Growing Healthy Kids: A School Enrichment Nutrition Education Program to Promote Healthy Behaviors for Children

The Growing Healthy Kids Program is a school-based nutrition education program that teaches students in Kindergarten through 2nd grade about healthy eating, physical activity, and how their body uses food. Pre- and post-knowledge data is collected from the students to measure changes in nutrition knowledge. In the first 2 years of the program, significant improvements in nutrition knowledge were found in all three grades. Teachers reported that students were more aware of the importance of nutrition and were making healthier meal and/or snack choices at the end of the program

Quantum Algorithms for the Approximate <i>k</i>-List Problem and their Application to Lattice Sieving

The Shortest Vector Problem (SVP) is one of the mathematical foundations of lattice based cryptography. Lattice sieve algorithms are amongst the foremost methods of solving SVP. The asymptotically fastest known classical and quantum sieves solve SVP in a $d$-dimensional lattice in 2^{\const d + \smallo(d)} time steps with 2^{\const' d + \smallo(d)} memory for constants $c, c'$. In this work, we give various quantum sieving algorithms that trade computational steps for memory.We first give a quantum analogue of the classical $k$-Sieve algorithm [Herold--Kirshanova--Laarhoven, PKC'18] in the Quantum Random Access Memory (QRAM) model, achieving an algorithm that heuristically solves SVP in $2^{0.2989d + o(d)}$ time steps using $2^{0.1395d + o(d)}$ memory. This should be compared to the state-of-the-art algorithm [Laarhoven, Ph.D Thesis, 2015] which, in the same model, solves SVP in $2^{0.2653d + o(d)}$ time steps and memory. In the QRAM model these algorithms can be implemented using \poly(d) width quantum circuits.Secondly, we frame the $k$-Sieve as the problem of $k$-clique listing in a graph and apply quantum $k$-clique finding techniques to the $k$-Sieve. Finally, we explore the large quantum memory regime by adapting parallel quantum search [Beals et al., Proc. Roy. Soc. A'13] to the $2$-Sieve and giving an analysis in the quantum circuit model. We show how to heuristically solve SVP in $2^{0.1037d + o(d)}$ time steps using $2^{0.2075d + o(d)}$ quantum memory

Hundreds of variants clustered in genomic loci and biological pathways affect human height

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

The effect of ABCA1 gene polymorphisms on ischaemic stroke risk and relationship with lipid profile

<p>Abstract</p> <p>Background</p> <p>Ischaemic stroke is a common disorder with genetic and environmental components contributing to overall risk. Atherothromboembolic abnormalities, which play a crucial role in the pathogenesis of ischaemic stroke, are often the end result of dysregulation of lipid metabolism. The ATP Binding Cassette Transporter (<it>ABCA1</it>) is a key gene involved in lipid metabolism. It encodes the cholesterol regulatory efflux protein which mediates the transfer of cellular phospholipids and cholesterol to acceptor apolipoproteins such as apolipoprotein A-I (ApoA-I). Common polymorphisms in this gene affect High Density Lipoprotein Cholesterol (HDL-C) and Apolipoprotein A-I levels and so influence the risk of atherosclerosis. This study has assessed the distribution of <it>ABCA1 </it>polymorphisms and haplotype arrangements in patients with ischaemic stroke and compared them to an appropriate control group. It also examined the relationship of these polymorphisms with serum lipid profiles in cases and controls.</p> <p>Methods</p> <p>We studied four common polymorphisms in <it>ABCA1 </it>gene: G/A-L158L, G/A-R219K, G/A-G316G and G/A-R1587K in 400 Caucasian ischaemic stroke patients and 487 controls. Dynamic Allele Specific Hybridisation (DASH) was used as the genotyping assay.</p> <p>Results</p> <p>Genotype and allele frequencies of all polymorphisms were similar in cases and controls, except for a modest difference in the <it>ABCA1 </it>R219K allele frequency (P-value = 0.05). Using the PHASE2 program, haplotype frequencies for the four loci (158, 219, 316, and 1587) were estimated in cases and controls. There was no significant difference in overall haplotypes arrangement in patients group compared to controls (p = 0.27). 2211 and 1211 haplotypes (1 = common allele, 2 = rare allele) were more frequent in cases (p = 0.05). Adjusted ORs indicated 40% and 46% excess risk of stroke for these haplotypes respectively. However, none of the adjusted ORs were statistically significant. Individuals who had R219K "22" genotype had a higher LDL level (p = 0.001).</p> <p>Conclusion</p> <p>Our study does not support a major role for the <it>ABCA1 </it>gene as a risk factor for ischaemic stroke. Some haplotypes may confer a minor amount of increased risk or protection. Polymorphisms in this gene may influence serum lipid profile.</p

