Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
269,503
result(s) for
"Biological development"
Sort by:
A brain for speech : a view from evolutionary neuroanatomy
This book discusses evolution of the human brain, the origin of speech and language. It covers past and present perspectives on the contentious issue of the acquisition of the language capacity. Divided into two parts, this insightful work covers several characteristics of the human brain including the language-specific network, the size of the human brain, its lateralization of functions and interhemispheric integration, in particular the phonological loop. Aboitiz argues that it is the phonological loop that allowed us to increase our vocal memory capacity and to generate a shared semantic space that gave rise to modern language. The second part examines the neuroanatomy of the monkey brain, vocal learning birds like parrots, emergent evidence of vocal learning capacities in mammals, mirror neurons, and the ecological and social context in which speech evolved in our early ancestors. This book's interdisciplinary topic will appeal to scholars of psychology, neuroscience, linguistics, biology and history -- Back cover.
Book
Injuries and illnesses in a cohort of elite youth alpine ski racers and the influence of biological maturity and relative age: a two-season prospective study
Studies on injuries and illnesses involving youth ski racers younger than 15 years are lacking in the literature. The aim of this study was prospectively to assess the incidence, prevalence, and severity of traumatic and overuse injuries, as well as illnesses of elite youth ski racers with regard to sex, biological maturity status, and relative age.
A prospective, longitudinal cohort design was used to monitor the anthropometrics, training characteristics, traumatic and overuse injuries, and illnesses of 82 elite youth ski racers (51 males, 31 females, age 9-14 years) over 2 consecutive years. The exact training exposure (skiing and athletic) was recorded. Relative age and estimated biological maturity status were assessed.
Relatively low injury incidence or prevalence (traumatic, 0.86/1,000 hours of training; overuse, 0.28/1,000 hours) and comparably high illness prevalence (2.4/athlete) were reported. The knee was the most commonly affected body part (traumatic injuries 36.5%, overuse injuries 82%). A high number of bone fractures were revealed (46%), while no stress fractures occurred; 66% of the illnesses were respiratory tract infections. No differences were found between males and females, the differing maturity groups, or relative age quartiles. Early-maturing athletes had comparably low traumatic and overuse-injury rates. Relatively younger athletes had low traumatic injury rates.
The injury-prevention measures implemented in the training process of youth ski racers seem to contribute to a low incidence of injury. Biological maturity status should be considered in the training process to prevent injuries in late-maturing athletes.
Journal Article
Critical period regulation across multiple timescales
Brain plasticity is dynamically regulated across the life span, peaking during windows of early life. Typically assessed in the physiological range of milliseconds (real time), these trajectories are also influenced on the longer timescales of developmental time (nurture) and evolutionary time (nature), which shape neural architectures that support plasticity. Properly sequenced critical periods of circuit refinement build up complex cognitive functions, such as language, from more primary modalities. Here, we consider recent progress in the biological basis of critical periods as a unifying rubric for understanding plasticity across multiple timescales. Notably, the maturation of parvalbumin-positive (PV) inhibitory neurons is pivotal. These fast-spiking cells generate gamma oscillations associated with critical period plasticity, are sensitive to circadian gene manipulation, emerge at different rates across brain regions, acquire perineuronal nets with age, and may be influenced by epigenetic factors over generations. These features provide further novel insight into the impact of early adversity and neurodevelopmental risk factors for mental disorders.
Journal Article
Single-cell epigenomics reveals mechanisms of human cortical development
During mammalian development, differences in chromatin state coincide with cellular differentiation and reflect changes in the gene regulatory landscape
1
. In the developing brain, cell fate specification and topographic identity are important for defining cell identity
2
and confer selective vulnerabilities to neurodevelopmental disorders
3
. Here, to identify cell-type-specific chromatin accessibility patterns in the developing human brain, we used a single-cell assay for transposase accessibility by sequencing (scATAC-seq) in primary tissue samples from the human forebrain. We applied unbiased analyses to identify genomic loci that undergo extensive cell-type- and brain-region-specific changes in accessibility during neurogenesis, and an integrative analysis to predict cell-type-specific candidate regulatory elements. We found that cerebral organoids recapitulate most putative cell-type-specific enhancer accessibility patterns but lack many cell-type-specific open chromatin regions that are found in vivo. Systematic comparison of chromatin accessibility across brain regions revealed unexpected diversity among neural progenitor cells in the cerebral cortex and implicated retinoic acid signalling in the specification of neuronal lineage identity in the prefrontal cortex. Together, our results reveal the important contribution of chromatin state to the emerging patterns of cell type diversity and cell fate specification and provide a blueprint for evaluating the fidelity and robustness of cerebral organoids as a model for cortical development.
