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So fast is the growth of a culture of E. coli that it led researchers to overlook a possible death rate. As a matter of fact, the experiments done in the first half of the 20th century were unable to detect any mortality. It is only at the beginning of the 21th century that positive evidence emerged which confirmed the existence of a sizeable (albeit small) mortality. In the present paper this mortality was measured at successive 45mn time intervals from early exponential growth into the stationary phase. Done with a flow cytometer, the successive measurements of the ratio dead/living also provided an estimate of the standard deviation of the mortality rate. In a forthcoming experiment we are planning to focus more closely on the stationary phase in order to find out if its mortality rate is lower or higher than in the exponential phase., Comment: 18 pages, 3 figures

We know that stress-factors, e.g. X-rays, have an effect on cells that is more lethal in rapid exponential growth than in stationary phase. It is this effect which makes radiotherapy effective in cancer treatment. This stress effect can be explained in two ways: (a) more vulnerability in the growth phase, (b) improved protection capacity and repair mechanisms in the stationary phase. Although the two explanations do not exclude each other, they are very different in the sense that (a) is a general mechanism whereas (b) is strain and stress-factor dependent. In this paper we explore major facets of (a). Firstly, we emphasize that (a) can account for known experimental stress-factor evidence. Secondly, we observe that (a) rightly predicts that slow exponential growth (meaning with a doubling time of several hours) results in a lower death rate than fast exponential growth (doubling time of a fraction of one hour), an effect that cannot be explained in the (b) framework because both organisms are in the same phase. Thirdly, we conjecture that the stress-factor effect can be extended to situations of chronic stress due to non-optimal environmental conditions. If correct, this conjecture would imply that even in normal culture conditions the natural death rate is lower in the stationary phase than in the growth phase. Finally, the paper closes with the description of several open questions and of appropriate test-experiments meant to address them., Comment: 21 pages, 4 figures

Named after Clio, the Greek goddess of history, cliophysics is a daughter (and in a sense an extension) of econophysics. Like econophysics it relies on the methodology of experimental physics. Its purpose is to conduct a scientific analysis of historical events. Such events can be of sociological, political or economic nature. In this last case cliophysics would coincide with econophysics. The main difference between cliophysics and econophysics is that the description of historical events may be qualitative as well as quantitative. For the handling of qualitative accounts cliophysics has developed an approach based on the identification of patterns. To detect a pattern the main challenge is to break the "noise barrier". The very existence of patterns is what makes cliophysics possible and ensures its success. Briefly stated, once a pattern is detected, it allows predictions to be made. As the capacity to make successful predictions is the hallmark of any science, it becomes easy to decide whether or not the claim made in the title of the paper is indeed fulfilled. A number of examples of clusters of similar events will be given which should convince readers that historical events can be simplified almost at will very much as in physics. One should not forget that physical effects are also subject to the environment. For instance, if tried at the equator, the experiment of the Foucault pendulum will fail. In the last part of the paper, we describe cliophysical investigations conducted over the past decades; they make us confident that cliophysics can be a valuable tool for decision makers., Comment: 15 pages, 1 figure, 3 tables

Infant deaths and old age deaths are very different. The former are mostly due to severe congenital malformations of one or a small number of specific organs. On the contrary, old age deaths are largely the outcome of a long process of deterioration which starts in the 20s and affects almost all organs. In terms of age-specific death rates, there is also a clear distinction: the infant death rate falls off with age, whereas the adult and old age death rate increases exponentially with age in conformity with Gompertz's law. Clearly, it would be satisfactory to explain the two phenomena as being two variants within the same explanatory framework. In other words, a mechanism providing a combined explanation for the two forms of mortality would be welcome. This is the purpose of the present paper. We show here that the same biological effects can account for the two cases provided there is a difference in their severity: death triggered by isolated lethal anomalies in one case and widespread wear-out anomalies in the second. We show that quite generally this mechanism leads indeed, respectively, to a declining and an upgoing death rate. Moreover, this theoretical framework leads to the conjecture that the severity of the death effects, whether in infancy or old age, are higher for organisms which are comprised of a larger number of organs. Finally, let us observe that the main focus of the paper is the drastic difference of the age-specific death rates (i.e. decreasing versus increasing) because this difference is found in many species, whereas the question of the best fit (e.g. Gompertz versus Weibull) is rather specific to human mortality., Comment: 11 pages, 3 figures

