Why sex matters: the biological mechanisms of cardiovascular disease

Cardiovascular disease (CVD) is the leading determinant of mortality and morbidity in women. However, a full understanding of the basic and clinical aspects of CVD in women is far from being accomplished. Sexual dimorphism in CVD has been reported both in humans and experimental animals. Menopause is a risk factor for CVD due to the reduction of endogenous estrogen, although the mechanisms underlying are poorly understood. Estrogens act through binding to vascular estrogen receptors and by non-genomic mechanisms. Advances in this field are essential to improve CVD diagnostic and clinical strategies in women, and to develop sex-specific prevention plans as much as female-oriented treatment algorithms. This paper reviews pathophysiology of CVD in women and its potential clinical implications. Particular emphasis is given to biochemical markers and to indicators of cardiovascular dysfunction and damage. Estimation of these parameters, central to cardiovascular pathophysiology, could represent a particularly relevant tool in female patients. More research is needed to identify women who will profit most of early intervention.     

Why disgust matters

The new synthesis about disgust is that it is a system that evolved to motivate infectious disease avoidance. There are vital practical and intellectual reasons why we need to understand disgust better. Practically, disgust can be harnessed to combat the behavioural causes of infectious and chronic disease such as diarrhoeal disease, pandemic flu and smoking. Disgust is also a source of much human suffering; it plays an underappreciated role in anxieties and phobias such as obsessive compulsive disorder, social phobia and post-traumatic stress syndromes; it is a hidden cost of many occupations such as caring for the sick and dealing with wastes, and self-directed disgust afflicts the lives of many, such as the obese and fistula patients. Disgust is used and abused in society, being both a force for social cohesion and a cause of prejudice and stigmatization of out-groups. This paper argues that a better understanding of disgust, using the new synthesis, offers practical lessons that can enhance human flourishing. Disgust also provides a model system for the study of emotion, one of the most important issues facing the brain and behavioural sciences today.     

Why bioimage informatics matters

Driven by the importance of spatial and physical factors in cellular processes and the size and complexity of modern image data, computational analysis of biological imagery has become a vital emerging sub-discipline of bioinformatics and computer vision.     

Why basic microbiology still matters

Microbiology has been a foundation of our investigation into the basic principles of life, but much remains to be discovered. Therefore, the focus on basic microbiology research cannot be lost.     

Why size matters: altering cell size

Several genes involved in growth control have lately been demonstrated to exhibit more potent effects on cell size than on cell proliferation. Many of these genes direct protein and ribosomal synthesis, highlighting the interdependence between cell size and macromolecular content. The failure to maintain normal cell size when these genes are deregulated suggests that, in certain contexts, cell growth and division are not coupled or coordinated. Several physiological repercussions of altering cell size have been identified.     

Why the stroma matters in breast cancer

Survival and recurrence rates in breast cancer are variable for common diagnoses, and therefore the biological underpinnings of the disease that determine those outcomes are yet to be fully understood. As a result, translational medicine is one of the fastest growing arenas of study in tumor biology. With advancements in genetic and imaging techniques, archived biopsies can be examined for purposes other than diagnosis. There is a great deal of evidence that points to the stroma as the major regulator of tumor progression following the initial stages of tumor formation, and the stroma may also contribute to risk factors determining tumor formation. Therefore, aspects of stromal biology are well-suited to be a focus for studies of patient outcome, where statistical differences in survival among patients provide evidence as to whether that stromal component is a signpost for tumor progression. In this review we summarize the latest research done where breast cancer patient survival was correlated with aspects of stromal biology, which have been put into four categories: reorganization of the extracellular matrix (ECM) to promote invasion, changes in the expression of stromal cell types, changes in stromal gene expression, and changes in cell biology signaling cascades to and from the stroma.     

Why intraspecific trait variation matters in community ecology

Natural populations consist of phenotypically diverse individuals that exhibit variation in their demographic parameters and intra- and inter-specific interactions. Recent experimental work indicates that such variation can have significant ecological effects. However, ecological models typically disregard this variation and focus instead on trait means and total population density. Under what situations is this simplification appropriate? Why might intraspecific variation alter ecological dynamics? In this review we synthesize recent theory and identify six general mechanisms by which trait variation changes the outcome of ecological interactions. These mechanisms include several direct effects of trait variation per se and indirect effects arising from the role of genetic variation in trait evolution.     

Why anisogamy drives ancestral sex roles

There is a clear tendency in nature for males to compete more strongly for fertilizations than females, yet the ultimate reasons for this are still unclear. Many researchers—dating back to Darwin and Bateman—have argued that the difference is ultimately driven by the fact that males (by definition) produce smaller and more numerous gametes than females. However, this view has recently been challenged, and a formal validation of the link between anisogamy and sex roles has been lacking. Here, we develop mathematical models that validate the intuition of Darwin and Bateman, showing that there is a very simple and general reason why unequal gamete numbers result in unequal investment in sexually competitive traits. This asymmetry does not require multiple mating by either sex, and covers traits such as mate searching, where the male bias has been difficult to explain. Furthermore, our models show males and females are predicted to diverge more strongly when the fertilization probability of each female gamete is high. Sex roles thus ultimately trace back to anisogamy and the resulting consequences for the fertilization process.