On Feedback Vertex Set: New Measure and New Structures

We present a new parameterized algorithm for the {feedback vertex set} problem ({\sc fvs}) on undirected graphs. We approach the problem by considering a variation of it, the {disjoint feedback vertex set} problem ({\sc disjoint-fvs}), which finds a feedback vertex set of size $k$ that has no overlap with a given feedback vertex set $F$ of the graph $G$. We develop an improved kernelization algorithm for {\sc disjoint-fvs} and show that {\sc disjoint-fvs} can be solved in polynomial time when all vertices in $G \setminus F$ have degrees upper bounded by three. We then propose a new branch-and-search process on {\sc disjoint-fvs}, and introduce a new branch-and-search measure. The process effectively reduces a given graph to a graph on which {\sc disjoint-fvs} becomes polynomial-time solvable, and the new measure more accurately evaluates the efficiency of the process. These algorithmic and combinatorial studies enable us to develop an $O^*(3.83^k)$-time parameterized algorithm for the general {\sc fvs} problem, improving all previous algorithms for the problem.Comment: Final version, to appear in Algorithmic

A Hierarchy of Polynomial Kernels

In parameterized algorithmics, the process of kernelization is defined as a polynomial time algorithm that transforms the instance of a given problem to an equivalent instance of a size that is limited by a function of the parameter. As, afterwards, this smaller instance can then be solved to find an answer to the original question, kernelization is often presented as a form of preprocessing. A natural generalization of kernelization is the process that allows for a number of smaller instances to be produced to provide an answer to the original problem, possibly also using negation. This generalization is called Turing kernelization. Immediately, questions of equivalence occur or, when is one form possible and not the other. These have been long standing open problems in parameterized complexity. In the present paper, we answer many of these. In particular, we show that Turing kernelizations differ not only from regular kernelization, but also from intermediate forms as truth-table kernelizations. We achieve absolute results by diagonalizations and also results on natural problems depending on widely accepted complexity theoretic assumptions. In particular, we improve on known lower bounds for the kernel size of compositional problems using these assumptions

Cone rod dystrophies

Cone rod dystrophies (CRDs) (prevalence 1/40,000) are inherited retinal dystrophies that belong to the group of pigmentary retinopathies. CRDs are characterized by retinal pigment deposits visible on fundus examination, predominantly localized to the macular region. In contrast to typical retinitis pigmentosa (RP), also called the rod cone dystrophies (RCDs) resulting from the primary loss in rod photoreceptors and later followed by the secondary loss in cone photoreceptors, CRDs reflect the opposite sequence of events. CRD is characterized by primary cone involvement, or, sometimes, by concomitant loss of both cones and rods that explains the predominant symptoms of CRDs: decreased visual acuity, color vision defects, photoaversion and decreased sensitivity in the central visual field, later followed by progressive loss in peripheral vision and night blindness. The clinical course of CRDs is generally more severe and rapid than that of RCDs, leading to earlier legal blindness and disability. At end stage, however, CRDs do not differ from RCDs. CRDs are most frequently non syndromic, but they may also be part of several syndromes, such as Bardet Biedl syndrome and Spinocerebellar Ataxia Type 7 (SCA7). Non syndromic CRDs are genetically heterogeneous (ten cloned genes and three loci have been identified so far). The four major causative genes involved in the pathogenesis of CRDs are ABCA4 (which causes Stargardt disease and also 30 to 60% of autosomal recessive CRDs), CRX and GUCY2D (which are responsible for many reported cases of autosomal dominant CRDs), and RPGR (which causes about 2/3 of X-linked RP and also an undetermined percentage of X-linked CRDs). It is likely that highly deleterious mutations in genes that otherwise cause RP or macular dystrophy may also lead to CRDs. The diagnosis of CRDs is based on clinical history, fundus examination and electroretinogram. Molecular diagnosis can be made for some genes, genetic counseling is always advised. Currently, there is no therapy that stops the evolution of the disease or restores the vision, and the visual prognosis is poor. Management aims at slowing down the degenerative process, treating the complications and helping patients to cope with the social and psychological impact of blindness

Recent Salmon Declines: A Result of Lost Feeding Opportunities Due to Bad Timing?

