Pre- and postcopulatory competition affect testes mass and organization differently in two monophyletic mole-rat species, Georychus capensis and Fukomys damarensis.

Sperm competition results from postcopulatory continuation of male-male competition for paternity. The level of sperm competition is predicted to be highest in species with greater polyandry and weakest in monogamous pairs. Sperm competition levels can be indexed using traits that reflect male investment in fertilization, particularly relative testes mass (RTM). However, the relationship between RTM and levels of sperm competition may also be influenced by precopulatory competition selecting for higher levels of testosterone, also produced by the testes. To test the relationship between RTM and both pre- and postcopulatory male-male competition we compared two bathyergid mole-rat species, the promiscuous Georychus capensis and the monogamous eusocial Fukomys damarensis. The promiscuous species had not only larger RTM, but also a greater proportion of spermatogenic tissue, maximizing germ cell production as well. Conversely, the eusocial species had smaller testes, but a higher proportion of interstitial tissue (which contains the androgenic Leydig cells) and higher levels of testosterone. Consequently, testicular traits as well as testes mass may be under selection, but these are not normally measured. More research is required on relative investment in different testicular traits in relation to both pre- and postcopulatory selection pressures.

The evolving value of older biomarkers in the clinical diagnosis of pediatric sepsis.

Sepsis remains the leading cause of childhood mortality worldwide. The evolving definition of pediatric sepsis is extrapolated from adult studies. Although lacking formal validation in the pediatric population, this working definition has historically proven its clinical utility. Prompt identification of pediatric sepsis is challenging as clinical picture is often variable. Timely intervention is crucial for optimal outcome, thus biomarkers are utilized to aid in immediate, yet judicious, diagnosis of sepsis. Over time, their use in sepsis has expanded with discovery of newer biomarkers that include genomic bio-signatures. Despite recent scientific advances, there is no biomarker that can accurately diagnose sepsis. Furthermore, older biomarkers are readily available in most institutions while newer biomarkers are not. Hence, the latter's clinical value in pediatric sepsis remains theoretical. Albeit promising, scarce data on newer biomarkers have been extracted from research settings making their clinical value unclear. As interest in newer biomarkers continue to proliferate despite their ambiguous clinical use, the literature on older biomarkers in clinical settings continue to diminish. Thus, revisiting the evolving value of these earliest biomarkers in optimizing pediatric sepsis diagnosis is warranted. This review focuses on the four most readily available biomarkers to bedside clinicians in diagnosing pediatric sepsis. IMPACT: The definition of pediatric sepsis remains an extrapolation from adult studies. Older biomarkers that include C-reactive protein, procalcitonin, ferritin, and lactate are the most readily available biomarkers in most pediatric institutions to aid in the diagnosis of pediatric sepsis. Older biomarkers, although in varying levels of reliability, remain to be useful clinical adjuncts in the diagnosis of pediatric sepsis if used in the appropriate clinical context. C-reactive protein and procalcitonin are more sensitive and specific among these older biomarkers in diagnosing pediatric sepsis although evidence varies in different age groups and clinical scenarios.

Sexual conflict in action: An antagonistic relationship between maternal and paternal sex allocation in the tammar wallaby, Notamacropus eugenii.

Sex ratio biases are often inconsistent, both among and within species and populations. While some of these inconsistencies may be due to experimental design, much of the variation remains inexplicable. Recent research suggests that an exclusive focus on mothers may account for some of the inconsistency, with an increasing number of studies showing variation in sperm sex ratios and seminal fluids. Using fluorescent in-situ hybridization, we show a significant population-level Y-chromosome bias in the spermatozoa of wild tammar wallabies, but with significant intraindividual variation between males. We also show a population-level birth sex ratio trend in the same direction toward male offspring, but a weaning sex ratio that is significantly female-biased, indicating that males are disproportionately lost during lactation. We hypothesize that sexual conflict between parents may cause mothers to adjust offspring sex ratios after birth, through abandonment of male pouch young and reactivation of diapaused embryos. Further research is required in a captive, controlled setting to understand what is driving and mechanistically controlling sperm sex ratio and offspring sex ratio biases and to understand the sexually antagonistic relationship between mothers and fathers over offspring sex. These results extend beyond sex allocation, as they question studies of population processes that assume equal input of sex chromosomes from fathers, and will also assist with future reproduction studies for management and conservation of marsupials.

Developmental sexual dimorphism and the evolution of mechanisms for adjustment of sex ratios in mammals.

Sex allocation theory predicts biased offspring sex ratios in relation to local conditions if they would maximize parental lifetime reproductive return. In mammals, the extent of the birth sex bias is often unpredictable and inconsistent, leading some to question its evolutionary significance. For facultative adjustment of sex ratios to occur, males and females would need to be detectably different from an early developmental stage, but classic sexual dimorphism arises from hormonal influences after gonadal development. Recent advances in our understanding of early, pregonadal sexual dimorphism, however, indicate high levels of dimorphism in gene expression, caused by chromosomal rather than hormonal differences. Here, we discuss how such dimorphism would interact with and link previously hypothesized mechanisms for sex-ratio adjustment. These differences between males and females are sufficient for offspring sex both to be detectable to parents and to provide selectable cues for biasing sex ratios from the earliest stages. We suggest ways in which future research could use the advances in our understanding of sexually dimorphic developmental physiology to test the evolutionary significance of sex allocation in mammals. Such an approach would advance our understanding of sex allocation and could be applied to other taxa.

Forgotten fathers: paternal influences on mammalian sex allocation.

Sex allocation research in mammals has focussed almost exclusively on mothers under the assumption that the male contribution is genetically determined during meiosis and therefore not under adaptive control. Although early studies on sperm traits suggested that sex ratios were at parity, technological advances have made analysis more reliable and cheaper. Subsequently, more studies have shown variation in the production of X-/Y-chromosome-bearing spermatozoa. We review the evidence that the X/Y ratio varies between and within individuals in mammals, and test whether there are consistent predictors of these sex ratio biases and finally discuss their implications for future studies on sex allocation.