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Cilia and flagella exhibit regular bending waves that perform mechanical work on the surrounding fluid, to propel cellular swimmers and pump fluids inside organisms. Here, we quantify a force-velocity relationship of the beating flagellum, by exposing flagellated emph{Chlamydomonas} cells to controlled microfluidic flows. A simple theory of flagellar limit-cycle oscillations, calibrated by measurements in the absence of flow, reproduces this relationship quantitatively. We derive a link between the chemo-mechanical efficiency of the flagellar beat and its ability to synchronize to oscillatory flows.
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Despite being of vital importance to the immune system, the mechanism by which cells engulf relatively large solid particles during phagocytosis is still poorly understood. From movies of neutrophil phagocytosis of polystyrene beads, we measure the fractional engulfment as a function of time and demonstrate that phagocytosis occurs in two distinct stages. During the first stage, engulfment is relatively slow and progressively slows down as phagocytosis proceeds. However, at approximately half-engulfment, the rate of engulfment increases dramatically, with complete engulfment attained soon afterwards. By studying simple mathematical models of phagocytosis, we suggest that the first stage is due to a passive mechanism, determined by receptor diffusion and capture, whereas the second stage is more actively controlled, perhaps with receptors being driven towards the site of engulfment. We then consider a more advanced model that includes signaling and captures both stages of engulfment. This model predicts that there is an optimum ligand density for quick engulfment. Further, we show how this model explains why non-spherical particles engulf quickest when presented tip-first. Our findings suggest that active regulation may be a later evolutionary innovation, allowing fast and robust engulfment even for large particles.
We present a theory of flagellar synchronization in the green alga Chlamydomonas, using full treatment of flagellar hydrodynamics. We find that two recently proposed synchronization mechanisms, basal coupling and flagellar waveform compliance, stabilize anti-phase synchronization if operative in isolation. Their nonlinear superposition, however, stabilizes in-phase synchronization as observed in experiments. Our theory predicts different synchronization dynamics in fluids of increased viscosity or external flow, suggesting a non-invasive way to control synchronization by hydrodynamic coupling.
Two distinct mechanisms for filtering noise in an input signal are identified in a class of adaptive sensory networks. We find that the high frequency noise is filtered by the output degradation process through time-averaging; while the low frequency noise is damped by adaptation through negative feedback. Both filtering processes themselves introduce intrinsic noises, which are found to be unfiltered and can thus amount to a significant internal noise floor even without signaling. These results are applied to E. coli chemotaxis. We show unambiguously that the molecular mechanism for the Berg-Purcell time-averaging scheme is the dephosphorylation of the response regulator CheY-P, not the receptor adaptation process as previously suggested. The high frequency noise due to the stochastic ligand binding-unbinding events and the random ligand molecule diffusion is averaged by the CheY-P dephosphorylation process to a negligible level in E.coli. We identify a previously unstudied noise source caused by the random motion of the cell in a ligand gradient. We show that this random walk induced signal noise has a divergent low frequency component, which is only rendered finite by the receptor adaptation process. For gradients within the E. coli sensing range, this dominant external noise can be comparable to the significant intrinsic noise in the system. The dependence of the response and its fluctuations on the key time scales of the system are studied systematically. We show that the chemotaxis pathway may have evolved to optimize gradient sensing, strong response, and noise control in different time scales
Mounting evidence for the role of oxidative stress in the degeneration of articular cartilage after an injurious impact requires our modeling & simulation efforts to temporarily shift from just describing the effect of mechanical stress and inflammation on osteoarthritis (OA). The hypothesis that the injurious impact causes irreversible damage to chondrocyte mitochondria, which in turn increase their production of free radicals, affecting their energy production and their ability to rebuild the extracellular matrix, has to be modeled and the processes quantified in order to further the understanding of OA, its causes, and viable treatment options. The current article presents a calibrated model that captures the damage oxidative stress incurs on the cell viability, ATP production, and cartilage stability in a cartilage explant after a drop-tower impact. The model validates the biological hypothesis and will be used in further efforts to identify possibilities for treatment and be a part of a bigger modeling & simulation framework for the development of OA.
Purpose: Experimental measurements of bone mineral density distributions (BMDDs) enable a determination of secondary mineralisation kinetics in bone, but the maximum degree of mineralisation and how this maximum is approached remain uncertain. We thus test computationally different hypotheses on late stages of bone mineralisation by simulating BMDDs in low turnover conditions. Materials and Methods: An established computational model of the BMDD that accounts for mineralisation and remodelling processes was extended to limit mineralisation to various maximum calcium capacities of bone. Simulated BMDDs obtained by reducing turnover rate from the reference trabecular BMDD under different assumptions on late stage mineralisation kinetics were compared with experimental BMDDs of low-turnover bone. Results: Simulations show that an abrupt stopping of mineralisation near a maximum calcium capacity induces a pile-up of minerals in the BMDD statistics that is not observed experimentally. With a smooth decrease of mineralisation rate, imposing low maximum calcium capacities helps to match peak location and width of simulated low turnover BMDDs with peak location and width of experimental BMDDs, but results in a distinctive asymmetric peak shape. No tuning of turnover rate and maximum calcium capacity was able to explain the differences found in experimental BMDDs between trabecular bone (high turnover) and femoral cortical bone (low turnover). Conclusions: Secondary mineralisation in human bone does not stop abruptly, but continues slowly up to a calcium content greater than 30 wt% Ca. The similar mineral heterogeneity seen in trabecular and femoral cortical bones at different peak locations was unexplained by turnover differences tested.
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