This manuscript proposes a significant step in our long-run investigation of infant mortality across species. Since 2016 (Berrut et al. 2016) a succession of studies (Bois et al. 2019) have traced infant mortality from organisms of high complexity (e.g. mammals) down to unicellular organisms. Infant mortality may be considered as a filtering process through which organisms with potentially lethal congenital defects are eliminated. Such defects may have many causes but here we focus particularly on mishaps resulting from non-optimal conditions in the production of proteins, enzymes and other crucial macromolecules. The statistical signature of infant mortality consists in a falling age-specific death rate. The question we address here is whether infant mortality episodes take place in bacteria in the minutes precededing or following cell division. It will be shown that while experiments carried out in the 20th century tried but failed to detect such an effect (mostly because of limited sample size), more recent observations provided consistent evidence of a sizeable mortality, with a rate of the order of 0.7 per 1,000 per hour, in the exponential growth phase of E. coli. A further crucial test will be to measure the age-specific, post-division death rate. An experiment is outlined for that purpose. It is based on the selection of stained cells through flow cytometry and the derivation of their ages at death from their sizes. If an infant mortality effect can be identified in E. coli it can be conjectured that a similar effect also exists in other unicellular organisms, both prokaryote and eukaryote., Comment: 16 p., 5 figures

The influence of per capita income on life expectancy is well documented, mostly through studies of multinational samples. However, one expects fairly weak correlations at both ends of the life span, that is to say in early infancy and in age groups of elderly from 85 to 100 years. The reason is that at both ends mortality is largely controled by biological factors rather than by socio-economic conditions. In order to test this conjecture, we explore the influence of income on age groups, separately in France, the United States and South Korea. More precisely in each country we compare income and mortality data in as many regional subunits as possible. One noteworthy constatation is that, contrary to a common view, personal income is only weakly correlated with infant mortality (i.e. mortality under the age of one year). More broadly, we propose as a conjecture that the common pattern revealed by the analysis of the three countries is also valid in other developed countries., Comment: 9 pages, 4 figures

Collective escaping is a ubiquitous phenomenon in animal groups. Symmetry breaking caused by panic escape exhibits a shared feature across species that one exit is used more than the other when agents escaping from a closed space with two symmetrically located exists. Intuitively, one exit will be used more by more individuals close to it, namely there is an asymmetric distribution initially. We used ant groups to investigate how initial distribution of colonies would influence symmetry breaking in collective escaping. Surprisingly, there was no positive correlation between symmetry breaking and the asymmetrically initial distribution, which was quite counter-intuitive. In the experiments, a flee stage was observed and accordingly a flee-pheromone model was introduced to depict this special behavior in the early stage of escaping. Simulation results fitted well with the experiment. Furthermore, the flee stage duration was calibrated quantitatively and the model reproduced the observation demonstrated by our previous work. This paper explicitly distinguished two stages in ant panic escaping for the first time, thus enhancing the understanding in escaping behavior of ant colonies.

