Learning, Social Intelligence and the Turing Test - why an "out-of-the-box" Turing Machine will not pass the Turing Test

The Turing Test (TT) checks for human intelligence, rather than any putative general intelligence. It involves repeated interaction requiring learning in the form of adaption to the human conversation partner. It is a macro-level post-hoc test in contrast to the definition of a Turing Machine (TM), which is a prior micro-level definition. This raises the question of whether learning is just another computational process, i.e. can be implemented as a TM. Here we argue that learning or adaption is fundamentally different from computation, though it does involve processes that can be seen as computations. To illustrate this difference we compare (a) designing a TM and (b) learning a TM, defining them for the purpose of the argument. We show that there is a well-defined sequence of problems which are not effectively designable but are learnable, in the form of the bounded halting problem. Some characteristics of human intelligence are reviewed including it's: interactive nature, learning abilities, imitative tendencies, linguistic ability and context-dependency. A story that explains some of these is the Social Intelligence Hypothesis. If this is broadly correct, this points to the necessity of a considerable period of acculturation (social learning in context) if an artificial intelligence is to pass the TT. Whilst it is always possible to 'compile' the results of learning into a TM, this would not be a designed TM and would not be able to continually adapt (pass future TTs). We conclude three things, namely that: a purely "designed" TM will never pass the TT; that there is no such thing as a general intelligence since it necessary involves learning; and that learning/adaption and computation should be clearly distinguished.Comment: 10 pages, invited talk at Turing Centenary Conference CiE 2012, special session on "The Turing Test and Thinking Machines

Model Analysis of Time Reversal Symmetry Test in the Caltech Fe-57 Gamma-Transition Experiment

The CALTECH gamma-transition experiment testing time reversal symmetry via the E2/M1 mulipole mixing ratio of the 122 keV gamma-line in Fe-57 has already been performed in 1977. Extending an earlier analysis in terms of an effective one-body potential, this experiment is now analyzed in terms of effective one boson exchange T-odd P-even nucleon nucleon potentials. Within the model space considered for the Fe-57 nucleus no contribution from isovector rho-type exchange is possible. The bound on the coupling strength phi_A from effective short range axial-vector type exchange induced by the experimental bound on sin(eta) leads to phi_A < 10^{-2}.Comment: 5 pages, RevTex 3.

CRISPR screens identify gene targets at breast cancer risk loci

Background: Genome-wide association studies (GWAS) have identified > 200 loci associated with breast cancer risk. The majority of candidate causal variants are in noncoding regions and likely modulate cancer risk by regulating gene expression. However, pinpointing the exact target of the association, and identifying the phenotype it mediates, is a major challenge in the interpretation and translation of GWAS. Results: Here, we show that pooled CRISPR screens are highly effective at identifying GWAS target genes and defining the cancer phenotypes they mediate. Following CRISPR mediated gene activation or suppression, we measure proliferation in 2D, 3D, and in immune-deficient mice, as well as the effect on DNA repair. We perform 60 CRISPR screens and identify 20 genes predicted with high confidence to be GWAS targets that promote cancer by driving proliferation or modulating the DNA damage response in breast cells. We validate the regulation of a subset of these genes by breast cancer risk variants. Conclusions: We demonstrate that phenotypic CRISPR screens can accurately pinpoint the gene target of a risk locus. In addition to defining gene targets of risk loci associated with increased breast cancer risk, we provide a platform for identifying gene targets and phenotypes mediated by risk variants.Natasha K. Tuano, Jonathan Beesley, Murray Manning, Wei Shi, Laura Perlaza, Jimenez, Luis F. Malaver, Ortega, Jacob M. Paynter, Debra Black, Andrew Civitarese, Karen McCue, Aaron Hatzipantelis, Kristine Hillman, Susanne Kaufmann, Haran Sivakumaran, Jose M. Polo, Roger R. Reddel, Vimla Band, Juliet D. French, Stacey L. Edwards, David R. Powell, Georgia Chenevix, Trench, and Joseph Rosenblu

The CASPR2 cell adhesion molecule functions as a tumor suppressor gene in glioma.

Contains fulltext : 89014.pdf (publisher's version ) (Closed access)Genomic translocations have been implicated in cancer. In this study, we performed a screen for genetic translocations in gliomas based on exon-level expression profiles. We identified a translocation in the contactin-associated protein-like 2 (CASPR2) gene, encoding a cell adhesion molecule. CASPR2 mRNA was fused to an expressed sequence tag that likely is part of the nuclear receptor coactivator 1 gene. Despite high mRNA expression levels, no CASPR2 fusion protein was detected. In a set of 25 glioblastomas and 22 oligodendrogliomas, mutation analysis identified two additional samples with genetic alterations in the CASPR2 gene and all three identified genetic alterations are likely to reduce CASPR2 protein expression levels. Methylation of the CASPR2 gene was also observed in gliomas and glioma cell lines. CASPR2-overexpressing cells showed decreased proliferation rates, likely because of an increase in apoptosis. Moreover, high CASPR2 mRNA expression level is positively correlated with survival and is an independent prognostic factor. These results indicate that CASPR2 acts as a tumor suppressor gene in glioma