The scientific heritage of Richard Henry Dalitz, FRS (1925-2006)

Professor Richard H. Dalitz passed away on January 13, 2006. He was almost 81 years old and his outstanding contributions are intimately connected to some of the major breakthroughs of the 20th century in particle and nuclear physics. These outstanding contributions go beyond the Dalitz Plot, Dalitz Pair and CDD poles that bear his name. He pioneered the theoretical study of strange baryon resonances, of baryon spectroscopy in the quark model, and of hypernuclei, to all of which he made lasting contributions. His formulation of the "$\theta-\tau$ puzzle" led to the discovery that parity is not a symmetry of the weak interactions. A brief scientific evaluation of Dalitz's major contributions to particle and nuclear physics is hereby presented, followed by the first comprehensive list of his scientific publications, as assembled from several sources. The list is divided into two categories: the first, main part comprises Dalitz's research papers and reviews, including topics in the history of particle physics, biographies and reminiscences; the second part lists book reviews, public lectures and obituaries authored by Dalitz, and books edited by him. This provides the first necessary step towards a more systematic research of the Dalitz heritage in modern physics. The present 2016 edition updates the original 2006 edition, published in Nucl. Phys. A 771 (2006) 2-7, doi:10.1016/j.nuclphysa.2006.03.007, and 8-25, doi:10.1016/j.nuclphysa.2006.03.008, by including for the first time a dozen or so of publications, found recently in a list submitted to the Royal Society by Dalitz in 2004, that escaped our attention in the original version.Comment: updates the original edition by including several publications, mostly in category III, that were unknown to us in 200

Inventories to insights

“In the long course of cell life on this earth it remained, for our age, for our generation, to receive the full ownership of our inheritance. We have entered the cell, the Mansion of our birth and started the inventory of our acquired wealth.” (Albert Claude, Nobel lecture, 1974

ODELAY: A Large-scale Method for Multi-parameter Quantification of Yeast Growth.

Growth phenotypes of microorganisms are a strong indicator of their underlying genetic fitness and can be segregated into 3 growth regimes: lag-phase, log-phase, and stationary-phase. Each growth phase can reveal different aspects of fitness that are related to various environmental and genetic conditions. High-resolution and quantitative measurements of all 3 phases of growth are generally difficult to obtain. Here we present a detailed method to characterize all 3 growth phases on solid media using an assay called One-cell Doubling Evaluation of Living Arrays of Yeast (ODELAY). ODELAY quantifies growth phenotypes of individual cells growing into colonies on solid media using time-lapse microscopy. This method can directly observe population heterogeneity with each growth parameter in genetically identical cells growing into colonies. This population heterogeneity offers a unique perspective for understanding genetic and epigenetic regulation, and responses to genetic and environmental perturbations. While the ODELAY method is demonstrated using yeast, it can be utilized on any colony forming microorganism that is visible by bright field microscopy

The Promise of Systems Biology Approaches for Revealing Host Pathogen Interactions in Malaria.

Despite global eradication efforts over the past century, malaria remains a devastating public health burden, causing almost half a million deaths annually (WHO, 2016). A detailed understanding of the mechanisms that control malaria infection has been hindered by technical challenges of studying a complex parasite life cycle in multiple hosts. While many interventions targeting the parasite have been implemented, the complex biology o

Abnormal Syntactic Comprehension Utilized by a Patient With Chronic Broca's Aphasia: Implications for Treatment

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Negative Autoregulation by FAS Mediates Robust Fetal Erythropoiesis

Tissue development is regulated by signaling networks that control developmental rate and determine ultimate tissue mass. Here we present a novel computational algorithm used to identify regulatory feedback and feedforward interactions between progenitors in developing erythroid tissue. The algorithm makes use of dynamic measurements of red cell progenitors between embryonic days 12 and 15 in the mouse. It selects for intercellular interactions that reproduce the erythroid developmental process and endow it with robustness to external perturbations. This analysis predicts that negative autoregulatory interactions arise between early erythroblasts of similar maturation stage. By studying embryos mutant for the death receptor FAS, or for its ligand, FASL, and by measuring the rate of FAS-mediated apoptosis in vivo, we show that FAS and FASL are pivotal negative regulators of fetal erythropoiesis, in the manner predicted by the computational model. We suggest that apoptosis in erythroid development mediates robust homeostasis regulating the number of red blood cells reaching maturity