Roundabout accident prediction model: random-parameter negative binomial approach

Roundabouts have been used widely on all road classes in the United Kingdom because they are considered safer than other types of intersections in general. The objective of this study was to examine geometric and traffic characteristics and their influences on the number of accidents. Data from each of 70 roundabouts (with 284 approaches) included all recorded vehicle accidents as well as geometric and traffic characteristics for the entire roundabout, within circulatory lanes, and at roundabout approaches. Resulting estimates were compared with those from random-parameter and fixed-parameter negative binomial count data models. The random-parameter results provided better goodness of fit than the fixed-parameter results, and more variables were found to be significant. Significant variables that influenced the number of accidents were total approach traffic, truck percentage, entry width, inscribed circle diameter, number of lanes, and presence of traffic signals

Pedestrian Injury and Human Behaviour: Observing Road-Rule Violations at High-Incident Intersections

Background Human behaviour is an obvious, yet under-studied factor in pedestrian injury. Behavioural interventions that address rule violations by pedestrians and motorists could potentially reduce the frequency of pedestrian injury. In this study, a method was developed to examine road-rule non-compliance by pedestrians and motorists. The purpose of the study was to examine the potential association between violations made by pedestrians and motorists at signalized intersections, and collisions between pedestrians and motor-vehicles. The underlying hypothesis is that high-incident pedestrian intersections are likely to vary with respect to their aetiology, and thus are likely to require individualized interventions – based on the type and rate of pedestrian and motorist violation. Methods High-incident pedestrian injury intersections in Vancouver, Canada were identified using geographic information systems. Road-rule violations by pedestrians and motorists were documented at each incident hotspot by a team of observers at several different time periods during the day. Results Approximately 9,000 pedestrians and 18,000 vehicles were observed in total. In total for all observed intersections, over 2000 (21%) pedestrians committed one of the observed pedestrian road-crossing violations, while approximately 1000 (5.9%) drivers committed one of the observed motorist violations. Great variability in road-rule violations was observed between intersections, and also within intersections at different observation periods. Conclusions Both motorists and pedestrians were frequently observed committing road-rule violations at signalized intersections, suggesting a potential human behavioural contribution to pedestrian injury at the study sites. These results suggest that each intersection may have unique mechanisms that contribute to pedestrian injury, and may require targeted behavioural interventions. The method described in this study provides the basis for understanding the relationship between violations and pedestrian injury risk at urban intersections. Findings could be applied to targeted prevention campaigns designed to reduce the number of pedestrian injuries at signalized intersections

In vitro degradation behavior and cytocompatibility of Mg–Zn–Zr alloys

Zinc and zirconium were selected as the alloying elements in biodegradable magnesium alloys, considering their strengthening effect and good biocompatibility. The degradation rate, hydrogen evolution, ion release, surface layer and in vitro cytotoxicity of two Mg–Zn–Zr alloys, i.e. ZK30 and ZK60, and a WE-type alloy (Mg–Y–RE–Zr) were investigated by means of long-term static immersion testing in Hank’s solution, non-static immersion testing in Hank’s solution and cell-material interaction analysis. It was found that, among these three magnesium alloys, ZK30 had the lowest degradation rate and the least hydrogen evolution. A magnesium calcium phosphate layer was formed on the surface of ZK30 sample during non-static immersion and its degradation caused minute changes in the ion concentrations and pH value of Hank’s solution. In addition, the ZK30 alloy showed insignificant cytotoxicity against bone marrow stromal cells as compared with biocompatible hydroxyapatite (HA) and the WE-type alloy. After prolonged incubation for 7 days, a stimulatory effect on cell proliferation was observed. The results of the present study suggested that ZK30 could be a promising material for biodegradable orthopedic implants and worth further investigation to evaluate its in vitro and in vivo degradation behavior

A bi-articular model for scapular-humeral rhythm reconstruction through data from wearable sensors

Patient-specific performance assessment of arm movements in daily life activities is fundamental for neurological rehabilitation therapy. In most applications, the shoulder movement is simplified through a socket-ball joint, neglecting the movement of the scapular-thoracic complex. This may lead to significant errors. We propose an innovative bi-articular model of the human shoulder for estimating the position of the hand in relation to the sternum. The model takes into account both the scapular-toracic and gleno-humeral movements and their ratio governed by the scapular-humeral rhythm, fusing the information of inertial and textile-based strain sensors

The BMP Antagonist Follistatin-Like 1 Is Required for Skeletal and Lung Organogenesis