Biologically, for any organism life does not start at birth but at fertilization of the embryo. Embryonic development is of great importance because it determines congenital anomalies and influences their severity. Whereas there is detailed qualitative knowledge of the successive steps of embryonic development, little is known about their probabilities of success or failure. Embryonic mortality as a function of post fertilization time provides a simple (albeit crude) way to identify major defects. We find that, in line with the few other species for which data are available, the embryonic mortality of zebrafish has a prominent peak shortly after fertilization. This is called the early embryonic mortality (EEM) effect. Although a number of immediate causes of death (e.g. infection, excess of carbon dioxide or of lactic acid, chromosomal defects) can be cited, the common underlying factor remains unknown. After reviewing embryonic mortality data available for chicken and a few other farm animals, we explain that zebrafish are particularly suited for such a study because embryogenesis can be followed from its very beginning and can be observed easily thanks to transparent egg shells. We report the following findings. (i) The mortality peak occurs in the first 15% of the 75-80 hours of embryogenesis and it is about 50 times higher than the low plateau which follows. (ii) The shape of the age-specific death rate is largely independent of the death level. Presently, little is known about the nature of embryonic defects. However, by reviewing two special cases we show that even small initial defects, e.g. spatial cellular asymmetries or irregularities in the timing of development, carry with them lethal effects in later stages of embryogenesis., Comment: 25 pages, 11 figures

Genetic and environmental factors are traditionally seen as the sole causes of congenital anomalies. In this paper we introduce a third possible cause, namely random "manufacturing" discrepancies with respect to ``design'' values. A clear way to demonstrate the existence of this component is to ``shut'' the two others and to see whether or not there is remaining variability. Perfect clones raised under well controlled laboratory conditions fulfill the conditions for such a test. Carried out for four different species, the test reveals a variability remainder of the order of 10%-20% in terms of coefficient of variation. As an example, the CV of the volume of E.coli bacteria immediately after binary fission is of the order of 10%. In short, ``manufacturing'' discrepancies occur randomly, even when no harmful mutation or environmental factors are involved. Not surprisingly, there is a strong connection between congenital defects and infant mortality. In the wake of birth there is a gradual elimination of defective units and this screening accounts for the post-natal fall of infant mortality. Apart from this trend, post-natal death rates also have humps and peaks associated with various inabilities and defects.\qL In short, infant mortality rates convert the case-by-case and mostly qualitative problem of congenital malformations into a global quantitative effect which, so to say, summarizes and registers what goes wrong in the embryonic phase. Based on the natural assumption that for simple organisms (e.g. rotifers) the manufacturing processes are shorter than for more complex organisms (e.g. mammals), fewer congenital anomalies are expected. Somehow, this feature should be visible on the infant mortality rate. How this conjecture can be tested is outlined in our conclusion., Comment: 43 pages, 9 figures

Infant mortality, by which we understand the postnatal stage during which mortality is declining, is a manifestation and embodiment of congenital abnormalities. Severe defects will translate into death occurring shortly after birth whereas slighter anomalies may contribute to death much later, possibly only in adult age. While for many species birth defects would be nearly impossible to identify, infant mortality provides a convenient global assessment. In the present paper we examine a broad range of species from mammals to fish to gastropods to insects. One of the objectives of our comparative analysis is to test a conjecture suggested by reliability engineering according to which the frequency of defects tends to increase together with the complexity of organisms. For that purpose, we set up experiments specially designed to measure infant mortality. In particular, we two species commonly used as model species in biological laboratories, namely the zebrafish Danio rerio and the rotifer Brachionus plicatilis. For the second, whose number of cells is about hundred times smaller than for the first, we find as expected that the screening effect of the infant phase is of much smaller amplitude. Our analysis also raises a number of challenging questions for which further investigation is necessary. For instance, why is the infant death rate of beetles and mollusks falling off exponentially rather than as a power law as observed for most other species? A possible research agenda is discussed in the conclusion of the paper., Comment: 31 pages, 16 figures

In earlier centuries kings and governments employed astrologists to help them take the best decisions. Present-day governments no longer employ astrologists but still have no clear analytical tool to replace them. Over the past two decades we have developed a methodology for the scientific investigation of recurrent historical events. It consists in two steps. (i) Identification and comparison of historical episodes driven by a common mechanism. (ii) Under the reasonable assumption that what has happened several times in the past is likely to happen again, one then derives testable predictions. This of course is nothing other than the protocol used in experimental science when exploring new phenomena. We believe such a tool can give decision makers much better insight. In the present paper we illustrate this analysis by considering challenges, that span more than a century, to US hegemony in the Pacific. The outcomes suggest that it is only through the sidelining of one of the contenders that the confrontation will end. At the time of writing (late 2018) early evidence of this confrontation is already visible at three levels. (i) Growing US concerns for domestic security that are leading to a new form of McCarthyism. (ii) Political instability due to China-US polarization in several Asian countries as well as in the countries participating in the Belt and Road Initiative. (iii) Tension and sanctions in procurement and trade., Comment: 38 pages, 5 figures

