Infections and autoimmunity--good or bad?

The relationship between infections and autoimmunity is complex. Current evidence indicates that microbes can initiate, enhance, or, conversely, abrogate autoimmunity. In this paper, we will review experimental examples illustrating mechanisms involved in these three scenarios. Microbial infections can act as environmental triggers inducing or promoting autoimmunity resulting in clinical manifestations of autoimmune disease in genetically predisposed individuals. However, increasing evidence suggests the opposite outcome, which is the prevention or amelioration of autoimmune processes following microbial encounters. These latter observations support conceptually the "hygiene hypothesis," suggesting that cleaner living conditions will lead to enhanced incidence of autoimmune disorders, asthma, and allergies. Because proof of concept in humans is difficult to obtain, we will discuss relevant animal model data in context with likely or proven human associations. Knowledge of mechanisms that underlie either positive or negative effects of infections on autoimmunity will facilitate exploration of molecular details for prospective clinical studies in the future.     

Auxin and ethylene: collaborators or competitors?

The individual roles of auxin and ethylene in controlling the growth and development of young seedlings have been well studied. In recent years, these two hormones have been shown to act synergistically to control specific growth and developmental processes, such as root elongation and root hair formation, as well as antagonistically in other processes, such as lateral root formation and hypocotyl elongation. This review examines the growth and developmental processes that are regulated by crosstalk between these two hormones and explores the mechanistic basis for the regulation of these processes. The emerging trend from these experiments is that ethylene modulates auxin synthesis, transport, and signaling with unique targets and responses in a range of tissues to fine-tune seedling growth and development.     

Media and breastfeeding: Friend or foe?

This short essay examines infant formula marketing and information sources for their representation of "choice" in the infant feeding context, and finds that while providing information about breast and bottle feeding, infant formula manufacturers focus on mothers' feelings and intuition rather than knowledge in making decisions. In addition, the essay considers how "choice" operates in the history of reproductive rights, shifting the discourse from a rights-based set of arguments to one based on a consumerist mentality. Utilizing the work of historian Rickie Solinger and a 2007 paper for the National Bureau of Labor Statistics, I argue that the structure of market work, and not abstract maternal decision making, determine mothers' choices and practices concerning infant feeding. For true freedoms for mothers to be achieved, freedoms that would include greater social provisions for mothers, our culture will have to confront how structural constraints make breastfeeding difficult, as well as how the concept of choice divides mothers into those who make good choices and those who do not.     

Fibulins and cancer: friend or foe?

The fibulins are a family of secreted glycoproteins, which are characterised by repeated epidermal-growth-factor-like domains and a unique C-terminal structure. Six distinct fibulin genes, encoding at least nine protein products generated by alternative splicing, have been identified. Considerable evidence is available pointing towards a structural role for fibulins within the extracellular matrix. Fibulins have been shown to modulate cell morphology, growth, adhesion and motility. The dysregulation of certain fibulins occurs in a range of human disorders, including cancer. Indeed, both tumour suppressive and oncogenic activities have been proposed for members of the fibulin family. Herein, we discuss the possible roles of fibulins in cancer, in addition to their diagnostic and therapeutic potential.     

Alzheimer's and Parkinson's disease--overlapping or synergistic pathologies?

Alzheimer's disease (AD) and Parkinson's disease (PD) are the two most common neurodegenerative disorders in humans. They are characterized by insoluble protein deposits; beta-amyloid plaques and tau-containing neurofibrillary lesions in AD, and alpha-synuclein-containing Lewy bodies in PD. As a significant percentage of patients have clinical and pathological features of both diseases, the patho-cascades of the two diseases might overlap. For the first time, new animal models that express multiple transgenes provide the tools to dissect the pathogenic pathways and to differentiate between additive and synergistic effects.     

Interactions between metals and alpha-synuclein--function or artefact?

alpha-synuclein is one of a family of proteins whose function remains unknown. This protein has become linked to a number of neurodegenerative disease although its potential causative role in these diseases remains mysterious. In diseases such as Parkinson's disease and Lewy body dementias, alpha-synuclein becomes deposited in aggregates termed Lewy bodies. Also, some inherited forms of Parkinson's diseases are linked to mutations in the gene for alpha-synuclein. Studies have mostly focussed on what causes the aggregation of the protein but, like many amyloidogenic proteins associated with a neurodegenerative disorder, this protein has now been suggested to bind copper. This finding is currently controversial. This review examines the evidence that alpha-synuclein is a copper binding protein and discusses whether this has any significance in determining the function of the protein or whether copper binding is at all necessary for aggregation.     

Homoplasy and homology: dichotomy or continuum?

