Compression as a universal principle of animal behavior

A key aim in biology and psychology is to identify fundamental principles underpinning the behavior of animals, including humans. Analyses of human language and the behavior of a range of non-human animal species have provided evidence for a common pattern underlying diverse behavioral phenomena: words follow Zipf's law of brevity (the tendency of more frequently used words to be shorter), and conformity to this general pattern has been seen in the behavior of a number of other animals. It has been argued that the presence of this law is a sign of efficient coding in the information theoretic sense. However, no strong direct connection has been demonstrated between the law and compression, the information theoretic principle of minimizing the expected length of a code. Here we show that minimizing the expected code length implies that the length of a word cannot increase as its frequency increases. Furthermore, we show that the mean code length or duration is significantly small in human language, and also in the behavior of other species in all cases where agreement with the law of brevity has been found. We argue that compression is a general principle of animal behavior, that reflects selection for efficiency of coding.Comment: This is the pre-proofed version. The published version will be available at http://onlinelibrary.wiley.com/journal/10.1111/%28ISSN%291551-670

Beth Levine in memoriam

Beth Levine was born on 7 April 1960 in Newark, New Jersey. She went to college at Brown University where she received an A.B. Magna Cum Laude, and she attended medical school at Cornell University Medical College, receiving her MD in 1986. She completed her internship and residency in Internal Medicine at Mount Sinai Hospital in New York, and her fellowship in Infectious Diseases at The Johns Hopkins Hospital. Most recently, Beth was a Professor of Internal Medicine and Microbiology, Director of the Center for Autophagy Research, and holder of the Charles Sprague Distinguished Chair in Biomedical Science at the University of Texas Southwestern Medical Center in Dallas. Beth died on 15 June 2020 from cancer. Beth is survived by her husband, Milton Packer, and their two children, Rachel (26 years old) and Ben (25 years old). Dr. Levine was as an international leader in the field of autophagy research. Her laboratory identified the mammalian autophagy gene BECN1/beclin 1; identified conserved mechanisms underlying the regulation of autophagy (e.g. BCL2-BECN1 complex formation, insulin-like signaling, EGFR, ERBB2/HER2 and AKT1-mediated BECN1 phosphosphorylation); and provided the first evidence that autophagy genes are important in antiviral host defense, tumor suppression, lifespan extension, apoptotic corpse clearance, metazoan development, Na,K-ATPase-regulated cell death, and the beneficial metabolic effects of exercise. She developed a potent autophagy-inducing cell permeable peptide, Tat-beclin 1, which has potential therapeutic applications in a range of diseases. She was a founding Associate Editor of the journal Autophagy and an editorial board member of Cell and Cell Host & Microbe. She has received numerous awards/honors in recognition of her scientific achievement, including: The American Cancer Society Junior Faculty Research Award (1994); election into the American Society of Clinical Investigation (2000); the Ellison Medical Foundation Senior Scholars Award in Global Infectious Diseases (2004); elected member, American Association of Physicians (2005); appointment as a Howard Hughes Medical Institute Investigator (2008); Edith and Peter O’Donnell Award in Medicine (2008); elected fellow, American Association for the Advancement of Science (2012); election into the National Academy of Sciences (2013); election into the Academy of Medicine, Engineering and Science of Texas (2013); the ASCI Stanley J. Korsmeyer Award (2014); Phyllis T. Bodel Women in Medicine Award, Yale University School of Medicine (2018); recipient, Barcroft Medal, Queen’s University Belfast (2018).Fil: An, Zhenyi. No especifíca;Fil: Ballabi, Andrea. No especifíca;Fil: Bennett, Lynda. No especifíca;Fil: Boya, Patricia. No especifíca;Fil: Cecconi, Francesco. No especifíca;Fil: Chiang, Wei Chung. No especifíca;Fil: Codogno, Patrice. No especifíca;Fil: Colombo, Maria Isabel. No especifíca;Fil: Cuervo, Ana Maria. No especifíca;Fil: Debnath, Jayanta. No especifíca;Fil: Deretic, Vojo. No especifíca;Fil: Dikic, Ivan. No especifíca;Fil: Dionne, Keith. No especifíca;Fil: Dong, Xiaonan. No especifíca;Fil: Elazar, Zvulun. No especifíca;Fil: Galluzzi, Lorenzo. No especifíca;Fil: Gentile, Frank. No especifíca;Fil: Griffin, Diane E.. No especifíca;Fil: Hansen, Malene. No especifíca;Fil: Hardwick, J. Marie. No especifíca;Fil: He, Congcong. No especifíca;Fil: Huang, Shu Yi. No especifíca;Fil: Hurley, James. No especifíca;Fil: Jackson, William T.. No especifíca;Fil: Jozefiak, Cindy. No especifíca;Fil: Kitsis, Richard N.. No especifíca;Fil: Klionsky, Daniel J.. No especifíca;Fil: Kroemer, Guido. No especifíca;Fil: Meijer, Alfred J.. No especifíca;Fil: Meléndez, Alicia. No especifíca;Fil: Melino, Gerry. No especifíca;Fil: Mizushima, Noboru. No especifíca;Fil: Murphy, Leon O.. No especifíca;Fil: Nixon, Ralph. No especifíca;Fil: Orvedahl, Anthony. No especifíca;Fil: Pattingre, Sophie. No especifíca;Fil: Piacentini, Mauro. No especifíca;Fil: Reggiori, Fulvio. No especifíca;Fil: Ross, Theodora. No especifíca;Fil: Rubinsztein, David C.. No especifíca;Fil: Ryan, Kevin. No especifíca;Fil: Sadoshima, Junichi. No especifíca;Fil: Schreiber, Stuart L.. No especifíca;Fil: Scott, Frederick. No especifíca;Fil: Sebti, Salwa. No especifíca;Fil: Shiloh, Michael. No especifíca;Fil: Shoji, Sanae. No especifíca;Fil: Simonsen, Anne. No especifíca;Fil: Smith, Haley. No especifíca;Fil: Sumpter, Kathryn M.. No especifíca;Fil: Thompson, Craig B.. No especifíca;Fil: Thorburn, Andrew. No especifíca;Fil: Thumm, Michael. No especifíca;Fil: Tooze, Sharon. No especifíca;Fil: Vaccaro, Maria Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Virgin, Herbert W.. No especifíca;Fil: Wang, Fei. No especifíca;Fil: White, Eileen. No especifíca;Fil: Xavier, Ramnik J.. No especifíca;Fil: Yoshimori, Tamotsu. No especifíca;Fil: Yuan, Junying. No especifíca;Fil: Yue, Zhenyu. No especifíca;Fil: Zhong, Qing. No especifíca

