Topological signature for periodic motion recognition

In this paper, we present an algorithm that computes the topological signature for a given periodic motion sequence. Such signature consists of a vector obtained by persistent homology which captures the topological and geometric changes of the object that models the motion. Two topological signatures are compared simply by the angle between the corresponding vectors. With respect to gait recognition, we have tested our method using only the lowest fourth part of the body's silhouette. In this way, the impact of variations in the upper part of the body, which are very frequent in real scenarios, decreases considerably. We have also tested our method using other periodic motions such as running or jumping. Finally, we formally prove that our method is robust to small perturbations in the input data and does not depend on the number of periods contained in the periodic motion sequence.Comment: arXiv admin note: substantial text overlap with arXiv:1707.0698

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Blood-based protein mediators of senility with replications across biofluids and cohorts

Dementia severity can be quantitatively described by the latent dementia phenotype 'δ' and its various composite 'homologues'. We have explored δ's blood-based protein biomarkers in the Texas Alzheimer's Research and Care Consortium. However, it would be convenient to replicate them in the Alzheimer's Disease Neuroimaging Initiative. To that end, we have engineered a δ homologue from the observed cognitive performance measures common to both projects [i.e. 'd:Texas Alzheimer's Research and Care Consortium to Alzheimer's Disease Neuroimaging Initiative' (dT2A)]. In this analysis, we confirm 13/22 serum proteins as partial mediators of age's effect on dementia severity as measured by dT2A in the Texas Alzheimer's Research and Care Consortium and then replicate 4/13 in the Alzheimer's Disease Neuroimaging Initiative's plasma data. The replicated mediators of age-specific effects on dementia severity are adiponectin, follicle-stimulating hormone, pancreatic polypeptide and resistin. In their aggregate, the 13 confirmed age-specific mediators suggest that 'cognitive frailty' pays a role in dementia severity as measured by δ. We provide both discriminant and concordant support for that hypothesis. Weight, calculated low-density lipoprotein and body mass index are partial mediators of age's effect in the Texas Alzheimer's Research and Care Consortium. Biomarkers related to other disease processes (e.g. cerebrospinal fluid Alzheimer's disease-specific biomarkers in the Alzheimer's Disease Neuroimaging Initiative) are not. It now appears that dementia severity is the sum of multiple independent processes impacting δ. Each may have a unique set of mediating biomarkers. Age's unique effect appears to be at least partially mediated through proteins related to frailty. Age-specific mediation effects can be replicated across cohorts and biofluids. These proteins may offer targets for the remediation of age-specific cognitive decline (aka 'senility'), help distinguish it from other determinants of dementia severity and/or provide clues to the biology of Aging Proper