Abnormal development of Sertoli cells, leading to abnormalities in other cell types, is our hypothesized explanation for the abnormal changes in DBP-exposed animals. As the testicular and other changes in DBP-exposed rats have all been reported in human TDS, DBP exposure in utero may provide a useful model for defining the cellular pathways in TDS.

Current neuropsychological models propose that some age-related cognitive changes are due to frontal-lobe deterioration. However, these models have not considered the possible subdivision of the frontal lobes into the dorsolateral and ventromedial regions. This study assessed the age effects on 3 tasks of executive function and working memory, tasks dependent on dorsolateral prefrontal dysfunction; and 3 tasks of emotion and social decision making, tasks dependent on ventromedial prefrontal dysfunction. Age-related differences in performance were found on all tasks dependent on dorsolateral prefrontal dysfunction. In contrast, age-related differences were not found on the majority of the tasks dependent on ventromedial prefrontal dysfunction. The results support a specific dorsolateral prefrontal theory of cognitive changes with age, rather than a global decline in frontal-lobe function.

Previous studies of dual-task coordination in working memory have shown a lack of dual-task interference when a verbal memory task is combined with concurrent perceptuomotor tracking. Two experiments are reported in which participants were required to perform pairwise combinations of (1) a verbal memory task, a visual memory task, and perceptuomotor tracking (Experiment 1), and (2) pairwise combinations of the two memory tasks and articulatory suppression (Experiment 2). Tracking resulted in no disruption of the verbal memory preload over and above the impact of a delay in recall and showed only minimal disruption of the retention of the visual memory load. Performing an ongoing verbal memory task had virtually no impact on retention of a visual memory preload or vice versa, indicating that performing two demanding memory tasks results in little mutual interference.Experiment 2 also showed minimal disruption when the two memory tasks were combined, although verbal memory (but not visual memory) was clearly disrupted by articulatory suppression interpolated between presentation and recall. These data suggest that a multiple-component working memory model provides a better account for performance in concurrent immediate memory tasks than do theories that assume a single processing and storage system or a limited-capacity attentional system coupled with activated memory traces.

The role(s) oestrogens play in male adult reproductive function remains uncertain. We have used antibodies specific for oestrogen receptor- alpha (ERalpha) and - beta (ERbeta) to investigate their distribution within the male. In testes from adult human, macaque and marmoset, ERbeta protein was detected in Sertoli cells, Leydig cells and peritubular myoid cells. In germ cells, the intensity of immunostaining for ERbeta was variable between species. Immunoexpression in preleptotene, leptotene and zygotene spermatocytes was low/absent in all species. Elongated spermatids were consistently immunonegative. No ERalpha immunoexpression was detected in testes. ERbeta was detected in epithelial and stromal cell nuclei throughout the male reproductive system [efferent ductules (ED), epididymis, vas deferens, seminal vesicles] and in the bladder. ERalpha was detected in non-ciliated epithelial cells in the ED, but rarely in epithelial and basal cells within the epididymis. Epithelial cells from seminal vesicles and bladder were immunonegative for ERalpha. Expression of ERalpha in stromal cells was rare in the ED, epididymis and bladder but more frequent in seminal vesicles. Expression of ERalpha, and long and short forms of ERbeta, was confirmed by Western blotting. The widespread expression of ERbeta suggests that it is the primary target for modulation of tissue function via oestrogenic ligands in the male reproductive system.

The programme went beyond many dementia activities. Despite no evidence for lasting effects, all involved wanted the programme to continue. A carer quote: You do it for the moment encapsulates a sense that an activity is worthwhile even if it gives benefit only whilst running. The programme is continuing and expanding.

The findings reveal a Theory of Mind deficit on a simple test that was dissociated from the presence of executive dysfunction and suggests a profile of cognitive and behavioral dysfunction indicative of a subclinical fvFTD syndrome. The relative contribution of prefrontal pathways to the cognitive profile in ALS is considered.

Immersive virtual reality (VR) emerges as a promising research and clinical tool. However, several studies suggest that VR induced adverse symptoms and effects (VRISE) may undermine the health and safety standards, and the reliability of the scientific results. In the current literature review, the technical reasons for the adverse symptomatology are investigated to provide suggestions and technological knowledge for the implementation of VR head-mounted display (HMD) systems in cognitive neuroscience. The technological systematic literature indicated features pertinent to display, sound, motion tracking, navigation, ergonomic interactions, user experience, and computer hardware that should be considered by the researchers. Subsequently, a meta-analysis of 44 neuroscientific or neuropsychological studies involving VR HMD systems was performed. The meta-analysis of the VR studies demonstrated that new generation HMDs induced significantly less VRISE and marginally fewer dropouts. Importantly, the commercial versions of the new generation HMDs with ergonomic interactions had zero incidents of adverse symptomatology and dropouts. HMDs equivalent to or greater than the commercial versions of contemporary HMDs accompanied with ergonomic interactions are suitable for implementation in cognitive neuroscience. In conclusion, researchers' technological competency, along with meticulous methods and reports pertinent to software, hardware, and VRISE, are paramount to ensure the health and safety standards and the reliability of neuroscientific results.

Fetal growth plays a role in programming of adult cardiometabolic disorders, which in men, are associated with lowered testosterone levels. Fetal growth and fetal androgen exposure can also predetermine testosterone levels in men, although how is unknown, because the adult Leydig cells (ALCs) that produce testosterone do not differentiate until puberty. To explain this conundrum, we hypothesized that stem cells for ALCs must be present in the fetal testis and might be susceptible to programming by fetal androgen exposure during masculinization. To address this hypothesis, we used ALC ablation/regeneration to identify that, in rats, ALCs derive from stem/progenitor cells that express chicken ovalbumin upstream promoter transcription factor II. These stem cells are abundant in the fetal testis of humans and rodents, and lineage tracing in mice shows that they develop into ALCs. The stem cells also express androgen receptors (ARs). Reduction in fetal androgen action through AR KO in mice or dibutyl phthalate (DBP) -induced reduction in intratesticular testosterone in rats reduced ALC stem cell number by ∼40% at birth to adulthood and induced compensated ALC failure (low/normal testosterone and elevated luteinizing hormone). In DBP-exposed males, this failure was probably explained by reduced testicular steroidogenic acute regulatory protein expression, which is associated with increased histone methylation (H3K27me3) in the proximal promoter. Accordingly, ALCs and ALC stem cells immunoexpressed increased H3K27me3, a change that was also evident in ALC stem cells in fetal testes. These studies highlight how a key component of male reproductive development can fundamentally reprogram adult hormone production (through an epigenetic change), which might affect lifetime disease risk.adult Leydig stem/progenitor cells | compensated Leydig cell failure | GATA4 | ethane dimethane sulfonate