As the timing of spring productivity blooms in near-shore areas advances due to warming trends in global climate, the selection pressures on out-migrating salmon smolts are shifting. Species and stocks that leave natal streams earlier may be favoured over later-migrating fish. The low post-release survival of hatchery fish during recent years may be in part due to static release times that do not take the timing of plankton blooms into account. This study examined the effects of release time on the migratory behaviour and survival of wild and hatchery-reared coho salmon (Oncorhynchus kisutch) using acoustic and coded-wire telemetry. Plankton monitoring and near-shore seining were also conducted to determine which habitat and food sources were favoured. Acoustic tags (n = 140) and coded-wire tags (n = 266,692) were implanted into coho salmon smolts at the Seymour and Quinsam Rivers, in British Columbia, Canada. Differences between wild and hatchery fish, and early and late releases were examined during the entire lifecycle. Physiological sampling was also carried out on 30 fish from each release group. The smolt-to-adult survival of coho salmon released during periods of high marine productivity was 1.5- to 3-fold greater than those released both before and after, and the fish's degree of smoltification affected their downstream migration time and duration of stay in the estuary. Therefore, hatchery managers should consider having smolts fully developed and ready for release during the peak of the near-shore plankton blooms. Monitoring chlorophyll a levels and water temperature early in the spring could provide a forecast of the timing of these blooms, giving hatcheries time to adjust their release schedule

School's out: what are urban children doing? The Summer Activity Study of Somerville Youth (SASSY)

Background: Research indicates that in the United States, children experience healthier BMI and fitness levels during school vs. summer, but research is limited. The primary goal of this pilot study was to assess where children spend their time during the months that school is not in session and to learn about the different types of activities they engage in within different care settings. A secondary goal of this pilot study was to learn what children eat during the summer months. Methods: A nine-week summer study of 57 parents of second and third grade students was conducted in an economically, racial/ethnically and linguistically diverse US urban city. Weekly telephone interviews queried time and activities spent on/in 1) the main caregiver’s care 2) someone else’s care 3) vacation 4) and camp. Activities were categorised as sedentary, light, moderate, or vigorous (0-3 scale). For each child, a mean activity level was calculated and weighted for proportion of time spent in each care situation, yielding a weighted activity index. On the last phone call, parents answered questions about their child’s diet over the summer. Two post-study focus groups were conducted to help interpret findings from the weekly activity interviews. Results: The mean activity index was 1.05 ± 0.32 and differed between gender (p = 0.07), education (p = 0.08) and primary language spoken in the household (p = 0.01). Children who spent a greater percentage of time in parent care had on average a lower activity index (β = -0.004, p = 0.01) while children who spent a greater percentage of time in camp had a higher activity index (β = 0.004, p = 0.03). When stratified into type of camp, percentage of time spent in active camp was also positively associated with mean activity index (β = 0.005, p =\u3c 0.001). With regards to diet, after adjusting for maternal education, children who attended less than five weeks of camp were four times more likely to eat their meals in front of the TV often/almost all of the time (OR = 4.0, 95%CI 1.0-16.2, p \u3c 0.06). Conclusions: Summer activities and some dietary behaviours are influenced by situation of care and sociodemographic characteristics. In particular, children who spend a greater proportion of time in structured environments appear to be more active. We believe that this pilot study is an important first step in our understanding of what children do during the summer months

Combined analysis of transcriptome and metabolite data reveals extensive differences between black and brown nearly-isogenic soybean (Glycine max) seed coats enabling the identification of pigment isogenes

<p>Abstract</p> <p>Background</p> <p>The <it>R </it>locus controls the color of pigmented soybean (<it>Glycine max</it>) seeds. However information about its control over seed coat biochemistry and gene expressions remains limited. The seed coats of nearly-isogenic black (<it>iRT</it>) and brown (<it>irT</it>) soybean (<it>Glycine max</it>) were known to differ by the presence or absence of anthocyanins, respectively, with genes for only a single enzyme (anthocyanidin synthase) found to be differentially expressed between isolines. We recently identified and characterized a UDP-glycose:flavonoid-3-<it>O</it>-glycosyltransferase (<it>UGT78K1</it>) from the seed coat of black (<it>iRT</it>) soybean with the aim to engineer seed coat color by suppression of an anthocyanin-specific gene. However, it remained to be investigated whether <it>UGT78K1 </it>was overexpressed with anthocyanin biosynthesis in the black (<it>iRT</it>) seed coat compared to the nearly-isogenic brown (<it>irT</it>) tissue.</p> <p>In this study, we performed a combined analysis of transcriptome and metabolite data to elucidate the control of the R locus over seed coat biochemistry and to identify pigment biosynthesis genes. Two differentially expressed late-stage anthocyanin biosynthesis isogenes were further characterized, as they may serve as useful targets for the manipulation of soybean grain color while minimizing the potential for unintended effects on the plant system.</p> <p>Results</p> <p>Metabolite composition differences were found to not be limited to anthocyanins, with specific proanthocyanidins, isoflavones, and phenylpropanoids present exclusively in the black (<it>iRT</it>) or the brown (<it>irT</it>) seed coat. A global analysis of gene expressions identified <it>UGT78K1 </it>and 19 other anthocyanin, (iso)flavonoid, and phenylpropanoid isogenes to be differentially expressed between isolines. A combined analysis of metabolite and gene expression data enabled the assignment of putative functions to biosynthesis and transport isogenes. The recombinant enzymes of two genes were validated to catalyze late-stage steps in anthocyanin biosynthesis <it>in vitro </it>and expression profiles of the corresponding genes were shown to parallel anthocyanin biosynthesis during black (<it>iRT</it>) seed coat development.</p> <p>Conclusion</p> <p>Metabolite composition and gene expression differences between black (<it>iRT</it>) and brown (<it>irT</it>) seed coats are far more extensive than previously thought. Putative anthocyanin, proanthocyanidin, (iso)flavonoid, and phenylpropanoid isogenes were differentially-expressed between black (<it>iRT</it>) and brown (<it>irT</it>) seed coats, and <it>UGT78K2 </it>and <it>OMT5 </it>were validated to code UDP-glycose:flavonoid-3-<it>O</it>-glycosyltransferase and anthocyanin 3'-<it>O</it>-methyltransferase proteins <it>in vitro</it>, respectively. Duplicate gene copies for several enzymes were overexpressed in the black (<it>iRT</it>) seed coat suggesting more than one isogene may have to be silenced to engineer seed coat color using RNA interference.</p

