Models of prey capture in larval fish

The food uptake of larval carp and pike is described from high speed movies with synchronous lateral and ventral views.During prey intake by larval fishes the velocities of the created suction flow are high relative to their own size: 0.3 m/s for carp larvae of 6 mm.Starting from the first feeding carp larvae have morphological adaptations to suction feeding: the suspensorium and opercula can be abducted, the hyoid lowered, the mouth edges can be sealed by a rotating maxillary and the opercular keeps the opercular slit closed till the moment of prey uptake.A model has been extended to calculate catch success of larval fishes from aiming inaccuracy (article 3). The absolute aiming inaccuracy (mm) increases during growth, the relative aiming inaccuracy (relative to the standard length) decreases. No causal relation exists between catch success and prey size (unless the prey is too large to pass the mouth aperture)During the time fish larvae cannot yet aim accurately, they must suck the water undirectedly. By swimming and protrusion a directed field of flow is created. Both are thus unfavorable in this respect, but they are the best ways to catch prey from larger distances. Film analysis showed that protrusion is absent in 6 mm carp larvae, but already 3.8% of the head length in 9 mm larvae. Young larvae have a larger relative increase (to body weight) during suction feeding than adult fishes. This is an optimization of suction feeding by enlarging the volume flow.A quantitative hydrodynamical model of suction feeding by larval fishes has been made. In the model the mouth cavity is treated as an expanding cylinder. the flow in and around the cylinder is calculated by numerically solving the Navier-Stokes equation in 2-D. Energy costs of suction feeding by larval fishes are negligible compared to the gains: 0.01% for large prey and 10% for very small prey. In an optimal foraging model energetic considerations during suction will be unimportant.The relation between muscle tension required for suction and fish size is determined. The relation between duration of the suction process, as measured from high speed films from 12-485 mm pikes, was used as input. The required muscle tension appeared to be minimal at hatching and increased with increasing size. Also at sizes smaller than hatching the calculated tension increased (with decreasing size), but the slope was much weaker. So on the basis of this relation no minimal size for the use of suction feeding seems to exist, at small size a freedom for architectural changes seems to be present.The interaction between suction flow and active escape movements of the prey determine which types of prey can be caught. For young larvae it is more important to postpone the moment of detection by the prey, than to maximize the water velocity. If the snap lasts longer (e.g. 20 ms) the velocity is important. The reason is that it takes 10 to 20 ms for a copepod or cladoceran to reach maximal velocity.During suction by carp larvae enormous accelerations of the water do occur (800 m/s 2in the mouth opening of a 6 mm larva). If a prey enters this region of high accelerations it is impossible to escape

An ionised/non-ionised dual porosity model of intervertebral disc tissue : an experimental quantification of parameters

The volume of the intrafibrillar water space – i.e. the water contained inside the collagen fibres – is a key parameter that is relevant to concepts of connective tissue structure and function. Confined compression and swelling experiments on annulus fibrosus samples are interpreted in terms of a dual porosity model that distinguishes between a non-ionised intrafibrillar porosity and an ionised extrafibrillar porosity. Both porosities intercommunicate and are saturated with a monovalent ionic solution, i.c. NaCl. The extrafibrillar fixed charge density of the samples is assessed using radiotracer techniques and the collagen content is evaluated by measurement of hydroxyproline concentration. The interpretation of the experimental data yields values for the intrafibrillar water content, the average activity coefficient of the ions, the Donnan osmotic coefficient, the fraction of intrafibrillar water, the stress-free deformation state, and an effective stress–strain relationship as a function of the radial position in the disc. A linear fit between the second Piola–Kirchhoff effective stress and Green–Lagrange strain yielded an effective stiffness: He=1.087 ± 0.657 MPa. The average fraction of intrafibrillar water was 1.16 g/g collagen. The results were sensitive to changes in the activity and osmotic coefficients and the fraction of intrafibrillar water. The fixed charge density increased with distance from the outer edge of the annulus, whereas the hydroxyproline decreased.The authors wish to thank Dr. Jill Urban for her advice concerning fixed charge density measurements, and Ing. Paul Willems for his assistance with the experiments. The research of Dr. J. M. Huyghe has been made possible through a fellowship of the Royal Netherlands Academy of Arts and Sciences

Partial hexokinase II knockout results in acute ischemia-reperfusion damage in skeletal muscle of male, but not female, mice

Cellular studies have demonstrated a protective role of mitochondrial hexokinase against oxidative insults. It is unknown whether HK protective effects translate to the in vivo condition. In the present study, we hypothesize that HK affects acute ischemia–reperfusion injury in skeletal muscle of the intact animal. Male and female heterozygote knockout HKII (HK(+/-)), heterozygote overexpressed HKII (HK(tg)), and their wild-type (WT) C57Bl/6 littermates mice were examined. In anesthetized animals, the left gastrocnemius medialis (GM) muscle was connected to a force transducer and continuously stimulated (1-Hz twitches) during 60 min ischemia and 90 min reperfusion. Cell survival (%LDH) was defined by the amount of cytosolic lactate dehydrogenase (LDH) activity still present in the reperfused GM relative to the contralateral (non-ischemic) GM. Mitochondrial HK activity was 72.6 ± 7.5, 15.7 ± 1.7, and 8.8 ± 0.9 mU/mg protein in male mice, and 72.7 ± 3.7, 11.2 ± 1.4, and 5.9 ± 1.1 mU/mg in female mice for HK(tg), WT, and HK(+/-), respectively. Tetanic force recovery amounted to 33 ± 7% for male and 17 ± 4% for female mice and was similar for HK(tg), WT, and HK(+/-). However, cell survival was decreased (p = 0.014) in male HK(+/-) (82 ± 4%LDH) as compared with WT (98 ± 5%LDH) and HK(tg) (97 ± 4%LDH). No effects of HKII on cell survival was observed in female mice (92 ± 2% LDH). In conclusion, in this mild model of acute in vivo ischemia–reperfusion injury, a partial knockout of HKII was associated with increased cell death in male mice. The data suggest for the first time that HKII mediates skeletal muscle ischemia–reperfusion injury in the intact male animal

Defects in 8-oxo-guanine repair pathway cause high frequency of C > A substitutions in neuroblastoma

Neuroblastomas are childhood tumors with frequent fatal relapses after induction treatment, which is related to tumor evolution with additional genomic events. Our whole-genome sequencing data analysis revealed a high frequency of somatic cytosine > adenine (C > A) substitutions in primary neuroblastoma tumors, which was associated with poor survival. We showed that increased levels of C > A substitutions correlate with copy number loss (CNL) of OGG1 or MUTYH. Both genes encode DNA glycosylases that recognize 8-oxo-guanine (8-oxoG) lesions as a first step of 8-oxoG repair. Tumor organoid models with CNL of OGG1 or MUTYH show increased 8-oxoG levels compared to wild-type cells. We used CRISPR-Cas9 genome editing to create knockout clones of MUTYH and OGG1 in neuroblastoma cells. Whole-genome sequencing of single-cell OGG1 and MUTYH knockout clones identified an increased accumulation of C > A substitutions. Mutational signature analysis of these OGG1 and MUTYH knockout clones revealed enrichment for C > A signatures 18 and 36, respectively. Clustering analysis showed that the knockout clones group together with tumors containing OGG1 or MUTYH CNL. In conclusion, we demonstrate that defects in 8-oxoG repair cause accumulation of C > A substitutions in neuroblastoma, which contributes to mutagenesis and tumor evolution