Variations in historical natural fertility patterns and the measurement of fertility control

This paper looks at 2 main issues: 1) Henry's definition of natural fertility--that which is not controlled within marriage in a parity-specific way; and 2) the use of standard age-specific marital fertility schedules to measure the extent of fertility control. The authors note a number of conceptual difficulties inherent in Henry's definition and which detract from its usefulness. In particular, prolonged lactation and taboos against sexual intercourse are capable of depressing fertility within marriage, while still allowing it to be described as natural. This paper explores some of the consequences of the identified difficulties for the measurement of fertility control within marriage. Regional as well as temporal variations are to be expected in the pattern of marital fertility. The factors affecting natural fertility may be broadly divided into the physical and the psychological. Needed are a variety of standard marital fertility schedules specific to the underlying fertility conditions of the particular population under investigation. The universal applicability of a single standard is placed in doubt. The greatest problem, however, with the application of the idea of natural fertility to historical populations is that its definition rests upon a number of behavioral characteristics amongst a population, whereas its identification must normally proceed in reverse, arguing backwards from the pattern observed to the behavioral processes and conditions which might have produced that pattern. The arguments presented are illustrated by a detailed example drawn from the fertility patterns of Britain, Denmark and Sweden.     

Specificities of antisera against estrogens linked to albumin at different positions (C6, C11, C16, C17)

Antisera were raised in rabbits using conjugates of albumin with 11-hemisuccinates of 11α-OH E₁ and 11α-OH E2. These antisera were compared with antisera to 6-oxo E₂ 6-CMO-, E₂ 17-succinyl- and E₃ 16, 17-disuccinyl-BSA by radioimmunoassay using a statistically designed three-point assay.Sheep anti-(rabbit γ-globulin) coupled to cellulose was used for the separation of antibody-bound and free labeled hapten.Antisera obtained with haptens linked to the carrier at the 17(16) position poorly discriminated between the various estrogens. Antisera obtained with 6- and 11-conjugates showed a much better specificity. In addition the specificity was influenced by using either estrone, estradiol or estriol as tritiated labels. This gives the possibility to determine different parameters by employing different labeled hormones.     

The role of Neuropilin-1 in COVID-19

Neuropilin-1 (NRP-1), a member of a family of signaling proteins, was shown to serve as an entry factor and potentiate SARS Coronavirus 2 (SARS-CoV-2) infectivity in vitro. This cell surface receptor with its disseminated expression is important in angiogenesis, tumor progression, viral entry, axonal guidance, and immune function. NRP-1 is implicated in several aspects of a SARS-CoV-2 infection including possible spread through the olfactory bulb and into the central nervous system and increased NRP-1 RNA expression in lungs of severe Coronavirus Disease 2019 (COVID-19). Up-regulation of NRP-1 protein in diabetic kidney cells hint at its importance in a population at risk of severe COVID-19. Involvement of NRP-1 in immune function is compelling, given the role of an exaggerated immune response in disease severity and deaths due to COVID-19. NRP-1 has been suggested to be an immune checkpoint of T cell memory. It is unknown whether involvement and up-regulation of NRP-1 in COVID-19 may translate into disease outcome and long-term consequences, including possible immune dysfunction. It is prudent to further research NRP-1 and its possibility of serving as a therapeutic target in SARS-CoV-2 infections. We anticipate that widespread expression, abundance in the respiratory and olfactory epithelium, and the functionalities of NRP-1 factor into the multiple systemic effects of COVID-19 and challenges we face in management of disease and potential long-term sequelae.     

One phase of the dormancy developmental pathway is critical for the evolution of insect seasonality

Evolutionary change in the timing of dormancy enables animals and plants to adapt to changing seasonal environments and can result in ecological speciation. Despite its clear biological importance, the mechanisms underlying the evolution of dormancy timing in animals remain poorly understood because of a lack of anatomical landmarks to discern which phase of dormancy an individual is experiencing. Taking advantage of the nearly universal characteristic of metabolic suppression during insect dormancy (diapause), we use patterns of respiratory metabolism to document physiological landmarks of dormancy and test which of the distinct phases of the dormancy developmental pathway contribute to a month‐long shift in diapause timing between a pair of incipient moth species. Here, we show that divergence in life cycle between the earlier‐emerging E‐strain and the later‐emerging Z‐strain of European corn borer (ECB) is clearly explained by a delay in the timing of the developmental transition from the diapause maintenance phase to the termination phase. Along with recent findings indicating that life‐cycle differences between ECB strains stem from allelic variation at a single sex‐linked locus, our results demonstrate how dramatic shifts in animal seasonality can result from simple developmental and genetic changes. Although characterizing the multiple phases of the diapause developmental programme in other locally adapted populations and species will undoubtedly yield surprises about the nature of animal dormancy, results in the ECB moth suggest that focusing on genetic variation in the timing of the dormancy termination phase may help explain how (or whether) organisms rapidly respond to global climate change, expand their ranges after accidental or managed introductions, undergo seasonal adaptation, or evolve into distinct species through allochronic isolation.     

Gene Expression-Based Classifiers Identify Staphylococcus aureus Infection in Mice and Humans

Staphylococcus aureus causes a spectrum of human infection. Diagnostic delays and uncertainty lead to treatment delays and inappropriate antibiotic use. A growing literature suggests the host’s inflammatory response to the pathogen represents a potential tool to improve upon current diagnostics. The hypothesis of this study is that the host responds differently to S. aureus than to E. coli infection in a quantifiable way, providing a new diagnostic avenue. This study uses Bayesian sparse factor modeling and penalized binary regression to define peripheral blood gene-expression classifiers of murine and human S. aureus infection. The murine-derived classifier distinguished S. aureus infection from healthy controls and Escherichia coli-infected mice across a range of conditions (mouse and bacterial strain, time post infection) and was validated in outbred mice (AUC>0.97). A S. aureus classifier derived from a cohort of 94 human subjects distinguished S. aureus blood stream infection (BSI) from healthy subjects (AUC 0.99) and E. coli BSI (AUC 0.84). Murine and human responses to S. aureus infection share common biological pathways, allowing the murine model to classify S. aureus BSI in humans (AUC 0.84). Both murine and human S. aureus classifiers were validated in an independent human cohort (AUC 0.95 and 0.92, respectively). The approach described here lends insight into the conserved and disparate pathways utilized by mice and humans in response to these infections. Furthermore, this study advances our understanding of S. aureus infection; the host response to it; and identifies new diagnostic and therapeutic avenues.