Posts Tagged ‘why0mg’

Sex Bias in Graduate Admissions: Data from Berkeley | Science

August 23, 2020

Sex Bias in Graduate Admissions: Data from Berkeley

P. J. Bickel1, E. A. Hammel1, J. W. O’Connell1

Science 07 Feb 1975:
Vol. 187, Issue 4175, pp. 398-404
DOI: 10.1126/science.187.4175.398

A type of Simpson’s paradox

Simpson’s paradox – Wikipedia

August 23, 2020‘s_paradox

Monty Hall problem – Wikipedia

August 9, 2020

collider bias

Case–control study – Wikipedia

April 13, 2020–control_study

Bradford Hill criteria – Wikipedia

April 13, 2020

In 1965, the English statistician Sir Austin Bradford Hill proposed a set of nine criteria to provide epidemiologic evidence of a causal relationship between a presumed cause and an observed effect. (For example, he demonstrated the connection between cigarette smoking and lung cancer.) The list of the criteria is as follows

Randomized controlled trial – Wikipedia

April 13, 2020

Low-density parity-check code – Wikipedia

February 17, 2020

turbo codes

2G cell phones used “soft decoding” (i.e., probabilities) but not belief propagation. 3G cell phones used Berrou’s turbo codes, and 4G phones used Gallager’s turbo-like codes.
[from book!]

Paternity Index – Wikipedia

February 16, 2020

Hidden Data and Surviving a Sinking Ship: Simpson’s Paradox – Select Statistical Consultants

April 26, 2019

continuous version of the paradox

Genetic susceptibility to lung cancer and co-morbidities

April 26, 2019

Genome-wide association studies (GWAS) have enabled significant progress in the past 5 years in investigating genetic susceptibility to lung cancer. Large scale, multi-cohort GWAS of mainly Caucasian, smoking, populations have identified strong associations for lung cancer mapped to chromosomal regions 15q [nicotinic acetylcholine receptor (nAChR) subunits: CHRNA3, CHRNA5], 5p (TERT-CLPTM1L locus) and 6p (BAT3-MSH5). Some studies in Asian populations of smokers have found similar risk loci, whereas GWAS in never smoking Asian females have identified associations in other chromosomal regions, e.g., 3q (TP63), that are distinct from smoking-related lung cancer risk loci. GWAS of smoking behaviour have identified risk loci for smoking quantity at 15q (similar genes to lung cancer susceptibility: CHRNA3, CHRNA5) and 19q (CYP2A6).