Memórias, criação e autoria no Design Contemporâneo

Este artigo apresenta e discute a presença da memória e sua relação com a criação e a autoria no design contemporâneo tanto no universo profissional quanto na formação superior em design a partir de discussões teóricas, análises e exemplos de ações, produtos, objetos e um projeto de ensino-aprendizagem de caráter interdisciplinar com o tema memória

Pulverização de glyphosate utilizando solução de uréia + sulfato de amônio

Several trials have been carried out for increasing glyphosate efficacy on weed burndown, including the addiction of ammonium sulfate and urea as adjuvants. On a physiological approach, there are explanations to complementary effect of these fertilizers when concomitantly added to herbicide spray solution. Therefore, three experiments were developed in field conditions with the objective of evaluating glyphosate efficacy for burning down different weed species by using solution of nitrogen fertilizers as spraying vehicles. Six treatments were evaluated, as follows: glyphosate (540 g a.e. ha-1) application using water, solution of ammonium sulfate – AMS (15 g L-1), solution of urea – U (5 g L-1), solution of U+AMS (2.5 + 7.5 g L-1) as spraying vehicles, glyphosate at 1080 g a.e. ha-1 sprayed with water, and check without application. Treatment’s efficacy was evaluated on mixed community of weeds, Brachiaria decumbens and Sorghum halepense. The use of nitrogen fertilizer solutions as glyphosate spraying vehicles did not increase B. decumbens control. The lower rate of glyphosate had higher efficacy over mixed weed community and over S. halepense due to the use of ammonium sulfate (15 g L-1) or U+AMS (2,5 + 7,5 g L-1) solution as spraying vehicles. The positive results reached after glyphosate application with nitrogen fertilizers were also observed on the reduction of the mixed weed community fresh mass and for S. halepense fresh and dry mass.Diversos experimentos têm sido realizados com intuito de elevar a eficácia do herbicida glyphosate na dessecação de plantas daninhas, incluindo-se o uso de sulfato de amônio ou ureia como adjuvantes. Em termos fisiológicos, existem explicações para o efeito complementar destes produtos quando adicionados concomitantemente à calda herbicida. Desta forma, três experimentos foram desenvolvidos em campo com o objetivo de avaliar a eficácia do herbicida glyphosate para dessecação de espécies de plantas daninhas utilizando solução de fertilizantes nitrogenados como veículos de pulverização. Foram avaliados seis tratamentos, sendo estes: aplicação de glyphosate (540 g e.a. ha-1) utilizando água, solução de sulfato de amônio – SA (15 g L-1), solução de uréia – U (5 g L-1), solução de U+SA (2,5 + 7,5 g L-1) como veículos de pulverização, glyphosate a 1080 g e.a. ha-1 aplicado com água, e testemunha sem aplicação. Avaliou-se a eficácia dos tratamentos sobre comunidade mista de plantas daninhas, Brachiaria decumbens e Sorghum halepense. O uso de solução de fertilizantes nitrogenados como veículo para pulverização do glyphosate não elevou o controle de B. decumbens. A menor dose do herbicida glyphosate teve maior eficácia sobre a comunidade mista de plantas daninhas e sobre S. halepense devido à pulverização com solução de SA (15 g L-1) ou de U+SA (2,5 + 7,5 g L-1). Os resultados positivos obtidos pela aplicação de glyphosate com fertilizantes nitrogenados também foram observados para a redução de massa fresca da comunidade mista e para massa fresca e seca de S. halepense

Ischemic neurons recruit natural killer cells that accelerate brain infarction

Brain ischemia and reperfusion activate the immune system. The abrupt development of brain ischemic lesions suggests that innate immune cells may shape the outcome of stroke. Natural killer (NK) cells are innate lymphocytes that can be swiftly mobilized during the earliest phases of immune responses, but their role during stroke remains unknown. Herein, we found that NK cells infiltrated the ischemic lesions of the human brain. In a mouse model of cerebral ischemia, ischemic neuron-derived fractalkine recruited NK cells, which subsequently determined the size of brain lesions in a T and B cell-independent manner. NK cell-mediated exacerbation of brain infarction occurred rapidly after ischemia via the disruption of NK cell tolerance, augmenting local inflammation and neuronal hyperactivity. Therefore, NK cells catalyzed neuronal death in the ischemic brain

Role of Fractalkine/CX3CR1 Interaction in Light-Induced Photoreceptor Degeneration through Regulating Retinal Microglial Activation and Migration

Background: Excessive exposure to light enhances the progression and severity of some human retinal degenerative diseases. While retinal microglia are likely to be important in neuron damage associated with these diseases, the relationship between photoreceptor damage and microglial activation remains poorly understood. Some recent studies have indicated that the chemokine fractalkine is involved in the pathogenesis of many neurodegenerative diseases. The present study was performed to investigate the cross-talk between injured photoreceptors and activated retinal microglia, focusing on the role of fractalkine and its receptor CX3CR1 in light-induced photoreceptor degeneration. Methodology/Principal Findings: Both in vivo and in vitro experiments were involved in the research. In vivo, Sprague– Dawley rats were exposed to blue light for 24 hours. In vitro, the co-culture of primary retinal microglia and a photoreceptor cell line (661W cell) was exposed to blue light for five hours. Some cultures were pretreated by the addition of anti-CX3CR1 neutralizing antibody or recombinant fractalkine. Expression of fractalkine/CX3CR1 and inflammatory cytokines was detected by immunofluorescence, real-time PCR, Western immunoblot analysis, and ELISA assay. TUNEL method was used to detect cell apoptosis. In addition, chemotaxis assay was performed to evaluate the impact of soluble fractalkine on microglial migration. Our results showed that the expression of fractalkine that was significantly upregulated after exposure to light, located mainly at the photoreceptors. The extent of photoreceptor degeneration and microglial migratio