Follistatin-like 1 (Fstl1) is a secreted protein of the BMP inhibitor class. During development, expression of Fstl1 is already found in cleavage stage embryos and becomes gradually restricted to mesenchymal elements of most organs during subsequent development. Knock down experiments in chicken and zebrafish demonstrated a role as a BMP antagonist in early development. To investigate the role of Fstl1 during mouse development, a conditional Fstl1 KO allele as well as a Fstl1-GFP reporter mouse were created. KO mice die at birth from respiratory distress and show multiple defects in lung development. Also, skeletal development is affected. Endochondral bone development, limb patterning as well as patterning of the axial skeleton are perturbed in the absence of Fstl1. Taken together, these observations show that Fstl1 is a crucial regulator in BMP signalling during mouse development

Intracellular iron uptake is favored in Hfe-KO mouse primary chondrocytes mimicking an osteoarthritis-related phenotype

HFE-hemochromatosis is a disease characterized by a systemic iron overload phenotype mainly associated with mutations in the HFE protein (HFE) gene. Osteoarthritis (OA) has been reported as one of the most prevalent complications in HFE-hemochromatosis patients, but the mechanisms associated with its onset and progression remain incompletely understood. In this study, we have characterized the response to high iron concentrations of a primary culture of articular chondrocytes isolated from newborn Hfe-KO mice and compared the results with that of a similar experiment developed in cells from C57BL/6 wild-type (wt) mice. Our data provide evidence that both wt- and Hfe-KO-derived chondrocytes, when exposed to 50 mu M iron, develop characteristics of an OA-related phenotype, such as an increased expression of metalloproteases, a decreased extracellular matrix production, and a lower expression level of aggrecan. In addition, Hfe-KO cells also showed an increased expression of iron metabolism markers and MMP3, indicating an increased susceptibility to intracellular iron accumulation and higher levels of chondrocyte catabolism. Accordingly, upon treatment with 50 mu M iron, these chondrocytes were found to preferentially differentiate toward hypertrophy with increased expression of collagen I and transferrin and downregulation of SRY (sex-determining region Y)-box containing gene 9 (Sox9). In conclusion, high iron exposure can compromise chondrocyte metabolism, which, when simultaneously affected by an Hfe loss of function, appears to be more susceptible to the establishment of an OA-related phenotype.European Regional Development FundEuropean Union (EU) [EMBRC.PT Alg-01-0145-FEDER-022121, Norte-01-0145-FEDER-000012]Fundacao para a Ciencia e a TecnologiaPortuguese Foundation for Science and Technology [SFRH/BD/77056/2011]Portuguese Foundation for Science and TechnologyPortuguese Foundation for Science and TechnologyPortuguese Science and Technology FoundationPortuguese Foundation for Science and Technologyinfo:eu-repo/semantics/publishedVersio

Interaction of TGFβ and BMP Signaling Pathways during Chondrogenesis

TGFβ and BMP signaling pathways exhibit antagonistic activities during the development of many tissues. Although the crosstalk between BMP and TGFβ signaling pathways is well established in bone development, the relationship between these two pathways is less well defined during cartilage development and postnatal homeostasis. We generated hypomorphic mouse models of cartilage-specific loss of BMP and TGFβ signaling to assess the interaction of these pathways in postnatal growth plate homeostasis. We further used the chondrogenic ATDC5 cell line to test effects of BMP and TGFβ signaling on each other's downstream targets. We found that conditional deletion of Smad1 in chondrocytes resulted in a shortening of the growth plate. The addition of Smad5 haploinsufficiency led to a more severe phenotype with shorter prehypertrophic and hypertrophic zones and decreased chondrocyte proliferation. The opposite growth plate phenotype was observed in a transgenic mouse model of decreased chondrocytic TGFβ signaling that was generated by expressing a dominant negative form of the TGFβ receptor I (ΔTβRI) in cartilage. Histological analysis demonstrated elongated growth plates with enhanced Ihh expression, as well as an increased proliferation rate with altered production of extracellular matrix components. In contrast, in chondrogenic ATDC5 cells, TGFβ was able to enhance BMP signaling, while BMP2 significantly reduces levels of TGF signaling. In summary, our data demonstrate that during endochondral ossification, BMP and TGFβ signaling can have antagonistic effects on chondrocyte proliferation and differentiation in vivo. We also found evidence of direct interaction between the two signaling pathways in a cell model of chondrogenesis in vitro