Classical Physics and Quantum Loops

The standard picture of the loop expansion associates a factor of h-bar with each loop, suggesting that the tree diagrams are to be associated with classical physics, while loop effects are quantum mechanical in nature. We discuss examples wherein classical effects arise from loop contributions and display the relationship between the classical terms and the long range effects of massless particles.Comment: 15 pages, 3 figure

Quantum Opacity, the RHIC HBT Puzzle, and the Chiral Phase Transition

We present a relativistic quantum mechanical treatment of opacity and refractive effects that allows reproduction of observables measured in two-pion (HBT) interferometry and pion spectra at RHIC. The inferred emission duration is substantial. The results are consistent with the emission of pions from a system that has a restored chiral symmetry.Comment: 4 pages, 2 figures. This version mentions shows the STAR 200 GeV data, and includes some technical improvements. The agreement with experiment is improved slightly, and the parameters of the model are changed slightl

Prospectus, March 16, 1992

https://spark.parkland.edu/prospectus_1992/1007/thumbnail.jp

Loss of glutathione homeostasis associated with neuronal senescence facilitates TRPM2 channel activation in cultured hippocampal pyramidal neurons

<p>Abstract</p> <p>Background</p> <p>Glutathione (GSH) plays an important role in neuronal oxidant defence. Depletion of cellular GSH is observed in neurodegenerative diseases and thereby contributes to the associated oxidative stress and Ca²⁺dysregulation. Whether depletion of cellular GSH, associated with neuronal senescence, directly influences Ca²⁺permeation pathways is not known. Transient receptor potential melastatin type 2 (TRPM2) is a Ca²⁺permeable non-selective cation channel expressed in several cell types including hippocampal pyramidal neurons. Moreover, activation of TRPM2 during oxidative stress has been linked to cell death. Importantly, GSH has been reported to inhibit TRPM2 channels, suggesting they may directly contribute to Ca²⁺dysregulation associated with neuronal senescence. Herein, we explore the relation between cellular GSH and TRPM2 channel activity in long-term cultures of hippocampal neurons.</p> <p>Results</p> <p>In whole-cell voltage-clamp recordings, we observe that TRPM2 current density increases in cultured pyramidal neurons over time in vitro. The observed increase in current density was prevented by treatment with NAC, a precursor to GSH synthesis. Conversely, treatment of cultures maintained for 2 weeks in vitro with L-BSO, which depletes GSH by inhibiting its synthesis, augments TRPM2 currents. Additionally, we demonstrate that GSH inhibits TRPM2 currents through a thiol-independent mechanism, and produces a 3.5-fold shift in the dose-response curve generated by ADPR, the intracellular agonist for TRPM2.</p> <p>Conclusion</p> <p>These results indicate that GSH plays a physiologically relevant role in the regulation of TRPM2 currents in hippocampal pyramidal neurons. This interaction may play an important role in aging and neurological diseases associated with depletion of GSH.</p

On “historical unity” of Russian and Ukrainian: A linguistic perspective on language conflict and change

This paper focuses on Putin’s (2021) misguided claim regarding “historical [linguistic] unity” of Russian and Ukrainian. Their being two distinct languages is not in question, as opposed (for example) to Serbian and Croatian. However, it is important to substantiate the objective reality of those differences, taking a strong stand against unjustified claims about linguistic [unity] where there are no grounds for them. Implementing a Python-coded algorithm, like those described in Nerbonne & Kretzschmar 2013, we calculate Levenshtein distance between frequency-based word lists, in a manner sensitive to both organic and contact-induced change, to fully reveal Ukrainian’s complex relationship with both Russian and Polish

Dependence of NMDA/GSK-3β Mediated Metaplasticity on TRPM2 Channels at Hippocampal CA3-CA1 Synapses

Transient receptor potential melastatin 2 (TRPM2) is a calcium permeable non-selective cation channel that functions as a sensor of cellular redox status. Highly expressed within the CNS, we have previously demonstrated the functional expression of these channels in CA1 pyramidal neurons of the hippocampus. Although implicated in oxidative stress-induced neuronal cell death, and potentially in neurodegenerative disease, the physiological role of TRPM2 in the central nervous system is unknown. