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Article ; Online: The emergence of egalitarianism in a model of early human societies

Guillaume Calmettes / James N. Weiss

Heliyon, Vol 3, Iss 11, Pp e00451- (2017)

2017

Abstract: How did egalitarianism emerge in early human societies? In contrast to dominance hierarchies in non-human primates, human simple forager bands are typically egalitarian, with male hunters often serving as the collective alpha. Here we present a ... ...

Abstract	How did egalitarianism emerge in early human societies? In contrast to dominance hierarchies in non-human primates, human simple forager bands are typically egalitarian, with male hunters often serving as the collective alpha. Here we present a thermodynamics-inspired simple population model, based on stochastic optimization of dominance relationships, in which a dominance hierarchy of individuals with exclusively self-centered characteristics (the desire to dominate, resentment at being dominated) transitions spontaneously to egalitarianism as their capacity for language develops. Language, specifically gossip, allows resentment against being dominated to promote the formation of antidominance coalitions which destabilize the alpha position for individuals, leading to a phase transition in which a coalition of the full population suddenly becomes dominant. Thus, egalitarianism emerges suddenly as the optimal power-sharing arrangement in a population of selfish individuals without any inherently altruistic qualities. We speculate that egalitarianism driven by punishment for exhibiting alpha-like behavior may then set the stage for genuinely altruistic traits to propagate as predicted by game theory models. Based on model simulations, we also predict that egalitarianism is a pre-condition for adaptation of tools as weapons. Potential implications for origins of human moral belief systems are discussed.
Keywords	Sociology ; Evolution ; Anthropology ; Science (General) ; Q1-390 ; Social sciences (General) ; H1-99
Language	English
Publishing date	2017-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A quantitative method to track protein translocation between intracellular compartments in real-time in live cells using weighted local variance image analysis.

Guillaume Calmettes / James N Weiss

PLoS ONE, Vol 8, Iss 12, p e

2013 Volume 81988

Abstract: The genetic expression of cloned fluorescent proteins coupled to time-lapse fluorescence microscopy has opened the door to the direct visualization of a wide range of molecular interactions in living cells. In particular, the dynamic translocation of ... ...

Abstract	The genetic expression of cloned fluorescent proteins coupled to time-lapse fluorescence microscopy has opened the door to the direct visualization of a wide range of molecular interactions in living cells. In particular, the dynamic translocation of proteins can now be explored in real time at the single-cell level. Here we propose a reliable, easy-to-implement, quantitative image processing method to assess protein translocation in living cells based on the computation of spatial variance maps of time-lapse images. The method is first illustrated and validated on simulated images of a fluorescently-labeled protein translocating from mitochondria to cytoplasm, and then applied to experimental data obtained with fluorescently-labeled hexokinase 2 in different cell types imaged by regular or confocal microscopy. The method was found to be robust with respect to cell morphology changes and mitochondrial dynamics (fusion, fission, movement) during the time-lapse imaging. Its ease of implementation should facilitate its application to a broad spectrum of time-lapse imaging studies.
Keywords	Medicine ; R ; Science ; Q
Subject code	612
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Long-Lasting Sparks

Zhen Song / Alain Karma / James N Weiss / Zhilin Qu

PLoS Computational Biology, Vol 12, Iss 1, p e

Multi-Metastability and Release Competition in the Calcium Release Unit Network.

2016 Volume 1004671

Abstract: Calcium (Ca) sparks are elementary events of biological Ca signaling. A normal Ca spark has a brief duration in the range of 10 to 100 ms, but long-lasting sparks with durations of several hundred milliseconds to seconds are also widely observed. ... ...

Abstract	Calcium (Ca) sparks are elementary events of biological Ca signaling. A normal Ca spark has a brief duration in the range of 10 to 100 ms, but long-lasting sparks with durations of several hundred milliseconds to seconds are also widely observed. Experiments have shown that the transition from normal to long-lasting sparks can occur when ryanodine receptor (RyR) open probability is either increased or decreased. Here, we demonstrate theoretically and computationally that long-lasting sparks emerge as a collective dynamical behavior of the network of diffusively coupled Ca release units (CRUs). We show that normal sparks occur when the CRU network is monostable and excitable, while long-lasting sparks occur when the network dynamics possesses multiple metastable attractors, each attractor corresponding to a different spatial firing pattern of sparks. We further highlight the mechanisms and conditions that produce long-lasting sparks, demonstrating the existence of an optimal range of RyR open probability favoring long-lasting sparks. We find that when CRU firings are sparse and sarcoplasmic reticulum (SR) Ca load is high, increasing RyR open probability promotes long-lasting sparks by potentiating Ca-induced Ca release (CICR). In contrast, when CICR is already strong enough to produce frequent firings, decreasing RyR open probability counter-intuitively promotes long-lasting sparks by decreasing spark frequency. The decrease in spark frequency promotes intra-SR Ca diffusion from neighboring non-firing CRUs to the firing CRUs, which helps to maintain the local SR Ca concentration of the firing CRUs above a critical level to sustain firing. In this setting, decreasing RyR open probability further suppresses long-lasting sparks by weakening CICR. Since a long-lasting spark terminates via the Kramers' escape process over a potential barrier, its duration exhibits an exponential distribution determined by the barrier height and noise strength, which is modulated differently by different ways of altering the Ca release ...
Keywords	Biology (General) ; QH301-705.5
Subject code	612
Language	English
Publishing date	2016-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Increased reactive oxygen species production during reductive stress: The roles of mitochondrial glutathione and thioredoxin reductases

