Magnetosphere-Ionosphere-Thermosphere Coupling Study at Jupiter Based on Juno's First 30 Orbits and Modeling Tools.

The dynamics of the Jovian magnetosphere is controlled by the interplay of the planet's fast rotation, its solar-wind interaction and its main plasma source at the Io torus, mediated by coupling processes involving its magnetosphere, ionosphere, and thermosphere. At the ionospheric level, these processes can be characterized by a set of parameters including conductances, field-aligned currents, horizontal currents, electric fields, transport of charged particles along field lines including the fluxes of electrons precipitating into the upper atmosphere which trigger auroral emissions, and the particle and Joule heating power dissipation rates into the upper atmosphere. Determination of these key parameters makes it possible to estimate the net transfer of momentum and energy between Jovian upper atmosphere and equatorial magnetosphere. A method based on a combined use of Juno multi-instrument data and three modeling tools was developed by Wang et al. (2021, https://doi.org/10.1029/2021ja029469) and applied to an analysis of the first nine orbits to retrieve these parameters along Juno's magnetic footprint. We extend this method to the first 30 Juno science orbits and to both hemispheres. Our results reveal a large variability of these parameters from orbit to orbit and between the two hemispheres. They also show dominant trends. Southern current systems are consistent with the generation of a region of sub-corotating ionospheric plasma flows, while both super-corotating and sub-corotating plasma flows are found in the north. These results are discussed in light of the previous space and ground-based observations and currently available models of plasma convection and current systems, and their implications are assessed.

Comparison of Multiplate, Platelet Function Analyzer-200, and Plateletworks in Healthy Dogs Treated with Aspirin and Clopidogrel.

BACKGROUND: Platelet function testing may be warranted to assess response to aspirin and clopidogrel. HYPOTHESIS/OBJECTIVES: To evaluate the effects of aspirin, clopidogrel, or combination therapy using 3 platelet function tests: Multiplate Analyzer (MP), Platelet Function Analyzer-200 (PFA), and Plateletworks (PW). ANIMALS: Six healthy laboratory Beagles. METHODS: Randomized double-blind placebo-controlled study (crossover design). Dogs were given aspirin 1 mg/kg, clopidogrel 2 mg/kg, or combination therapy for 1 week each, with a washout period of 2 weeks. Platelet function was assessed on days 0 and 7 of each phase using MP (adenosine diphosphate [ADP], arachidonic acid [AA], collagen [COL] agonists), PFA (P2Y, COL-ADP [CADP], COL-Epinephrine [CEPI] cartridges), and PW (ADP, AA, COL agonists). Platelet counts were obtained with impedance and optical counters. RESULTS: For MP, mean aggregation was decreased for COL and AA with combination therapy and for ADP with all treatments. For PFA, mean CT was increased for the CEPI cartridge with aspirin; and for the P2Y and CADP cartridges with clopidogrel or combination therapy. More dogs receiving clopidogrel showed an increase in PFA CT using the P2Y than the CADP cartridge. For PW, mean aggregation was decreased for AA with all treatments; for ADP with clopidogrel or combination therapy; and for COL with clopidogrel. The PW results with the 2 hematology counters showed almost perfect agreement. CONCLUSION AND CLINICAL IMPORTANCE: All platelet function tests detected treatment effects in some dogs and may have utility for monitoring therapy.

Cloning and analysis of two new isoforms of multifunctional Ca2+/calmodulin-dependent protein kinase. Expression in multiple human tissues.

Multifunctional Ca2+/calmodulin-dependent protein kinase (CaM kinase) is a mediator of calcium signals in diverse signaling pathways. In human lymphocytes and epithelial tissues, CaM kinase activates a chloride channel via a Ca(2+)-dependent pathway which is preserved in cystic fibrosis. To characterize the CaM kinase present in these tissues we have cloned an isoform of this kinase from human T lymphocytes. We show the cDNA structure of two variants of this human CaM kinase, gamma B and gamma C, which are predicted to translate to 518 and 495 amino acids, respectively. Amino acid differences between these isoforms and the rat brain gamma isoform (which we refer to as gamma A) are localized to the variable domain. We used RNase protection of this variable region to reveal the level of expression of gamma B and gamma C CaM kinase mRNAs in nine human tissues and cell lines. When transfected into Jurkat T cells, the gamma B cDNA encoded a functional kinase which cosedimented on sucrose gradients with endogenous T cell CaM kinase activity and formed a large multimeric enzyme. The recombinant gamma B isoform displayed two phases of autophosphorylation characteristic of CaM kinases, including the phase which converts it to a partially Ca(2+)-independent species. Site-directed mutagenesis of the predicted autoinhibitory domain yielded a mutant which was approximately 37% active in the absence of Ca2+/calmodulin, confirming the region as critical for autoregulation, and suggesting this mutant as a tool for studying the role of CaM kinase in nonneuronal tissues.

Cataloging altered gene expression in young and senescent cells using enhanced differential display.

Recently, a novel PCR-based technique, differential display (DD), has facilitated the study of differentially expressed genes at the mRNA level. We report here an improved version of DD, which we call Enhanced Differential Display (EDD). We have modified the technique to enhance reproducibility and to facilitate sequencing and cloning. Using EDD, we have generated and verified a catalog of genes that are differentially expressed between young and senescent human diploid fibroblasts (HDF). From 168 genetags that were identified initially, 84 could be sequenced directly from PCR amplified bands. These sequences represent 27 known genes and 37 novel genes. By Northern blot analysis we have confirmed the differential expression of a total of 23 genes (12 known, 11 novel), while 19 (seven known, 12 novel) did not show differential expression. Several of the known genes were previously observed by others to be differentially expressed between young and senescent fibroblasts, thereby validating the technique.