Homology is the presence of the same feature in two organisms whose most recent common ancestor also possessed the feature. I discuss the bases on which we can tell that two features being compared share sufficient elements of sameness to allow them to be treated as homologous and therefore to be legitimately compared with one another in a way that informs comparative, evolutionary, and phylogenetic analysis. To do so, I discuss the relationship(s) between homology and homoplasy to conclude that we are dealing neither with a dichotomy between homoplasy as parallelism/convergence and homology as common descent nor with a dichotomy of homoplasy as the interrupted presence of the character in a lineage and homology as the continuous presence of the character. Rather, we are dealing with common descent with varying degrees of modification. Homoplasy and homology are not dichotomies but the extremes of a continuum, reflecting deep or more recent shared ancestry based on shared cellular mechanisms and processes and shared genes and gene pathways and networks. The same genes can be used to initiate the development of homoplastic and homologous structures. Consequently, structures may be lost but their developmental bases retained, providing the potential for homoplasy. It should not be surprising that similar features persist when a feature is present in the nearest common ancestor (homology). Neither should it be surprising to find that different environments or selective pressures can trigger the reappearance of similar features in organisms that do not share a recent common ancestor (homoplasy).     

Endocytosis and Autophagy: Exploitation or Cooperation?

Autophagy is a lysosome-mediated degradative system that is a highly conserved pathway present in all eukaryotes. In all cells, double-membrane autophagosomes form and engulf cytoplasmic components, delivering them to the lysosome for degradation. Autophagy is essential for cell health and can be activated to function as a recycling pathway in the absence of nutrients or as a quality-control pathway to eliminate damaged organelles or even to eliminate invading pathogens. Autophagy was first identified as a pathway in mammalian cells using morphological techniques, but the Atg (autophagy-related) genes required for autophagy were identified in yeast genetic screens. Despite tremendous advances in elucidating the function of individual Atg proteins, our knowledge of how autophagosomes form and subsequently interact with the endosomal pathway has lagged behind. Recent progress toward understanding where and how both the endocytotic and autophagic pathways overlap is reviewed here.Autophagy is a lysosome-mediated pathway for the degradation of cytosolic proteins and organelles, which is essential for cell homeostasis, development, and for the prevention of several human diseases and infection (Choi et al. 2013). Importantly, autophagy cannot occur without an active lysosome. However, it is becoming increasingly recognized that the endosomal pathway plays a greater role than just providing the degradative enzymes found in the lysosome. Recent data suggest that in mammalian cells multiple contributions from several stages of the endocytic pathway are essential for efficient autophagy. Here we outline the autophagic pathway and then address the recent data on how different endosomal compartments contribute to autophagy, and the molecular machinery required for the interaction of the endosome and lysosome during the formation, and consumption of the autophagosome. Given the model emerging that the amino-acid-sensitive autophagic pathway originates from the endoplasmic reticulum (ER), several questions arise, including how do recognition and productive interaction occur between an ER-derived membrane and endosomes? How are these interactions mediated, and which are essential for efficient autophagy?     

Punish or perish? Retaliation and collaboration among humans

A spate of recent investigations on reciprocation and social enforcement in humans has brought together (and sometimes divided) economists, psychologists, anthropologists, social scientists and evolutionary biologists, in addition to neurologists and students of animal behavior. Experimental work on public goods and social incentives has addressed a wealth of questions on the emotional and cognitive (proximal) factors, and also on the genetic and cultural (ultimate) evolutionary mechanisms involved in this essential aspect of human nature.     

Should Associations between HIV-Related Risk Perceptions and Behaviors or Intentions Be Positive or Negative?

Risk perceptions are important in HIV research and interventions; mixed results were found between HIV-related perceptions and behaviors. We interviewed 377 sexually active injecting drug users in China, finding mixed associations between HIV-related risk perception assessed by two general measures and two previous risk behaviors (syringe sharing: p<.05; unprotected sex: p>.05) – partially supporting the ‘reflective hypothesis’ that reflection on previous behaviors increases risk perceptions. When we use specific measures for risk perceptions (HIV transmission via unprotected sex with specific types of sex partner and via syringe sharing) and use behavioral intention to adopt protective risk behaviors (condom use and avoid syringe sharing totally) as dependent variables, positive significant associations were observed – supporting the motivational hypothesis that risk perceptions motivate one to adopt protective behaviors. The direction and significance of the associations of concern depends on types of measures used. It has important implications on research design, data interpretation and services.     

Psychopathology or adaptation? Genetic and evolutionary perspectives on individual differences and psychopathology

A greater understanding of psychopathology will be found in the integration of genetic and evolutionary perspectives on adaptation and function. Evolutionary theory proposes that adaptive traits are reproduced more successfully than maladaptive ones. However, some traits, while contributing to fitness in the ancestral environment, may contribute to fitness no longer. This is known as mismatch theory. Evolutionarily informed research into various "pathologies" has yielded interesting results, some based on this theory. This paper serves to distinguish between genetic and evolutionary perspectives on psychopathology as well as to examine some recent research on the selective forces that may be implicated in psychopathy, anorexic behavior, and ADHD. We suggest that research into psychopathy in general would benefit from an evolutionary perspective and an examination of the assumptions behind past research.