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The causal association between cardiovascular proteins and diabetic nephropathy: a Mendelian randomization study.
Int Urol Nephrol
January 2025
Department of Nephrology, Jiangxi Medical College, The Second Affiliated Hospital, Nanchang University, Nanchang, Jiangxi, China.
Purpose: To clarify the causal association between cardiovascular proteins and diabetic nephropathy (DN) in Europeans.
Methods: The large genome-wide association study data of cardiovascular proteins and DN were used for this two-sample Mendelian randomization (MR) analysis. We took the Inverse variance weighted (IVW) as the primary method.
Robust differentiation and potent immunomodulation of human mesenchymal stromal cells cultured with a xeno-free GMP protein supplement.
Cytotherapy
January 2025
Institute for Bioengineering of Catalonia (IBEC), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. Electronic address:
Background/aims: Human mesenchymal stromal cells (hMSC) are multipotent adult cells commonly used in regenerative medicine as advanced therapy medicinal products. The expansion of these cells in xeno-free supplements is highly encouraged by regulatory agencies due to safety concerns. However, the number of supplements with robust performance and consistency for hMSC expansion are limited.
View Article and Find Full Text PDFSpin-Orbit Coupling and Admixture Coefficients in SA-CASSCF and MS-CASPT2, and Triplet Excitation Yield Simulated via Trajectory Surface Hopping and Calibrated SA-CASSCF in 1,2-Dioxetane Derivatives.
J Phys Chem A
January 2025
Department of Chemistry and Supercomputing Institute, University of Minnesota, Minneapolis, Minnesota 55455-0431, United States.
The energy gaps, spin-orbit coupling (SOC), and admixture coefficients over a series of the configurations are evaluated by the SA-CASSCF/6-31G, SA-CASSCF/6-31G*, SA-CASSCF/ANO-RCC-VDZP, and MS-CASPT2/ANO-RCC-VDZP to reveal the extent of the inaccuracy of the SA-CASSCF. By comparing the mean absolute errors for the energy gaps and the admixture coefficient magnitudes (ACMs) measured between the SA-CASSCF/6-31G, SA-CASSCF/6-31G*, or SA-CASSCF/ANO-RCC-VDZP and the MS-CASPT2/ANO-RCC-VDZP, the SA-CASSCF/6-31G is selected as the electronic structure method in the nonadiabatic molecular dynamics simulation. The major components of the ACMs of the SA-CASSCF/6-31G and MS-CASPT2/ANO-RCC-VDZP are identified and compared; we find that the ACMs are underestimated by the SA-CASSCF/6-31G, which is verified by the reasonable triplet quantum yield simulated by the trajectory surface hopping and the calibrated SA-CASSCF/6-31G.
View Article and Find Full Text PDFSigma1 inhibitor suppression of adaptive immune resistance mechanisms mediated by cancer cell derived extracellular vesicles.
Cancer Biol Ther
December 2025
Department of Pharmacology, Physiology, and Cancer Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Adaptive immune resistance in cancer describes the various mechanisms by which tumors adapt to evade anti-tumor immune responses. IFN-γ induction of programmed death-ligand 1 (PD-L1) was the first defined and validated adaptive immune resistance mechanism. The endoplasmic reticulum (ER) is central to adaptive immune resistance as immune modulatory secreted and integral membrane proteins are dependent on ER.
View Article and Find Full Text PDFMetabolic adaptations to acute glucose uptake inhibition converge upon mitochondrial respiration for leukemia cell survival.
Cell Commun Signal
January 2025
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA.
One hallmark of cancer is the upregulation and dependency on glucose metabolism to fuel macromolecule biosynthesis and rapid proliferation. Despite significant pre-clinical effort to exploit this pathway, additional mechanistic insights are necessary to prioritize the diversity of metabolic adaptations upon acute loss of glucose metabolism. Here, we investigated a potent small molecule inhibitor to Class I glucose transporters, KL-11743, using glycolytic leukemia cell lines and patient-based model systems.
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