Quantitative Models and Implicit Complexity

We give new proofs of soundness (all representable functions on base types lies in certain complexity classes) for Elementary Affine Logic, LFPL (a language for polytime computation close to realistic functional programming introduced by one of us), Light Affine Logic and Soft Affine Logic. The proofs are based on a common semantical framework which is merely instantiated in four different ways. The framework consists of an innovative modification of realizability which allows us to use resource-bounded computations as realisers as opposed to including all Turing computable functions as is usually the case in realizability constructions. For example, all realisers in the model for LFPL are polynomially bounded computations whence soundness holds by construction of the model. The work then lies in being able to interpret all the required constructs in the model. While being the first entirely semantical proof of polytime soundness for light logi cs, our proof also provides a notable simplification of the original already semantical proof of polytime soundness for LFPL. A new result made possible by the semantic framework is the addition of polymorphism and a modality to LFPL thus allowing for an internal definition of inductive datatypes.Comment: 29 page

Structure of the TPR Domain of AIP: Lack of Client Protein Interaction with the C-Terminal alpha-7 Helix of the TPR Domain of AIP Is Sufficient for Pituitary Adenoma Predisposition

PMCID: PMC3534021This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Unreliable numbers: error and harm induced by bad design can be reduced by better design

Number entry is a ubiquitous activity and is often performed in safety- and mission-critical procedures, such as healthcare, science, finance, aviation and in many other areas. We show that Monte Carlo methods can quickly and easily compare the reliability of different number entry systems. A surprising finding is that many common, widely used systems are defective, and induce unnecessary human error. We show that Monte Carlo methods enable designers to explore the implications of normal and unexpected operator behaviour, and to design systems to be more resilient to use error. We demonstrate novel designs with improved resilience, implying that the common problems identified and the errors they induce are avoidable

Dehalogenation of polychlorinated biphenyls and polybrominated diphenyl ethers using a hybrid bioinorganic catalyst

The environmentally prevalent polybrominated diphenyl ether (PBDE) #47 and polychlorinated biphenyls (PCBs) #28 and #118 were challenged for 24 hours with a novel biomass-supported Pd catalyst (BioPd0). Analysis of the products via GC/MS revealed the BioPd0 to cause the challenged compounds to undergo stepwise dehalogenation with preferential loss of the least sterically hindered halogen atom. A mass balance for PCB #28 showed that it is degraded to three dichlorobiphenyls (33.9 %), two monochlorobiphenyls (12 %), and biphenyl (30.7 %). The remaining mass was starting material. In contrast, while PCB #118 underwent degradation to yield five tetra- and five trichlorinated biphenyls; no less chlorinated products or biphenyl were detected, and the total mass of degraded products was 0.3 %. Although the BioPd0 material was developed for treatment of PCBs, a mass balance for PBDE #47 showed that the biocatalyst could prove a useful method for treatment of PBDEs. Specifically, 10 % of PBDE # 47 was converted to identifiable lower brominated congeners, predominantly the tribrominated BDE 17, and the dibrominated BDE 4, 75 % remained intact, while 15 % of the starting mass was unaccounted for

Cover to Volume 3

The fibroblast mitogen platelet-derived growth factor -BB (PDGF-BB) induces a transient expression of the orphan nuclear receptor NR4A1 (also named Nur77, TR3 or NGFIB). The aim of the present study was to investigate the pathways through which NR4A1 is induced by PDGF-BB and its functional role. We demonstrate that in PDGF-BB stimulated NIH3T3 cells, the MEK1/2 inhibitor CI-1040 strongly represses NR4A1 expression, whereas Erk5 downregulation delays the expression, but does not block it. Moreover, we report that treatment with the NF-κB inhibitor BAY11-7082 suppresses NR4A1 mRNA and protein expression. The majority of NR4A1 in NIH3T3 was found to be localized in the cytoplasm and only a fraction was translocated to the nucleus after continued PDGF-BB treatment. Silencing NR4A1 slightly increased the proliferation rate of NIH3T3 cells; however, it did not affect the chemotactic or survival abilities conferred by PDGF-BB. Moreover, overexpression of NR4A1 promoted anchorage-independent growth of NIH3T3 cells and the glioblastoma cell lines U-105MG and U-251MG. Thus, whereas NR4A1, induced by PDGF-BB, suppresses cell growth on a solid surface, it increases anchorage-independent growth