Analysis of chromatin state at a single-cell level in samples of developing human forebrain demonstrate both cell-type-specific and region-specific changes during neurogenesis.
Journal Article
Astrocyte senescence promotes glutamate toxicity in cortical neurons
Neurodegeneration is a major age-related pathology. Cognitive decline is characteristic of patients with Alzheimer's and related dementias and cancer patients after chemo- or radio-therapies. A recently emerged driver of these and other age-related pathologies is cellular senescence, a cell fate that entails a permanent cell cycle arrest and pro-inflammatory senescence-associated secretory phenotype (SASP). Although there is a link between inflammation and neurodegenerative diseases, there are many open questions regarding how cellular senescence affects neurodegenerative pathologies. Among the various cell types in the brain, astrocytes are the most abundant. Astrocytes have proliferative capacity and are essential for neuron survival. Here, we investigated the phenotype of primary human astrocytes made senescent by X-irradiation, and identified genes encoding glutamate and potassium transporters as specifically downregulated upon senescence. This down regulation led to neuronal cell death in co-culture assays. Unbiased RNA sequencing of transcripts expressed by non-senescent and senescent astrocytes confirmed that glutamate homeostasis pathway declines upon senescence. Our results suggest a key role for cellular senescence, particularly in astrocytes, in excitotoxicity, which may lead to neurodegeneration including Alzheimer's disease and related dementias.
Journal Article
Single-cell reconstruction of developmental trajectories during zebrafish embryogenesis
As embryos develop, numerous cell types with distinct functions and morphologies arise from pluripotent cells. Three research groups have used single-cell RNA sequencing to analyze the transcriptional changes accompanying development of vertebrate embryos (see the Perspective by Harland). Wagner et al. sequenced the transcriptomes of more than 90,000 cells throughout zebrafish development to reveal how cells differentiate during axis patterning, germ layer formation, and early organogenesis. Farrell et al. profiled the transcriptomes of tens of thousands of embryonic cells and applied a computational approach to construct a branching tree describing the transcriptional trajectories that lead to 25 distinct zebrafish cell types. The branching tree revealed how cells change their gene expression as they become more and more specialized. Briggs et al. examined whole frog embryos, spanning zygotic genome activation through early organogenesis, to map cell states and differentiation across all cell lineages over time. These data and approaches pave the way for the comprehensive reconstruction of transcriptional trajectories during development. Science , this issue p. 981 , p. eaar3131 , p. eaar5780 ; see also p. 967 Single-cell RNA sequencing and a computational technique reveal cell trajectories that form the complex body plan of the zebrafish embryo. During embryogenesis, cells acquire distinct fates by transitioning through transcriptional states. To uncover these transcriptional trajectories during zebrafish embryogenesis, we sequenced 38,731 cells and developed URD, a simulated diffusion-based computational reconstruction method. URD identified the trajectories of 25 cell types through early somitogenesis, gene expression along them, and their spatial origin in the blastula. Analysis of Nodal signaling mutants revealed that their transcriptomes were canalized into a subset of wild-type transcriptional trajectories. Some wild-type developmental branch points contained cells that express genes characteristic of multiple fates. These cells appeared to trans-specify from one fate to another. These findings reconstruct the transcriptional trajectories of a vertebrate embryo, highlight the concurrent canalization and plasticity of embryonic specification, and provide a framework with which to reconstruct complex developmental trees from single-cell transcriptomes.
