RESUMEN
A significant growth of research on adaptive liquid lens is achieved over the past decades, and the field is still attracting increasing attentions, focusing on the transition from the current stage to the commercialized stage. The challenges faced are not limited to fabrication, material, small tuning range in focal lengths, additional control systems, limitations in special actuation methods and so on. In addition, the use of external driving parts or systems induce extra problem on bulky appearance, high cost, low reliability etc. Therefore, adaptive liquid lens will be an interesting research focus in both microfluidics and optofluidics science. This review attempts to summarize and focus on the droplet profile deformation under different driving mechanisms in tunable liquid microlens as well as the application in cameras, cell phone and so on. The driving techniques are generally categorized in terms of mechanisms and driving sources.
RESUMEN
The seemly paradoxical Gq agonist-stimulated phosphoinositide production has long been known, but the underlying mechanism and its physiological significance are not known. In this study, we studied cardiac phosphoinositide levels in both cells and whole animals under the stimulation of norepinephrine (NE), angiotensin II (Ang II), and other physiologically relevant interventions. The results demonstrated that activation of membrane receptors related to NE or Ang II caused an initial increase and a later fall in phosphatidylinositol 4,5-bisphosphate (PIP2) levels in the primary cultured cardiomyocytes from adult rats. The possible mechanism underlying this increase in PIP2 was found to be through an enhanced activity of phosphatidylinositol 4-kinase IIIß, which was mediated by an up-regulated interaction between phosphatidylinositol 4-kinase IIIß and PKC; the increased activity of phosphatidylinositol 4-phosphate 5-kinase γ was also involved for NE-induced increase of PIP2. When the systolic functions of the NE/Ang II-treated cells were measured, a maintained or failed contractility was found to be correlated with a rise or fall in corresponding PIP2 levels. In two animal models of cardiac hypertrophy, PIP2 levels were significantly reduced in hypertrophic hearts induced by isoprenaline but not in those induced by swimming exercise. This study describes a novel mechanism for phosphoinositide metabolism and modulation of cardiac function.
Asunto(s)
Angiotensina II/fisiología , Cardiomegalia/fisiopatología , Norepinefrina/fisiología , Fosfatidilinositol 4,5-Difosfato/metabolismo , Fosfatidilinositol-4-Fosfato 3-Quinasa/fisiología , Angiotensina II/farmacología , Animales , Cardiomegalia/inducido químicamente , Cardiomegalia/enzimología , Modelos Animales de Enfermedad , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/enzimología , Miocitos Cardíacos/fisiología , Norepinefrina/farmacología , Ratas , Ratas Sprague-DawleyRESUMEN
To study the effects of Smad4 on liver fibrosis and hepatocarcinogenesis in mice treated with CCl(4)/ethanol. The wild-type mice (Smad4 +/+) and the Smad4 knockout mice (Smad4 +/-) were injected subcutaneously with carbon tetrachloride(CCl(4))/ethanol twice a week for twenty weeks. The expression of Smad4, TGFbeta1, Smad2, Smad3, Smad6, TIMP1, MMP2 and MMP9 was detected by RT-PCR. In the cirrhotic liver, the expression of Smad4 mRNA was significantly higher than that in the normal liver. Comparing with wild-type mice (Smad4 +/+), the TGFbeta1-Smad4 signaling was markedly attenuated in the Smad4 knockout mice (Smad4 +/-). After induction by CCl(4)/ethanol, the hepatic fibrosis in the Smad4 knockout mice (Smad4 +/-) was obviously alleviated compared with the wild-type mice (Smad4 +/+), and the incidence rate of hepatocarcinogenesis of the former was also lower than that of the latter(32.0% vs 41.9%). These results indicate that knocking out Smad4 can delay the progression of liver fibrosis and liver cancer.
Asunto(s)
Cirrosis Hepática Experimental/patología , Neoplasias Hepáticas Experimentales/patología , Transducción de Señal , Proteína Smad4/genética , Factor de Crecimiento Transformador beta1/metabolismo , Animales , Tetracloruro de Carbono/administración & dosificación , Modelos Animales de Enfermedad , Etanol/administración & dosificación , Femenino , Cirrosis Hepática Experimental/inducido químicamente , Cirrosis Hepática Experimental/metabolismo , Neoplasias Hepáticas Experimentales/inducido químicamente , Neoplasias Hepáticas Experimentales/metabolismo , Masculino , Ratones , Ratones Noqueados , ARN Mensajero/genética , ARN Mensajero/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Proteínas Smad/genética , Proteínas Smad/metabolismo , Proteína Smad4/metabolismo , Inhibidor Tisular de Metaloproteinasa-1/genética , Inhibidor Tisular de Metaloproteinasa-1/metabolismo , Factor de Crecimiento Transformador beta1/genéticaRESUMEN
BACKGROUND: The incidence of hepatic portal cholangiocarcinoma is increasing and it is always associated with poor survival. This study analyzed an effective therapeutic method. METHODS: A retrospective analysis was made on 70 patients with hepatic portal cholangiocarcinoma admitted between January 2004 and February 2007 to the General Hospital of Air Force PLA. RESULTS: Forty-seven patients had hepatic duct-jejunum anastomosis after resection of hepatic portal cholangiocarcinoma. Internal or external biliary drainage and canals for internal radiation were performed in those patients unfit for operation. Among the 70 patients, 5 died within 15 months, 27 survived more than 24 months, and the others survived 4-18 months. CONCLUSION: Surgery is the primary therapeutic method for hepatic portal cholangiocarcinoma. Internal or external biliary drainage can prolong the life-span.