Adjunctive Dexamethasone Affects the Expression of Genes Related to Inflammation, Neurogenesis and Apoptosis in Infant Rat Pneumococcal Meningitis

Streptococcus pneumoniae is the most common pathogen causing non-epidemic bacterial meningitis worldwide. The immune response and inflammatory processes contribute to the pathophysiology. Hence, the anti-inflammatory dexamethasone is advocated as adjuvant treatment although its clinical efficacy remains a question at issue. In experimental models of pneumococcal meningitis, dexamethasone increased neuronal damage in the dentate gyrus. Here, we investigated expressional changes in the hippocampus and cortex at 72 h after infection when dexamethasone was given to infant rats with pneumococcal meningitis. Nursing Wistar rats were intracisternally infected with Streptococcus pneumoniae to induce experimental meningitis or were sham-infected with pyrogen-free saline. Besides antibiotics, animals were either treated with dexamethasone or saline. Expressional changes were assessed by the use of GeneChip® Rat Exon 1.0 ST Arrays and quantitative real-time PCR. Protein levels of brain-derived neurotrophic factor, cytokines and chemokines were evaluated in immunoassays using Luminex xMAP® technology. In infected animals, 213 and 264 genes were significantly regulated by dexamethasone in the hippocampus and cortex respectively. Separately for the cortex and the hippocampus, Gene Ontology analysis identified clusters of biological processes which were assigned to the predefined categories “inflammation”, “growth”, “apoptosis” and others. Dexamethasone affected the expression of genes and protein levels of chemokines reflecting diminished activation of microglia. Dexamethasone-induced changes of genes related to apoptosis suggest the downregulation of the Akt-survival pathway and the induction of caspase-independent apoptosis. Signalling of pro-neurogenic pathways such as transforming growth factor pathway was reduced by dexamethasone resulting in a lack of pro-survival triggers. The anti-inflammatory properties of dexamethasone were observed on gene and protein level in experimental pneumococcal meningitis. Further dexamethasone-induced expressional changes reflect an increase of pro-apoptotic signals and a decrease of pro-neurogenic processes. The findings may help to identify potential mechanisms leading to apoptosis by dexamethasone in experimental pneumococcal meningitis

Neuronal Chemokines: Versatile Messengers In Central Nervous System Cell Interaction

Whereas chemokines are well known for their ability to induce cell migration, only recently it became evident that chemokines also control a variety of other cell functions and are versatile messengers in the interaction between a diversity of cell types. In the central nervous system (CNS), chemokines are generally found under both physiological and pathological conditions. Whereas many reports describe chemokine expression in astrocytes and microglia and their role in the migration of leukocytes into the CNS, only few studies describe chemokine expression in neurons. Nevertheless, the expression of neuronal chemokines and the corresponding chemokine receptors in CNS cells under physiological and pathological conditions indicates that neuronal chemokines contribute to CNS cell interaction. In this study, we review recent studies describing neuronal chemokine expression and discuss potential roles of neuronal chemokines in neuron–astrocyte, neuron–microglia, and neuron–neuron interaction

Defective microglial development in the hippocampus of Cx3cr1 deficient mice

Microglial cells participate in brain development and influence neuronal loss and synaptic maturation. Fractalkine is an important neuronal chemokine whose expression increases during development and that can influence microglia function via the fractalkine receptor, CX3CR1. Mice lacking Cx3cr1 show a variety of neuronal defects thought to be the result of deficient microglia function. Activation of CX3CR1 is important for the proper migration of microglia to sites of injury and into the brain during development. However, little is known about how fractalkine modulates microglial properties during development. Here we examined microglial morphology, response to ATP, and K(+) current properties in acute brain slices from Cx3cr1 knockout mice across postnatal hippocampal development. We found that fractalkine signaling is necessary for the development of several morphological and physiological features of microglia. Specifically, we found that the occurrence of an outward rectifying K(+) current, typical of activated microglia, that peaked during the second and third postnatal week, was reduced in Cx3cr1 knockout mice. Fractalkine signaling also influenced microglial morphology and ability to extend processes in response to ATP following its focal application to the slice. Our results reveal the developmental profile of several morphological and physiological properties of microglia and demonstrate that these processes are modulated by fractalkine signaling

Combining Galantamine and Memantine in Multitargeted, New Chemical Entities Potentially Useful in Alzheimer’s Disease

Herein we report on a novel series of multitargeted compounds obtained by linking together galantamine and memantine. The compounds were designed by taking advantage of the crystal structures of acetylcholinesterase (AChE) in complex with galantamine derivatives. Sixteen novel derivatives were synthesized, using spacers of different lengths and chemical composition. The molecules were then tested as inhibitors of AChE and as binders of the N-methyl-d-aspartate (NMDA) receptor (NMDAR). Some of the new compounds were nanomolar inhibitors of AChE and showed micromolar affinities for NMDAR. All compounds were also tested for selectivity toward NMDAR containing the 2B subunit (NR2B). Some of the new derivatives showed a micromolar affinity for NR2B. Finally, selected compounds were tested using a cell-based assay to measure their neuroprotective activity. Three of them showed a remarkable neuroprotective profile, inhibiting the NMDA-induced neurotoxicity at subnanomolar concentrations (e.g., 5, named memagal, IC(50) = 0.28 nM)