Journal Article
Opportunities and limitations of genetically modified nonhuman primate models for neuroscience research
The recently developed new genome-editing technologies, such as the CRISPR/Cas system, have opened the door for generating genetically modified nonhuman primate (NHP) models for basic neuroscience and brain disorders research. The complex circuit formation and experience-dependent refinement of the human brain are very difficult to model in vitro, and thus require use of in vivo whole-animal models. For many neurodevelopmental and psychiatric disorders, abnormal circuit formation and refinement might be at the center of their pathophysiology. Importantly, many of the critical circuits and regional cell populations implicated in higher human cognitive function and in many psychiatric disorders are not present in lower mammalian brains, while these analogous areas are replicated in NHP brains. Indeed, neuropsychiatric disorders represent a tremendous health and economic burden globally. The emerging field of genetically modified NHP models has the potential to transform our study of higher brain function and dramatically facilitate the development of effective treatment for human brain disorders. In this paper, we discuss the importance of developing such models, the infrastructure and training needed to maximize the impact of such models, and ethical standards required for using these models.
Journal Article
Lattice light-sheet microscopy
Animation defines life, and the three-dimensional (3D) imaging of dynamic biological processes occurring within living specimens is essential to understand life. However, in vivo imaging, especially in 3D, involves inevitable tradeoffs of resolution, speed, and phototoxicity. Chen et al. describe a microscope that can address these concerns. They used a class of nondiffracting beams, known as 2D optical lattices, which spread the excitation energy across the entire field of view while simultaneously eliminating out-of-focus excitation. Lattice light sheets increase the speed of image acquisition and reduce phototoxicity, which expands the range of biological problems that can be investigated. The authors illustrate the power of their approach using 20 distinct biological systems ranging from single-molecule binding kinetics to cell migration and division, immunology, and embryonic development. Science , this issue 10.1126/science.1257998 A new microscope allows three-dimensional imaging of living systems at very high resolution in real time. Although fluorescence microscopy provides a crucial window into the physiology of living specimens, many biological processes are too fragile, are too small, or occur too rapidly to see clearly with existing tools. We crafted ultrathin light sheets from two-dimensional optical lattices that allowed us to image three-dimensional (3D) dynamics for hundreds of volumes, often at subsecond intervals, at the diffraction limit and beyond. We applied this to systems spanning four orders of magnitude in space and time, including the diffusion of single transcription factor molecules in stem cell spheroids, the dynamic instability of mitotic microtubules, the immunological synapse, neutrophil motility in a 3D matrix, and embryogenesis in Caenorhabditis elegans and Drosophila melanogaster . The results provide a visceral reminder of the beauty and the complexity of living systems.
Journal Article
A gp130–Src–YAP module links inflammation to epithelial regeneration
Inflammation promotes regeneration of injured tissues through poorly understood mechanisms, some of which involve interleukin (IL)-6 family members, the expression of which is elevated in many diseases including inflammatory bowel diseases and colorectal cancer. Here we show in mice and human cells that gp130, a co-receptor for IL-6 cytokines, triggers activation of YAP and Notch, transcriptional regulators that control tissue growth and regeneration, independently of the gp130 effector STAT3. Through YAP and Notch, intestinal gp130 signalling stimulates epithelial cell proliferation, causes aberrant differentiation and confers resistance to mucosal erosion. gp130 associates with the related tyrosine kinases Src and Yes, which are activated on receptor engagement to phosphorylate YAP and induce its stabilization and nuclear translocation. This signalling module is strongly activated upon mucosal injury to promote healing and maintain barrier function.
This study demonstrates the activation of a STAT3-independent healing pathway in response to mucosal injury which involves the co-receptor for IL-6 cytokines gp130 and downstream effectors Src, Yes, YAP and Notch.
Beneficial effects of inflammation
As well as activating innate and adaptive immunity, inflammation triggers tissue repair and regeneration through mechanisms that are largely unknown. This study demonstrates the activation of a STAT3-independent healing pathway in a mouse model of experimental colitis through a process involving gp130 (a co-receptor for interleukin-6 family cytokines) and the downstream effectors Src, Yes, YAP and Notch.
Journal Article