Investigating the ``physics'' of food crises consists in identifying features which are common to all large-scale food crises. One element which stands out is the fact that during a food crisis there is not only a surge in deaths but also a correlative temporary decline in conceptions and subsequent births. As a matter of fact, birth reduction may even start several months before the death surge and can therefore serve as an early warning signal of an impending crisis. This scenario is studied in three cases of large-scale food crises. Finland (1868), India (1867--1907), China (1960--1961). It turns out that between the regional amplitudes of death spikes and birth troughs there is a power law relationship. This confirms what was already observed for the epidemic of 1918 in the United States (Richmond et al. 2018b). In a second part of the paper we explain how this relationship can be used for the investigation of mass-mortality episodes in cases where direct death data are either uncertain or nonexistent., Comment: 29 pages, 11 figures

Herteliu et al. (2015) have elsewhere analyzed the impact of religious festivals on births in Romania. Here we broaden the analysis (i) by studying the effect of Lent on marriages as well as births (ii) by analyzing a number of other countries which allows a comparison with non-Orthodox countries. We also introduce a new methodology which treats the data in a way that frees the analysis from bias related to seasonal patterns of births and marriages. The comparison between the effects on marriages and conceptions appears of particular interest for it permits to assess the respective weighs of social pressure on one hand and personal leanings on the other hand. Our analysis reveals a strong effect of Lent on marriages with a reduction by 80% in Orthodox countries and 40% in West European Catholic and Protestant countries. Since the influence of Lent on conceptions is independent of any form of direct social control one might expect the effect to be much smaller. In percentage terms it is roughly 10 times smaller than the effect on marriage. The present methodology opens the way to the accurate investigation of the impact of other mobile religious periods (e.g. Ramadan) on various social phenomena (e.g. suicide)., Comment: 16 pages, 7 figures

In the same way as tree rings give us useful information about the climate many decades ago (or even centuries ago in the case of big trees), population pyramids allow us to know birth or death rates several decades earlier. Naturally, they can fulfill such promises only if they have been recorded accurately. That is why we start this study by listing a number of pitfalls that may occur in the process of taking censuses. In this paper our main goal is to show how it is possible to "read" population pyramids. Sudden changes in birth rate give rise to the clearest signatures. This indicator reveals that major tragedies like famines, wars, or epidemics are generally accompanied by a fall in birth rates. Thanks to this observation, population pyramids can be used to identify and gauge the blows suffered by populations and nations. As an illustration of how this works, we compare the population pyramids of North and South Korea. This allows us, among other things, to gauge the scale of the food shortage that North Korea experienced at the end of the 1990s., Comment: 17 pages, 10 figures

Investigations of a possible connection between population density and the propagation and magnitude of epidemics have so far led to mixed and unconvincing results. There are three reasons for that. (i) Previous studies did not focus on the appropriate density interval. (ii) For the density to be a meaningful variable the population must be distributed as uniformly as possible. If an area has towns and cities where a majority of the population is concentrated its average density is meaningless. (iii) In the propagation of an epidemic the initial proportion of susceptibles (that is to say persons who have not developed an immunity) is an essential, yet usually unknown, factor. The assumption that most of the population is susceptible holds only for new strain of diseases. It will be shown that when these requirements are taken care of, the size of epidemics is indeed closely connected with the population density. This empirical observation comes as a welcome confirmation of the classical KMK (Kermack-McKendrick 1927) model. Indeed, one of its key predictions is that the size of the epidemic increases strongly (and in a non linear way) with the initial density of susceptibles. An interesting consequence is that, contrary to common beliefs, in sparsely populated territories, like Alaska, Australia or the west coast of the United states the size of epidemics among native populations must have been limited by the low density even for diseases for which the natives had no immunity (i.e., were susceptibles)., Comment: 16 pages, 7 figures

