Endogent: Centre for Anatomy and Invasive Techniques

The invention of new endoscopical techniques for surgery and interventional radiology demand improved training at postgraduate level. The Endogent Centre for Anatomy and Invasive Techniques support these requirements by establishing hands-on practical training courses by using new procedures for cadaver embalming. Cadavers fixed by conventional procedures using formalin for conservation, are of limited use for practical surgical courses due to the profound changes of colour, strength and fragility of organs and tissues. The new Thiel embalming technique is based on the use of 4-chloro-3- methylenphenol, various salts for fixation, boric acid for disinfecting, and ethylene glycol for preservation of tissue plasticity, while the concentration of formalin is kept to the strict minimum (0.8%). This results in well preserved organs and tissues concerning colour, consistency, flexibility and plasticity. The articular joints remain freely movable and the peritoneal cavity can be inflated for laparoscopic procedures. Up to now this cadaver model was used in our institute for laparoscopic bariatric surgery, colon surgery, arthroscopy and thorax surgery. Another feature is that the lungs can be ventilated during surgical procedures. Preliminary findings seem to indicate that the corpses also serve as a suitable phantom for assessing thorax radiological equipment. Expert clinicians work as tutors and give intensive instructions before the participants start with hands-on surgery. We intend to expose also our undergraduate medical students to demonstrations of surgical approaches on Thiel embalmed corpses, in order to reveal the need for detailed anatomical knowledge in the clinic at an early stage in the medical curriculum

3D computerized model for measuring strain and displacement of the brachial plexus following placement of reverse shoulder prosthesis

The aim of the present study was to develop a method for three-dimensional (3D) reconstruction of the brachial plexus to study its morphology and to calculate strain and displacement in relation to changed nerve position. The brachial plexus was finely dissected and injected with contrast medium and leaden markers were implanted into the nerves at predefined places. A reverse shoulder prosthesis was inserted in a cadaveric specimen what induced positional change in the upper limb nerves. Computed tomography (CT) was performed before and after this surgical intervention. The computer assisted image processing package Mimics (R) was used to reconstruct the pre- and postoperative brachial plexus in 3D. The results show that the current interactive model is a realistic and detailed representation of the specimen used, which allows 3D study of the brachial plexus in different configurations. The model estimated strains up to 15.3% and 19.3% for the lateral and the medial root of the median nerve as a consequence of placing a reverse shoulder prosthesis. Furthermore, the model succeeded in calculating the displacement of the brachial plexus by tracking each implanted lead marker. The presented brachial plexus 3D model currently can be used in vitro for cadaver biomechanical analyses of nerve movement to improve diagnosis and treatment of peripheral neuropathies. The model can also be applied to study the exact location of the plexus in unusual upper limb positions like during axillary radiation therapy and it is a potential tool to optimize the approaches of brachial plexus anesthetic blocks

Artificial beach nourishment on Belgian east coast

For several decades, the Belgian East Coast has posed problems of a sedimentological nature. Off the coast, a gully (called “Appelzak”) has developed to a depth of 8 m below low-water and has shifted dangerously near the existing seadike, causing severe beach erosion. In 1976 the Belgian Government decided to sizeably enlarge the outer harbor of Zeebrugge seaward to a distance of 3.5 km from the coast, and to proceed with a significant beach restoration of about 8.5 million m³ of sand. An extensive observation program is carried out to study beach changes and to indicate unexpected developments, so that counter-measures can be taken in good time. Results of observations over the period June 1979 until February 1981 are examined using survey data from bathymetric soundings, aerial photogrammetry and terrestrial beach measurem

Cell transformation assays for prediction of carcinogenic potential: State of the science and future research needs

