Closed-Form Solution and Experimental Verification for the Axisymmetric Deformation Problem of Blistering Circular Thin Polymer Films under Uniformly Distributed Gas Pressure.

The existing studies indicate that the measurement formulas used in blister test techniques, which are used to measure the mechanical properties of thin-film/substrate systems, are usually given based on an approximation-that is, the applied direction of the uniformly distributed transverse load is always vertical, while the applied direction of the uniformly distributed gas pressure is always perpendicular to the surface of the thin film. This approximation will lead to a large measurement error. In this study, we obtained the analytical solution to the problem of axisymmetric deformation of blistering circular thin polymer films under the action of uniformly distributed gas pressure via the power series method. An example is given to illustrate the error caused by the approximation mentioned above, and the validity of the solution presented here is verified. The result shows that the chance of error caused by the approximation increases with the increase in the applied load, and it far exceeds the allowable error of measurement when the applied load is relatively large. In addition, the related experiments of the blistering circular thin polymer film under uniformly distributed gas pressure are carried out, and the experimental results are compared with the theoretical results. The comparison results show that the analytical solution given in this paper is correct. The solution presented here is of great significance to improve the measurement accuracy of the blister test technique.

Activation of ß2-adrenoceptor enhances synaptic potentiation and behavioral memory via cAMP-PKA signaling in the medial prefrontal cortex of rats.

The prefrontal cortex (PFC) plays a critical role in cognitive functions, including working memory, attention regulation, behavioral inhibition, as well as memory storage. The functions of PFC are very sensitive to norepinephrine (NE), and even low levels of endogenously released NE exert a dramatic influence on the functioning of the PFC. Activation of ß-adrenoceptors (ß-ARs) facilitates synaptic potentiation and enhances memory in the hippocampus. However, little is known regarding these processes in the PFC. In the present study, we investigate the role of ß2-AR in synaptic plasticity and behavioral memory. Our results show that ß2-AR selective agonist clenbuterol facilitates spike-timing-dependent long-term potentiation (tLTP) under the physiological conditions with intact GABAergic inhibition, and such facilitation is prevented by co-application with the cAMP inhibitor Rp-cAMPS. Loading postsynaptic pyramidal cells with Rp-cAMPS, the PKA inhibitor PKI(5-24), or the G protein inhibitor GDP-ß-S significantly decreases, but does not eliminate, the effect of clenbuterol. Clenbuterol suppresses the GABAergic transmission, while blocking GABAergic transmission by the GABA(A) receptor blocker partially mimics the effect of clenbuterol. In behavioral tests, a post-training infusion of clenbuterol into mPFC enhances 24-h trace fear memory. In summary, we observed that prefrontal cortical ß2-AR activation by clenbuterol facilitates tLTP and enhances trace fear memory. The mechanism underlying tLTP facilitation involves stimulating postsynaptic cAMP-PKA signaling cascades and suppressing GABAergic circuit activities.

Association between Bmi1 and clinicopathological status of esophageal squamous cell carcinoma.

AIM: To investigate the clinicopathological roles of Bmi1 in esophageal squamous cell carcinoma (ESCC). METHODS: Quantitative real-time polymerase chain reaction and immunohistochemical staining for Bmi1 were performed in cancerous and adjacent non-cancerous paraffin-embedded esophageal specimens. RESULTS: The Bmi1 expression level was unaffected by gender and age. The level of Bmi1 mRNA in ESCC was significantly higher than that in the adjacent non-cancerous tissues (2.181 +/- 2.158 vs 0.931 +/- 0.894, P = 0.0152), and its over-expression was aggressively associated with lymph node metastasis (3.580 +/- 2.487 vs 1.703 +/- 0.758, P = 0.0003), poorer cell differentiation (P = 0.0000) and advanced pathological stage (3.827 +/- 2.673 vs 1.590 +/- 0.735, P = 0.0001). The patients were divided into high-expression and low-expression groups based on the median expression level of Bmi1 mRNA, and a shorter overall survival time in the former group was observed. Immunohistochemistry for Bmi1 oncoprotein showed diffusely positive, focally positive and negative expression in 44, 16 and 10 of 70 ESCC cases, respectively, compared with three, two and five of 10 adjacent non-cancerous cases (P = 0.027). The positive rate of the oncoprotein in samples of histological grade III was higher than that of grade II (P = 0.031), but its expression had no relation to the lymph node metastasis and pathological staging. In 70 ESCC samples, Bmi1 showed high intense expression in the cytoplasm and less or even no expression in the nucleus. CONCLUSION: Bmi1 was over-expressed in ESCC. Increased Bmi1 mRNA expression was significantly associated with ESCC progression, and the oncoprotein was largely distributed in the cytoplasm of tumor cells.