The conservation status of the world's freshwater molluscs

With the biodiversity crisis continuing unchecked, we need to establish levels and drivers of extinction risk, and reassessments over time, to effectively allocate conservation resources and track progress towards global conservation targets. Given that threat appears particularly high in freshwaters, we assessed the extinction risk of 1428 randomly selected freshwater molluscs using the IUCN Red List Categories and Criteria, as part of the Sampled Red List Index project. We show that close to one-third of species in our sample are estimated to be threatened with extinction, with highest levels of threat in the Nearctic, Palearctic and Australasia and among gastropods. Threat levels were higher in lotic than lentic systems. Pollution (chemical and physical) and the modification of natural systems (e.g. through damming and water abstraction) were the most frequently reported threats to freshwater molluscs, with some regional variation. Given that we found little spatial congruence between species richness patterns of freshwater molluscs and other freshwater taxa, apart from crayfish, new additional conservation priority areas emerged from our study. We discuss the implications of our findings for freshwater mollusc conservation, the adequacy of a sampled approach and important next steps to estimate trends in freshwater mollusc extinction risk over time

Dual targeting of p53 and c-MYC selectively eliminates leukaemic stem cells

e Glasgow and Manchester Experimental Cancer Medicine Centres (ECMC), which are funded by CR-UK and the Chief Scientist’s Office (Scotland). We acknowledge the funders who have contributed to this work: MRC stratified medicine infrastructure award (A.D.W.), CR-UK C11074/A11008 (F.P., L.E.M.H., T.L.H., A.D.W.); LLR08071 (S.A.A., E.C.); LLR11017 (M.C.); SCD/04 (M.C.); LLR13035 (S.A.A., K.D., A.D.W., and A.P.); LLR14005 (M.T.S., D.V.); KKL690 (L.E.P.); KKL698 (P.B.); LLR08004 (A.D.W., A.P. and A.J.W.); MRC CiC (M.E.D.); The Howat Foundation (FACS support); Friends of Paul O’Gorman (K.D. and FACS support); ELF 67954 (S.A.A.); BSH start up fund (S.A.A.); MR/K014854/1 (K.D.)

Return of GGH15: Provable Security Against Zeroizing Attacks

The GGH15 multilinear maps have served as the foundation for a number of cutting-edge cryptographic proposals. Unfortunately, many schemes built on GGH15 have been explicitly broken by so-called ``zeroizing attacks,\u27\u27 which exploit leakage from honest zero-test queries. The precise settings in which zeroizing attacks are possible have remained unclear. Most notably, none of the current indistinguishability obfuscation (iO) candidates from GGH15 have any formal security guarantees against zeroizing attacks. In this work, we demonstrate that all known zeroizing attacks on GGH15 implicitly construct algebraic relations between the results of zero-testing and the encoded plaintext elements. We then propose a ``GGH15 zeroizing model as a new general framework which greatly generalizes known attacks. Our second contribution is to describe a new GGH15 variant, which we formally analyze in our GGH15 zeroizing model. We then construct a new iO candidate using our multilinear map, which we prove secure in the GGH15 zeroizing model. This implies resistance to all known zeroizing strategies. The proof relies on the Branching Program Un-Annihilatability (BPUA) Assumption of Garg et al. [TCC 16-B] (which is implied by PRFs in NC^1 secure against P/Poly) and the complexity-theoretic p-Bounded Speedup Hypothesis of Miles et al. [ePrint 14] (a strengthening of the Exponential Time Hypothesis)

Sex Reversal in Zebrafish fancl Mutants Is Caused by Tp53-Mediated Germ Cell Apoptosis

The molecular genetic mechanisms of sex determination are not known for most vertebrates, including zebrafish. We identified a mutation in the zebrafish fancl gene that causes homozygous mutants to develop as fertile males due to female-to-male sex reversal. Fancl is a member of the Fanconi Anemia/BRCA DNA repair pathway. Experiments showed that zebrafish fancl was expressed in developing germ cells in bipotential gonads at the critical time of sexual fate determination. Caspase-3 immunoassays revealed increased germ cell apoptosis in fancl mutants that compromised oocyte survival. In the absence of oocytes surviving through meiosis, somatic cells of mutant gonads did not maintain expression of the ovary gene cyp19a1a and did not down-regulate expression of the early testis gene amh; consequently, gonads masculinized and became testes. Remarkably, results showed that the introduction of a tp53 (p53) mutation into fancl mutants rescued the sex-reversal phenotype by reducing germ cell apoptosis and, thus, allowed fancl mutants to become fertile females. Our results show that Fancl function is not essential for spermatogonia and oogonia to become sperm or mature oocytes, but instead suggest that Fancl function is involved in the survival of developing oocytes through meiosis. This work reveals that Tp53-mediated germ cell apoptosis induces sex reversal after the mutation of a DNA–repair pathway gene by compromising the survival of oocytes and suggests the existence of an oocyte-derived signal that biases gonad fate towards the female developmental pathway and thereby controls zebrafish sex determination