RESUMEN
Continuous monitoring of heart-rate is expected to lead to early detection of physical discomfort. In this study, we propose a non-contact heart-rate measurement method which can be used in an environment such as driver heart-rate monitoring with body movement. The method is based on the electric field strength transmitted through the human body that changes with the diastole and systole of the heart. Unlike conventional displacement detection of the skin surface, we attempted to capture changes in the internal structure of the human body by irradiating the human body with microwaves and acquiring microwaves that pass through the heart. We first estimated the electric field strength transmitted through the heart using three receiving sensors to reduce the body movement effect. Then we decomposed the estimated transmitted electric field using stationary wavelet transform to eliminate significant distortion due to body movement. As a result, we achieved an estimation accuracy of heart-rate as high as 98% in a verification experiment with normal body movement.
Asunto(s)
Algoritmos , Análisis de Ondículas , Frecuencia Cardíaca , Humanos , Monitoreo Fisiológico , MovimientoRESUMEN
Using cDNA microarray technology, the expression of chemokine genes in the elicitation site of 2,4,6-trinitrochlorobenzene-induced contact hypersensitivity (CHS) was examined in mice. Of the 33 genes analyzed, levels of 11 gene expressions changed, and these can be assigned to four groups based on their kinetic patterns; (1) LARC/CCL20 whose mRNA level increased rapidly at 3 h post-challenge and then gradually decreased, (2) JE/CCL2, MARC/CCL7, MIP-1gamma/CCL9, monocyte chemoattractant protein (MCP)-5/CCL12, ELC/CCL19 and BRAK/CXCL14 whose mRNA levels increased with time and reached the maximum at 6-9 h post-challenge, (3) LIX/CXCL5, Mig/CXCL9 and IP-10/CXCL10 whose mRNA levels increased gradually at least up to 12 h post challenge, and (4) SLC/CCL21 whose mRNA level decreased gradually with time after challenge. The findings suggest that sequential expression of chemokine genes is essential for orientating non-specific skin response to hapten-specific CHS response through the recruitment of inflammatory cells such as neutrophils, monocytes/macrophages and T-cells from the circulation into the tissue site.
Asunto(s)
Quimiocinas CXC/metabolismo , Quimiocinas/metabolismo , Dermatitis por Contacto/inmunología , Animales , Quimiocinas/genética , Quimiocinas CXC/genética , Dermatitis por Contacto/genética , Dermatitis por Contacto/patología , Oído/patología , Expresión Génica , Perfilación de la Expresión Génica , Interferón gamma/metabolismo , Interleucina-1/metabolismo , Cinética , Ratones , Ratones Endogámicos BALB C , Análisis de Secuencia por Matrices de Oligonucleótidos , Cloruro de Picrilo , ARN Mensajero/metabolismo , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
Effects of a topical corticosteroid drug, diflucortolone valerate, on the mRNA expressions for four CC- and four CXC-chemokines, which have been reported to be associated with recruitment of different kinds of proinflammatory and inflammatory cells, were investigated by RT-PCR in mice with 2,4,6-trinitrochlorobenzene (TNCB)-induced contact hypersensitivity (CHS) response. All of the eight gene expressions were clearly up-regulated in the lesion site of the CHS response up to 24 h post-challenge of TNCB at which ear swelling response reached a peak, so that heavy infiltration of inflammatory cells consisting mainly of mononuclear cells and neutrophils was likely induced by these chemokines. Topical treatment with diflucortolone valerate suppressed completely the infiltrates as well as the ear swelling response. In addition, the up-regulation of gene expressions for these eight chemokines were suppressed by the treatment, indicating that the corticosteroid drug attenuates the expression of chemokine genes essential for orientating nonspecific skin response to hapten-specific CHS response through the recruitment of inflammatory cells from the circulation into the tissue site.
Asunto(s)
Antiinflamatorios/farmacología , Quimiocinas/biosíntesis , Dermatitis por Contacto/metabolismo , Diflucortolona/análogos & derivados , Diflucortolona/farmacología , Administración Cutánea , Animales , Antiinflamatorios/administración & dosificación , Quimiocinas/genética , Dermatitis por Contacto/genética , Dermatitis por Contacto/patología , Diflucortolona/administración & dosificación , Oído/patología , Expresión Génica , Masculino , Ratones , Ratones Endogámicos BALB C , ARN Mensajero/biosíntesis , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factores de TiempoRESUMEN
Using computer-based, motif-trap screening, we have identified a third member of the mammalian fat family, fat3. Human and rat fat3 are also similar to the Drosophila tumor suppressor gene fat. The rat fat3 gene encodes a large protein of 4555 amino acids with 34 cadherin domains, 4 epidermal growth factor (EGF)-like motifs, a laminin A-G motif, and a cytoplasmic domain. Each member of the fat family is differentially expressed in the central nervous system during development. While both fat3 mRNA and fat1 mRNA are abundantly expressed in the fetal brain, the expression of MEGF1/fat2 mRNA is restricted to the postnatal cerebellum. fat3 mRNA and protein expression in the brain peaks at E15 during embryonic development. During this time, robust fat3 immunoreactivity is also observed in the spinal cord. These data suggest that the fat3 protein plays an important role in axon fasciculation and modulation of the extracellular space surrounding axons during embryonic development.