On the intersection of tolerance and cocomparability graphs.

It has been conjectured by Golumbic and Monma in 1984 that the intersection of tolerance and cocomparability graphs coincides with bounded tolerance graphs. Since cocomparability graphs can be efficiently recognized, a positive answer to this conjecture in the general case would enable us to efficiently distinguish between tolerance and bounded tolerance graphs, although it is NP-complete to recognize each of these classes of graphs separately. The conjecture has been proved under some – rather strong – structural assumptions on the input graph; in particular, it has been proved for complements of trees, and later extended to complements of bipartite graphs, and these are the only known results so far. Furthermore, it is known that the intersection of tolerance and cocomparability graphs is contained in the class of trapezoid graphs. In this article we prove that the above conjecture is true for every graph G, whose tolerance representation satisfies a slight assumption; note here that this assumption concerns only the given tolerance representation R of G, rather than any structural property of G. This assumption on the representation is guaranteed by a wide variety of graph classes; for example, our results immediately imply the correctness of the conjecture for complements of triangle-free graphs (which also implies the above-mentioned correctness for complements of bipartite graphs). Our proofs are algorithmic, in the sense that, given a tolerance representation R of a graph G, we describe an algorithm to transform R into a bounded tolerance representation R  ∗  of G. Furthermore, we conjecture that any minimal tolerance graph G that is not a bounded tolerance graph, has a tolerance representation with exactly one unbounded vertex. Our results imply the non-trivial result that, in order to prove the conjecture of Golumbic and Monma, it suffices to prove our conjecture. In addition, there already exists evidence in the literature that our conjecture is true

European mtDNA Variants Are Associated With Differential Responses to Cisplatin, an Anticancer Drug: Implications for Drug Resistance and Side Effects.

Background: Cisplatin, a powerful antitumor agent, causes formation of DNA adducts, and activation of apoptotic pathways. Presently, cisplatin resistance develops in up to 70% of patients but the underlying molecular mechanism(s) are unclear and there are no markers to determine which patients will become resistant. Mitochondria play a significant role not only in energy metabolism but also retrograde signaling (mitochondria to nucleus) that modulates inflammation, complement, and apoptosis pathways. Maternally inherited mitochondrial (mt) DNA can be classified into haplogroups representing different ethnic populations that have diverse susceptibilities to diseases and medications. Methods: Transmitochondrial cybrids, where all cell lines possess identical nuclear genomes but either the H (Southern European) or J (Northern European) mtDNA haplogroups, were treated with cisplatin and analyzed for differential responses related to viability, oxidative stress, and expression levels of genes associated with cancer, cisplatin-induced nephrotoxicity and resistance, apoptosis and signaling pathways. Results: The cisplatin-treated-J cybrids showed greater loss of cell viability along with lower levels of reactive oxygen species and mitochondrial membrane potential compared to cisplatin-treated-H cybrids. After cisplatin treatment, J cybrids showed increased gene expression of BAX, CASP3, and CYP51A, but lower levels of SFRP1 compared to untreated-J cybrids. The cisplatin-treated-H cybrids had elevated expression of CDKN1A/P21, which has a role in cisplatin toxicity, compared to untreated-H cybrids. The cisplatin-treated H had higher transcription levels of ABCC1, DHRS2/HEP27, and EFEMP1 compared to cisplatin-treated-J cybrids. Conclusions: Cybrid cell lines that contain identical nuclei but either H mtDNA mitochondria or J mtDNA mitochondria respond differently to cisplatin treatments suggesting involvement of the retrograde signaling (from mitochondria to nucleus) in the drug-induced cell death. Varying toxicities and transcription levels of the H vs. J cybrids after cisplatin treatment support the hypothesis that mtDNA variants play a role in the expression of genes affecting resistance and side effects of cisplatin

Engineering Art Galleries

The Art Gallery Problem is one of the most well-known problems in Computational Geometry, with a rich history in the study of algorithms, complexity, and variants. Recently there has been a surge in experimental work on the problem. In this survey, we describe this work, show the chronology of developments, and compare current algorithms, including two unpublished versions, in an exhaustive experiment. Furthermore, we show what core algorithmic ingredients have led to recent successes

Mitochondrial Dysfunction Links Ceramide Activated HRK Expression and Cell Death

Cell death is an essential process in normal development and homeostasis. In eyes, corneal epithelial injury leads to the death of cells in underlying stroma, an event believed to initiate corneal wound healing. The molecular basis of wound induced corneal stromal cell death is not understood in detail. Studies of others have indicated that ceramide may play significant role in stromal cell death following LASIK surgery. We have undertaken the present study to investigate the mechanism of death induced by C6 ceramide in cultures of human corneal stromal (HCSF) fibroblasts.Cultures of HCSF were established from freshly excised corneas. Cell death was induced in low passage (p<4) cultures of HCSF by treating the cells with C6 ceramide or C6 dihydroceramide as a control. Cell death was assessed by Live/Dead cell staining with calcein AM and ethidium homodimer-1 as well as Annexin V staining, caspase activation and TUNEL staining Mitochondrial dysfunction was assessed by Mito Sox Red, JC-1 and cytochrome C release Gene expression was examined by qPCR and western blotting.Our data demonstrate ceramide caused mitochondrial dysfunction as evident from reduced MTT staining, cyto c release from mitochondria, enhanced generation of ROS, and loss in mitochondrial membrane potential (ΔΨm). Cell death was evident from Live -Dead Cell staining and the inability to reestablish cultures from detached cells. Ceramide induced the expression of the harikari gene(HRK) and up-regulated JNK phosphorylation. In ceramide treated cells HRK was translocated to mitochondria, where it was found to interact with mitochondrial protein p32. The data also demonstrated HRK, p32 and BAD interaction. Ceramide-induced expression of HRK, mitochondrial dysfunction and cell death were reduced by HRK knockdown with HRK siRNA.Our data document that ceramide is capable of inducing death of corneal stromal fibroblasts through the induction of HRK mediated mitochondria dysfunction

Image metamorphosis with scattered feature constraints

This paper describes an image metamorphosis technique to handle scattered feature constraints specified with points, polylines, and splines. Solutions to the following three problems are presented: feature specification, warp generation, and transition control. We demonstrate the use of snakes to reduce the burden of feature specification. Next, we propose the use of multilevel free-form deformations (MFFD) to compute C-2-continuous and one-to-one mapping functions among the specified features. The resulting technique, based on B-spline approximation, is simpler and faster than previous warp generation methods. Furthermore, it produces smooth image transformations without undesirable ripples and foldovers. Finally, we simplify the MFFD algorithm to derive transition functions to control geometry and color blending. Implementation details are furnished and comparisons among Various metamorphosis techniques are presented.X11127sciescopu

Casting an Object with a Core

This paper addresses geometric problems in manufacturing objects by casting. In casting, molten material is poured into the cavity of the cast and allowed to solidify, after which the cast is removed. The cast has two cast parts to be removed in opposite directions. To manufacture more complicated objects, the cast may also have a side core to be removed in a direction skewed to the removal directions for the cast parts. We address the following problem: Given an object and the removal directions for the cast parts and the side core, can a cast be constructed such that the cast parts and the side core can be removed in the directions specified without colliding with the object or each other? We give necessary and sufficient conditions for the problem, as well as a discrete algorithm to perform the test in O(n(3) log n) time for polyhedral objects, where n is the number of vertices, edges, and facets. If the test result is positive, a cast with complexity O(n(3)) can be constructed within the same time bound. We also present an example to show that a cast may have Omega(n(3)) complexity in the worst case.X11sciescopu