Aerospace medicine and biology: A continuing bibliography with indexes (supplement 355)

This bibliography lists 147 reports, articles and other documents introduced into the NASA Scientific and Technical Information System during October, 1991. Subject coverage includes: aerospace medicine and psychology, life support systems and controlled environments, safety equipment, exobiology and extraterrestrial life, and flight crew behavior and performance

Closure of Loop-Mediated Isothermal Amplification Chamber on Lab-On-Chip Using Thermal-Responsive Valve

Point-of-care tests for nucleic acids are important for the diagnosis and management of infectious and genetic diseases, biowarfare agents, and for drug research. Recent integration of loop-mediated isothermal amplification (LAMP) onto a lab-on-chip (LOC) platform allows sensitive and specific, detection of target DNA or RNA sequences for point-of-care (POC) applications. However, because of the high risk of contamination to LAMP products, robust and simple methods of hermetically sealing the reaction chamber are essential. In addition, having a method for isolation of nucleic acids at the level of the chip is more effective for POC applications because a laboratory setting is not required to complete the analysis. This report describes an integrated, polymer-based cassette which was designed for detection of DNA/RNA target-sequences by using LAMP and a solid-state nucleic acid purification membrane. The LAMP chamber seals using a self-actuated thermalresponsive valve made from expandable microspheres suspended in Polydimethylsiloxane (PDMS). A flow-through, Flinders Technology Associates membrane (Whatman FT A®) was installed on the cassette with the expectation of providing isolation and purification of nucleic acids. The cassette was designed, fabricated and the efficacy of the valve to seal the LAMP chamber was investigated. The valve underwent expansion and held pressures of233 +/- 5.0 kPa without signs of leakage. A portable, battery-powered, polyimide-based thin film heater, placed outside the cassette, provided thermal control. In addition, a LAMP primer set was designed for the serotonin receptor 5HTRIA promoter gene using Primer Explorer V 4 software (http:/ /primerexplorer.jp/elamp4.0.0/index.html) for LAMP detection of neurotransmitter serotonin. The integrated, portable LAMP cassette will be attractive in global health-care challenges, mainly in resource-poor locations, where the availability of laboratory equipment and/or trained personal is restricted.Digitized from a paper copy provided by the Physiological Sciences Graduate Interdisciplinary Program

Technology 2001: The Second National Technology Transfer Conference and Exposition, volume 2

Proceedings of the workshop are presented. The mission of the conference was to transfer advanced technologies developed by the Federal government, its contractors, and other high-tech organizations to U.S. industries for their use in developing new or improved products and processes. Volume two presents papers on the following topics: materials science, robotics, test and measurement, advanced manufacturing, artificial intelligence, biotechnology, electronics, and software engineering

Characterization of an aryl hydrocarbon receptor from a cetacean : an approach for assessing contaminant susceptibility in protected species

Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy at the Massachusetts Institute of Technology and the Woods Hole Oceanographic Institution September 2000Some cetaceans bioaccumulate substantial concentrations of halogenated aromatic hydrocarbons (HAH) in their tissues, but little is known about the effects of such burdens on cetacean health. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related HAH cause toxicity via activation of the aryl hydrocarbon receptor (AHR), a member of the bHLH-PAS family of transcription factors. Differences in AHR structure and function are known to contribute to species-specific differences in susceptibility to HAH toxicity, and targets for HAH toxicity are related to the tissue-specific expression of AHR. The goal of these studies was to ascertain the potential for HAH effects in cetaceans by characterizing the AHR from the beluga, Delphinapterus leucas. The beluga AHR was characterized by its molecular structure, capacity for ligand binding, structure-binding relationships with various classes of HAH, as well as tissue-specific expression. These results show that: 1) in an in vitro system, the beluga AHR possesses binding affinities similar to AHRs of other mammals that are considered sensitive to toxic effects of HAH, 2) Structure-activity relationships are consistent with a common mechanism of coplanar HAH action among cetaceans and rodent species, and 3) the AHR protein is expressed in many tissues of the beluga, and is present at high levels in lymphoid organs, liver and lung. Together, these data suggest that cetaceans can be considered sensitive to the action of coplanar HAH. Further, using in vitro expressed proteins is a promising approach for addressing molecular and biochemical questions about PHAH toxicity in endangered and protected species where logistical and ethical concerns preclude testing in live animals.This work was supported by NIH Grant No. ES06272, NOAA National Sea Grant College Program Grant Nos. NA46RG0470, (WHO! Sea Grant Project No. R/B-137), NA86RG0075 (WHO! Sea Grant Project No. R/B-15l), NA86RG0075 (WHOI Sea Grant Project No. R/P-64) and the Ocean Ventures Fund