High-resolution analysis of copy number alterations and associated expression changes in ovarian tumors

<p>Abstract</p> <p>Background</p> <p>DNA copy number alterations are frequently observed in ovarian cancer, but it remains a challenge to identify the most relevant alterations and the specific causal genes in those regions.</p> <p>Methods</p> <p>We obtained high-resolution 500K SNP array data for 52 ovarian tumors and identified the most statistically significant minimal genomic regions with the most prevalent and highest-level copy number alterations (recurrent CNAs). Within a region of recurrent CNA, comparison of expression levels in tumors with a given CNA to tumors lacking that CNA and to whole normal ovary samples was used to select genes with CNA-specific expression patterns. A public expression array data set of laser capture micro-dissected (LCM) non-malignant fallopian tube epithelia and LCM ovarian serous adenocarcinoma was used to evaluate the effect of cell-type mixture biases.</p> <p>Results</p> <p>Fourteen recurrent deletions were detected on chromosomes 4, 6, 9, 12, 13, 15, 16, 17, 18, 22 and most prevalently on X and 8. Copy number and expression data suggest several apoptosis mediators as candidate drivers of the 8p deletions. Sixteen recurrent gains were identified on chromosomes 1, 2, 3, 5, 8, 10, 12, 15, 17, 19, and 20, with the most prevalent gains localized to 8q and 3q. Within the 8q amplicon, <it>PVT1</it>, but not <it>MYC</it>, was strongly over-expressed relative to tumors lacking this CNA and showed over-expression relative to normal ovary. Likewise, the cell polarity regulators <it>PRKCI </it>and <it>ECT2 </it>were identified as putative drivers of two distinct amplicons on 3q. Co-occurrence analyses suggested potential synergistic or antagonistic relationships between recurrent CNAs. Genes within regions of recurrent CNA showed an enrichment of Cancer Census genes, particularly when filtered for CNA-specific expression.</p> <p>Conclusion</p> <p>These analyses provide detailed views of ovarian cancer genomic changes and highlight the benefits of using multiple reference sample types for the evaluation of CNA-specific expression changes.</p

Osteo-Chondroprogenitor–Specific Deletion of the Selenocysteine tRNA Gene, Trsp, Leads to Chondronecrosis and Abnormal Skeletal Development: A Putative Model for Kashin-Beck Disease

Kashin-Beck disease, a syndrome characterized by short stature, skeletal deformities, and arthropathy of multiple joints, is highly prevalent in specific regions of Asia. The disease has been postulated to result from a combination of different environmental factors, including contamination of barley by mold mycotoxins, iodine deficiency, presence of humic substances in drinking water, and, importantly, deficiency of selenium. This multifunctional trace element, in the form of selenocysteine, is essential for normal selenoprotein function, including attenuation of excessive oxidative stress, and for the control of redox-sensitive molecules involved in cell growth and differentiation. To investigate the effects of skeletal selenoprotein deficiency, a Cre recombinase transgenic mouse line was used to trigger Trsp gene deletions in osteo-chondroprogenitors. Trsp encodes selenocysteine tRNA[Ser]Sec, required for the incorporation of selenocysteine residues into selenoproteins. The mutant mice exhibited growth retardation, epiphyseal growth plate abnormalities, and delayed skeletal ossification, as well as marked chondronecrosis of articular, auricular, and tracheal cartilages. Phenotypically, the mice thus replicated a number of the pathological features of Kashin-Beck disease, supporting the notion that selenium deficiency is important to the development of this syndrome