Using role-based control to produce locomotion in chain-type self-reconfigurable robots

This paper presents a role-based approach to the problem of controlling locomotion of chain-type self-reconfigurable robots. In role-based control, all modules are controlled by identical controllers. Each controller consists of several playable roles and a role-selection mechanism. A role represents the motion of a module and how it synchronizes with connected modules. A controller selects which role to play depending on the local configuration of the module and the roles being played by connected modules. We use role-based control to implement a sidewinder and a caterpillar gait in the CONRO self-reconfigurable robot. The robot is made from up to nine modules connected in a chain. We show that the locomotion speed of the caterpillar gait is constant even with loss of 75% of the communication signals. Furthermore, we show that the speed of the caterpillar gait decreases gracefully with a decreased number of modules. We also implement a quadruped gait and show that without changing the controller the robot can be extended with an extra pair of legs and produce a hexapod gait. Based on these experiments, we conclude that role-based control is robust to signal loss, scales with an increased number of modules, and is a simple approach to the control of locomotion of chain-type self-reconfigurable robots.     

From the Politics of Urgency to the Governance of Preparedness: A Research Agenda on Urban Vulnerability

To date, little social science understanding has been developed about what it would mean to strategically build resilience in the context of such rich interdependencies between social, technical and natural worlds. We argue that shifts in strategies to deal with urban crises marks a turn from the politics of urgency, characteristic of crisis management, towards a governance of preparedness, characterised by strategies to build urban resilience. Social science needs to develop research agendas that critically engage with different understandings of resilience and the challenges of building resilience across different scales of urban governance.     

Comparison of biochemical markers of bone turnover in Paget disease treated with pamidronate and a proposed model for the relationships between measurements of the different forms of pyridinoline cross-links

We have compared the use of new markers of bone turnover in the assessment and treatment of Paget disease and made observations on the mechanisms of bone resorption. Urine hydroxyproline (Hyp) as a bone resorption marker and serum alkaline phosphatase (ALP) as a bone formation marker have traditionally been used to biochemically assess and monitor treatment of Paget disease. Hyp and total ALP were compared with total urine pyridinoline (Pyd) and deoxypyridinoline (Dpd), free urine Pyd and Dpd, urine type I collagen N-terminal cross-linked telopeptide (NTX), type I collagen C-terminal propeptide (PICP), serum osteocalcin, and bone ALP in Paget patients treated with pamidronate. Patients were divided into three biochemical severity-based treatment groups by their fasting urine hydroxyprolline excretion (HypE) levels (Le., group 1, HypE < 5.0 mumol/l of glomerular filtrate [GF]; group 2, HypE of 5.0-9.9 mumol/l of GF; group 3, HypE > 10 mumol/l of GF). Group 1 received one 60 mg intravenous infusion of pamidronate, and groups 2 and 3 received four and six 60 mg infusions at weekly intervals, respectively. Fasting serum and morning urine specimens were taken before and at 2, 6, 13, and 26 weeks after starting treatment. Baseline Z scores were used to compare separation of patient results from normal, and the difference in Z scores from baseline to 13 weeks was used to compare response to treatment. Baseline discrimination and response to treatment at all disease activity levels was greatest for NTX and was poor for osteocalcin, PICP, and C-terminal cross-linked telopeptide of type I collagen (ICTP). The other markers showed good discrimination and response at medium and high levels of disease activity. NTX, total Pyd and Dpd, free Pyd and Dpd, and ICTP are all pyridinoline cross-link-based markers, but discrimination and response by NTX was generally much greater than for the others. Determination of the mechanism of the difference between NTX and other cross-link measures is necessary for appropriate use of the markers and may also lead to a better understanding of the bone resorption process. It has been proposed that the greater sensitivity and discrimination of NTX is because it is more bone-specific than the other cross-link markers with significant amounts of free Pyd and Dpd coming from nonbone sources. We propose another model where the proportion of peptide-bound cross-links such as NTX may be increased in high bone turnover states partly due to a rate-limiting step in their degradation to free cross-links. Conditions with high bone resorption rates would have high levels of NTX that would decline rapidly when resorption rates fall to a level where the capacity to degrade NTX matches the rate of production.     

The role of bile and bile acids in bacterial translocation in obstructive jaundice in rats

Eight independent chl (chromosome loss) mutants were isolated using yeast haploid strain disomic for chromosome III. In these mutants, chromosome III is lost during mitosis 50-fold more frequently than in the wild-type strains. chl mutants are also incapable of stable maintenance of circular and linear artificial chromosomes. Seven of the eight mutations are recessive, and one is semidominant. Complementation tests placed these mutants into six complementation groups (chl11 through chl16). Based on tetrad analysis, chl12, chl14 and chl15 correspond to mutations in single nuclear genes. Tetrad analysis of the other mutants was not possible due to poor spore viability. Complementation analysis was also carried out between collection of chl mutants and ctf mutants (chromosome transmission fidelity) (Spencer et al., 1990). The chl3, chl4, chl8, chl12 and chl15 mutants were unable to complement ctf3, ctf17, ctf12, ctf18 and ctf4, respectively. Three CHL genes were mapped by tetrad analysis. The CHL3 gene is placed on the right arm of chromosome XII, between the ILV5 (33.3 cM) and URA4 (21.8 cM) loci. The CHL10 gene is located on the left arm of chromosome VI, 12.5 cM from the centromere. The CHL15 gene is tightly linked to the KAR3 marker of the right arm of chromosome XVI (8.8 cM). The mapping data indicate that these three genes differ from other genes known to affect chromosome stability in mitosis. Therefore, the total number of the CHL genes identified (including those described by us earlier) is 13 (CHL1-CHL10, CHL12, CHL14 and CHL15).