Several ion–molecule reactions of ionospheric interest have been studied in a drift-tube–mass-spectrometer apparatus for ions of mean energy from thermal energies to ∼ 1 eV. The measured rate coefficients in cubic centimeters/second are N++O2: 5 × 10−10 from 0.039–0.9 eV; N2++O2: 6 × 10−11 at 0.039 eV, decreasing to ∼ 8 × 10−12 at 0.9 eV; O2++NO: 3 × 10−10 from 0.039–1.6 eV; O++CO2: 1 × 10−9 at 0.039 eV, decreasing to 5 × 10−10 cm3/sec at 1.3 eV. The relevance of the first three reactions for the Earth's ionosphere and of the last reaction for the Martian atmosphere is discussed briefly.
Ion–molecule reactions of sodium, potassium, and barium ions with O2, NO, and H2O have been studied in a drift tube–mass spectrometer apparatus. The following rate constants or upper limits were obtained: Na+,K, +, Ba++O2(NO)→products, k < 10−13cm3/sec (0.04 − ∼ 5 eV), Na++H2O+M→Na+·H2O+M, k(3) = 1.0(+ 0.5, − 0.3) × 10−28cm6/secfor M = H2O, k(3) = 4.7(+ 1.2, − 1.0) × 10−30cm6/secfor M = He, K++H2O+M→K+·H2O+M, k(3) = 4.5(+ 2.3, − 1.5) × 10−29cm6/secfor M = H2O, k(3) = 2.6(+ 0.7, − 0.5) × 10−30cm6/secfor M = He. The consequences of these results for the D and E region of the upper atmosphere are briefly described.
T cell-based cellular therapies benefit from a product with reduced differentiation and enhanced oxidative metabolism. Methods to achieve this balance without negatively impacting T cell expansion or impairing T cell function have proven elusive. AMP-activated protein kinase (AMPK) is a cellular energy sensor which promotes mitochondrial health and improves oxidative metabolism. We hypothesized that increasing AMPK activity in human T cells would augment their oxidative capacity, creating an ideal product for adoptive cellular therapies. Lentiviral transduction of the regulatory AMPKγ2 subunit stably enhanced intrinsic AMPK signaling and promoted mitochondrial respiration with increased basal oxygen consumption rates (OCR), higher maximal OCR, and augmented spare respiratory capacity. These changes were accompanied by increased mitochondrial density and elevated expression of proteins involved in mitochondrial fusion. AMPKγ2-transduction also increased T cell glycolytic activity. This combination of metabolic reprogramming enhanced in vitro T cell expansion while promoting memory T cell yield. Finally, when activated under decreasing glucose conditions, AMPKγ2-transduced T cells maintained higher levels of both proliferation and inflammatory cytokine production. Together, these data suggest that augmenting intrinsic AMPK signaling via overexpression of AMPKγ2 can improve the expansion and function of human T cells for subsequent use in adoptive cellular therapies.
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