We analyse more than 500 000 songs released in the UK between 1985 and 2015 to understand the dynamics of success (defined as ‘making it’ into the top charts), correlate success with acoustic features and explore the predictability of success. Several multi-decadal trends have been uncovered. For example, there is a clear downward trend in ‘happiness’ and ‘brightness’, as well as a slight upward trend in ‘sadness’. Furthermore, songs are becoming less ‘male’. Interestingly, successful songs exhibit their own distinct dynamics. In particular, they tend to be ‘happier’, more ‘party-like’, less ‘relaxed’ and more ‘female’ than most. The difference between successful and average songs is not straightforward. In the context of some features, successful songs pre-empt the dynamics of all songs, and in others they tend to reflect the past. We used random forests to predict the success of songs, first based on their acoustic features, and then adding the ‘superstar’ variable (informing us whether the song’s artist had appeared in the top charts in the near past). This allowed quantification of the contribution of purely musical characteristics in the songs’ success, and suggested the time scale of fashion dynamics in popular music.

The question of stem cell control is at the center of our understanding of tissue functioning, both in healthy and cancerous conditions. It is well accepted that cellular fate decisions (such as divisions, differentiation, apoptosis) are orchestrated by a network of regulatory signals emitted by different cell populations in the lineage and the surrounding tissue. The exact regulatory network that governs stem cell lineages in a given tissue is usually unknown. Here we propose an algorithm to identify a set of candidate control networks that are compatible with (a) measured means and variances of cell populations in different compartments, (b) qualitative information on cell population dynamics, such as the existence of local controls and oscillatory reaction of the system to population size perturbations, and (c) statistics of correlations between cell numbers in different compartments. Using the example of human colon crypts, where lineages are comprised of stem cells, transit amplifying cells, and differentiated cells, we start with a theoretically known set of 32 smallest control networks compatible with tissue stability. Utilizing near-equilibrium stochastic calculus of stem cells developed earlier, we apply a series of tests, where we compare the networks’ expected behavior with the observations. This allows us to exclude most of the networks, until only three, very similar, candidate networks remain, which are most compatible with the measurements. This work demonstrates how theoretical analysis of control networks combined with only static biological data can shed light onto the inner workings of stem cell lineages, in the absence of direct experimental assessment of regulatory signaling mechanisms. The resulting candidate networks are dominated by negative control loops and possess the following properties: (1) stem cell division decisions are negatively controlled by the stem cell population, (2) stem cell differentiation decisions are negatively controlled by the transit amplifying cell population.

Successful maintenance of cellular lineages critically depends on the fate decision dynamics of stem cells (SCs) upon division. There are three possible strategies with respect to SC fate decision symmetry: (a) asymmetric mode, when each and every SC division produces one SC and one non-SC progeny; (b) symmetric mode, when 50% of all divisions produce two SCs and another 50%—two non-SC progeny; (c) mixed mode, when both the asymmetric and two types of symmetric SC divisions co-exist and are partitioned so that long-term net balance of the lineage output stays constant. Theoretically, either of these strategies can achieve lineage homeostasis. However, it remains unclear which strategy(s) are more advantageous and under what specific circumstances, and what minimal control mechanisms are required to operate them. Here we used stochastic modeling to analyze and quantify the ability of different types of divisions to maintain long-term lineage homeostasis, in the context of different control networks. Using the example of a two-component lineage, consisting of SCs and one type of non-SC progeny, we show that its tight homeostatic control is not necessarily associated with purely asymmetric divisions. Through stochastic analysis and simulations we show that asymmetric divisions can either stabilize or destabilize the lineage system, depending on the underlying control network. We further apply our computational model to biological observations in the context of a two-component lineage of mouse epidermis, where autonomous lineage control has been proposed and notable regional differences, in terms of symmetric division ratio, have been noted—higher in thickened epidermis of the paw skin as compared to ear and tail skin. By using our model we propose a possible explanation for the regional differences in epidermal lineage control strategies. We demonstrate how symmetric divisions can work to stabilize paw epidermis lineage, which experiences high level of micro-injuries and a lack of hair follicles as a back-up source of SCs.

Understanding the dynamics of stem cell lineages is of central importance both for healthy and cancerous tissues. We study stochastic population dynamics of stem cells and differentiated cells, where cell decisions, such as proliferation vs differentiation decisions, or division and death decisions, are under regulation from surrounding cells. The goal is to understand how different types of control mechanisms affect the means and variances of cell numbers. We use the assumption of weak dependencies of the regulatory functions (the controls) on the cell populations near the equilibrium to formulate moment equations. We then study three different methods of closure, showing that they all lead to the same results for the highest order terms in the expressions for the moments. We derive simple explicit expressions for the means and the variances of stem cell and differentiated cell numbers. It turns out that the variance is expressed as an algebraic function of partial derivatives of the controls with respect to the population sizes at the equilibrium. We demonstrate that these findings are consistent with the results previously obtained in the context of particular systems, and also present two novel examples with negative and positive control of division and differentiation decisions. This methodology is formulated without any specific assumptions on the functional form of the controls, and thus can be used for any biological system.