Here the term "high frequency" refers to daily, weekly or monthly birth data. The fluctuations of daily birth numbers show a succession of spikes and dips which, at least at first sight, looks almost as random as white noise. However in recent times several studies were published, including by the present authors, which have given better insight into how birth is affected by exogenous factors. One of them concerns the way adverse conditions (e.g. famines, diseases, earthquakes, heat waves) temporarily affect the conception capacity of populations, thus producing birth rate troughs 9 months after mortality waves. In addition, religious interdicts (e.g. during the Lent period) lead to reduced conceptions. These as well as other effects raise the hope that we will soon be able to "read" and interpret birth rate patterns just as the Egyptologist Jean-Francois Champollion managed to decipher many (though not all) hieroglyphs., Comment: 23 pages, 10 figures

In a general way at all ages and for almost all diseases, male death rates are higher than female death rates. Here we report a case in which the opposite holds, namely for tuberculosis (TB) mortality between the ages of 5 and 25, female death rates are about two times higher than male rates. What makes this observation of interest is that it occurs in all countries for which data are available (e.g. Britain, Switzerland and United States), and in all years from the end of the 19th century up to the time in the 1960s when TB became a very rare disease in all developed countries. The fact that this regularity holds despite a drastic reduction in the number of deaths is also noteworthy. What is the practical usefulness of this investigation? So far, the reason of this anomaly remains an open question but the effect is so accurate that it can be used for probing the reliability and accuracy of mortality records. This will be explained in the case of developing countries. For instance, it turns out that in South African TB death data as published (and revised) by the "World Health Organization", female deaths were certainly under-estimated by a factor of two., Comment: 13 pages, 4 figures

In 2015 in the United States 612,000 persons died from cancer whereas only 470 died from tuberculosis (TB), a disease which was the main cause of death around 1900. How can one explain such a key discrepancy in treatment progress? A statistical comparison between TB and cancer will give some clues. However, TB and cancer also share several important features. Both TB and cancer can affect several organs, e.g. lungs, brain, bones, intestines, skin. What in cancer is called malignant neoplasm (tumor) is called granuloma in TB. By isolating malignant cells (versus bacteria) from the rest of the body, such clusters protect the host's organism but at the same time they are "secure beachheads" from where malignant cells (versus infected macrophages) can wander off to new locations. Thus, metastatic tumors have a TB parallel in the form of secondary granulomas. In order to investigate more closely this parallel we use the age-specific response of organs. Called spectrometric analysis in a previous paper (Berrut et al. 2017), this method provides information about how fast tumors develop and how serious they become. A convenient characterization of the response to TB of organ j is given by the following (age-dependent) death ratio: Tj(t)=(death by TB of type j)/(all TB deaths) The development of cancer tumors can be described by a similar function Cj(t). We compare the organs' responses in all cases for which specific death data are available. It appears that for the same organ Tj(t) is similar in shape to Cj(t). For instance, with regard to brain tumors, both TB and cancer mortality peak around the age of 10. Such observations may bring to light vulnerabilities in the way the immune system provides protection to various organs., Comment: 22p, 8 figures. An old version was replaced by a new one which is about twice as long. At first the new version was submitted as a new paper, but at the request of the administration a replacement seemed a more appropriate solution

In part 1 we identified a new coupling between death spikes and birth dips that occurs following catastrophic events such as influenza pandemics and earthquakes. Here we seek to characterize some of the key features. We introduce a transfer function defined as the amplitude of the birth trough (the output) divided by the amplitude of the death spike (the input). This has two features: it is always smaller than one so is an attenuation factor and as a function of the amplitude of the death spike, it may be characterized by a power law with exponent close to unity. Since many countries do not publish monthly data, merely annual data, we attempt to extend the analysis to cover such data and how to identify the death-birth coupling. Finally we compare the response to unexpected death spikes and regular seasonal death peaks, such as winter death peaks which occur annually in many countries., Comment: 16 pages, 4 figures

