of the most significant selenoenzymes in mammals, corroborated by early embryonic lethality of PHGPx null mice. PHGPx is one of five selenium-dependent glutathione peroxidases and the second glutathione peroxidase to be discovered in 1982. PHGPx has a particular position within this family owing to its peculiar structural and catalytic properties, its multifaceted roles during male gametogenesis, and its necessity for early mouse development. Interestingly, mice devoid of endogenous glutathione die at the same embryonic stage as PHGPx-deficient mice compatible with the hypothesis that a similar phenotype of embryonic lethality may be provoked by PHGPx deficiency and lack of its reducing substrate glutathione. Various gain- and loss-of-function approaches in mice have provided some insights into the physiological functions of PHGPx. These include a protective role for PHGPx in response to irradiation, increased resistance of transgenic PHGPx mice to toxin-induced liver damage, a putative role in various steps of embryogenesis, and a contribution to sperm chromatin condensation. The expression of three forms of PHGPx and early embryonic lethality call for more specific studies, such as tissue-specific disruption of PHGPx, to precisely understand the contribution of PHGPx to mammalian physiology and under pathological conditions. 相似文献
180.
Mutation in the Scyl1 gene encoding amino-terminal kinase-like protein causes a recessive form of spinocerebellar neurodegeneration
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Schmidt WM Kraus C Höger H Hochmeister S Oberndorfer F Branka M Bingemann S Lassmann H Müller M Macedo-Souza LI Vainzof M Zatz M Reis A Bittner RE 《EMBO reports》2007,8(7):691-697
Here, we show that the murine neurodegenerative disease mdf (autosomal recessive mouse mutant 'muscle deficient') is caused by a loss-of-function mutation in Scyl1, disrupting the expression of N-terminal kinase-like protein, an evolutionarily conserved putative component of the nucleocytoplasmic transport machinery. Scyl1 is prominently expressed in neurons, and enriched at central nervous system synapses and neuromuscular junctions. We show that the pathology of mdf comprises cerebellar atrophy, Purkinje cell loss and optic nerve atrophy, and therefore defines a new animal model for neurodegenerative diseases with cerebellar involvement in humans. 相似文献