Dance movement therapy in Australia : a survey of practitioners and practice

This article reports the results of a survey of 41 dance-movement therapy practitioners in Australia. Issues for dance-movement therapy practice in Australia were investigated within the themes of practitioners; programs and clients, and philosophical and industrial concerns. Overall, it was apparent that the dance-movement therapy profession in Australia is both diverse and homogenous: therapists&rsquo; professional orientations and backgrounds, and the types of settings in which they work, are very diverse, but therapists are much more similar in their ages, gender, cultural backgrounds and geographic location. The issues raised by the variation and lack of diversity are discussed, along with possible strategies to address them. <br /

Press Conference - Senator Edmund S. Muskie Endorsed by Senators Eagleton and Symington and Governor Hearnes

Press conference following the announcement of the endorsement of Senator Edmund S. Muskie for the Democratic nomination in 1972 by Governor Hearnes, and Senators Symington and Eagleton

Regression based predictor for p53 transactivation

<p>Abstract</p> <p>Background</p> <p>The p53 protein is a master regulator that controls the transcription of many genes in various pathways in response to a variety of stress signals. The extent of this regulation depends in part on the binding affinity of p53 to its response elements (REs). Traditional profile scores for p53 based on position weight matrices (PWM) are only a weak indicator of binding affinity because the level of binding also depends on various other factors such as interaction between the nucleotides and, in case of p53-REs, the extent of the spacer between the dimers.</p> <p>Results</p> <p>In the current study we introduce a novel <it>in-silico </it>predictor for p53-RE transactivation capability based on a combination of multidimensional scaling and multinomial logistic regression. Experimentally validated known p53-REs along with their transactivation capabilities are used for training. Through cross-validation studies we show that our method outperforms other existing methods. To demonstrate the utility of this method we (a) rank putative p53-REs of target genes and target microRNAs based on the predicted transactivation capability and (b) study the implication of polymorphisms overlapping p53-RE on its transactivation capability.</p> <p>Conclusion</p> <p>Taking into account both nucleotide interactions and the spacer length of p53-RE, we have created a novel <it>in-silico </it>regression-based transactivation capability predictor for p53-REs and used it to analyze validated and novel p53-REs and to predict the impact of SNPs overlapping these elements.</p

Characterization of genome-wide p53-binding sites upon stress response

The tumor suppressor p53 is a sequence-specific transcription factor, which regulates the expression of target genes involved in different stress responses. To understand p53's essential transcriptional functions, unbiased analysis of its DNA-binding repertoire is pivotal. In a genome-wide tiling ChIP-on-chip approach, we have identified and characterized 1546 binding sites of p53 upon Actinomycin D treatment. Among those binding sites were known as well as novel p53 target sites, which included regulatory regions of potentially novel transcripts. Using this collection of genome-wide binding sites, a new high-confidence algorithm was developed, p53scan, to identify the p53 consensus-binding motif. Strikingly, this motif was present in the majority of all bound sequences with 83% of all binding sites containing the motif. In the surrounding sequences of the binding sites, several motifs for potential regulatory cobinders were identified. Finally, we show that the majority of the genome-wide p53 target sites can also be bound by overexpressed p63 and p73 in vivo, suggesting that they can possibly play an important role at p53 binding sites. This emphasizes the possible interplay of p53 and its family members in the context of target gene binding. Our study greatly expands the known, experimentally validated p53 binding site repertoire and serves as a valuable knowledgebase for future research

Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences

Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53R273H in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53R273H targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin

TP63 and TP73 in cancer, an unresolved “family” puzzle of complexity, redundancy and hierarchy

AbstractTP53 belongs to a small gene family that includes, in mammals, two additional paralogs, TP63 and TP73. The p63 and p73 proteins are structurally and functionally similar to p53 and their activity as transcription factors is regulated by a wide repertoire of shared and unique post-translational modifications and interactions with regulatory cofactors. p63 and p73 have important functions in embryonic development and differentiation but are also involved in tumor suppression. The biology of p63 and p73 is complex since both TP63 and TP73 genes are transcribed into a variety of different isoforms that give rise to proteins with antagonistic properties, the TA-isoforms that act as tumor-suppressors and DN-isoforms that behave as proto-oncogenes. The p53 family as a whole behaves as a signaling “network” that integrates developmental, metabolic and stress signals to control cell metabolism, differentiation, longevity, proliferation and death. Despite the progress of our knowledge, the unresolved puzzle of complexity, redundancy and hierarchy in the p53 family continues to represent a formidable challenge

Noncanonical DNA Motifs as Transactivation Targets by Wild Type and Mutant p53

Sequence-specific binding by the human p53 master regulator is critical to its tumor suppressor activity in response to environmental stresses. p53 binds as a tetramer to two decameric half-sites separated by 0–13 nucleotides (nt), originally defined by the consensus RRRCWWGYYY (n = 0–13) RRRCWWGYYY. To better understand the role of sequence, organization, and level of p53 on transactivation at target response elements (REs) by wild type (WT) and mutant p53, we deconstructed the functional p53 canonical consensus sequence using budding yeast and human cell systems. Contrary to early reports on binding in vitro, small increases in distance between decamer half-sites greatly reduces p53 transactivation, as demonstrated for the natural TIGER RE. This was confirmed with human cell extracts using a newly developed, semi–in vitro microsphere binding assay. These results contrast with the synergistic increase in transactivation from a pair of weak, full-site REs in the MDM2 promoter that are separated by an evolutionary conserved 17 bp spacer. Surprisingly, there can be substantial transactivation at noncanonical ½-(a single decamer) and ¾-sites, some of which were originally classified as biologically relevant canonical consensus sequences including PIDD and Apaf-1. p53 family members p63 and p73 yielded similar results. Efficient transactivation from noncanonical elements requires tetrameric p53, and the presence of the carboxy terminal, non-specific DNA binding domain enhanced transactivation from noncanonical sequences. Our findings demonstrate that RE sequence, organization, and level of p53 can strongly impact p53-mediated transactivation, thereby changing the view of what constitutes a functional p53 target. Importantly, inclusion of ½- and ¾-site REs greatly expands the p53 master regulatory network

CHARACTERIZATION OF SOME GENERATIVE PHASES OF BLACK RICE ORIGIN OF WEST KALIMANTAN ON RED YELLOW PODZOLIC SOIL

Characterization of black rice is needed to know the character information of the plant. This study aims to determine the generative phase morphology characteristic and the level of similarity of some black rice from West Kalimantan on RYP soil. This research was conducted in experimental garden of Faculty of Agriculture of Tanjungpura University. The study used Completely Randomized Design (CRD), consisting of 4 treatments A = Nanga Taman, B = Sanggau, C = Senakin and D = Ensalang. Each treatment were replicated 6 times and each replication consisted of 3 plant samples.  The observed  measurement were stem strength, plant height, leaf maturity (yellowing), panicle emergence, grain fertility, plant age, leaf color, number of productive tillers, stem color, number of grain per panicle, pannicle type, secondary panicle, males, lemma and palea, hair on lemma and palea, color of grain tip, grain tip, grain end, long grain, diameter of stem segment, length of panicle, seed width and weight of 100 grains. Character observation data were analyzed using MVSP program to obtain dendogram. Based on the analysis of generative phase character, the plant was divided into 3 groups. The first group consists of Senakin black rice. The second group consisted of the black rice species of Ensalang and Sanggau. The third group consists of Nanga Taman black rice

Near-optimal intelligent control for continuous set-point regulator problems via approximate dynamic programming

Ph.D.Augustine O. Esogbu