Aggregate planning through the imprecise goal programming model: integration of the manager's preferences

Aggregate planning involves planning the best quantity to be produced during time periods in the medium‐range horizon at the lowest cost. Usually, the production manager seeks a plan that simultaneously optimizes several incommensurable and conflicting objectives, such as total cost, level of inventories, level of customer service, fluctuation in workforce, and utilization level of the physical facility and equipment. The goal programming (GP) model is one of the best known multi‐objective programming models that considers simultaneously several conflicting objectives to select the most satisfactory solution among a set of feasible solutions. In the production planning problem, the goals and the technological parameters are naturally imprecise. Moreover, the existing GP formulations developed in industrial engineering and aggregate production planning do not explicitly incorporate the manager's preferences. The aim of this paper is to develop a GP formulation within an imprecise environment where the concept of satisfaction function will be utilized to explicitly introduce the manager's preferences into the aggregate planning model.     

An intensional approach for periodic data in relational databases

Periodic data play a major role in many application domains, spanning from manufacturing to office automation, from scheduling to data broadcasting. In many of such domains, the huge number of repetitions make the goal of extesionally storing and accessing such data very challenging. In this paper, we propose a new methodology, based on an intensional representation of periodic data. The representation model we propose captures the notion of periodic granularity provided by the temporal database glossary, and is an extension of the TSQL2 temporal relational data model. We define the algebraic operators, and introduce access algorithms to cope with them, proving that they are correct with respect to the traditional extesional approach. We also provide an experimental evaluation of our approach.     

Enhancing Urban Façades via LiDAR‐Based Sculpting

Buildings with symmetrical façades are ubiquitous in urban landscapes and detailed models of these buildings enhance the visual realism of digital urban scenes. However, a vast majority of the existing urban building models in web‐based 3D maps such as Google earth are either less detailed or heavily rely on texturing to render the details. We present a new framework for enhancing the details of such coarse models, using the geometry and symmetry inferred from the light detection and ranging (LiDAR) scans and 2D templates. The user‐defined 2D templates, referred to as coded planar meshes (CPMs), encodes the geometry of the smallest repeating 3D structures of the façades via face codes. Our encoding scheme, take into account the directions, type as well as the offset distance of the sculpting to be applied at the respective locations on the coarse model. In our approach, LiDAR scan is registered with the coarse models taken from Google earth 3D or Bing maps 3D and decomposed into dominant planar segments (each representing the frontal or lateral walls of the building). The façade segments are then split into horizontal and vertical tiles using a weighted point count function defined over the window or door boundaries. This is followed by an automatic identification of CPM locations with the help of a template fitting algorithm that respects the alignment regularity as well as the inter‐element spacing on the façade layout. Finally, 3D boolean sculpting operations are applied over the boxes induced by CPMs and the coarse model, and a detailed 3D model is generated. The proposed framework is capable of modelling details even with occluded scans and enhances not only the frontal façades (facing to the streets) but also the lateral façades of the buildings. We demonstrate the potentials of the proposed framework by providing several examples of enhanced Google earth models and highlight the advantages of our method when designing photo‐realistic urban façades.     

Incremental Labelling of Voronoi Vertices for Shape Reconstruction

We present an incremental Voronoi vertex labelling algorithm for approximating contours, medial axes and dominant points (high curvature points) from 2D point sets. Though there exist many number of algorithms for reconstructing curves, medial axes or dominant points, a unified framework capable of approximating all the three in one place from points is missing in the literature. Our algorithm estimates the normals at each sample point through poles (farthest Voronoi vertices of a sample point) and uses the estimated normals and the corresponding tangents to determine the spatial locations (inner or outer) of the Voronoi vertices with respect to the original curve. The vertex classification helps to construct a piece‐wise linear approximation to the object boundary. We provide a theoretical analysis of the algorithm for points non‐uniformly (ε‐sampling) sampled from simple, closed, concave and smooth curves. The proposed framework has been thoroughly evaluated for its usefulness using various test data. Results indicate that even sparsely and non‐uniformly sampled curves with outliers or collection of curves are faithfully reconstructed by the proposed algorithm.     

