Towards a Better Prediction of Cell Settling on Nanostructure Arrays—Simple Means to Complicated Ends

Vertical arrays of nanostructures (NSs) are emerging as promising platforms for probing and manipulating live mammalian cells. The broad range of applications requires different types of interfaces, but cell settling on NS arrays is not yet fully controlled and understood. Cells are both seen to deform completely into NS arrays and to stay suspended like tiny fakirs, which have hitherto been explained with differences in NS spacing or density. Here, a better understanding of this phenomenon is provided by using a model that takes into account the extreme membrane deformation needed for a cell to settle into a NS array. It is shown that, in addition to the NS density, cell settling depends strongly on the dimensions of the single NS, and that the settling can be predicted for a given NS array geometry. The predictive power of the model is confirmed by experiments and good agreement with cases from the literature. Furthermore, the influence of cell‐related parameters is evaluated theoretically and a generic method of tuning cell settling through surface coating is demonstrated experimentally. These findings allow a more rational design of NS arrays for the numerous exciting biological applications where the mode of cell settling is crucial.     

The effect of annealing on the elastoplastic and viscoelastic responses of isotactic polypropylene

Observations are reported on isotactic polypropylene (i) in a series of tensile tests with a constant strain rate on specimens annealed for 24 h at various temperatures in the range from 110 to 150 °C, (ii) in two series of creep tests in the subyield region of deformations on samples not subjected to thermal treatment and on specimens annealed at 140 °C, and (iii) in a series of tensile relaxation tests on non-annealed specimens. Constitutive equations are derived for the elastoplastic and non-linear viscoelastic responses of semicrystalline polymers. A polymer is treated as an equivalent transient network of macro-molecules bridged by junctions (physical cross-links, entanglements and lamellar blocks). The network is assumed to be highly heterogeneous, and it is thought of as an ensemble of meso-regions with different activation energies for separation of strands from temporary nodes. The elastoplastic behavior is modelled as sliding of junctions in meso-domains with respect to their reference positions driven by macro-deformation. The viscoelastic response is attributed to detachment of active strands from temporary junctions and attachment of dangling chains to the network. Constitutive equations for isothermal deformations with small strains are derived by using the laws of thermodynamics. Adjustable parameters in the stress–strain relations are found by fitting the experimental data.     

Sequential Decoding of Convolutional Codes for Rayleigh Fading Channels

The performance of sequential decoding of long constraint length convolutional codes is evaluated for Rayleigh fading channels. Sequential decoding is not practical below a certain theoretical signal-to-noise ratio, and these theoretical limits are calculated for a number of modulation methods and code rates. As an example, with BPSK modulation, soft decisions and code rate 1/2, the theoretical signal-to-noise ratio per information bit is 5.7 dB. Above this limit the bit error rate can be made arbitrarily small by increasing the constraint length at no significant complexity cost. Furthermore, it is shown that with carefully chosen quantization steps, 8 level uniform quantization gives a negligible loss also for sequential decoding on a Rayleigh fading channel. Simulation results using 8 level quantization correspond well with the theoretical performance bounds. Also, the performance on a correlated channel with finite interleaving has been obtained. With an interleaver depth of 50×50 and a normalized doppler frequency equal to 0.01 we are only 0.5 dB away from the performance with perfect interleaving. Finally, bit error rate results show this scheme to compete well with Turbo codes.     

Effects of experimental muscle pain on muscle activity and co-ordination during static and dynamic motor function

The relation between muscle pain, muscle activity, and muscle co-ordination is still controversial. The present human study investigates the influence of experimental muscle pain on resting, static, and dynamic muscle activity. In the resting and static experiments, the electromyography (EMG) activity and the contraction force of m. tibialis anterior were assessed before and after injection of 0.5 ml hypertonic saline (5%) into the same muscle. In the dynamic experiment, injections of 0.5 ml hypertonic saline (5%) were performed into either m. tibialis anterior (TA) or m. gastrocnemius (GA) and the muscle activity and co-ordination were investigated during gait on a treadmill by EMG recordings from m. TA and m. GA. At rest no evidence of EMG hyperactivity was found during muscle pain. The maximal voluntary contraction (MVC) during muscle pain was significantly lower than the control condition (P < 0.05). During a static contraction at 80% of the pre-pain MVC muscle pain caused a significant reduction in endurance time (P < 0.043). During dynamic contractions, muscle pain resulted in a significant decrease of the EMG activity in the muscle, agonistic to the painful muscle (P < 0.05), and a significant increase of the EMG activity of the muscle, antagonistic to the painful muscle (P < 0.05). Muscle pain seems to cause a general protection of painful muscles during both static and dynamic contractions. The increased EMG activity of the muscle antagonistic to the painful muscle is probably a functional adaptation of muscle co-ordination in order to limit movements. Modulation of muscle activity by muscle pain could be controlled via inhibition of muscles agonistic to the movement and/or excitation of muscles antagonistic to the movement. The present results are in accordance with the pain-adaptation model (Lund, J.P., Stohler, C.S. and Widmer, C.G. In: H. Vaer?y and H. Merskey (Eds.), Progress in Fibromyalgia and Myofascial Pain. Elsevier, Amsterdam, 1993, pp. 311-327.) which predicts increased activity of antagonistic muscle and decreased activity of agonistic muscle during experimental and clinical muscle pain.