Korge, Paavo / Guillaume Calmettes / James N. Weiss

Biochimica et biophysica acta. 2015 June, July, v. 1847, no. 6-7

2015

Abstract: Both extremes of redox balance are known to cause cardiac injury, with mounting evidence revealing that the injury induced by both oxidative and reductive stress is oxidative in nature. During reductive stress, when electron acceptors are expected to be ... ...

Abstract	Both extremes of redox balance are known to cause cardiac injury, with mounting evidence revealing that the injury induced by both oxidative and reductive stress is oxidative in nature. During reductive stress, when electron acceptors are expected to be mostly reduced, some redox proteins can donate electrons to O2 instead, which increases reactive oxygen species (ROS) production. However, the high level of reducing equivalents also concomitantly enhances ROS scavenging systems involving redox couples such as NADPH/NADP+ and GSH/GSSG. Here our objective was to explore how reductive stress paradoxically increases net mitochondrial ROS production despite the concomitant enhancement of ROS scavenging systems. Using recombinant enzymes and isolated permeabilized cardiac mitochondria, we show that two normally antioxidant matrix NADPH reductases, glutathione reductase and thioredoxin reductase, generate H2O2 by leaking electrons from their reduced flavoprotein to O2 when electron flow is impaired by inhibitors or because of limited availability of their natural electron acceptors, GSSG and oxidized thioredoxin. The spillover of H2O2 under these conditions depends on H2O2 reduction by peroxiredoxin activity, which may regulate redox signaling in response to endogenous or exogenous factors. These findings may explain how ROS production during reductive stress overwhelms ROS scavenging capability, generating the net mitochondrial ROS spillover causing oxidative injury. These enzymes could potentially be targeted to increase cancer cell death or modulate H2O2-induced redox signaling to protect the heart against ischemia/reperfusion damage.
Keywords	NADP (coenzyme) ; antioxidants ; cell death ; electrons ; flavoproteins ; glutathione ; glutathione-disulfide reductase ; heart ; hydrogen peroxide ; ischemia ; mitochondria ; neoplasms ; oxidative stress ; oxygen ; peroxiredoxin
Language	English
Dates of publication	2015-06
Size	p. 514-525.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	282711-6
ISSN	0005-2728 ; 0304-4173
ISSN	0005-2728 ; 0304-4173
DOI	10.1016/j.bbabio.2015.02.012
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Mechanisms of Arrhythmogenicity of Hypertrophic Cardiomyopathy-Associated Troponin T (TNNT2) Variant I79N

Sanam Shafaattalab / Alison Y Li / Marvin G Gunawan / BaRun Kim / Farah Jayousi / Yasaman Maaref / Zhen Song / James N Weiss / R. John Solaro / Zhilin Qu / Glen F Tibbits

Frontiers in Cell and Developmental Biology, Vol

2021 Volume 9

Abstract: Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiovascular disease and often results in cardiac remodeling and an increased incidence of sudden cardiac arrest (SCA) and death, especially in youth and young adults. Among thousands of ... ...

