Deformation and reverse snapping of a circular shallow shell under uniform edge tension

AbstractIn this paper we study the deformation and stability of a shallow shell under uniform edge tension, both theoretically and experimentally. Von Karman’s plate model is adopted to formulate the equations of motion. For a shell with axisymmetrical initial shape, the equilibrium positions can be classified into axisymmetrical and unsymmetrical solutions. While there may exist both stable and unstable axisymmetrical solutions, all the unsymmetrical solutions are unstable. Since the unsymmetrical solutions will not affect the stability of the axisymmetrical solutions, it is concluded that for quasi-static analysis, there is no need to include unsymmetrical assumed modes in the calculation. If the shell is initially in the unstrained configuration, it will only be flattened smoothly when the edge tension is applied. No snap-through buckling is possible in this case. On the other hand, if the shell is initially in the strained position, it will be snapped back to the stable position on the other side of the base plane when the edge tension reaches a critical value. Experiment is conducted on several free brass shells of different initial heights to verify the theoretical predictions. Generally speaking, for the range of initial height H<10 the experimental measurements of the deformation and the reverse snapping load agree well with theoretical predictions

Control of the SCOLE configuration using distributed parameter models

A continuum model for the SCOLE configuration has been derived using transfer matrices. Controller designs for distributed parameter systems have been analyzed. Pole-assignment controller design is considered easy to implement but stability is not guaranteed. An explicit transfer function of dynamic controllers has been obtained and no model reduction is required before the controller is realized. One specific LQG controller for continuum models had been derived, but other optimal controllers for more general performances need to be studied

Motor neuron-derived Thsd7a is essential for zebrafish vascular development via the Notch-dll4 signaling pathway.

BackgroundDevelopment of neural and vascular systems displays astonishing similarities among vertebrates. This parallelism is under a precise control of complex guidance signals and neurovascular interactions. Previously, our group identified a highly conserved neural protein called thrombospondin type I domain containing 7A (THSD7A). Soluble THSD7A promoted and guided endothelial cell migration, tube formation and sprouting. In addition, we showed that thsd7a could be detected in the nervous system and was required for intersegmental vessels (ISV) patterning during zebrafish development. However, the exact origin of THSD7A and its effect on neurovascular interaction remains unclear.ResultsIn this study, we discovered that zebrafish thsd7a was expressed in the primary motor neurons. Knockdown of Thsd7a disrupted normal primary motor neuron formation and ISV sprouting in the Tg(kdr:EGFP/mnx1:TagRFP) double transgenic zebrafish. Interestingly, we found that Thsd7a morphants displayed distinct phenotypes that are very similar to the loss of Notch-delta like 4 (dll4) signaling. Transcript profiling further revealed that expression levels of notch1b and its downstream targets, vegfr2/3 and nrarpb, were down-regulated in the Thsd7a morphants. These data supported that zebrafish Thsd7a could regulate angiogenic sprouting via Notch-dll4 signaling during development.ConclusionsOur results suggested that motor neuron-derived Thsd7a plays a significant role in neurovascular interactions. Thsd7a could regulate ISV angiogenesis via Notch-dll4 signaling. Thus, Thsd7a is a potent angioneurin involved in the development of both neural and vascular systems

Coalescence of small bubbles with surfactants

Bubble coalescence is central to many important technological processes, such as separations, cleaning of oil spills, microfluidics, emulsification and foaming. It is well known that surfactants, which are frequently present as additives or contaminants, delay coalescence by slowing the drainage of the liquid film separating the approaching bubbles before they make contact. However, the coalescence and surfactant transport mechanisms developed after surfactant-laden bubbles make initial contact remain poorly understood. Here, we characterize these mechanisms using high-fidelity numerical simulations to predict the evolution of bubble interfaces, surfactant spreading, and induced Marangoni flows. Our results show that the surfactant initially accumulates on the tiny meniscus bridge formed between the coalescing bubbles due to the rapid and highly localized contraction of meniscus area. At the same time, a Marangoni-driven convective flow is generated at the interface, which drags the accumulated surfactant away from the joining meniscus and toward the back of the bubbles. Together, these transport mechanisms affect the rate bubble coalescence by dynamically modifying the local pull of surface tension on the bubble interfaces

Indirect Identification of Linear Stochastic Systems with Known Feedback Dynamics

An algorithm is presented for identifying a state-space model of linear stochastic systems operating under known feedback controller. In this algorithm, only the reference input and output of closed-loop data are required. No feedback signal needs to be recorded. The overall closed-loop system dynamics is first identified. Then a recursive formulation is derived to compute the open-loop plant dynamics from the identified closed-loop system dynamics and known feedback controller dynamics. The controller can be a dynamic or constant-gain full-state feedback controller. Numerical simulations and test data of a highly unstable large-gap magnetic suspension system are presented to demonstrate the feasibility of this indirect identification method