In the wake of the influenza pandemic of 1889-1890 Jacques Bertillon, a pioneer of medical statistics, noticed that after the massive death spike there was a dip in birth numbers around 9 months later which was significantly larger than that which could be explained by the population change as a result of excess deaths. In addition it can be noticed that this dip was followed by a birth rebound a few months later. However having made this observation, Bertillon did not explore it further. Since that time the phenomenon was not revisited in spite of the fact that in the meanwhile there have been several new cases of massive death spikes. The aim here is to analyze these new cases to get a better understanding of this death-birth coupling phenomenon. The largest death spikes occurred in the wake of more recent influenza pandemics in 1918 and 1920, others were triggered by the 1923 earthquakes in Tokyo and the Twin Tower attack on September 11, 2001. We shall see that the first of these events indeed produced an extra dip in births whereas the 9/11 event did not. This disparity highlights the pivotal role of collateral sufferers. In the last section it is shown how the present coupling leads to predictions; it can explain in a unified way effects which so far have been studied separately, as for instance the impact on birth rates of heat waves. Thus, it appears that behind the random appearance of birth rate fluctuations there are in fact hidden explanatory factors., Comment: 27 pages, 13 figures

Separatism is examined in a long-run perspective. Accordingly, many political or economic factors which may be crucial in dealing with short-term episodes can be safely disregarded. Extending an approach pioneered by J. Jenkins, the paper assesses the role of spatial and historical factors. It shows that the means used to stage a separatist struggle are to a notable extent borrowed from former historical episodes, an analysis which supports and illustrates Charles Tilly's thesis of restricted repertoires of action. The purpose of the present paper is to introduce the model, to make it plausible and to demonstrate its potential usefulness by examining a number of critical examples. A more systematic analysis is carried out in a follow-up paper by using a data set that includes about 40 cases of separatist struggles., Comment: 28 pages, 3 figures

In part 1 we have discussed the role played by geographical and historical conditions. Here we wish to test our model and to estimate its parameters. Ti this effect two indexes are introduced. The geographical index is aimed at characterizing the degree of separateness of a given region with respect to the national state to which it belongs. This index turns out to be closely connected to the number of minority-speakers; it is also correlated with the level of separatist disturbances, at least for samples having the same historical background. The purpose of the second index is precisely to specify the role of past episodes in shaping current separatist outbreaks. To a large extent, current episodes are modeled on former ones; typically this process of semi-replication appears to be characterized by a "memory" that extends over at least one and a half century. Note that this study concentrates on the occurrence and forms of separatist struggles rather than on their short-term political causes. In so doing, it follows a methodological track that has been pioneered by Stanley Lieberson (1985, the "stardom" paradigm) and Charles Tilly (1993, the "traffic jam" paradigm)., Comment: 26 pages, 9 figures

Ever since the studies of Louis-Adolphe Bertillon in the late 19th century it has been known that marital status and number of children markedly affect death and suicide rates. This led in 1898 Emile Durkheim to conjecture a connection between social isolation (especially at family level) and suicide. However, further progress was long hampered by the limited statistical data available from death certificates. Recently, it was shown by the present authors that disability data from census records can be used as a reliable substitute for mortality data. This opens a new route to investigations of family ties because census information goes much beyond the limited data reported on death certificates. It is shown that the disability rate of adults decreases when they have more family links. More precisely, the reduction of the parents' disability brought about by the presence of a child reveals that the strength of ties between parents and child is highest in the first year after birth and then weakens steadily as the child ages. It will also be seen that the strength of the bond between husband and wife is highest when they are of same age and decreases fairly steadily when the age gap increases., Comment: 20 p., 10 figures