Cumulative index to NASA Tech Briefs, 1986-1990, volumes 10-14

Tech Briefs are short announcements of new technology derived from the R&D activities of the National Aeronautics and Space Administration. These briefs emphasize information considered likely to be transferrable across industrial, regional, or disciplinary lines and are issued to encourage commercial application. This cumulative index of Tech Briefs contains abstracts and four indexes (subject, personal author, originating center, and Tech Brief number) and covers the period 1986 to 1990. The abstract section is organized by the following subject categories: electronic components and circuits, electronic systems, physical sciences, materials, computer programs, life sciences, mechanics, machinery, fabrication technology, and mathematics and information sciences

RGS14 (414)-mediated prevention of an episodic memory loss: a study of molecular mechanism

A large proportion of human populations suffer memory impairments either caused by normal aging or afflicted by diverse neurological and neurodegenerative diseases. Memory enhancers and other drugs tested so far against memory loss have failed to produce therapeutic efficacy in clinical trials and thus, there is a need to find remedy for this mental disorder. In search for cure of memory loss, our laboratory discovered a robust memory enhancer called RGS14(414). A treatment in brain with its gene produces an enduring effect on memory that lasts for lifetime of rats. Therefore, current thesis work was designed to investigate whether RGS14(414) treatment can prevent memory loss and furthermore, explore through biological processes responsible for RGS-mediated memory enhancement. We found that RGS14(414) gene treatment prevented episodic memory loss in rodent models of normal aging and Alzheimer´s disease. A memory loss was observed in normal rats at 18 months of age; however, when they were treated with RGS14(414) gene at 3 months of age, they abrogated this deficit and their memory remained intact till the age of 22 months. In addition to normal aging rats, effect of memory enhancer treatment in mice model of Alzheimer´s disease (AD-mice) produced a similar effect. AD-mice subjected to treatment with RGS14(414) gene at the age of 2 months, a period when memory was intact, showed not only a prevention in memory loss observed at 4 months of age but also they were able to maintain normal memory after 6 months of the treatment. We posit that long-lasting effect on memory enhancement and prevention of memory loss mediated through RGS14(414) might be due to a permanent structural change caused by a surge in neuronal connections and enhanced neuronal remodeling, key processes for long-term memory formation. A neuronal arborization analysis of both pyramidal and non-pyramidal neurons in brain of RGS14(414)-treated rats exhibited robust rise in neurites outgrowth of both kind of cells, and an increment in number of branching from the apical dendrite of pyramidal neurons, reaching to almost three times of the control animals. To further understand of underlying mechanism by which RGS14(414) induces neuronal arborization, we investigated into neurotrophic factors. We observed that RGS14 treatment induces a selective increase in BDNF. Role of BDNF in neuronal arborization, as well as its implication in learning and memory processes is well described. In addition, our results showing a dynamic expression pattern of BDNF during ORM processing that overlapped with memory consolidation further support the idea of the implication of this neurotrophin in formation of long-term memory in RGS-animals. On the other hand, in studies of expression profiling of RGS-treated animals, we have demonstrated that 14-3-3ζ protein displays a coherent relationship to RGS-mediated ORM enhancement. Recent studies have demonstrated that the interaction of receptor for activated protein kinase 1 (RACK1) with 14-3-3ζ is essential for its nuclear translocation, where RACK1-14-3-3ζ complex binds at promotor IV region of BDNF and promotes an increase in BDNF gene transcription. These observations suggest that 14-3-3ζ might regulate the elevated level of BDNF seen in RGS14(414) gene treated animals. Therefore, it seems that RGS-mediated surge in 14-3-3ζ causes elevated BDNF synthesis needed for neuronal arborization and enhanced ORM. The prevention of memory loss might be mediated through a restoration in BDNF and 14-3-3ζ protein levels, which are significantly decreased in aging and Alzheimer’s disease. Additionally, our results demonstrate that RGS14(414) treatment could be a viable strategy against episodic memory loss