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1.
Dysphagia ; 36(4): 719-728, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-32979096

RESUMO

Diet modification is an important intervention in the management of patients with dysphagia. Food entering the airway, same as oral bacterium, causes pulmonary inflammation; therefore, the elucidation of inflammatory responses to different foods is important. This study aimed to investigate the differences in the severity of inflammatory response induced by intratrachial injection of foods with different nutritional components. Two jelly products, the one containing only carbohydrates (KURIN jelly: Isocal Jelly KURIN®) and the other containing carbohydrates, proteins, and lipids (HC jelly: Isocal Jelly HC®), were prepared. These jelly products (dilution with saline, 50% volume/volume) and saline, as control, were intratracheally administered to Sprague-Dawley rats at a dose of 1 ml/kg (KURIN group (n = 15), HC group (n = 15), Saline group (n = 15)). At 1, 2 and 7 days after administration, lungs were harvested and histological analysis was performed. The severity of induced inflammation was evaluated using the Acute Lung Injury (ALI) score with hematoxylin-eosin staining, and the expression of IL-1ß, IL-6 and TNF-α, markers of airway inflammation, were observed with immunostaining. The ALI score in the HC jelly group was significantly higher than the KURIN jelly group and the Saline group (P < 0.01) at 1 and 2 days after administration, while the ALI score in the KURIN jelly group was higher than Saline group only at 2 day after administration. Numerous positive cells for IL-1ß, IL-6 and TNF-α were observed only in the HC jelly group at 1 and 2 days after administration. There were no significant histological differences between the three groups at 7 days after administration. Our data suggests that the severity of inflammation caused by aspiration differs depending on the ingredients of the foods, and the nutrients contained in foods might be considered in dietary management for the patients with dysphagia.


Assuntos
Lesão Pulmonar Aguda , Pneumonia , Animais , Humanos , Pulmão , Ratos , Ratos Sprague-Dawley , Fator de Necrose Tumoral alfa
2.
Dalton Trans ; 47(8): 2543-2548, 2018 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-29384534

RESUMO

A dinuclear helical iron(ii) complex of a new ditopic thiazolylimine ligand (L) has been synthesised via supramolecular assembly. The resulting dinuclear helical cylinder [Fe2L3]·4BF4 was investigated by variable temperature X-ray crystallography, ESI high resolution mass spectrometry, CHN analysis, FT-IR and UV-Vis spectroscopy. The nature of the spin transition was investigated by magnetic susceptibility measurements, and confirmed by VT-SCXRD and X-ray photoelectron spectroscopy. [Fe2L3]·4BF4 displays a complete spin transition with a gradual-abrupt character at T1/2 = 348 K and represents a new example of a dinuclear iron(ii) complex exhibiting a spin transition at high temperature. Both VT-SCXRD and XPS measurements show excellent correlation with the magnetic susceptibility experiments, demonstrating the power of XPS not just to confirm, but also to clearly follow the spin-state transition in Fe(ii) SCO complexes.

3.
eNeuro ; 3(3)2016.
Artigo em Inglês | MEDLINE | ID: mdl-27390772

RESUMO

Microglia survey and directly contact neurons in both healthy and damaged brain, but the mechanisms and functional consequences of these contacts are not yet fully elucidated. Combining two-photon imaging and patch clamping, we have developed an acute experimental model for studying the role of microglia in CNS excitotoxicity induced by neuronal hyperactivity. Our model allows us to simultaneously examine the effects of repetitive supramaximal stimulation on axonal morphology, neuronal membrane potential, and microglial migration, using cortical brain slices from Iba-1 eGFP mice. We demonstrate that microglia exert an acute and highly localized neuroprotective action under conditions of neuronal hyperactivity. Evoking repetitive action potentials in individual layer 2/3 pyramidal neurons elicited swelling of axons, but not dendrites, which was accompanied by a large, sustained depolarization of soma membrane potential. Microglial processes migrated to these swollen axons in a mechanism involving both ATP and glutamate release via volume-activated anion channels. This migration was followed by intensive microglial wrapping of affected axons and, in some cases, the removal of axonal debris that induced a rapid soma membrane repolarization back to resting potentials. When the microglial migration was pharmacologically blocked, the activity-induced depolarization continued until cell death ensued, demonstrating that the microglia-axon contact served to prevent pathological depolarization of the soma and maintain neuronal viability. This is a novel aspect of microglia surveillance: detecting, wrapping, and rescuing neuronal soma from damage due to excessive activity.


Assuntos
Potenciais da Membrana/fisiologia , Microglia/fisiologia , Neuroproteção/fisiologia , Células Piramidais/fisiologia , Trifosfato de Adenosina/metabolismo , Animais , Axônios/efeitos dos fármacos , Axônios/patologia , Axônios/fisiologia , Movimento Celular/efeitos dos fármacos , Movimento Celular/fisiologia , Tamanho Celular , Dendritos/efeitos dos fármacos , Dendritos/patologia , Dendritos/fisiologia , Feminino , Ácido Glutâmico/metabolismo , Canais Iônicos/metabolismo , Masculino , Potenciais da Membrana/efeitos dos fármacos , Camundongos Transgênicos , Microglia/efeitos dos fármacos , Microglia/patologia , Neuroproteção/efeitos dos fármacos , Células Piramidais/efeitos dos fármacos , Células Piramidais/patologia , Técnicas de Cultura de Tecidos
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