NASA Ames Institutional Scientific Collection (ISC)

NASA's current human space flight research is directed towards enabling human space exploration beyond Low Earth Orbit (LEO). The Space Flight Payload Projects; Rodent Research, Cell Science, and Microbial Labs, flown on the International Space Station (ISS), benefit both the global life sciences and commercial space communities. Verified data sets, science results, peer-reviewed publications, and returned biospecimens, collected and analyzed for flight and ground investigations, are all part of the knowledge base within NASAs Human Exploration and Operations Mission Directorates Space Life and Physical Sciences Research and Applications (SLPSRA) Division, specifically the Human Research and Space Biology Programs. These data and biospecimens are made available through the public LSDA website. The Ames Institutional Scientific Collection (ISC), or ARC Biobank, stores flight and ground biospecimens from Space Shuttle and ISS programs. These specimens are curated and managed by the Ames Life Sciences Data Archive (ALSDA), an internal node of NASA's Life Sciences Data Archive (LSDA). The ARC Biolbank stores over 15,000 specimens from experiments dating from 1984 to present. Currently available specimens include tissues from the circulatory, digestive, endocrine, excretory, integumentary, muscular, neurosensory, reproductive, respiratory and skeletal systems. The most recent contributions include RNA, DNA and protein extracts from Rodent Research 1 and tissues from Rodent Research 4. NASA's biospecimen collection represents a unique and limited resource. The use of these biospecimens maximizes utilization and scientific return from these unique spaceflight payload and ground control research subjects. These biospecimens are harvested following complex, costly NASA research activities to meet primary scientific objectives. Once the primary scientific objectives have been met, the remaining specimens are made available to provide secondary opportunities for complementary studies or new investigations to broaden research without large expenditures of time or resources. Innovative ways of sharing this information ultimately advances the frontiers of human space exploration as well as scientific understanding of the effects of gravity on life on earth

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

Preliminary Report

this paper we prove the existence of self-similar solutions to the anisotropic curve shortening equatio

Morphological diversification and functional maturation of human astrocytes in glia-enriched cortical organoid transplanted in mouse brain

Astrocytes, the most abundant glial cell type in the brain, are underrepresented in traditional cortical organoid models due to the delayed onset of cortical gliogenesis. Here we introduce a new glia-enriched cortical organoid model that exhibits accelerated astrogliogenesis. We demonstrated that induction of a gliogenic switch in a subset of progenitors enabled the rapid derivation of astroglial cells, which account for 25-31% of the cell population within 8-10 weeks of differentiation. Intracerebral transplantation of these organoids reliably generated a diverse repertoire of cortical neurons and anatomical subclasses of human astrocytes. Spatial transcriptome profiling identified layer-specific expression patterns among distinct subclasses of astrocytes within organoid transplants. Using an in vivo acute neuroinflammation model, we identified a subpopulation of astrocytes that rapidly activates pro-inflammatory pathways upon cytokine stimulation. Additionally, we demonstrated that CD38 signaling has a crucial role in mediating metabolic and mitochondrial stress in reactive astrocytes. This model provides a robust platform for investigating human astrocyte function

NGLY1 mutations cause protein aggregation in human neurons.

Biallelic mutations in the gene that encodes the enzyme N-glycanase 1 (NGLY1) cause a rare disease with multi-symptomatic features including developmental delay, intellectual disability, neuropathy, and seizures. NGLY1s activity in human neural cells is currently not well understood. To understand how NGLY1 gene loss leads to the specific phenotypes of NGLY1 deficiency, we employed direct conversion of NGLY1 patient-derived induced pluripotent stem cells (iPSCs) to functional cortical neurons. Transcriptomic, proteomic, and functional studies of iPSC-derived neurons lacking NGLY1 function revealed several major cellular processes that were altered, including protein aggregate-clearing functionality, mitochondrial homeostasis, and synaptic dysfunctions. These phenotypes were rescued by introduction of a functional NGLY1 gene and were observed in iPSC-derived mature neurons but not astrocytes. Finally, laser capture microscopy followed by mass spectrometry provided detailed characterization of the composition of protein aggregates specific to NGLY1-deficient neurons. Future studies will harness this knowledge for therapeutic development

NGLY1 mutations cause protein aggregation in human neurons

Summary: Biallelic mutations in the gene that encodes the enzyme N-glycanase 1 (NGLY1) cause a rare disease with multi-symptomatic features including developmental delay, intellectual disability, neuropathy, and seizures. NGLY1’s activity in human neural cells is currently not well understood. To understand how NGLY1 gene loss leads to the specific phenotypes of NGLY1 deficiency, we employed direct conversion of NGLY1 patient-derived induced pluripotent stem cells (iPSCs) to functional cortical neurons. Transcriptomic, proteomic, and functional studies of iPSC-derived neurons lacking NGLY1 function revealed several major cellular processes that were altered, including protein aggregate-clearing functionality, mitochondrial homeostasis, and synaptic dysfunctions. These phenotypes were rescued by introduction of a functional NGLY1 gene and were observed in iPSC-derived mature neurons but not astrocytes. Finally, laser capture microscopy followed by mass spectrometry provided detailed characterization of the composition of protein aggregates specific to NGLY1-deficient neurons. Future studies will harness this knowledge for therapeutic development

Innovators And Instigators: Feminist Contributions To American Abortion Technology, 1963-1973

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