RESUMO
Electroepitaxy is recognized as an effective approach to prepare metal electrodes with nearly complete reversibility. Nevertheless, large-scale manipulation is still not attainable owing to complicated interfacial chemistry. Here, the feasibility of extending Zn electroepitaxy toward the bulk phase over a mass-produced mono-oriented Cu(111) foil is demonstrated. Interfacial Cu-Zn alloy and turbulent electroosmosis are circumvented by adopting a potentiostatic electrodeposition protocol. The as-prepared Zn single-crystalline anode enables stable cycling of symmetric cells at a stringent current density of 50.0 mA cm-2 . The assembled full cell further sustaines a capacity retention of 95.7% at 5.0 A g-1 for 1500 cycles, accompanied by a controllably low N/P ratio of 7.5. In addition to Zn, Ni electroepitaxy can be realized by using the same approach. This study may inspire rational exploration of the design of high-end metal electrodes.
Assuntos
Ligas , Galvanoplastia , Eletrodos , ZincoRESUMO
OBJECTIVE: To transform eukaryotic expression vector pEGFP-PDX-1 into marrow stromal cells by liposome and to optimize the conditions of transformation. METHODS: The recombinant vector was identified by enzyme digestion analysis and sequencing. The recombinant plasmid was transformed into bone marrow stromal cells and it changed the quantity of DNA or liposome. The expression of PDX-1 gene in the transformed cells was detected by immunocytochemical staining. RESULTS: Enzyme digestion analysis and sequencing showed that the interesting gene was integreted into the recombinant vector. We obtained satisfactory efficiency of transfection when the ratio of DNA and liposome was 1 : 1 or 1 : 2. The PDX-1 in the transformed cells was expressed by immunocytochemical staining. CONCLUSION: The eukaryotic expression vector pEGFP-PDX-1 was constructed for the first time in China. We have enhanced the efficiency of transfection by optimizing the transformation conditions. It is possible to use the bone marrow stromal cells as seed cells in tissue-engineering.
Assuntos
Células da Medula Óssea/metabolismo , Proteínas de Homeodomínio/biossíntese , Células Estromais/metabolismo , Transativadores/biossíntese , Transfecção , Animais , Sequência de Bases , Células da Medula Óssea/citologia , Células Cultivadas , Células Eucarióticas/metabolismo , Proteínas de Homeodomínio/genética , Lipossomos , Masculino , Dados de Sequência Molecular , Ratos , Ratos Sprague-Dawley , Proteínas Recombinantes/biossíntese , Proteínas Recombinantes/genética , Células Estromais/citologia , Engenharia Tecidual , Transativadores/genéticaRESUMO
OBJECTIVE: To investigate the effect of intraventricular injection of human dental pulp stem cells (DPSCs) on hypoxic-ischemic brain damage (HIBD) in neonatal rats. METHODS: Thirty-six neonatal rats (postnatal day 7) were assigned to control, HIBD, or HIBD+DPSC groups (nâ=â12 each group). For induction of HIBD, rats underwent left carotid artery ligation and were exposed to 8% to 10% oxygen for 2 h. Hoechst 33324-labeled human DPSCs were injected into the left lateral ventricle 3 days after HIBD. Behavioral assays were performed to assess hypoxic-ischemic encephalopathy (HIE), and on postnatal day 45, DPSC survival was assessed and expression of neural and glial markers was evaluated by immunohistochemistry and Western blot. RESULTS: The HIBD group showed significant deficiencies compared to control on T-maze, radial water maze, and postural reflex tests, and the HIBD+DPSC group showed significant improvement on all behavioral tests. On postnatal day 45, Hoechst 33324-labeled DPSC nuclei were visible in the injected region and left cortex. Subsets of DPSCs showed immunostaining for neuronal (neuron-specific enolase [NSE], Nestin) and glial markers (glial fibrillary acidic protein [GFAP], O4). Significantly decreased staining/expression for NSE, GFAP, and O4 was found in the HBID group compared to control, and this was significantly increased in the HBID+DPSC group. CONCLUSION: Intraventricular injection of human DPSCs improves HIBD in neonatal rats.