Mixed-species aggregations in arthropods

This review offers the first synthesis of the research on mixed-species groupings of arthropods and highlights the behavioural and evolutionary questions raised by such behaviour. Mixed-species groups are commonly found in mammals and birds. Such groups are also observed in a large range of arthropod taxa independent of their level of sociality. Several examples are presented to highlight the mechanisms underlying such groupings, particularly the evidence for phylogenetic proximity between members that promotes cross-species recognition. The advantages offered by such aggregates are described and discussed. These advantages can be attributed to the increase in group size and could be identical to those of non-mixed groupings, but competition-cooperation dynamics might also be involved, and such effects may differ between homo- and heterospecific groups. We discuss three extreme cases of interspecific recognition that are likely involved in mixed-species groups as vectors for cross-species aggregation: tolerance behaviour between two social species, one-way mechanism in which one species is attractive to others and two-way mechanism of mutual attraction. As shown in this review, the study of mixed-species groups offers biologists an interesting way to explore the frontiers of cooperation-competition, including the process of sympatric speciation.PostprintPeer reviewe

Association between HIV infection and mitochondrial DNA copy number in peripheral blood: A population-based, prospective cohort study

Background. Low mitochondrial DNA (mtDNA) copy number (CN) is a predictor of adverse aging outcomes, and its status may be altered in human immunodefciency virus (HIV)-infected persons. Tis study evaluated the cross-sectional and longitudinal change of mtDNA CN by HIV markers. Methods. mtDNA CN was measured in the ALIVE (AIDS Linked to the Intravenous Experience) cohort of persons with a history of injecting drugs. Multivariable linear regression models controlling for demographic characteristics, behavior, and hepatitis C virus (HCV) seropositivity assessed the relationship of mtDNA CN to HIV markers (CD4+ T-cell counts, viral load, antiretroviral therapy [ART] use). Linear mixed models tested the association between HIV markers and age-related mtDNA CN trajectories. Results. Among 741 individuals at baseline, 436 (59%) were infected with HIV. HIV-infected individuals who had lower CD4+ T-cell counts (P =.01), had higher viral loads (P \u3c.01), and were not receiving ART (P \u3c.01) had signifcantly lower mtDNA CNs than uninfected persons; there was no difference between participants who were uninfected and HIV-infected individuals who had well-controlled HIV levels. In longitudinal follow-up of 507 participants, from age 50 years onward, mtDNA CN declined signifcantly faster among HIV-infected individuals than among HIV-uninfected persons (-0.03 units of change/year vs 0.006 units of change/year; P =.04), even among infected individuals with well-controlled HIV. Conclusion. Before 50 years of age, mtDNA CN is similar between HIV-infected individuals with well-controlled HIV and uninfected persons, but from age 50 onward, mtDNA CN declines signifcantly faster among all infected individuals than among HIV-uninfected persons

Commission on Russian-American Relations 2010

Created as part of the 2010 Jackson School for International Studies SIS 495: Task Force. Robert Huber, Task Force Advisor; Martin Sletzinger, Evaluator

Evaluation of mitochondrial DNA copy number estimation techniques.

Mitochondrial DNA copy number (mtDNA-CN), a measure of the number of mitochondrial genomes per cell, is a minimally invasive proxy measure for mitochondrial function and has been associated with several aging-related diseases. Although quantitative real-time PCR (qPCR) is the current gold standard method for measuring mtDNA-CN, mtDNA-CN can also be measured from genotyping microarray probe intensities and DNA sequencing read counts. To conduct a comprehensive examination on the performance of these methods, we use known mtDNA-CN correlates (age, sex, white blood cell count, Duffy locus genotype, incident cardiovascular disease) to evaluate mtDNA-CN calculated from qPCR, two microarray platforms, as well as whole genome (WGS) and whole exome sequence (WES) data across 1,085 participants from the Atherosclerosis Risk in Communities (ARIC) study and 3,489 participants from the Multi-Ethnic Study of Atherosclerosis (MESA). We observe mtDNA-CN derived from WGS data is significantly more associated with known correlates compared to all other methods (p < 0.001). Additionally, mtDNA-CN measured from WGS is on average more significantly associated with traits by 5.6 orders of magnitude and has effect size estimates 5.8 times more extreme than the current gold standard of qPCR. We further investigated the role of DNA extraction method on mtDNA-CN estimate reproducibility and found mtDNA-CN estimated from cell lysate is significantly less variable than traditional phenol-chloroform-isoamyl alcohol (p = 5.44x10-4) and silica-based column selection (p = 2.82x10-7). In conclusion, we recommend the field moves towards more accurate methods for mtDNA-CN, as well as re-analyze trait associations as more WGS data becomes available from larger initiatives such as TOPMed