The Roles of Internal Representation and Processing in Problem Solving Involving Insight: A Computational Complexity Perspective

In human problem solving, there is a wide variation between individuals in problem solution time and success rate, regardless of whether or not this problem solving involves insight. In this paper, we apply computational and parameterized analysis to a plausible formalization of extended representation change theory (eRCT), an integration of problem solving by problem space search and insight as problem restructuring which proposes that this variation may be explainable by individuals having different problem representations and search heuristic choices. Our analyses establish not only the intractability of eRCT in general, but also sets of restrictions under which eRCT-based problem solving can and cannot be done quickly. As such, our analyses both prove that several conjectures about what makes problem solving under eRCT possible in practice are incomplete, in the sense that not all factors in the model whose restriction is responsible for efficient solvability are part of the explanation, and provide several new explanations that are complete

Deep Analogical Inference as the Origin of Hypotheses

The ability to generate novel hypotheses is an important problem-solving capacity of humans. This ability is vital for making sense of the complex and unfamiliar world we live in. Often, this capacity is characterized as an inference to the best explanation—selecting the “best” explanation from a given set of candidate hypotheses. However, it remains unclear where these candidate hypotheses originate from. In this paper we contribute to computationally explaining these origins by providing the contours of the computational problem solved when humans generate hypotheses. The origin of hypotheses, otherwise known as abduction proper, is hallmarked by seven properties: (1) isotropy, (2) open-endedness, (3) novelty, (4) groundedness, (5) sensibility, (6) psychological realism, and (7) computational tractability. In this paper we provide a computational-level theory of abduction proper that unifies the first six of these properties and lays the groundwork for the seventh property of computational tractability. We conjecture that abduction proper is best seen as a process of deep analogical inference

Intentional Communication: Computationally Easy or Difficult?

Human intentional communication is marked by its flexibility and context sensitivity. Hypothesized brain mechanisms can provide convincing and complete explanations of the human capacity for intentional communication only insofar as they can match the computational power required for displaying that capacity. It is thus of importance for cognitive neuroscience to know how computationally complex intentional communication actually is. Though the subject of considerable debate, the computational complexity of communication remains so far unknown. In this paper we defend the position that the computational complexity of communication is not a constant, as some views of communication seem to hold, but rather a function of situational factors. We present a methodology for studying and characterizing the computational complexity of communication under different situational constraints. We illustrate our methodology for a model of the problems solved by receivers and senders during a communicative exchange. This approach opens the way to a principled identification of putative model parameters that control cognitive processes supporting intentional communication

Ignorance is Bliss: A Complexity Perspective on Adapting Reactive Architectures

Abstract-We study the computational complexity of adapting a reactive architecture to meet task constraints. This computational problem has application in a wide variety of fields, including cognitive and evolutionary robotics and cognitive neuroscience. We show that-even for a rather simple world and a simple task-adapting a reactive architecture to perform a given task in the given world is N P -hard. This result implies that adapting reactive architectures is computationally intractable regardless the nature of the adaptation process (e.g., engineering, development, evolution, learning, etc.) unless very special conditions apply. In order to find such special conditions for tractability, we have performed parameterized complexity analyses. One of our main findings is that architectures with limited sensory and perceptual abilities are efficiently adaptable

Mild-to-Moderate Kidney Dysfunction and Cardiovascular Disease: Observational and Mendelian Randomization Analyses

BACKGROUND: End-stage renal disease is associated with a high risk of cardiovascular events. It is unknown, however, whether mild-to-moderate kidney dysfunction is causally related to coronary heart disease (CHD) and stroke. METHODS: Observational analyses were conducted using individual-level data from 4 population data sources (Emerging Risk Factors Collaboration, EPIC-CVD [European Prospective Investigation into Cancer and Nutrition-Cardiovascular Disease Study], Million Veteran Program, and UK Biobank), comprising 648 135 participants with no history of cardiovascular disease or diabetes at baseline, yielding 42 858 and 15 693 incident CHD and stroke events, respectively, during 6.8 million person-years of follow-up. Using a genetic risk score of 218 variants for estimated glomerular filtration rate (eGFR), we conducted Mendelian randomization analyses involving 413 718 participants (25 917 CHD and 8622 strokes) in EPIC-CVD, Million Veteran Program, and UK Biobank. RESULTS: There were U-shaped observational associations of creatinine-based eGFR with CHD and stroke, with higher risk in participants with eGFR values 105 mL·min-1·1.73 m-2, compared with those with eGFR between 60 and 105 mL·min-1·1.73 m-2. Mendelian randomization analyses for CHD showed an association among participants with eGFR 105 mL·min-1·1.73 m-2. Results were not materially different after adjustment for factors associated with the eGFR genetic risk score, such as lipoprotein(a), triglycerides, hemoglobin A1c, and blood pressure. Mendelian randomization results for stroke were nonsignificant but broadly similar to those for CHD. CONCLUSIONS: In people without manifest cardiovascular disease or diabetes, mild-to-moderate kidney dysfunction is causally related to risk of CHD, highlighting the potential value of preventive approaches that preserve and modulate kidney function

