IBM Watson Health has formed a medical imaging collaborative with more than 15 leading healthcare organizations. The goal: To take on some of the most deadly diseases. The collaborative, which includes health systems, academic medical centers, ambulatory radiology providers and imaging technology companies, aims to help doctors address breast, lung, and other cancers; diabetes; eye health; brain disease; and heart disease and related conditions, such as stroke. Watson will mine insights from what IBM calls previously invisible unstructured imaging data and combine it with a broad variety of data from other sources, such as data from electronic health records, radiology and pathology reports, lab results, doctors' progress notes, medical journals, clinical care guidelines and published outcomes studies. As the work of the collaborative evolves, Watson's rationale and insights will evolve, informed by the latest combined thinking of the participating organizations.
We have, up to this point, had decades of benefits accrued through computing -- but what innovations will push the envelope for our seniors? Artificial intelligence (AI) is the information of science. AI is misunderstood and glamorized by some, making it out to be something other than what it really is. It gives us the ability to use computers to perform tasks that usually require human intelligence. What was dubbed "artificial" is coming to be more appropriately thought to be cognitive intelligence, giving us tremendous benefits in all fields including aging, health, and safety.
Historically, AI research has understandably focused on those aspects of cognition that distinguish humans from other animals - in particular, our capacity for complex problem solving. However, with a few notable exceptions, narratives in popular media generally focus on those aspects of human experience that we share with other social animals: attachment, mating and child rearing, violence, group affiliation, and inter-group and inter-individual conflict. Moreover, the stories we tell often focus on the ways in which these processes break down. In this paper, I will argue that current agent architectures don't offer particularly good models of these phenomena, and discuss specific phenomena that I think it would be illuminating to understand at a computational level.
The human cerebral cortex has undergone an extraordinary increase in size and complexity during mammalian evolution. Cortical cell lineages are specified in the embryo, and genetic and epidemiological evidence implicates early cortical development in the etiology of neuropsychiatric disorders such as autism spectrum disorder (ASD), intellectual disabilities, and schizophrenia. Most of the disease-implicated genomic variants are located outside of genes, and the interpretation of noncoding mutations is lagging behind owing to limited annotation of functional elements in the noncoding genome. We set out to discover gene-regulatory elements and chart their dynamic activity during prenatal human cortical development, focusing on enhancers, which carry most of the weight upon regulation of gene expression. We longitudinally modeled human brain development using human induced pluripotent stem cell (hiPSC)–derived cortical organoids and compared organoids to isogenic fetal brain tissue. Fetal fibroblast–derived hiPSC lines were used to generate cortically patterned organoids and to compare oganoids' epigenome and transcriptome to that of isogenic fetal brains and external datasets. Organoids model cortical development between 5 and 16 postconception weeks, thus enabling us to study transitions from cortical stem cells to progenitors to early neurons. The greatest changes occur at the transition from stem cells to progenitors. The regulatory landscape encompasses a total set of 96,375 enhancers linked to target genes, with 49,640 enhancers being active in organoids but not in mid-fetal brain, suggesting major roles in cortical neuron specification. Enhancers that gained activity in the human lineage are active in the earliest stages of organoid development, when they target genes that regulate the growth of radial glial cells. Parallel weighted gene coexpression network analysis (WGCNA) of transcriptome and enhancer activities defined a number of modules of coexpressed genes and coactive enhancers, following just six and four global temporal patterns that we refer to as supermodules, likely reflecting fundamental programs in embryonic and fetal brain. Correlations between gene expression and enhancer activity allowed stratifying enhancers into two categories: activating regulators (A-regs) and repressive regulators (R-regs).