Copyright @ 2011 The Authors. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.Cell transformation assays (CTAs) have long been proposed as in vitro methods for the identification of potential chemical carcinogens. Despite showing good correlation with rodent bioassay data, concerns over the subjective nature of using morphological criteria for identifying transformed cells and a lack of understanding of the mechanistic basis of the assays has limited their acceptance for regulatory purposes. However, recent drivers to find alternative carcinogenicity assessment methodologies, such as the Seventh Amendment to the EU Cosmetics Directive, have fuelled renewed interest in CTAs. Research is currently ongoing to improve the objectivity of the assays, reveal the underlying molecular changes leading to transformation and explore the use of novel cell types. The UK NC3Rs held an international workshop in November 2010 to review the current state of the art in this field and provide directions for future research. This paper outlines the key points highlighted at this meeting

Mechanisms of c-Myc Degradation by Nickel Compounds and Hypoxia

Nickel (Ni) compounds have been found to cause cancer in humans and animal models and to transform cells in culture. At least part of this effect is mediated by stabilization of hypoxia inducible factor (HIF1a) and activating its downstream signaling. Recent studies reported that hypoxia signaling might either antagonize or enhance c-myc activity depending on cell context. We investigated the effect of nickel on c-myc levels, and demonstrated that nickel, hypoxia, and other hypoxia mimetics degraded c-myc protein in a number of cancer cells (A549, MCF-7, MDA-453, and BT-474). The degradation of the c-Myc protein was mediated by the 26S proteosome. Interestingly, knockdown of both HIF-1α and HIF-2α attenuated c-Myc degradation induced by Nickel and hypoxia, suggesting the functional HIF-1α and HIF-2α was required for c-myc degradation. Further studies revealed two potential pathways mediated nickel and hypoxia induced c-myc degradation. Phosphorylation of c-myc at T58 was significantly increased in cells exposed to nickel or hypoxia, leading to increased ubiquitination through Fbw7 ubiquitin ligase. In addition, nickel and hypoxia exposure decreased USP28, a c-myc de-ubiquitinating enzyme, contributing to a higher steady state level of c-myc ubiquitination and promoting c-myc degradation. Furthermore, the reduction of USP28 protein by hypoxia signaling is due to both protein degradation and transcriptional repression. Nickel and hypoxia exposure significantly increased the levels of dimethylated H3 lysine 9 at the USP28 promoter and repressed its expression. Our study demonstrated that Nickel and hypoxia exposure increased c-myc T58 phosphorylation and decreased USP28 protein levels in cancer cells, which both lead to enhanced c-myc ubiquitination and proteasomal degradation

BCL6 degradation caused by the interaction with the C-terminus of pro-HB-EGF induces cyclin D2 expression in gastric cancers

BCL6 is a transcriptional repressor that has important functions in lymphocyte differentiation and lymphomagenesis, but there have been no reports of BCL6 expression in gastric cancers. In the present study, we investigated the BCL6 function in gastric cancers. Treatment with TPA resulted in BCL6 degradation and cyclin D2 upregulation. This phenomenon was inhibited by the suppression of the nuclear translocation of HB-EGF-CTF (C-terminal fragment of pro-HB-EGF). The HB-EGF-CTF nuclear translocation leads to the interaction of BCL6 with HB-EGF-CTF and the nuclear export of BCL6, and after that BCL6 degradation was mediated by ubiquitin/proteasome pathway. Real-time RT–PCR and siRNA targeting BCL6 revealed that BCL6 suppresses cyclin D2 expression. Our data indicate that BCL6 interacts with nuclear-translocated HB-EGF-CTF and that the nuclear export and degradation of BCL6 induces cyclin D2 upregulation. We performed immunohistochemical analyses of BCL6, HB-EGF and cyclin D2 in human gastric cancers. The inverse correlation between BCL6 and cyclin D2 was also found in HB-EGF-positive human gastric cancers. BCL6 degradation caused by the HB-EGF-CTF also might induce cyclin D2 expression in human gastric cancers. Inhibition of HB-EGF-CTF nuclear translocation and maintenance of BCL6 function are important for the regulation of gastric cancer progression