ABSTRACT
Imaging systems are widely used in many fields. However, there is an inherent compromise between field of view (FOV) and resolution. In this paper, we propose an optofluidic zoom system with increased FOV and less chromatic aberration, which can realize switching between large FOV and high resolution. The proposed system consists of a liquid prism, a zoom objective, an image sensor and image processing module, which can realize optical zoom and deflection. The proposed system achieves non-mechanical optical zoom from f = 40.5 mm to f = 84.0 mm. Besides, the angular resolution of zoom objective is up to 26"18 at f = 84.0 mm. The deflection range is ±10°, and the whole FOV of proposed system can reach up to 30.3°. The proposed system is compact and easy to machine. In addition, we reduce chromatic aberration produced by the liquid prism significantly. The proposed system can be used in monitor system, target tracking system, telescope system and so on.
ABSTRACT
High levels of transforming growth factor-ß (TGFß) correlate with poor prognosis for patients with prostate cancer and other cancers. TGFß is a multifunctional cytokine and crucial regulator of cell fate, such as epithelial to mesenchymal transition (EMT), which is implicated in cancer invasion and progression. TGFß conveys its signals upon binding to type I and type II serine/threonine kinase receptors (TßRI/II); phosphorylation of Smad2 and Smad3 promotes their association with Smad4, which regulates expression of targets genes, such as Smad7, p21, and c-Jun. TGFß also activates the ubiquitin ligase tumor necrosis factor receptor-associated factor 6 (TRAF6), which associates with TßRI and activates the p38 mitogen-activated protein kinase (MAPK) pathway. Snail1 is a key transcription factor, induced by TGFß that promotes migration and invasion of cancer cells. In this study, we have identified a novel binding site for c-Jun in the promoter of the Snail1 gene and report that the activation of the TGFß-TRAF6-p38 MAPK pathway promotes both c-Jun expression and its activation via p38α-dependent phosphorylation of c-Jun at Ser63. The TRAF6-dependent activation of p38 also leads to increased stability of c-Jun, due to p38-dependent inactivation of glycogen synthase kinase (GSK) 3ß by phosphorylation at Ser9. Thus, our findings elucidate a novel role for the p38 MAPK pathway in stimulated cells, leading to activation of c-Jun and its binding to the promoter of Snail1, thereby triggering motility and invasiveness of aggressive human prostate cancer cells.
Subject(s)
JNK Mitogen-Activated Protein Kinases/metabolism , Prostatic Neoplasms/genetics , Prostatic Neoplasms/pathology , Transcription Factors/genetics , Transcriptional Activation , Transforming Growth Factor beta/metabolism , Breast Neoplasms/genetics , Breast Neoplasms/pathology , Cell Line, Tumor , Female , Humans , MAP Kinase Signaling System , Male , Neoplasm Invasiveness/genetics , Promoter Regions, Genetic , Serine/metabolism , Snail Family Transcription Factors , TNF Receptor-Associated Factor 6/metabolism , Transcription Factors/metabolismABSTRACT
OBJECTIVE: To investigate the changes in angiotensinogen (AGT), angiotensin II type 1 receptor (AT(1)R), endothelial nitric oxide synthase (eNOS) mRNA and protein expressions and nitric oxide (NO) content in the rat glomeruli in response to leptin stimulation. METHODS: The glomeruli isolated from male SD rats were stimulated with 3 nmol/L leptin for 2 h. Real-time PCR and Western blotting were performed to analyze the mRNA and protein expressions of AGT, AT(1)R and eNOS in the glomeruli, and nitrite concentration in the glomeruli was measured by nitrate reductase assay. RESULTS: In comparison with the control group, exposure to leptin increased the mRNA levels of AGT, ATR(1) and eNOS in the isolated glomeruli by 2.69-/+0.17, 3.77-/+0.16 and 2.56-/+0.29 folds (P=0.024, 0.018 and 0.044), and their protein levels by 2.06-/+0.10, 2.67-/+0.08 and 1.61-/+0.13 folds (P=0.021, 0.015 and 0.032), respectively. The NO production in the glomeruli was also increased by 2.77-/+0.14 folds (P=0.000) following leptin exposure. CONCLUSION: Leptin exposure of isolated rat glomeruli directly causes activation of the internal renal renin-angiotensin system and enhanced NO production, suggesting that leptin plays a role in the pathogenesis of maladaptation in renal hemodynamics in obesity.
