Evidence map›Paper›PMID 21828277›Full record

ArticleGenetics2011

Is life law-like?

Kenneth M Weiss, Anne V Buchanan

Abstract read
In one paragraph

Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Kenneth M WeissDepartment of Anthropology, Pennsylvania State University, University Park, Pennsylvania 16802, USA. kmw4@psu.edu
Anne V Buchanan

Funding

ANALYZE: Software for Joint Linkage and LD AnalysisR01MH063749 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TERWILLIGER, JOSEPH D · 2001 to 2005
$1.7M
Inferring phenogentic mechanisms in psychiatric and other complex traitsR01MH084995 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TERWILLIGER, JOSEPH DOUGLAS · 2009 to 2012
$1.6M
NIMH NIH HHS MH063749NIMH NIH HHS MH084995NIMH NIH HHS R01 MH063749NIMH NIH HHS R01 MH084995
6 · The paper itself

Abstract

Genes are generally assumed to be primary biological causes of biological phenotypes and their evolution. In just over a century, a research agenda that has built on Mendel's experiments and on Darwin's theory of natural selection as a law of nature has had unprecedented scientific success in isolating and characterizing many aspects of genetic causation. We revel in these successes, and yet the story is not quite so simple. The complex cooperative nature of genetic architecture and its evolution include teasingly tractable components, but much remains elusive. The proliferation of data generated in our "omics" age raises the question of whether we even have (or need) a unified theory or "law" of life, or even clear standards of inference by which to answer the question. If not, this not only has implications for the widely promulgated belief that we will soon be able to predict phenotypes like disease risk from genes, but also speaks to the limitations in the underlying science itself. Much of life seems to be characterized by ad hoc, ephemeral, contextual probabilism without proper underlying distributions. To the extent that this is true, causal effects are not asymptotically predictable, and new ways of understanding life may be required.

Indexed as

Biological EvolutionLifeAnimalsHumansNatureSelection, Genetic

Identifiers

PMID21828277
PMCPMC3176095

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.