Analyzing Epidemics in New France: The Measles Epidemic of 1714-15

@font-face { font-family: Cambria Math ; }@font-face { font-family: Calibri ; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0cm 0cm 0.0001pt; font-size: 12pt; font-family: Times New Roman ; }p.MsoNoSpacing, li.MsoNoSpacing, div.MsoNoSpacing { margin: 0cm 0cm 0.0001pt; font-size: 11pt; font-family: Cambria; }.MsoChpDefault { font-family: Cambria; }div.WordSection1 { page: WordSection1; } ABSTRACT Few epidemics have been documented in the context of historical Quebec. The rich epidemiological and demographic data contained in the Registre de population du Québec ancien makes it possible to conduct detailed analyses of historical epidemics and can be beneficial to filling in gaps in modern knowledge. The historical studies of measles have a distinct advantage over modern ones, in that epidemics can be analyzed in a natural state unhindered by modern medical treatment and vaccine campaigns. This dissertation attempts to fill this knowledge gap of infectious diseases through the development of methods to analyze epidemics in the absence of cause of death records. The results show the suitability of these methods to investigate the 1714-15 measles epidemic and its impact on the children in the population. The first study examined the general dynamics of the epidemic that provisioned the baseline for the subsequent studies. Measles entry to the Montreal area was from Colonial America circa late-March of 1714. The epidemic spread eastwards to most other parts of the colony by late-August of the same year and disappeared early in 1715. Measles was virulent with an estimated death rate of 52.8 per thousand for children under age 15. Infants and toddlers were the main victims, while females were slightly more likely than males to have died from the virus. Although the epidemic originated in the Western parishes, severity finally turned out to be higher in the Eastern parishes of the colony. The second study identified several measles-specific risk factors among children under age 5 were identified with case/control comparisons, which revealed that the effects of these factors were only significant and intensified during the acute phase of the epidemic. Contrary to what was reported in modern studies, singletons or children with fewer siblings had higher odds of dying than children in larger sibships. The age difference between siblings appeared to be a more important predictor of death than the size of the sibship, as a larger average difference led to an increased likelihood of death. As well, children with a sibling who died during the epidemic and children with immigrant parents were at higher risk. In the third study, exposed children who survived the acute episode of the epidemic were followed for 25 months past the estimated date of infection. It was found that children exposed before age 3 had higher long-term mortality than the unexposed children. The difference remained significant while assessing the effects of the demographic and sibship risk factors. For the exposed cohort, the risk of death also varied by age and sex. Only females exposed during infancy had a significantly higher risk of dying, while both exposed male and female toddlers had higher mortality during the follow-up period. In this case, the effect was slightly stronger for males. No significant long-term mortality difference was found among children exposed between 36 and 59 months of age

Familial and Environmental Influences on Longevity in a Pre-industrial Population

Data from historical populations provide an adequate context for the examination of the familial and environmental components of longevity. We have investigated the relation between sibling survivorship and longevity through French-Canadian children of a completed fertility cohort born between 1625 and 1704. The Cox regression model was used to analyze the effects of sibling survivorship on the survival time of these early Canadian inhabitants. Other covariates such as regional variation, secular trends (i.e. period effects), parental and spousal survival were also taken into consideration. Our findings show that individuals with at least one sibling surviving beyond 85 years of age had a life-long sustained mortality advantage over the general population. The risks of death after age 50 was 55% and 60% lower for females and males, respectively, having a long-lived sibling. In comparison, the parental of origin effects were negligible. Only the mother-son association in age at death was found significant among the four possible parent-child pairs. Overall, the various models provided better fit to male than to female data. Biological as well as social explanations are explored in order to account for the various results