Mild-to-Moderate Kidney Dysfunction and Cardiovascular Disease: Observational and Mendelian Randomization Analyses

BACKGROUND: End-stage renal disease is associated with a high risk of cardiovascular events. It is unknown, however, whether mild-to-moderate kidney dysfunction is causally related to coronary heart disease (CHD) and stroke. METHODS: Observational analyses were conducted using individual-level data from 4 population data sources (Emerging Risk Factors Collaboration, EPIC-CVD [European Prospective Investigation into Cancer and Nutrition-Cardiovascular Disease Study], Million Veteran Program, and UK Biobank), comprising 648 135 participants with no history of cardiovascular disease or diabetes at baseline, yielding 42 858 and 15 693 incident CHD and stroke events, respectively, during 6.8 million personyears of follow-up. Using a genetic risk score of 218 variants for estimated glomerular filtration rate (eGFR), we conducted Mendelian randomization analyses involving 413 718 participants (25917 CHD and 8622 strokes) in EPIC-CVD, Million Veteran Program, and UK Biobank. RESULTS: There were U-shaped observational associations of creatinine-based eGFR with CHD and stroke, with higher risk in participants with eG FR values 105 mL.min(-1).1.73 m(-2), compared with those with eG FR between 60 and 105 mL.min(-1).1.73 m(-2). Mendelian randomization analyses for CHD showed an association among participants with eGFR 105 mL.min(-1).1.73 m(-2). Results were not materially different after adjustment for factors associated with the eGFR genetic risk score, such as lipoprotein(a), triglycerides, hemoglobin Alc, and blood pressure. Mendelian randomization results for stroke were nonsignificant but broadly similar to those for CHD. CONCLUSIONS: In people without manifest cardiovascular disease or diabetes, mild-to-moderate kidney dysfunction is causally related to risk of CHD, highlighting the potential value of preventive approaches that preserve and modulate kidney function

Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci.

We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease

Rare and low-frequency coding variants alter human adult height

Height is a highly heritable, classic polygenic trait with ~700 common associated variants identified so far through genome - wide association studies . Here , we report 83 height - associated coding variants with lower minor allele frequenc ies ( range of 0.1 - 4.8% ) and effects of up to 2 16 cm /allele ( e.g. in IHH , STC2 , AR and CRISPLD2 ) , >10 times the average effect of common variants . In functional follow - up studies, rare height - increasing alleles of STC2 (+1 - 2 cm/allele) compromise d proteolytic inhibition of PAPP - A and increased cleavage of IGFBP - 4 in vitro , resulting in higher bioavailability of insulin - like growth factors . The se 83 height - associated variants overlap genes mutated in monogenic growth disorders and highlight new biological candidates ( e.g. ADAMTS3, IL11RA, NOX4 ) and pathways ( e.g . proteoglycan/ glycosaminoglycan synthesis ) involved in growth . Our results demonstrate that sufficiently large sample sizes can uncover rare and low - frequency variants of moderate to large effect associated with polygenic human phenotypes , and that these variants implicate relevant genes and pathways

The genetic architecture of type 2 diabetes

The genetic architecture of common traits, including the number, frequency, and effect sizes of inherited variants that contribute to individual risk, has been long debated. Genome-wide association studies have identified scores of common variants associated with type 2 diabetes, but in aggregate, these explain only a fraction of heritability. To test the hypothesis that lower-frequency variants explain much of the remainder, the GoT2D and T2D-GENES consortia performed whole genome sequencing in 2,657 Europeans with and without diabetes, and exome sequencing in a total of 12,940 subjects from five ancestral groups. To increase statistical power, we expanded sample size via genotyping and imputation in a further 111,548 subjects. Variants associated with type 2 diabetes after sequencing were overwhelmingly common and most fell within regions previously identified by genome-wide association studies. Comprehensive enumeration of sequence variation is necessary to identify functional alleles that provide important clues to disease pathophysiology, but large-scale sequencing does not support a major role for lower-frequency variants in predisposition to type 2 diabetes