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Y ou could be forgiven for thinking that the turn of the millennium was a golden age for the life sciences. After the halcyon days of the 1950s and ’60s when the structure of DNA, the true nature of genes and the genetic code itself were discovered, the Human Genome Project, launched in 1990 and culminating with a preliminary announcement of the entire genome sequence in 2000, looked like – and was presented as – a comparably dramatic leap forward in our understanding of the basis of life itself. As Bill Clinton put it when the draft sequence was unveiled: ‘Today we are learning the language in which God created life.’ Portentous stuff.

The genome sequence reveals the order in which the chemical building blocks (of which there are four distinct types) that make up our DNA are arranged along the molecule’s double-helical strands. Our genomes each have around 3 billion of these ‘letters’; reading them all is a tremendous challenge, but the Human Genome Project (HGP) transformed genome sequencing within the space of a couple of decades from a very slow and expensive procedure into something you can get done by mail order for the price of a meal for two.

Since that first sequence was unveiled in 2000, hundreds of thousands of human genomes have now been decoded, giving an indication of the person-to-person variation in sequence. This information has provided a vital resource for biomedicine, enabling us, for example, to identify which parts of the genome correlate with which diseases and traits. And all that investment in gene-sequencing technology was more than justified merely by its use for studying and tracking the SARS-CoV-2 virus during the COVID-19 pandemic.

Here we report on the collaboration of Open AI and Retro Biotech using GPT-4b to investigate ways to improve the efficacy of the Yamanaka factors in reprogramming cells.
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Health claims Disclosure: Information provided on this video is not a substitute for direct, individual medical treatment or advice. Please consult with your doctor first. Products or services mentioned in this video are not a recommendation.

Audio Copyright Disclaimer.
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Environmental Gerontology & Vulnerability Science For Health And Well-Being — Dr. Amir Baniassadi, Ph.D. — Marcus Institute for Aging Research, Hebrew SeniorLife / Harvard Medical School.


Dr. Amir Baniassadi, Ph.D. is an Instructor of Medicine at Harvard Medical School and an Assistant Scientist in Marcus Institute for Aging Research (https://www.marcusinstituteforaging.o… where he works on environmental impacts on health and well-being of older populations.

Dr. Baniassadi works on the impacts of ambient air temperature and air quality (both indoors and outdoors) on outcomes related to the health and well-being of physiologically and socioeconomically vulnerable populations. His research applies novel environmental modeling and measurement techniques along with remote and long-term physiological and functional monitoring of individuals to establish relationships between exposure and outcome variables of interest outside clinical lab settings. The ultimate goal of his research is to develop environmental interventions that optimize the environment for health and longevity of older adults.

Dr. Baniassadi has a Ph.D. in Civil, Environmental, and Sustainable Engineering from Arizona State University and a B.Sc. degree in Mechanical Engineering from the University of Tehran. His post-doctoral training includes a three-year T32 fellowship in Translational Research in Older adults, and a two-year postdoctoral fellowship at Harvard University Graduate School of Design.

#AmirBaniassadi #HarvardMedicalSchool #MarcusInstituteForAgingResearch #EnvironmentalGerontology #VulnerabilityScience #Exposome #Health #WellBeing #Wearables #SmartHome #AgingInPlace #Thermoregulation #HeatIslands.

Uniquely human features of neocortical development and maturation are not only intriguing for their implications in human-specific cognitive abilities, but they are also vulnerable to dysregulation which could cause or contribute to distinctly human brain disorder pathophysiology. The human cerebral cortex is essential for both cognition and emotional processing and dysregulation of these processes of the cortex are associated with a wide range of brain disorders including schizophrenia (SZ), autism spectrum disorder (ASD), Parkinson’s disease (PD), and Alzheimer’s disease (AD) (Berman and Weinberger, 1991; Rubenstein, 2011; Xu et al., 2019). Much remains to be learned about the mechanisms governing cortical expansion and responses to pathogenesis between human and non-human primates (NHPs) (Otani et al., 2016). Understanding these differences could shed light on the underlying mechanisms responsible for human-specific brain disorders and lead to the identification of key targets for the development of effective therapies.

