Significant changes have occurred in the anthropogenic emissions of many compounds related to the Kyoto and Montreal Protocols within the past 20 years and many of their atmospheric abundances have responded dramatically. Additionally, there are a number of related natural compounds with underdetermined source or sink budgets. A new instrument, Medusa, was developed to make the high frequency in situ measurements required for the determination of the atmospheric lifetimes and emissions of these compounds. This automated system measures a wide range of halocarbons, hydrocarbons, and sulfur compounds involved in ozone depletion and/or climate forcing, from the very volatile perfluorocarbons (PFCs, e.g., CF(4) and CH(3)CF(3)) and hydrofluorocarbons (HFCs, e.g., CH(3)CF(3)) to the higher-boiling point solvents (such as CH(3)Cl(3) and CCl(2)=CCl(2)) and CHBr(3). A network of Medusa systems worldwide provides 12 in situ ambient air measurements per day of more than 38 compounds of part per trillion mole fractions and precisions up to 0.1% RSD at the five remote field stations operated by the Advanced Global Atmospheric Gases Experiment (AGAGE). This custom system couples gas chromatography/mass spectrometry (GC/MSD) with a novel scheme for cryogen-free low-temperature preconcentration (-165 degrees C) of analytes from 2 L samples in a two-trap process using HayeSep D adsorbent.
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http://dx.doi.org/10.1021/ac702084k | DOI Listing |
Biosens Bioelectron
December 2024
Shenzhen Bay Laboratory, Shenzhen, 518132, China. Electronic address:
Here, we developed nanobody-assisted nanoluciferase fragment complementation for in situ measurement and visualization of endogenous protein-protein interaction (NanaPPI). When an interaction occurs, primary antibodies for two proteins bring the proximity of secondary nanobody-fused small/large fragment to reassemble into an intact NanoLuc variant, thus transforming interaction events to luminescent signals in situ with high sensitivity. Compared to proximity ligation assay, NanaPPI has a similar signal-to-background ratio, but it is more convenient with faster procedures, easier readout and lower cost.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Background: Emerging evidence support the notion that loss of splicing repression by TDP-43, an RNA binding protein that was first implicated in ALS-FTD, underlies their pathogenesis. Previously, we showed that delivery of an AAV9 vector at early postnatal day expressing a fusion protein, termed CTR comprised of the N-terminal region of TDP-43 and an unrelated splicing repressor termed RAVER1 complemented the loss of TDP-43 in mice lacking TDP-43 in spinal motor neurons (ChAT-IRES-Cre;tardbp mice). To translate this potential therapeutic strategy to the clinic, it will be important to demonstrate benefit of such AAV delivery of CTR to motor neurons in adult mice.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Emory University School of Medicine, Atlanta, GA, USA.
Background: Circular RNA represents a distinctive form of noncoding RNA resulting from back-splicing of exons and introns in mRNA. CircRNA has been shown play important roles in neurological diseases, such as Alzheimer's disease (AD). Some recent studies also have demonstrated circRNA is enriched in the mammal brain and differentially altered during AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: A case study on a PSEN1 (E280A) carrier with APOECh (R136S) mutation revealed changes in APOE protein function led to a protective effect on AD outcomes. Notably, there is an intriguing disparity between the two hallmark pathologies: a reduction in tauopathy but no change in plaque burden. Given that the APOE protein is predominantly produced by astrocytes and activated microglia, and the APOE gene is among the disease-associated microglia (DAM) genes, it is conceivable that the variance in pathological outcomes may be rooted in the glial response.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Sanders-Brown Center on Aging, Lexington, KY, USA.
Background: Compared to the 'neutral' E3, the E4 allele of Apolipoprotein E (APOE) confers up to a 15-fold increase in Alzheimer's Disease (AD) risk. Conversely, the neuroprotective E2 allele decreases AD risk by a similar degree. Here, we aimed to assess the therapeutic potential of cell-type specific allelic 'switching' by investigating the physiological and neuropathological changes associated with an inducible, in vivo APOE4 to APOE2 transition in astrocytes using a novel transgenic mouse model METHOD: The APOE "switch mouse" (APOE4s2) uses the Cre-loxP system to allow for inducible APOE allele switching from E4 to E2.
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