Practical Productivity Analysis for Management: Part II. Measurement and Interpretation

In Part I, a framework for the analysis and measurement of productivity was provided, along with a sample of some empirical findings obtained with this framework. In this paper, the array of factors which must be examined in order to account for the observed findings is reviewed. Problems encountered in the application of this framework in different kinds of plants are discussed, including problems with the development of managerial ability to interpret the results of the analysis.     

Deglycosylation Increases the Aggregation and Angiogenic Properties of Mutant Tissue Inhibitor of Metalloproteinase 3 Protein: Implications for Sorsby Fundus Dystrophy

Sorsby fundus dystrophy (SFD) is an autosomal dominant macular disorder caused by mutations in tissue Inhibitor of the metalloproteinase-3 (TIMP3) gene with the onset of symptoms including choroidal neovascularization as early as the second decade of life. We have previously reported that wild-type TIMP3 is an endogenous angiogenesis inhibitor that inhibits Vascular Endothelial Growth Factor (VEGF)-mediated signaling in endothelial cells. In contrast, SFD-related S179C-TIMP3 when expressed in endothelial cells, does not have angiogenesis-inhibitory properties. To evaluate if this is a common feature of TIMP3 mutants associated with SFD, we examined and compared endothelial cells expressing S179C, Y191C and S204C TIMP3 mutants for their angiogenesis-inhibitory function. Western blot analysis, zymography and reverse zymography and migration assays were utilized to evaluate TIMP3 protein, Matrix Metalloproteinase (MMP) and MMP inhibitory activity, VEGF signaling and in vitro migration in endothelial cells expressing (VEGF receptor-2 (VEGFR-2) and wild-type TIMP3 or mutant-TIMP3. We demonstrate that mutant S179C, Y191C- and S204C-TIMP3 all show increased glycosylation and multimerization/aggregation of the TIMP3 protein. In addition, endothelial cells expressing TIMP3 mutations show increased angiogenic activities and elevated VEGFR-2. Removal of N-glycosylation by mutation of Asn¹⁸⁴, the only potential N-glycosylation site in mutant TIMP3, resulted in increased aggregation of TIMP3, further upregulation of VEGFR-2, VEGF-induced phosphorylation of VEGFR2 and VEGF-mediated migration concomitant with reduced MMP inhibitory activity. These results suggest that even though mutant TIMP3 proteins are more glycosylated, post-translational deglycosylation may play a critical role in the aggregation of mutant TIMP3 and contribute to the pathogenesis of SFD. The identification of factors that might contribute to changes in the glycome of patients with SFD will be useful. Future studies will evaluate whether variations in the glycosylation of mutant TIMP3 proteins are contributing to the severity of the disease.     

Nucleotide sequence of the murine leukaemia virus amphotropic strain 4070A integrase (IN) coding region and comparative structural analysis of the inferred polypeptide

The complete nucleotide sequence of the integrase (IN) protein coding region of the murine leukaemia virus (MLV) amphotropic strain 4070A is presented. The sequence comprises 1,224 nucleotides, encoding a 408-residue polypeptide of M(r) 46,312. Alignment of the inferred 4070A IN amino acid sequence with the IN proteins of other MLV showed that substitutions are confined largely to segments within the N- and C-terminal domains. In the N-terminal domain the majority of substitutions occur as contiguous 2- to 6-residue blocks, whereas in the C-terminal domain they occur as isolated entities except within a short segment characterized by deletions/insertions. Selection appears to act on the C-terminal 19 residues of IN rather than on the N-terminal residues of ENV (encoded by overlapping reading frames), suggesting a functional role for this segment. Phylogenetic analyses grouped the sequences into two clusters, one comprising IN from the amphotropic strain 4070A and three ecotropic MLV (CAS-BR-E, Moloney and Friend), the other consisting of IN from three ecotropic MLV (two radiation-induced viruses and AKV) and a mink cell focus-forming (MCF) MLV virus. The same dichotomy and cluster composition was obtained from analysis of the long terminal repeat (LTR) regions from these viruses (consistent with the functional interrelationship of IN and LTR) but not from analysis of envelope protein sequences (consistent with the functional independence of ENV proteins from both IN and LTR). Secondary structure predictions supported features determined from the catalytic domain of human immunodeficiency virus and avian sarcoma virus IN, and identified probable structures within the relatively long N- and C-terminal domains of MLV IN proteins.