Influences of Early Life Conditions on Old Age Mortality in Old Québec

Increasingly, bio-demographers are turning to infancy and childhood to gain a better understanding of old age mortality. However, evidence of a link between early life conditions and survival until old age is fragmentary, and the intervening mechanisms remain unclear. Drawing from data on a cohort of French-Canadian children born in the 17th and 18th centuries, we study the effects of infant exposure to infectious diseases (as revealed by the infant mortality rate in the year of birth) on later life mortality. A series of Cox proportional hazard models are used and we control for other familial and environmental conditions prevalent in childhood, as well as in adulthood. Results point to a slight, but not significant effect of a disease load in infancy for females born in years of exceptionally high infant mortality. The results are also not conclusive for males. More generally, a trend of increasing infant mortality over time correlates with general decreases in post-reproductive mortality rates, which are probably due to period improvements in later life conditions. Our study supports the view that period changes have stronger relevance than cohort effects in the study of historical variations in old age mortality

The Measles Epidemic of 1714-1715 in New-France

Abstract not availabl

Post-reproductive Longevity in a Natural Fertility Population

Fertility patterns may be useful markers for rates of biological aging. Based on evolutionary and socio-demographic approaches to historical data from the population of Québec (taken from the Registre de population du Québec ancien at the University of Montreal), we examine the effects of reproduction on longevity. Using Cox hazard models on about 2,000 couples married in the colony before 1740, we show that women bearing their last child late in life had longer post-reproductive lives, suggesting that late menopause is associated with an overall slower rate of aging. Increased parity had an opposite, detrimental effect on women’s post-reproductive survival. On the other hand, husband’s longevity was less sensitive to parity and reproductive history. For husbands increased effective family size (EFS; the number of children who survived up to age 18) in a “compressed” reproductive time-span meant higher chances for survival past age 60. Children may serve as strong economical assets on farmstead during colonization, which would mostly benefit fathers. In a collaborative effort to unveil post-reproductive aging patterns in historical populations, the results are compared to previous analyses conducted on the Utah population database and evolutionary and socio-demographic theories addressed in light of the results

Familial Aggregation of Survival and Late Female Reproduction

Abstract not availabl

Contrasting requirements during disease evolution identify EZH2 as a therapeutic target in AML

This study demonstrates that EZH2 has stage-specific and diametrically opposite roles during the induction and maintenance stages of AML. However, different transcriptional programs are affected at each stage, identifying mutant EZH2 as a prognostic marker and paradoxically wild-type EZH2 as a potential therapeutic targetThe Huntly laboratory is funded by CRUK (Programme C18680/A25508), ERC (Grant 647685 COMAL), KKLF, MRC, Bloodwise, the Wellcome Trust (WT) and the Cambridge NIHR BRC. F.B. is a recipient of a Wellcome Trust PhD for Clinicians award. P.G. is funded by the Wellcome Trust (109967/Z/15/Z). We acknowledge the WT/MRC centre grant (097922/Z/11/Z) and support from WT strategic award 100140. Research in the laboratory is also supported by core funding from Wellcome and MRC to the Wellcome-MRC Cambridge Stem Cell Institute. We are grateful to Chiara Cossetti, Gabriela Grondys-Kotarba and Reiner Schulte at the CIMR Flow Cytometry Core for their invaluable help and advice with cell sorting. This research was supported by the Cambridge NIHR BRC Cell Phenotyping Hub. Patient samples were received from the UK NCRI AML trials. The authors declare no competing financial interests

Does exposure to infectious diseases in infancy affect old-age mortality? Evidence from a pre-industrial population

Many studies have shown that health conditions experienced in childhood play an important role on an individual's adult mortality. Recent research suggests that past reductions in early life exposure to infectious diseases have been a major contributor to the historical decline in old-age mortality. Drawing on French-Canadian data from cohorts born in the 17th and 18th centuries, we test whether a progressive deterioration in early life conditions (as revealed by an increasing infant mortality rate) translates into a decrease in survival prospects in late life. We use traditional demographic measures such as the age-specific probability of death, and a series of proportional hazard models to control for familial and environmental conditions. Results point toward little evidence of any early life effects. The trend of increasing infant mortality does not correlate with a general increase of mortality in older ages within the same cohorts. Period changes affecting survival at older ages (war, epidemics) as well as demographic and biological characteristics shared within families have a much larger role in old-age mortality than early life characteristics shared within the same cohorts.Canada Epidemics Infant mortality Cohort effects Historical demography Longevity Period effects