The Farr-Bertillon law states that the mortality rate of single and widowed persons is about three times the rate of married people of same age. This excess mortality can be measured with good accuracy for all ages except for young widowers. The reason is that, at least nowadays, very few people become widowed under the age of 30. Here we show that disability data from census records can also be used as a reliable substitute for mortality rates. In fact excess-disability and excess-mortality go hand in hand. Moreover, as there are about ten times more cases of disability than deaths, the disability variable is able to offer more accurate measurements in all cases where the number of deaths is small. This allows a more accurate investigation of the young widower effect; it confirms that, as already suspected from death rate data, there is a huge spike between the ages of 20 and 30. By using disability rates we can also study additional features not accessible using death rate data. For example we can examine the health impact of a change in living place. The observed temporary inflated disability rate confirms what could be expected by invoking the "Transient Shock" conjecture formulated by the authors in a previous paper., Comment: 14 pages, 5 figures

The purpose of this note is to explain what is "analytical history", a modular and testable analysis of historical events introduced in a book published in 2002 (Roehner and Syme 2002). Broadly speaking, it is a comparative methodology for the analysis of historical events. Comparison is the keystone and hallmark of science. For instance, the extrasolar planets are crucial for understanding our own solar system. Until their discovery, astronomers could observe only one instance. Single instances can be described but they cannot be understood in a testable way. In other words, if one accepts that, as many historians say, "historical events are unique", then no testable understanding can be developed., Comment: 16 pages, 3 figures

After birth setting up an effective immune system is a major challenge for all living organisms. In this paper we show that this process can be explored by using the age-specific infant death rate as a kind of sensor. This is made possible because, as shown by the authors in Berrut et al. (2016), between birth and a critical age t_c, for all mammals the death rate decreases with age as an hyperbolic function. For humans t_c is equal to 10 years. At some ages the hyperbolic fall displays spikes which, it is assumed, correspond to specific events in the organism's response to exogenous factors. One of these spikes occurs 10 days after birth and there is another at the age of about 300 days. It is shown that the first spike is related to viral infections whereas the second is related to bacterial diseases. By going back to former time periods during which infant mortality was much higher than currently, it is possible to get a magnified view of these peaks which in turn may give us useful information about how an organism adapts to new conditions. Apart from pathogens, the same methodology can be used to study the response to changes in other external conditions, e.g. supply of food, temperature or oxygen level., Comment: 13 pages, 6 figures

Is cancer a disease that can be cured or a degenerative disease which comes predominantly with old age? We give an answer based on a two-dimensional representation of diseases. These two dimensions are defined as follows. In mortality curves there is an age, namely a_c = 10 years, which plays a crucial role in the sense that the mortality rate decreases in the interval I1=(aa_c). The respective trends in I1 and I2 are the two parameters used in our classification of diseases. Within the framework of reliability analysis, I1 and I2 would be referred to as the "burn-in" and "wear-out" phases. This leads to define three broad groups of diseases. (AS1) Asymmetry with prevalence of I1. (AS2) Asymmetry with prevalence of I2. (S) Symmetry, with I1 and I2 both playing roles of comparable importance. Not surprisingly, among AS1-cases one finds all diseases due to congenital malformations. In the AS2-class one finds degenerative diseases, e.g. Alzheimer's disease. Among S-cases one finds most diseases due to external pathogens or to wear-out processes. Cancer is one of those mixed cases and it is closer to (AS2) than to (AS1). This representation also explains what we call an OVERKILL EFFECT in old age. It tells us that even an effective cancer therapy would have no influence whatsoever on the extent of human life unless ALL other diseases are cured simultaneously. We conclude that whilst one might develop a cure for many of the known diseases of old age, new diseases will arise and the quest for the ultimate cure will be never ending. Death before the age of 120 seems firmly written in our genetic code and the best we shall be able to do is to help people cope with the inevitability of death as and when it arises., Comment: 16 pages, 8 figures

