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The pretension of building membrane structures may relax over its service lifetime, which may cause engineering failure under external loads. Therefore, the pretension of building membrane structures should be monitored or estimated regularly to compare the actual pretension to its design pretension and then to adopt some strengthening measures to mitigate future problems. Based on the geometrically nonlinear vibration of a rectangular orthotropic membrane structure, a nondestructive detection method for monitoring its pretension is developed in this article. This method is achieved by impacting a low-velocity pellet onto the membrane surface to generate vibration and detecting its response amplitude. Then the detected amplitude is converted into a pretension estimate via a derived formula. In addition, experiments for three kinds of conventional membrane material (Heytex H5573, Xing Yi Da, and ZZF 3010) were carried out according to the theoretical idea. The experimental results proved this method is feasible and verified the theoretical derivation is reasonable.

The pretension of building membrane structures may relax over its service lifetime, which may cause engineering failure under external loads. Therefore, the pretension of building membrane structures should be monitored or estimated regularly to compare the actual pretension to its design pretension and then to adopt some strengthening measures to mitigate future problems. Based on the geometrically nonlinear vibration of a rectangular orthotropic membrane structure, a nondestructive detection method for monitoring its pretension is developed in this article. This method is achieved by impacting a low-velocity pellet onto the membrane surface to generate vibration and detecting its response amplitude. Then the detected amplitude is converted into a pretension estimate via a derived formula. In addition, experiments for three kinds of conventional membrane material (Heytex H5573, Xing Yi Da, and ZZF 3010) were carried out according to the theoretical idea. The experimental results proved this method is feasible and verified the theoretical derivation is reasonable.

© 2015 Springer Science+Business Media New York Solid-state processes of bonding 1 mm copper (Cu) wires on Cu substrates and silicon (Si) chips, respectively, were developed. To overcome Cu oxidation issue, the bonding surface on the wire was plated a silver (Ag) layer. An annealing step followed to make the Ag layer much easier to deform and conform to the Cu or Si bonding surfaces. The bonding process was performed at 300 °C with 6.89 MPa. Wire-bond cross sections were studied using optical and electron microscopy, respectively. The images obtained exhibit nearly perfect Ag–Cu bonding interface. For wire-bonds made on Cu substrate, in-plane (shear) pull test measured a breaking of force 20.7–23.7 kg, comparable to the 22.5 kg breaking force of the Cu wire itself. Breaking forces on vertical (peel) pull test are about one-half of in-plane pull test results. For wire-bonds made on Si chip, breaking forces are about 80 % of those made on Cu substrate. Fracture modes were evaluated in details. 90 % of the wire-bonds broke with three modes mixed together: near Cu–Ag plating interface, inside Ag layer, and Ag–Cu bonding interface. Thus, the bonding interface is as strong as other regions of the wire-bond. This solid-state wire bonding process is expected to have valuable applications in high power and high temperature devices and modules where the wire-bonds have to stand alone without protection due to lack of high temperature molding compound and reinforcing materials.

© 2015 Springer Science+Business Media New York Solid-state processes of bonding 1 mm copper (Cu) wires on Cu substrates and silicon (Si) chips, respectively, were developed. To overcome Cu oxidation issue, the bonding surface on the wire was plated a silver (Ag) layer. An annealing step followed to make the Ag layer much easier to deform and conform to the Cu or Si bonding surfaces. The bonding process was performed at 300 °C with 6.89 MPa. Wire-bond cross sections were studied using optical and electron microscopy, respectively. The images obtained exhibit nearly perfect Ag–Cu bonding interface. For wire-bonds made on Cu substrate, in-plane (shear) pull test measured a breaking of force 20.7–23.7 kg, comparable to the 22.5 kg breaking force of the Cu wire itself. Breaking forces on vertical (peel) pull test are about one-half of in-plane pull test results. For wire-bonds made on Si chip, breaking forces are about 80 % of those made on Cu substrate. Fracture modes were evaluated in details. 90 % of the wire-bonds broke with three modes mixed together: near Cu–Ag plating interface, inside Ag layer, and Ag–Cu bonding interface. Thus, the bonding interface is as strong as other regions of the wire-bond. This solid-state wire bonding process is expected to have valuable applications in high power and high temperature devices and modules where the wire-bonds have to stand alone without protection due to lack of high temperature molding compound and reinforcing materials.