Abstract	Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiovascular disease and often results in cardiac remodeling and an increased incidence of sudden cardiac arrest (SCA) and death, especially in youth and young adults. Among thousands of different variants found in HCM patients, variants of TNNT2 (cardiac troponin T—TNNT2) are linked to increased risk of ventricular arrhythmogenesis and sudden death despite causing little to no cardiac hypertrophy. Therefore, studying the effect of TNNT2 variants on cardiac propensity for arrhythmogenesis can pave the way for characterizing HCM in susceptible patients before sudden cardiac arrest occurs. In this study, a TNNT2 variant, I79N, was generated in human cardiac recombinant/reconstituted thin filaments (hcRTF) to investigate the effect of the mutation on myofilament Ca2+ sensitivity and Ca2+ dissociation rate using steady-state and stopped-flow fluorescence techniques. The results revealed that the I79N variant significantly increases myofilament Ca2+ sensitivity and decreases the Ca2+ off-rate constant (koff). To investigate further, a heterozygous I79N+/−TNNT2 variant was introduced into human-induced pluripotent stem cells using CRISPR/Cas9 and subsequently differentiated into ventricular cardiomyocytes (hiPSC-CMs). To study the arrhythmogenic properties, monolayers of I79N+/− hiPSC-CMs were studied in comparison to their isogenic controls. Arrhythmogenesis was investigated by measuring voltage (Vm) and cytosolic Ca2+ transients over a range of stimulation frequencies. An increasing stimulation frequency was applied to the cells, from 55 to 75 bpm. The results of this protocol showed that the TnT-I79N cells had reduced intracellular Ca2+ transients due to the enhanced cytosolic Ca2+ buffering. These changes in Ca2+ handling resulted in beat-to-beat instability and triangulation of the cardiac action potential, which are predictors of arrhythmia risk. While wild-type (WT) hiPSC-CMs were accurately entrained to frequencies of at least 150 bpm, the I79N ...
Keywords	human iPSC-derived cardiomyocyte (hiPSC-CM) ; troponin T ; hypertrophic cardiomyopathy ; optical mapping of calcium and action potentials ; cardiomyocyte calcium ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Ca2+ transient as a feedback sensor controlling cardiomyocyte ionic conductances in mouse populations

Colin M Rees / Jun-Hai Yang / Marc Santolini / Aldons J Lusis / James N Weiss / Alain Karma

eLife, Vol

2018 Volume 7

Abstract: Conductances of ion channels and transporters controlling cardiac excitation may vary in a population of subjects with different cardiac gene expression patterns. However, the amount of variability and its origin are not quantitatively known. We propose ... ...

Abstract	Conductances of ion channels and transporters controlling cardiac excitation may vary in a population of subjects with different cardiac gene expression patterns. However, the amount of variability and its origin are not quantitatively known. We propose a new conceptual approach to predict this variability that consists of finding combinations of conductances generating a normal intracellular Ca2+ transient without any constraint on the action potential. Furthermore, we validate experimentally its predictions using the Hybrid Mouse Diversity Panel, a model system of genetically diverse mouse strains that allows us to quantify inter-subject versus intra-subject variability. The method predicts that conductances of inward Ca2+ and outward K+ currents compensate each other to generate a normal Ca2+ transient in good quantitative agreement with current measurements in ventricular myocytes from hearts of different isogenic strains. Our results suggest that a feedback mechanism sensing the aggregate Ca2+ transient of the heart suffices to regulate ionic conductances.
Keywords	cardiac electrophysiology ; cardiac homeostasis ; computational biology ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2018-09-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Subcellular localization of hexokinases I and II directs the metabolic fate of glucose.

Scott John / James N Weiss / Bernard Ribalet

PLoS ONE, Vol 6, Iss 3, p e

2011 Volume 17674

Abstract: The first step in glucose metabolism is conversion of glucose to glucose 6-phosphate (G-6-P) by hexokinases (HKs), a family with 4 isoforms. The two most common isoforms, HKI and HKII, have overlapping tissue expression, but different subcellular ... ...

Abstract	The first step in glucose metabolism is conversion of glucose to glucose 6-phosphate (G-6-P) by hexokinases (HKs), a family with 4 isoforms. The two most common isoforms, HKI and HKII, have overlapping tissue expression, but different subcellular distributions, with HKI associated mainly with mitochondria and HKII associated with both mitochondrial and cytoplasmic compartments. Here we tested the hypothesis that these different subcellular distributions are associated with different metabolic roles, with mitochondrially-bound HK's channeling G-6-P towards glycolysis (catabolic use), and cytoplasmic HKII regulating glycogen formation (anabolic use).To study subcellular translocation of HKs in living cells, we expressed HKI and HKII linked to YFP in CHO cells. We concomitantly recorded the effects on glucose handling using the FRET based intracellular glucose biosensor, FLIPglu-600 mM, and glycogen formation using a glycogen-associated protein, PTG, tagged with GFP. Our results demonstrate that HKI remains strongly bound to mitochondria, whereas HKII translocates between mitochondria and the cytosol in response to glucose, G-6-P and Akt, but not ATP. Metabolic measurements suggest that HKI exclusively promotes glycolysis, whereas HKII has a more complex role, promoting glycolysis when bound to mitochondria and glycogen synthesis when located in the cytosol. Glycogen breakdown upon glucose removal leads to HKII inhibition and dissociation from mitochondria, probably mediated by increases in glycogen-derived G-6-P.These findings show that the catabolic versus anabolic fate of glucose is dynamically regulated by extracellular glucose via signaling molecules such as intracellular glucose, G-6-P and Akt through regulation and subcellular translocation of HKII. In contrast, HKI, which activity and regulation is much less sensitive to these factors, is mainly committed to glycolysis. This may be an important mechanism by which HK's allow cells to adapt to changing metabolic conditions to maintain energy balance and avoid ...
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2011-03-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Apamin does not inhibit human cardiac Na+ current, L-type Ca2+ current or other major K+ currents.