Iterative LQG Controller Design Through Closed-Loop Identification

This paper presents an iterative Linear Quadratic Gaussian (LQG) controller design approach for a linear stochastic system with an uncertain open-loop model and unknown noise statistics. This approach consists of closed-loop identification and controller redesign cycles. In each cycle, the closed-loop identification method is used to identify an open-loop model and a steady-state Kalman filter gain from closed-loop input/output test data obtained by using a feedback LQG controller designed from the previous cycle. Then the identified open-loop model is used to redesign the state feedback. The state feedback and the identified Kalman filter gain are used to form an updated LQC controller for the next cycle. This iterative process continues until the updated controller converges. The proposed controller design is demonstrated by numerical simulations and experiments on a highly unstable large-gap magnetic suspension system

Pronounced activation of protein kinase C, ornithine decarboxylase and c-jun proto-oncogene by paraquat-generated active oxygen species in WI-38 human lung cells

AbstractParaquat (methyl viologen, PQ) is a widely used herbicide that produces oxygen-derived free radicals and severely injures human lungs. In this study we examined the effects of PQ on the protein kinase C (PKC), ornithine decarboxylase (ODC) and c-jun oncogene expression in WI-38 human lung cells. Exposure of cells to 25–200 μM PQ resulted in an increase of [3H]phorbol dibutyrate (PDBu) binding and PKC redistribution in a dose-dependent manner. Interestingly, a superoxide dismutase mimic, 4-hydroxyl-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol, 2.5 mM) and catalase (400 μg/ml) could significantly reduce the PQ-stimulated increase of phorbol ester binding and particular PKC phosphorylatiog activity, but dimethylsulfoxide (DMSO, 1.5%), an effective ·OH trapping agent, failed to prevent this stimulation. In addition, an endogenous substrate of PKC, 80 kDa protein, was found to be highly phosphorylated in intact WI-38 cells treated with 50 AM PQ. The increase of phosphorylated proteins could be completely or partly abolished by Tempol or catalase, but only the phosphorylation of 80 kDa protein was diminished by protein kinase C inhibitor, 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine (H-7). A maximal peak of ODC activity was observed at 6 h of treatment with 50 μM PQ. PQ induced activity was reduced at the following rates, Tempol 85%, DMSO 80% and catalase 45%, but H-7 failed to do so. Furthermore, we found that the level of c-jun mRNA was transiently increased by PQ and the peak appeared at 1 h of treatment. When correlated with the PKC result, Tempol, catalase and H-7 all effectively blocked PQ-elicited c-jun transcript expression, but DMSO only exhibited a weakly inhibitory effect. We therefore propose that superoxide anion (O2− and H2O2 generated by PQ could activate PKC and lead to induction of c-jun gene expression; on the other hand, O2− and ·OH might trigger other kinase pathways to elevate ODC activity. Finally, the sequential expression of c-jun oncogene, and ODC may cooperate to relieve the oxidative damages elicited by PQ

Modeling and Identification of a Large Gap Magnetic Suspension System

This paper presents the results of modeling and system identification efforts on the NASA Large-Angle Magnetic Suspension Test Fixture (LAMSTF). The LAMSTF consists of a cylindrical permanent magnet which is levitated above a planar array of five electromagnets mounted in a circular configuration. The analytical model is first developed and open-loop characteristics are described. The system is shown to be highly unstable and requires feedback control in order to apply system identification. Limitations on modeling accuracy due to the effect of eddy-currents on the system are discussed. An algorithm is derived to identify a state-space model for the system from input/output data acquired during closed-loop operation. The algorithm is tested on both the baseline system and a perturbed system which has an increased presence of eddy currents. It is found that for the baseline system the analytic model adequately captures the dynamics, although the identified model improves the simulation accuracy. For the system perturbed by additional unmodeled eddy-currents the analytic model is no longer adequate and a higher-order model, determined through system identification, is required to accurately predict the system's time response

Inhibition effect of a custom peptide on lung tumors

Cecropin B is a natural antimicrobial peptide and CB1a is a custom, engineered modification of it. In vitro, CB1a can kill lung cancer cells at concentrations that do not kill normal lung cells. Furthermore, in vitro, CB1a can disrupt cancer cells from adhering together to form tumor-like spheroids. Mice were xenografted with human lung cancer cells; CB1a could significantly inhibit the growth of tumors in this in vivo model. Docetaxel is a drug in present clinical use against lung cancers; it can have serious side effects because its toxicity is not sufficiently limited to cancer cells. In our studies in mice: CB1a is more toxic to cancer cells than docetaxel, but dramatically less toxic to healthy cells