Evaluating the effectiveness of road mitigation measures

The last 20 years have seen a dramatic increase in efforts to mitigate the negative effects of roads and traffic on wildlife, including fencing to prevent wildlife-vehicle collisions and wildlife crossing structures to facilitate landscape connectivity. While not necessarily explicitly articulated, the fundamental drivers behind road mitigation are human safety, animal welfare, and/or wildlife conservation. Concomitant with the increased effort to mitigate has been a focus on evaluating road mitigation. So far, research has mainly focussed on assessing the use of wildlife crossing structures, demonstrating that a broad range of species use them. However, this research has done little to address the question of the effectiveness of crossing structures, because use of a wildlife crossing structure does not necessarily equate to its effectiveness. The paucity of studies directly examining the effectiveness of crossing structures is exacerbated by the fact that such studies are often poorly designed, which limits the level of inference that can be made. Without well performed evaluations of the effectiveness of road mitigation measures, we may endanger the viability of wildlife populations and inefficiently use financial resources by installing structures that are not as effective as we think they are. In this paper we outline the essential elements of a good experimental design for such assessments and prioritize the parameters to be measured. The framework we propose will facilitate collaboration between road agencies and scientists to undertake research programs that fully evaluate effectiveness of road mitigation measures. We discuss the added value of road mitigation evaluations for policy makers and transportation agencies and provide recommendations on how to incorporate such evaluations in road planning practices.     

Genomic imbalances are confined to non-proliferating cells in paediatric patients with acute myeloid leukaemia and a normal or incomplete karyotype

Leukaemia is often associated with genetic alterations such as translocations, amplifications and deletions, and recurrent chromosome abnormalities are used as markers of diagnostic and prognostic relevance. However, a proportion of acute myeloid leukaemia (AML) cases have an apparently normal karyotype despite comprehensive cytogenetic analysis. Based on conventional cytogenetic analysis of banded chromosomes, we selected a series of 23 paediatric patients with acute myeloid leukaemia and performed whole genome array comparative genome hybridization (aCGH) using DNA samples derived from the same patients. Imbalances involving large chromosomal regions or entire chromosomes were detected by aCGH in seven of the patients studied. Results were validated by fluorescence in situ hybridization (FISH) to both interphase nuclei and metaphase chromosomes using appropriate bacterial artificial chromosome (BAC) probes. The majority of these copy number alterations (CNAs) were confirmed by FISH and found to localize to the interphase rather than metaphase nuclei. Furthermore, the proliferative states of the cells analyzed by FISH were tested by immunofluorescence using an antibody against the proliferation marker pKi67. Interestingly, these experiments showed that, in the vast majority of cases, the changes appeared to be confined to interphase nuclei in a non-proliferative status.     

Human periosteum-derived progenitor cells express distinct chemokine receptors and migrate upon stimulation with CCL2, CCL25, CXCL8, CXCL12, and CXCL13

For bone repair, transplantation of periosteal progenitor cells (PCs), which had been amplified within supportive scaffolds, is applied clinically. More innovative bone tissue engineering approaches focus on the in situ recruitment of stem and progenitor cells to defective sites and their subsequent use for guided tissue repair. Chemokines are known to induce the directed migration of bone marrow CD34(-) mesenchymal stem cells (MSCs). The aim of our study was to determine the chemokine receptor expression profile of human CD34(-) PCs and to demonstrate that these cells migrate upon stimulation with selected chemokines. PCs were isolated from periosteum of the mastoid bone and displayed a homogenous cell population presenting an MSC-related cell-surface antigen profile (ALCAM(+), SH2(+), SH3(+), CD14(-), CD34(-), CD44(+), CD45(-), CD90(+)). The expression profile of chemokine receptors was determined by real-time PCR and immunohistochemistry. Both methods consistently demonstrated that PCs express receptors of all four chemokine subfamilies CC, CXC, CX(3)C, and C. Migration of PCs and a dose-dependent migratory effect of the chemokines CCL2 (MCP1), CCL25 (TECK), CXCL8 (IL8), CXCL12 (SDF1alpha), and CXCL13 (BCA1), but not CCL22 (MDC) were demonstrated using a 96-multiwell chemotaxis assay. In conclusion, for the first time, here we report that human PCs express chemokine receptors, present their profile, and demonstrate a dose-dependent migratory effect of distinct chemokines on these cells. These results are promising towards in situ bone repair therapies based on guiding PCs to bone defects, and encourage further in vivo studies.     

Feinstruktur der Protonephridien von Paromalostomum proceracauda (Plathelminthes,Macrostomida)

Zusammenfassung Die Protonephridien von Paromalostomum proceracauda bestehen aus je einem Terminalkomplex und einem ausleitenden Kanal. Jeder Terminalkomplex setzt sich aus drei multiciliären Terminalzellen mit jeweils separatem Filtrationsapparat zusammen; die Zellen sind gestaffelt hintereinander angeordnet und bilden ein gemeinsames Reusenlumen. Der Nephridialkanal, der nicht an der Ultrafiltration, sondern nur an Resorptionsvorgängen beteiligt ist, besteht aus mindestens zwei röhrenförmigen, hintereinander liegenden ciliären Zellen. Die jeweils letzte Kanalzelle bildet auch den Nephridialporus. Proximal sind die Protonephridien bis zur Basis der Epidermis vollständig von einer interzellulären Matrix umhüllt.

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Fine structure of the protonephridia of Paromalostomum proceracauda (Plathelminthes, Macrostomida)

Summary The protonephridia of Paromalostomum proceracaud consist, respectively, of a terminal complex and a draining canal. Each terminal complex is composed of three multiciliary terminal cells with separate filtration apparatuses; the cells are staggered, forming a joint basket lumen. The nephridial canal consists of two or more tube-shaped ciliary cells, which are arranged in series; these cells do not participate in ultrafiltration but in resorption processes. The last canal cell also forms the nephroporus. Up to the epidermis, the protonephridia are proximally surrounded by an intercellular matrix.

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Abkürzungen cw Cilienwurzel - ep Epidermiszelle - i Interzellularsubstanz - k Kanalzelle - kl Kanallumen - l Leptotrichien - m Muskulatur des Hautmuskelschlauches - n Kern einer Terminaloder Kanalzelle - r Reusenapparat - rl Reusenlumen - rs Reusenstab - t1, 2, 3 Terminalzelle 1, 2, 3 - v Vakuole     

Functional characterization of the Staphylococcus carnosus SecA protein in Escherichia coli and Bacillus subtilissecA mutant strains

Abstract The cell wall of Candida albicans contains mannoproteins that are covalently associated with β-1,6-glucan. When spheroplasts were allowed to regenerate a new cell wall, initially non-glucosylated cell wall proteins accumulated in the medium. While the spheroplasts became osmotically stable, β-1,6-glucosylated proteins could be identified in their cell wall by SDS-extraction or β-1,3-glucanase digestion. At later stages of regeneration, β-1,3-glucosylated proteins were also found. Hence, incorporation of proteins into the cell wall is accompanied by extracellular coupling to β-1,6-/β-l,3-glucan. The SDS-extractable glucosylated proteins probably represent degradation products of wall proteins rather than their precursors. Tunicamycin delayed, but did not prevent the formation of β-1,6-glucosylated proteins, demonstrating that β-1,6-glucan is not attached to N -glycosidic side-chains of wall proteins.     

Local and landscape responses of biodiversity in calcareous grasslands

Biodiversity and Conservation - Across Europe, calcareous grasslands become increasingly fragmented and their quality deteriorates through abandonment and land use intensification, both affecting...