Between 2003 and 2015 the prices of apartments in Hong Kong (adjusted for inflation) increased by a factor of 3.8. This is much higher than in the United States prior to the so-called subprime crisis of 2007. The analysis of this speculative episode confirms the mechanism and regularities already highlighted by the present authors in similar episodes in other countries. Based on these regularities, it is possible to predict the price trajectory over the time interval 2016-2025. It suggests that, unless appropriate relief is provided by the mainland, Hong Kong will experience a decade-long slump. Possible implications for its relations with Beijing are discussed at the end of the paper., Comment: 21 pages, 8 figures

The expression "wage transition" refers to the fact that over the past two or three decades in all developed economies wage increases have levelled off. There has been a widening divergence and decoupling between wages on the one hand and GDP per capita on the other hand. Yet, in China wages and GDP per capita climbed in sync (at least up to now). In the first part of the paper we present comparative statistical evidence which measures the extent of the wage transition effect. In a second part we consider the reasons of this phenomenon, in particular we explain how the transfers of labor from low productivity sectors (such as agriculture) to high productivity sectors (such as manufacturing) are the driver of productivity growth, particularly through their synergetic effects. Although rural flight represents only one of these effects, it is certainly the most visible because of the geographical relocation that it implies; it is also the most well-defined statistically. Moreover, it will be seen that it is a good indicator of the overall productivity and attractivity of the non-agricultural sector. Because this model accounts fairly well for the observed evolution in industrialized countries, we use it to predict the rate of Chinese economic growth in the coming decades. Our forecast for the average annual growth of real wages ranges from 4% to 6% depending on how well China will control the development of its healthcare industry., Comment: 32 pages, 9 figures

This paper is not (or at least not only) about human infant mortality. In line with reliability theory, "infant" will refer here to the time interval following birth during which the mortality (or failure) rate decreases. This definition provides a systems science perspective in which birth constitutes a sudden transition which falls within the field of application of the "Transient Shock" (TS) conjecture put forward in Richmond et al. (2016c). This conjecture provides predictions about the timing and shape of the death rate peak. (i) It says that there will be a death rate spike whenever external conditions change abruptly and drastically. (ii) It predicts that after a steep rising there will be a much longer hyperbolic relaxation process. These predictions can be tested by considering living organisms for which birth is a multi-step process. Thus, for fish there are three states: egg, yolk-sac phase, young adult. The TS conjecture predicts a mortality spike at the end of the yolk-sac phase, and this timing is indeed confirmed by observation. Secondly, the hyperbolic nature of the relaxation process can be tested using high accuracy Swiss statistics which give postnatal death rates from one hour after birth up to the age of 10 years. It turns out that since the 19th century despite a great overall reduction in infant mortality, the shape of the age-specific death rate has remained basically unchanged. This hyperbolic pattern is not specific to humans. It can also be found in small primates as recorded in the archives of zoological gardens. Our ultimate objective is to set up a chain of cases which starts from simple systems and then moves up step by step to more complex organisms. The cases discussed here can be seen as initial landmarks., Comment: 46 pages, 14 figures, 4 tables

Gompertz's law tells us that for humans above the age of 35 the death rate increases exponentially with a doubling time of about 10 years. Here, we show that the same law continues to hold even for ages over 100. Beyond 106 there is so far no statistical evidence available because the number of survivors is too small even in the largest nations. However assuming that Gompertz's law continues to hold beyond 106, we conclude that the mortality rate becomes equal to 1 at age 120 (meaning that there are 1,000 deaths in a population of one thousand). In other words, the upper bound of human life is near 120. The existence of this fixed-point has interesting implications. It allows us to predict the form of the relationship between death rates at age 35 and the doubling time of Gompertz's law. In order to test this prediction, we first carry out a transversal analysis for a sample of countries comprising both industrialized and developing nations. As further confirmation, we also develop a longitudinal analysis using historical data over a time period of almost two centuries. Another prediction arising from this fixed-point model, is that, above a given population threshold, the lifespan of the oldest person is independent of the size of her national community. This prediction is supported by available empirical evidence., Comment: 14 pages, 7 figures