Chih-Chieh Yu / Tomohiko Ai / James N Weiss / Peng-Sheng Chen

PLoS ONE, Vol 9, Iss 5, p e

2014 Volume 96691

Abstract: Apamin is commonly used as a small-conductance Ca2+-activated K+ (SK) current inhibitor. However, the specificity of apamin in cardiac tissues remains unclear.To test the hypothesis that apamin does not inhibit any major cardiac ion currents.We studied ... ...

Abstract	Apamin is commonly used as a small-conductance Ca2+-activated K+ (SK) current inhibitor. However, the specificity of apamin in cardiac tissues remains unclear.To test the hypothesis that apamin does not inhibit any major cardiac ion currents.We studied human embryonic kidney (HEK) 293 cells that expressed human voltage-gated Na+, K+ and Ca2+ currents and isolated rabbit ventricular myocytes. Whole-cell patch clamp techniques were used to determine ionic current densities before and after apamin administration.Ca2+ currents (CACNA1c+CACNB2b) were not affected by apamin (500 nM) (data are presented as median [25th percentile;75th percentile] (from -16 [-20;-10] to -17 [-19;-13] pA/pF, P = NS), but were reduced by nifedipine to -1.6 [-3.2;-1.3] pA/pF (p = 0.008). Na+ currents (SCN5A) were not affected by apamin (from -261 [-282;-145] to -268 [-379;-132] pA/pF, P = NS), but were reduced by flecainide to -57 [-70;-47] pA/pF (p = 0.018). None of the major K+ currents (IKs, IKr, IK1 and Ito) were inhibited by 500 nM of apamin (KCNQ1+KCNE1, from 28 [20]; [37] to 23 [18]; [32] pA/pF; KCNH2+KCNE2, from 28 [24]; [30] to 27 [24]; [29] pA/pF; KCNJ2, from -46 [-48;-40] to -46 [-51;-35] pA/pF; KCND3, from 608 [505;748] to 606 [454;684]). Apamin did not inhibit the INa or ICaL in isolated rabbit ventricular myocytes (INa, from -67 [-75;-59] to -68 [-71;-59] pA/pF; ICaL, from -16 [-17;-14] to -14 [-15;-13] pA/pF, P = NS for both).Apamin does not inhibit human cardiac Na+ currents, L-type Ca2+ currents or other major K+ currents. These findings indicate that apamin is a specific SK current inhibitor in hearts as well as in other organs.
Keywords	Medicine ; R ; Science ; Q
Subject code	572
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A personalized, multiomics approach identifies genes involved in cardiac hypertrophy and heart failure

Marc Santolini / Milagros C. Romay / Clara L. Yukhtman / Christoph D. Rau / Shuxun Ren / Jeffrey J. Saucerman / Jessica J. Wang / James N. Weiss / Yibin Wang / Aldons J. Lusis / Alain Karma

npj Systems Biology and Applications, Vol 4, Iss 1, Pp 1-

2018 Volume 13

Abstract: Personalized medicine: uncovering missed disease genes A multitude of genes associated with complex diseases are revealed by a novel personalized, as opposed to population-level, analysis of differential gene expression. While traditional investigations ... ...

Abstract	Personalized medicine: uncovering missed disease genes A multitude of genes associated with complex diseases are revealed by a novel personalized, as opposed to population-level, analysis of differential gene expression. While traditional investigations of the genetic basis of complex diseases assume homogeneity across individuals and identify genes differentially expressed between a diseased and a healthy population, Northeastern University and University of California Los Angeles researchers have identified a different class of disease genes that exhibit heterogeneous up and down-regulation across 100 genetically distinct mouse strains subject to a stressor inducing heart failure, but show no significant change of expression at the population level. The results, validated by in vitro knockdown, demonstrate that individualized approaches are crucial to unmask all genes involved in complex diseases, opening new avenues for the development of personalized therapies.
Keywords	Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2018-02-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Defibrillation Failure and Tachycardia-Induced Early Afterdepolarizations

Richard Samade / James N. Weiss / Kalyanam Shivkumar / Boris Y. Kogan

Lecture Notes in Engineering and Computer Science, Vol 2173, Iss 1, Pp 1-

A Simulation Study

2008 Volume 6

Keywords	Electronic computers. Computer science ; QA75.5-76.95 ; Instruments and machines ; QA71-90 ; Mathematics ; QA1-939 ; Science ; Q
Language	English
Publishing date	2008-10-01T00:00:00Z
Publisher	Newswood and International Association of Engineers
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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