Forensic samples are among the most complex encountered. Blood is best known, but other biological matrices also carry genetic information. Cheek swabs (buccal swabs) collect cells from the inside of the mouth and have the advantage of being a non-invasive sample collection compared to a blood draw. Hair, depending on the presence of the root, is amenable to DNA typing. Semen, vaginal fluids, and vaginal swabs are collected in sexual assault cases. Any surface on which biological fluids (blood, oral fluid, vaginal fluid, etc.) are deposited becomes a potential DNA source.

The initial deposition (called the primary transfer) occurs from a person to a surface. It is the deposition of blood, saliva, semen, or other biological substance directly from the body onto a surface. This process could be a victim’s blood dripping onto an assailant’s clothing, saliva on a cigarette, or seminal fluid on a bedsheet.

In this unashamed polemic I argue that most extant plant species currently represented by a Linnean binomial exist only at the most basic level of a primary hypothesis that has not yet been subjected to the crucial test of circumscription. Rigorous circumscription requires sampling of numerous populations across the full range of a putative species and its supposed close relatives for several properties, including analytical morphology and genetics, preferably supported by gene exchange experiments and autecological observations. In the absence of genuine, demonstrable discontinuities in at least one biologically meaningful property, perceived species boundaries remain entirely arbitrary, thereby hindering rather than assisting every kind of biological investigation. The term 'cryptic species' has many implied definitions, but in my opinion it simply boils down to the many situations where limited morphological and molecular differentiation leave the analyst unsure whether credible species boundaries exist among the representative individuals analysed. The lack of obvious discontinuities typically reflects ongoing gene-flow and/or low levels of extinction of intermediate lineages. At present, the status of a putative species is rarely subjected to critical appraisal through the lens of any specified species concept or evolutionary mechanism, despite the widely accepted primacy of species in systematic biology.

Developmental language disorder (DLD) is estimated to affect 8 per cent of primary school-aged children, and has lasting impacts on academic achievement and social-emotional and behavioural outcomes. DLD is classified as a severe and persistent impairment in the acquisition, understanding, production or use of language, occurring in the absence of comorbid neurodevelopmental disorder. The phenotype of DLD is well established, yet there is relatively limited understanding of its aetiology. A complex interaction of genetic variants and environmental factors is thought to be the cause. To date, linkage and association analyses have implicated a handful of genes in DLD populations, including CMIP and ATP2C2. While many of these variants are common in DLD, they are not consistently associated with severe language impairment, and many overlap with chromosome regions commonly associated with neurodevelopmental disorders such as intellectual disability. The effects of alternate genetic models such as copy number and rare variants may provide a gateway to understanding the complex genetic pathways of this disorder. Pleiotropy and generalisation are also important considerations in understanding the genetic architecture of DLD. Here we outline the phenotype of DLD and provide an overview of recently identified gene pathways implicated in this disorder.

Human beings are one of the innumerable products of the process of evolution by natural selection. As such, understanding our psychological makeup requires an appreciation of the mechanism of natural selection itself. When a population of reproducing entities has (1) variation in traits, (2) inheritance of variation, and (3) nonrandom differential reproduction, entities with traits that are good at making themselves more numerous will, by definition, tend to be better represented in future generations. Organisms that are best able to interact with their environment in a way that promotes their own reproduction are favored automatically. Under consistent environmental conditions, small changes in inherited traits can add up to complex adaptations by adding incremental improvements to the organisms’ fit with the environment. The relationship between variation and inheritance is complex in organisms because variation is manifest in the phenotype, but inheritance occurs between genotypes. The relationship between these two aspects of organisms is complex because genes must act through interaction with the environment. Further complications arise due to the blindness of natural selection to changes in future environments and available variation. Despite these intricacies, natural selection has crafted vastly complex and diverse organisms over the course of billions of years, with no foresight or thought.

Frailty is an important geriatric syndrome that is common and commonly missed, and affects more than a third of people over age 85. Frailty is characterized by diminished physiologic reserves and function, leading to decreased capacity to withstand stressors. Frail adults are at a higher risk of dependency, institutionalization, and death. Multiple interventions have been attempted, including physical activity, improving nutrition, and hormonal therapy, but there are no curative interventions for frailty and it is not clear if frailty can be reversed. Several issues have limited the advancement of frailty research and translation into practice, including the lack of consensus regarding the definition of frailty, the proliferation of assessment tools, and the gaps in validated best practice guidance for frail patients. The recognition of frailty, especially in its early stages, offers the possibility of preventing or mitigating adverse clinical outcomes. Older adults who are frail may benefit most from a comprehensive geriatric evaluation to help elucidate a plan of care that is consistent with patient's goals, values, and preferences.

This chapter will set the table for your personal decisions when considering taking a leadership position and what should go into your thinking as you’re weighing your options. It covers what goes into understanding the position itself and how to find out the crucial details and duties it requires. It then discusses the leadership “phenotype” – what personal skills you bring to the role and whether the role will be a good “fit” for you. It probes what motivates you to be a leader and why, and whether that will give you a durable effect. Finally, it helps you to look at the career move in the context of your overall career, and whether the position will bridge you to something greater in the long run, or whether it’s a dead end. This chapter sets the stage for what comes next, an understanding of your personality as a leader.

The abnormal animal featured here is the Siamese cat, whose color pattern is due to a mutation in the tyrosinase gene, which makes the tyrosinase protein sensitive to temperature. We talk about how some species use temperature to dictate their coloration and how this can happen developmentally.

This commentary reflects on Jang and Choi’s (this volume) chapter summarizing the extent work on behavior and molecular genetic studies of personality disorder (PD). The authors argue that more work needs to be done on refining the PD phenotype, as most work in genetics to date has utilized categorical definitions of PD, even though clinical psychology generally and the field of PDs specifically is moving resolutely toward a dimensional conceptualization (as represented in the alternative model of PDs in the DSM-5). They also argue that the real benefit of both quantitative and measured gene approaches to studying PDs might not be the elucidation of more precise heritability estimates or even the identification of specific genes, but the contribution of environmental influences to maladaptive personality traits.

This rejoinder uses the neuroimaging literature on affect regulation to exemplify how integration of complementary methods suggested by the commentaries could advance neurobiological understanding of personality disorders. It illustrates progressive insights gained from incorporating multiple sources of evidence including neuroimaging, genetics, and behavioral data associated with affect regulation. It also demonstrates the use of brain pattern activation analysis in addition to studying individual regions of interest to better understand the complex relationships between biological genotype, brain activity, and behavioral phenotype. The ways in which neuroimaging can serve as an endophenotype to bridge the gap between genes and distant phenotypes are highlighted.