Subtle differences observed by comparing human neurodevelopment to that of our closest evolutionary relatives could reveal underlying mechanisms, including genomic or transcriptional differences, contributing to varied phenotypes (Pollen et al., 2019). Human-specific responses to pathogenesis might be elucidated in a similar manner; by comparing brain pathophysiology of humans to our non-human primate counterparts (Hof et al., 2004). Although rodent models have taught us much about basic mammalian brain development and disorders (Fernando and Robbins, 2011), comparing governing processes and responses to species more closely related to humans can reduce the number of variables allowing for the identification of specific mechanisms responsible for observed deviations. Studies analyzing induced pluripotent stem cells (iPSCs) derived from humans, chimpanzees, and bonobos (Pan paniscus) show large sets of differentially expressed genes between human and NHP iPSCs. Perhaps the most compelling differentially expressed genes are those related to increased long interspersed element-1 (LINE-1) mobility in chimpanzees and bonobos, which could have implications on the rates of genetic divergence among species, and alternative mechanisms of pluripotency maintenance in chimpanzees (Marchetto et al., 2013; Gallego Romero et al., 2015). Furthermore, when human and NHP iPSCs were differentiated to neurons, they displayed distinctive migratory patterns at the neural progenitor cell (NPC) stage followed by contrasting morphology and timing of maturation in neurons (Marchetto et al., 2019). Despite the ability of two-dimensional (2D) PSC-derived neural cultures to demonstrate basic organization and transcriptomic changes of early brain development (Yan et al., 2013), while retaining the genetic background of the somatic cells from which they are reprogrammed, they lack the ability to develop complex cytoarchitecture, recapitulate advanced spatiotemporal transcriptomics, and brain region interconnectivity (including migration and axon guidance) of ensuing primate brain development (Soldner and Jaenisch, 2019). Intricate cellular heterogeneity, complex architecture, and interconnectivity of neurodevelopment, in addition to pathogenic responses, could be observed by comparing human and NHP brain tissues; however, ethical concerns and the inaccessibility of pre-and postnatal primate brain tissues limits the feasibility of such studies.

While brain organoids might be a long way from forming or sharing thoughts with us, they could still teach us much about ourselves. Brain organoids are three-dimensional (3D), PSC-derived structures that display complex radial organization of expanding neuroepithelium following embedding in an extracellular matrix like Matrigel and can recapitulate some subsequent processes of neurodevelopment including neurogenesis, gliogenesis, synaptogenesis, heterogenous cytoarchitecture, cell and axon migration, myelination of axons, and spontaneously-active neuronal networks (Lancaster et al., 2013; Bagley et al., 2017; Birey et al., 2017; Quadrato et al., 2017; Xiang et al., 2017; Marton et al., 2019; Shaker et al., 2021). It is likely that all these features of neurodevelopment are governed by some degree of specifies-specific dynamics. Brain organoids can be generated from human and NHP PSCs and, since some pathways regulating neural induction and brain region specification are well conserved in primates, both unguided cerebral organoids and guided brain region specific organoids can be generated (Mora-Bermúdez et al., 2016; Field et al., 2019; Kanton et al., 2019). Additional protocols have been established for the derivation of brain region specific organoids from human PSCs (hPSCs), including dorsal forebrain, ventral forebrain, midbrain, thalamus, basal ganglia, cerebellum, and telencephalic organoids (Muguruma et al., 2015; Sakaguchi et al., 2015; Jo et al., 2016; Bagley et al., 2017; Birey et al., 2017; Watanabe et al., 2017; Xiang et al., 2017, 2019; Qian et al., 2018). With some modifications, these methods could prove to be successful in establishing brain region-specific organoids from a variety of NHP PSC lines allowing for the reproducible comparison of homogeneous, human-specific neurodevelopment and brain disorder pathophysiology in brain regions beyond the cortex.