Publications by authors named "Maria A Holland"

Cortical folding is a critical process during brain development, resulting in morphologies that are both consistent and distinct between individuals and species. While earlier studies have highlighted important aspects of cortical folding, most existing computational models, based on the differential growth theory, fall short of explaining why folds tend to appear in particular locations. The axon tension hypothesis may provide insight into this conundrum; however, there has been significant controversy about a potential role of axonal tension during the gyrification.

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Across mammalia, brain morphology follows specific scaling patterns. Bigger bodies have bigger brains, with surface area outpacing volume growth, resulting in increased foldedness. We have recently studied scaling rules of cortical thickness, both local and global, finding that the cortical thickness difference between thick gyri and thin sulci also increases with brain size and foldedness.

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Cranial dura mater is a dense interwoven vascularized connective tissue that helps regulate neurocranial remodeling by responding to strains from the growing brain. Previous ex vivo experimentation has failed to account for the role of prestretch in the mechanical behavior of the dura. Here we aim to estimate the prestretch in mouse cranial dura mater and determine its dependency on direction and age.

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Humans are known to have significant and consistent differences in thickness throughout the cortex, with thick outer gyral folds and thin inner sulcal folds. Our previous work has suggested a mechanical basis for this thickness pattern, with the forces generated during cortical folding leading to thick gyri and thin sulci, and shown that cortical thickness varies along a gyral-sulcal spectrum in humans. While other primate species are expected to exhibit similar patterns of cortical thickness, it is currently unknown how these patterns scale across different sizes, forms, and foldedness.

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Brain development involves precisely orchestrated genetic, biochemical, and mechanical events. At the cellular level, neuronal proliferation in the innermost zone of the brain followed by migration towards the outermost layer results in a rapid increase in brain surface area, outpacing the volumetric growth of the brain, and forming the highly folded cortex. This work aims to provide mechanistic insights into the process of brain development and cortical folding using a biomechanical model that couples cell division and migration with volumetric growth.

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Cortical thickness varies throughout the cortex in a systematic way. However, it is challenging to investigate the patterns of cortical thickness due to the intricate geometry of the cortex. The cortex has a folded nature both in radial and tangential directions which forms not only gyri and sulci but also tangential folds and intersections.

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The process of gyrification, by which the brain develops the intricate pattern of gyral hills and sulcal valleys, is the result of interactions between biological and mechanical processes during brain development. Researchers have developed a vast array of computational models in order to investigate cortical folding. This review aims to summarize these studies, focusing on five essential elements of the brain that affect development and gyrification and how they are represented in computational models: (i) the constraints of skull, meninges, and cerebrospinal fluid; (ii) heterogeneity of cortical layers and regions; (iii) anisotropic behavior of subcortical fiber tracts; (iv) material properties of brain tissue; and (v) the complex geometry of the brain.

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Tissues are not stress-free. As we grow, our tissues adapt to different physiological and disease conditions through growth and remodeling. This adaptation occurs at the microscopic scale, where cells control the microstructure of their immediate extracellular environment to achieve homeostasis.

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Cortical folding-the process of forming the characteristic gyri (hills) and sulci (valleys) of the cortex-is a highly dynamic process that results from the interaction between gene expression, cellular mechanisms, and mechanical forces. Like many other cells, neurons are sensitive to their mechanical environment. Because of this, cortical growth may not happen uniformly throughout gyri and sulci after the onset of cortical folding, which is accompanied by patterns of tension and compression in the surrounding tissue.

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The cortical thickness is a characteristic biomarker for a wide variety of neurological disorders. While the structural organization of the cerebral cortex is tightly regulated and evolutionarily preserved, its thickness varies widely between 1.5 and 4.

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Tissue growth and remodeling are known to govern mechanical homeostasis in biological tissue, but their relative contributions to homeostasis remain unclear. Here, we use mechanical models, fueled by experimental findings, to demonstrate that growth and remodeling have different effects on heart valve stretch homeostasis during physiological postnatal development. Two developmental stages were considered: early-stage (from infant to adolescent) and late-stage (from adolescent to adult) development.

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Understanding the characteristic morphology of our brain remains a challenging, yet important task in human evolution, developmental biology, and neurosciences. Mathematical modeling shapes our understanding of cortical folding and provides functional relations between cortical wavelength, thickness, and stiffness. Yet, current mathematical models are phenomenologically isotropic and typically predict non-physiological, periodic folding patterns.

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Many living structures are coated by thin films, which have distinct mechanical properties from the bulk. In particular, these thin layers may grow faster or slower than the inner core. Differential growth creates a balanced interplay between tension and compression and plays a critical role in enhancing structural rigidity.

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Skin is a highly dynamic, autoregulated, living system that responds to mechanical stretch through a net gain in skin surface area. Tissue expansion uses the concept of controlled overstretch to grow extra skin for defect repair in situ. While the short-term mechanics of stretched skin have been studied intensely by testing explanted tissue samples ex vivo, we know very little about the long-term biomechanics and mechanobiology of living skin in vivo.

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