Car Design and Road Crossing Behaviour

Humans possess a highly developed sensitivity for facial features. This sensitivity is also deployed to non-human beings and inanimate objects such as cars. In the present study we aimed to investigate whether car design has a bearing on the behaviour of pedestrians. Methods: An immersive virtual reality environment with a zebra crossing was used to determine a) whether the minimum accepted distance for crossing the street is bigger for cars with dominant appearance than for cars with friendly appearance (Block 1) and b) whether the speed of dominant cars are overestimated compared to friendly cars (Block 2). In Block 1, the participant's task was to cross the road in front of an approaching car at the latest moment. The point of time when entering and leaving the street was measured. In Block 2 they were asked to estimate the speed of each passing car. An independent sample rated dominant cars as being more dominant, angry and hostile than friendly cars. Results: None of the predictions regarding the car design was confirmed. Instead, there was an effect of starting position: From the centre island, participants entered the road significantly later (smaller accepted distance) and left the road later than when starting from the pavement. Consistently, the speed of the cars was estimated significantly lower when standing on the centre island compared to the pavement. When entering the visual size of the cars as factor (instead of dominance), we found that participants started to cross the road significantly later in front of small cars compared to big cars and that the speed of smaller cars was overestimated compared to big cars (size-speed bias). Conclusions: Car size and starting position, not car design seem to have an influence on road crossing behaviour.

Two variants in the KIT gene as candidate causative mutations for a dominant white and a white spotting phenotype in the donkey.

White spotting phenotypes have been intensively studied in horses, and although similar phenotypes occur in the donkey, little is known about the molecular genetics underlying these patterns in donkeys. White spotting in donkeys can range from only a few white areas to almost complete depigmentation and is characterised by a loss of pigmentation usually progressing from a white spot in the hip area. Completely white-born donkeys are rare, and the phenotype is characterised by the complete absence of pigment resulting in pink skin and a white coat. A dominant mode of inheritance has been demonstrated for spotting in donkeys. Although the mode of inheritance for the completely white phenotype in donkeys is not clear, the phenotype shows similarities to dominant white in horses. As variants in the KIT gene are known to cause a range of white phenotypes in the horse, we investigated the KIT gene as a potential candidate gene for two phenotypes in the donkey, white spotting and white. A mutation analysis of all 21 KIT exons identified a missense variant in exon 4 (c.662A>C; p.Tyr221Ser) present only in a white-born donkey. A second variant affecting a splice donor site (c.1978+2T>A) was found exclusively in donkeys with white spotting. Both variants were absent in 24 solid-coloured controls. To the authors' knowledge, this is the first study investigating genetic mechanisms underlying white phenotypes in donkeys. Our results suggest that two independent KIT alleles are probably responsible for white spotting and white in donkeys.

When the prey gets too big: an uncommon road accident involving a motorcyclist, a car and a bird

We present the postmortem findings of a fatal road accident involving a motorcyclist, a car, and a common buzzard. Both the motorcyclist and the bird died on the scene of the accident and were examined by postmortem full-body CT and autopsy. In addition, a facial injury of the motorcyclist was compared with the dimensions of the buzzard’s beak and claws by 3D scan technologies. Blood splatters collected on the bird’s beak, feet, and tail were examined by DNA analysis. The overall findings suggested a collision of a common buzzard with a motorcyclist in full speed, causing the motorcyclist to lose control of his vehicle and crash with an approaching car on the oncoming lane.

On the road. Der Pilgerweg der Gerechtigkeit und des Friedens als transformative Herausforderung

Am Leitfaden der Geschichte der Emmaus-Jünger (Lk 24,13-35) wird die Botschaft der Ökumenischen Weltversammlung von Busan von 2013 in ihrer Verbindung von geistlicher Transformation der Glaubenden und politischer Transformation durch die Glaubenden am Beispiel der Nachhaltigkeitsthematik ausgelegt.

The Kepler Problem (the road to Bohr)

The classical Kepler problem is reviewed in depth in preparation to studying the Bohr model of the atom.

Role and regulation of c-KIT gene expression in tumor growth and metastasis of human melanoma

The purpose of this study was to investigate the role of the c-KIT receptor in the progression of human melanoma and the mechanism(s) for the regulation of c-KIT gene expression in human melanoma.^ The molecular changes associated with the transition of melanoma cells from radial growth phase (RGP) to vertical growth phase (VGP) (metastatic phenotype) are not well-defined. Expression of the tyrosine-kinase receptor c-KIT progressively decreases during local tumor growth and invasion of human melanomas. To provide direct evidence that the metastasis of human melanoma is associated with the loss of c-KIT expression, highly metastatic A375SM cells, which express very low or undetectable levels of c-KIT, were tranduced with the human c-KIT gene. We demonstrated that enforced c-KIT expression in highly metastatic human melanoma cells significantly suppressed their tumorigenicity and metastatic propensity in nude mice. In addition, we showed that the ligand for c-KIT, SCF, induces apoptosis in human melanoma cells expressing c-KIT under both in vitro and in vivo conditions. These results suggest that loss of c-KIT receptor may allow malignant melanoma cells to escape SCF/c-KIT-mediated apoptosis, thus contributing to tumor growth and eventually metastasis.^ Furthermore, we investigated the possible mechanism(s) for the down-regulation of c-KIT gene expression in malignant melanoma. Sequence analysis of the c-KIT promoter indicated that this promoter contains several consensus binding-site sequences including three putative AP2 and two Myb sites. Although Myb was shown to be associated with c-KIT expression in human hemotopoietic cells, we found no correlation between c-KIT expression and Myb expression in human melanoma cell lines. In contrast, we showed that c-KIT expression directly correlates with expression of AP2 in human melanoma cells. We found that highly metastatic cells do not express the transcription factor AP2. Expression of AP2 in A375SM cells (c-KIT-negative and AP2-negative) was enough to restore luciferase activity driven by the c-KIT promoter in a dose-dependent manner. On the other hand, co-expression of the dominant-negative form of AP2 (AP2B) in Mel-501 cells (c-KIT-positive and AP2-positive) resulted in two-fold reduction in luciferase activity. Electrophoretic mobility shift assays revealed that the c-KIT promoter contains functional AP2 binding sites which could associate with AP2 protein. Endogenous c-KIT gene expression levels were elevated in AP2 stably-transfected human melanoma A375SM cells. Expression of exogenous AP2 in A375SM cells inhibited their tumorigenicity and metastatic potential in nude mice. The c-KIT ligand, SCF, also induced apoptosis in the AP2 stably-transfected A375SM cells. The identification of AP2 as an important regulator for c-KIT expression suggests that AP2 may have tumor growth and metastasis inhibitory properties, possibly mediated through c-KIT/SCF effects on apoptosis of human melanoma cells. Since AP2 binding sites were found in the promoters of other genes involved in the progression of human melanoma, such as MMP2 (72 kDa collagenase), MCAM/MUC18 and P21/WAF-1, our findings suggest that loss of AP2 expression might be a crucial event in the development of malignant melanoma. ^