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1.
J Synchrotron Radiat ; 2024 Sep 01.
Artículo en Inglés | MEDLINE | ID: mdl-39116008

RESUMEN

Addressing the demand for high stability of beamline instruments at the SHINE facility, a high stability mirror regulating mechanism has been developed for mirror adjustments. Active mass damping was adopted to attenuate pitch angle vibrations of mirrors caused by structural vibrations. An internal absolute velocity feedback was used to reduce the negative impact of spillover effects and to improve performance. The experiment was conducted on a prototype structure of a mirror regulating mechanism, and results showed that the vibration RMS of the pitch angle was effectively attenuated from 47 nrad to 27 nrad above 1 Hz.

2.
Neurotoxicology ; 72: 85-94, 2019 05.
Artículo en Inglés | MEDLINE | ID: mdl-30769002

RESUMEN

In view of the wide application of fluoroquinolones (FQs), a group of broad-spectrum synthetic antibacterial agents, and their large ingress into the environment, the toxic effects on non-target organisms caused by FQs have received great attention. In this study, we used zebrafish embryo as a model, measured the general toxic effects of norfloxacin, a commonly used FQs, and investigated the effects of norfloxacin on the neurodevelopment of zebrafish embryos. Our data showed that norfloxacin significantly inhibited the hatching rate of zebrafish embryos, and increased the mortality and malformation rate of the embryos. To discuss the developmental neurotoxicity of norfloxacin, we measured the expression of several stem cell and neuron lineage markers in the zebrafish embryos. We found that norfloxacin exposure inhibited the expression of GFAP (glial cell marker), and enhanced the expression of Sox 2 (stem cell marker) and Eno2 (mature neuron marker). By measuring the level of active Caspase 3 and the expression ratio of Bax to Bcl2, we discovered that norfloxacin induced obvious cell apoptosis in the brain of zebrafish embryos. To explore the mechanism of the developmental neurotoxic effects of norfloxacin, we applied MK-801, a non-competitive NMDA receptors antagonist, to block the actions of NMDA receptors. The results indicated that MK-801 could rescue the upregulated cell apoptosis and disrupted balance of neuro-glial differentiation induced by norfloxacin in the brain of zebrafish embryos. Our results suggest that the activation of NMDA receptors mediates the developmental neurotoxicity of norfloxacin.


Asunto(s)
Antibacterianos/toxicidad , Encéfalo/efectos de los fármacos , Encéfalo/embriología , Desarrollo Embrionario/efectos de los fármacos , Neuronas/efectos de los fármacos , Norfloxacino/toxicidad , Células Madre/efectos de los fármacos , Animales , Apoptosis/efectos de los fármacos , Embrión no Mamífero/efectos de los fármacos , Pez Cebra
3.
Stem Cell Res ; 17(3): 489-497, 2016 11.
Artículo en Inglés | MEDLINE | ID: mdl-27771497

RESUMEN

The continuous growth of mouse incisors depends on epithelial stem cells (SCs) residing in the SC niche, called labial cervical loop (LaCL). The homeostasis of the SCs is subtly regulated by complex signaling networks. In this study, we focus on retinoic acid (RA), a derivative of Vitamin A and a known pivotal signaling molecule in controlling the functions of stem cells (SCs). We analyzed the expression profiles of several key molecules of the RA signaling pathway in cultured incisor explants upon exogenous RA treatment. The expression patterns of these molecules suggested a negative feedback regulation of RA signaling in the developing incisor. We demonstrated that exogenous RA had negative effects on incisor SCs and that this was accompanied by downregulation of Fgf10, a mesenchymally expressed SC survival factor in the mouse incisor. Supplement of Fgf10 in incisor cultures completely blocked RA effects by antagonizing apoptosis and increasing proliferation in LaCL epithelial SCs. In addition, Fgf10 obviously antagonized RA-induced downregulation of the SC marker Sox2 in incisor epithelial SCs. Our findings suggest that the negative effects of RA on incisor SCs result from inhibition of mesenchymal Fgf10.


Asunto(s)
Incisivo/citología , Incisivo/efectos de los fármacos , Nicho de Células Madre/efectos de los fármacos , Tretinoina/toxicidad , Animales , Apoptosis/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Factor 10 de Crecimiento de Fibroblastos/biosíntesis , Incisivo/metabolismo , Ratones , Transducción de Señal
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