The recent publication by Wylie et al. is reviewed, demonstrating that the p53 protein regulates the movement of transposons. While this work presents genetic evidence for a piRNA‐mediated p53 interaction with transposons in Drosophila and zebrafish, it is herein placed in the context of a decade or so of additional work that demonstrated a role for p53 in regulating transposons and other repetitive elements. The line of thought in those studies began with the observation that transposons damage DNA and p53 (...) regulates DNA damage. The presence of transposon movement can increase the rate of evolution in the germ line and alter genes involved in signal transduction pathways. Transposition can also play an important role in cancers where the p53 gene function is often mutated. This is particularly interesting as recent work has shown that de‐repression of repetitive elements in cancer has important consequences for the immune system and tumor microenvironment. (shrink)

The retinoblastoma sensitivity protein (Rb) and the p53 gene product both appear to function as negative regulators of cell division or abnormal cellular growth in some differentiated cell types. Several types of cancers have been shown to be derived from cells that have extensively mutated both alleles of one or both of these genes, resulting in a loss‐of‐function mutation. In the case of the p53 gene, this mutational process appears to occur in two steps, with the first mutation at the (...) p53 locus resulting in a trans‐dominant phenotype. The mutant p53 gene product enters into an oligomeric protein complex with the wild‐type p53 protein derived from the other normal allele and such a complex is inactive or less efficient in its negative regulation of growth control. This intermediate stage of carcinogenesis selects for the proliferation of cells with one mutant allele, enhancing the probability of obtaining a cancer cell with both alleles damaged.The DNA tumor viruses have evolved mechanisms to interact with the Rb and p53 negative regulators of cellular growth in order to enhance their own replication in growing cells. SV40 and adenovirus type 5 produce viral encoded proteins that also form oligomeric protein complexes with p53 and Rb, presumably inactivating their functions. These viral proteins are also the oncogene products of these viruses. Thus, the mechanisms by which cancer may arise in a host, via mutations or virus infections, have fundamental common pathways effecting the same cellular genes and gene products; Rb and p53. (shrink)

Fodor argued that in contrast to input systems which are informationally encapsulated, general intelligence is unencapsulated and hence non-modular; for this reason, he suggested, prospects for understanding it are not bright. It is argued that an additional property, primitive functionality, is required for non-modularity. A functionally primitive computational model for quantifier scoping, limited to some scoping influences, is then motivated, and an implementation described. It is argued that only such a model can be faithful to intuitive scope preferences. But it (...) is also argued that an extended model which includes all scoping influences is a hopeless prospect from a developmental perspective. Fodor's views are concluded to have some independent support: quantifier scoping is a mental ability parasitic on general intelligence that is non-modular though in a revised sense, warranting pessimism about our ability of model it. (shrink)

In On What We Mean, Arnold Chien discusses the meaning of a speaker, a notion we use in everyday conversation. Speaker's meaning is a fundamental notion of pragmatics, i.e. the study of the relation between words and speakers. Yet everyday speaker's meaning has not been systematically studied in philosophy or linguistics. Chien's approach to these issues is to take a speaker's meaning as an answer to "what do you (s/he) mean" (WDYM) questions. He then analyzes WDYM-questions in terms of (...) Bas van Fraassen's analysis of why-questions, according to which, a question consists of a set of parameters whose values vary according to the context. The constraints on speaker's meanings are analyzed in terms of certain constraints on answers to WDYM-questions. The account is extended to metaphor, understood to be a kind of conceptual indeterminacy. (shrink)

In this article, we review approaches to modeling a connection between spatial and mathematical thinking across development. We critically evaluate the strengths and weaknesses of factor analyses, meta-analyses, and experimental literatures. We examine those studies that set out to describe the nature and number of spatial and mathematical skills and specific connections between these abilities, especially those that included children as participants. We also find evidence of strong spatial-mathematical connections and transfer from spatial interventions to mathematical understanding. Finally, we map (...) out the kinds of studies that could enhance our understanding of the mechanisms by which spatial and mathematical processing are connected and the principles by which mathematical outcomes could be enhanced through spatial training in educational settings. (shrink)

Studies have failed to yield definitive evidence for the existence and/or role of well-defined chaotic attractors in real brain systems. Tsuda's transients stabilized on unstable manifolds of unstable fixed points using mechanisms similar to Ott's algorithmic “control of chaos” are demonstrable. Grebogi's order in preserving “strange nonchaotic” attractor with fractal dimension but Lyapounov is suggested for neural network tasks dependent on sequence.

Even if we recognize that the delta-lognormal model provides an excellent fit to a large variety of data, the question remains as to what we actually learn from such a model, which could be seen as merely another multiparameter account? Do we welcome such an encompassing account, or do we expect to learn more from the limitations that become apparent when applying dedicated models addressing specific classes of movements?

Book Reviews in This Article:William J. curran Larry Gostin, and Mary Clark, Acquired Immunodeficiency Syndrome: Legal and Regulatory Policy.

The very high genome copy number in cytoplasmic organelles is a puzzling fact in cell biology. It is proposed here that high copy number reflects an increased need for organellar ribosomes that can only be satisfied by the increased ribosomal RNA gene number that results from genome multiplication.

From cytological examination, the size and form of the chromosomes in the eukaryotic nucleus are invariant across generations, leading to the expectation that constancy of inheritance likely depends on constancy of the chromosomal DNA molecule conveying the constant phenotype. Indeed, except for rare mutations, major phenotypic traits appear largely without change from generation to generation. Thus, when it was discovered that the inheritance of traits for bacteria, mitochondria and chloroplasts was also constant, it was assumed that chromosomes in those locations (...) were also constant. Such has not turned out to be the case, however; those chromosomes are highly variable in structure. I propose, therefore, that only for the nucleus is there a requirement that a chromosome be “finished” (contain only fully replicated genomes) before it may segregate to daughter cells. This requirement does not apply to the variable chromosomes among chloroplasts, mitochondria and bacteria. BioEssays 29:474–483, 2007. © 2007 Wiley Periodicals, Inc. (shrink)

The very high genome copy number in cytoplasmic organelles is a puzzling fact in cell biology. It is proposed here that high copy number reflects an increased need for organellar ribosomes that can only be satisfied by the increased ribosomal RNA gene number that results from genome multiplication.

The concept of quantum spontaneity is introduced to provide a non-deterministic, non-indeterministic, and non-random model of consciousness that can accommodate our intuitive sense of self, intentionality, and creativity.