Sodium orthovanadate, an inhibitor of protein tyrosine phosphatases, causes increased levels of tyrosine phosphorylation and blocks, at noncytotoxic concentrations, the differentiative response of rat pheochromocytoma (PC12) cells to beta-nerve growth factor (beta NGF) and basic fibroblast growth factor (bFGF) in a reversible manner. It also prevents growth factor-induced neurite proliferation in primed cells and causes the retraction of previously formed neurites, even in the presence of beta NGF or bFGF. It is equally effective in blocking neurite proliferation by 8-Br-cAMP. Zinc chloride and ammonium molybdate, two other inhibitors of tyrosine phosphatases, also cause parallel decreases in neurite proliferation. Orthovanadate generally reduces the transcription of immediate early response genes (TIS 8 and c-fos) and secondary response genes (ornithine decarboxylase (ODC), acetyl-cholinesterase (AChE) and SCG 10) induced by beta NGF, bFGF, EGF, and PMA, albeit in a variable fashion. There was no observed effect on the kinetics of expression as judged by TIS 8 induction by beta NGF and protein kinase C (PKC) downregulation did not change the levels of inhibition by orthovanadate seen in control cells. Orthovanadate does not affect the production of diacylglycerol induced by beta NGF or bFGF. These observations are consistent with the view that growth factor stimulation of differentiation in PC12 cells involves at least one other PKC independent pathway, and that cAMP and PMA (and their active analogs) activate tyrosine kinases (albeit probably secondarily), which are at least partially responsible for their actions. Although the exact site(s) of action of orthovanadate that lead to the inhibition of growth factor-induced neurite proliferation are unknown, the results presented suggest that it prolongs tyrosine phosphorylations by nonreceptor tyrosine kinases that act downstream from the receptor kinases.

Sodium orthovanadate, an inhibitor of protein tyrosine phosphatases, causes increased levels of tyrosine phosphorylation and blocks, at noncytotoxic concentrations, the differentiative response of rat pheochromocytoma (PC12) cells to beta-nerve growth factor (beta NGF) and basic fibroblast growth factor (bFGF) in a reversible manner. It also prevents growth factor-induced neurite proliferation in primed cells and causes the retraction of previously formed neurites, even in the presence of beta NGF or bFGF. It is equally effective in blocking neurite proliferation by 8-Br-cAMP. Zinc chloride and ammonium molybdate, two other inhibitors of tyrosine phosphatases, also cause parallel decreases in neurite proliferation. Orthovanadate generally reduces the transcription of immediate early response genes (TIS 8 and c-fos) and secondary response genes (ornithine decarboxylase (ODC), acetyl-cholinesterase (AChE) and SCG 10) induced by beta NGF, bFGF, EGF, and PMA, albeit in a variable fashion. There was no observed effect on the kinetics of expression as judged by TIS 8 induction by beta NGF and protein kinase C (PKC) downregulation did not change the levels of inhibition by orthovanadate seen in control cells. Orthovanadate does not affect the production of diacylglycerol induced by beta NGF or bFGF. These observations are consistent with the view that growth factor stimulation of differentiation in PC12 cells involves at least one other PKC independent pathway, and that cAMP and PMA (and their active analogs) activate tyrosine kinases (albeit probably secondarily), which are at least partially responsible for their actions. Although the exact site(s) of action of orthovanadate that lead to the inhibition of growth factor-induced neurite proliferation are unknown, the results presented suggest that it prolongs tyrosine phosphorylations by nonreceptor tyrosine kinases that act downstream from the receptor kinases.