In the stag beetle family (Lucanidae), males have diverged from females by sexual selection. The males fight each other for mating opportunities with their enlarged mandibles. It is known that owners of larger fighting apparatuses are favoured to win the male-male fights, but it was unclear whether male stag beetles also need to produce high bite forces while grabbing and lifting opponents in fights. We show that male Cyclommatus metallifer stag beetles bite three times as forcefully as females. This is not entirely unexpected given the spectacular nature of the fights, but all the more impressive given the difficulty of achieving this with their long mandibles (long levers). Our results suggest no increase in male intrinsic muscle strength to accomplish this. However, morphological analyses show that the long mandibular output levers in males are compensated by elongated input levers (and thus a wider anterior side of the head). The surplus of male bite force capability is realized by enlargement of the closer muscles of the mandibles, while overall muscle force direction remained optimal. To enable the forceful bites required to ensure male reproductive success, male head size and shape are adapted for long input levers and large muscles. Therefore, the entire head should be regarded as an integral part of male armature.
A new software package called Octopus was developed for tomographic reconstruction of parallel beam projection data and fan beam data. It was written entirely in LabView®. It has a full graphical user interface and a high level of automation while allowing every processing step to be manually controlled. Octopus displays some unique features such as dual-energy tomography for element-sensitive investigations. Most importantly it features distributed reconstruction over a network using a server–client architecture with negligible network delays reducing reconstruction times almost proportionally to the number of clients. Octopus runs independently in a Windows® environment.
Although a full understanding of the hepatic circulation is one of the keys to successfully perform liver surgery and to elucidate liver pathology, relatively little is known about the functional organization of the liver vasculature. Therefore, we materialized and visualized the human hepatic vasculature at different scales, and performed a morphological analysis by combining vascular corrosion casting with novel micro-computer tomography (CT) and image analysis techniques. A human liver vascular corrosion cast was obtained by simultaneous resin injection in the hepatic artery (HA) and portal vein (PV). A high resolution (110 lm) micro-CT scan of the total cast allowed gathering detailed macrovascular data. Subsequently, a mesocirculation sample (starting at generation 5; 88 9 68 9 80 mm³) and a microcirculation sample (terminal vessels including sinusoids; 2.0 9 1.5 9 1.7 mm³) were dissected and imaged at a 71-lm and 2.6-lm resolution, respectively. Segmentations and 3D reconstructions allowed quantifying the macro-and mesoscale branching topology, and geometrical features of HA, PV and hepatic venous trees up to 13 generations (radii ranging from 13.2 mm to 80 lm; lengths from 74.4 mm to 0.74 mm), as well as microvascular characteristics (mean sinusoidal radius of 6.63 lm). Combining corrosion casting and micro-CT imaging allows quantifying the branching topology and geometrical features of hepatic trees using a multiscale approach from the macro-down to the microcirculation. This may lead to novel insights into liver circulation, such as internal blood flow distributions and anatomical consequences of pathologies (e.g. cirrhosis).
UGCT is a user facility for multidisciplinary micro-CT research. The scanners at UGCT are custom designed and built by the Radiation Physics research group (UGent). This paper describes the two latest scanners that were developed in collaboration with XRE: HECTOR, a high energy micro-CT scanner, and EMCT, a gantry based micro-CT scanner with variable magnification. HECTOR is a 240 kV 280 W system with a nominal resolution of 4 micrometer. A 40x40 cm² flat panel detector which can be tiled results in a field of view of 80x80 cm². The sample positioning stage can carry samples up to 80 kg. The second scanner, EMCT, is a gantry based micro-focus system with a variable magnification. Unlike medical or small-animal scanners, the rotation axis is mounted vertically. It was designed to allow scans of objects that are hard to rotate in a standard micro-CT scanner, such as samples that are wired to peripheral equipment or samples in a fluid environment. The source is a 130 kV 15 W microfocus source (nominal resolution 5µm) with integrated high-voltage supply. The standard detector is a 15x15 cm² flat panel detector resulting in a maximal field-of-view of 12cm diameter. In addition a high-speed detector is available which can be installed on both scanners for micro-CT of dynamic processes. To further extend the effective X-ray energy at HECTOR a high sensitivity line detector will be installed in the near future.
Bruck syndrome (BS) is a disorder characterized by joint flexion contractures and skeletal dysplasia that shows strong clinical overlap with the brittle bone disease Osteogenesis Imperfecta (OI). BS is caused by bi-allelic mutations in either the FKBP10 or the PLOD2 gene. PLOD2 encodes the lysyl hydroxylase 2 (LH2) enzyme, which is responsible for the hydroxylation of lysine residues in fibrillar collagen telopeptides. This hydroxylation directs cross-linking of collagen fibrils in the extracellular matrix, which is necessary to provide stability and tensile integrity to the collagen fibrils. To further elucidate the function of LH2 in vertebrate skeletal development, we created a zebrafish model harboring a homozygous plod2 nonsense mutation resulting in reduced telopeptide hydroxylation and cross-linking of bone type I collagen. Adult plod2 mutants present with a shortened body axis and severe skeletal abnormalities with evidence of bone fragility and fractures. The vertebral column of plod2 mutants is short and scoliotic with compressed vertebrae that show excessive bone formation at the vertebral end plates, and increased tissue mineral density in the vertebral centra. The muscle fibers of mutant zebrafish have a reduced diameter near the horizontal myoseptum. The endomysium, a layer of connective tissue ensheathing the individual muscle fibers, is enlarged. Transmission electron microscopy of mutant vertebral bone shows type I collagen fibrils that are less organized with loss of the typical plywood-like structure. In conclusion, plod2 mutant zebrafish show molecular and tissue abnormalities in the musculoskeletal system that are concordant with clinical findings in BS patients. Therefore, the plod2 zebrafish mutant is a promising model for the elucidation of the underlying pathogenetic mechanisms leading to BS and the development of novel therapeutic avenues in this syndrome.
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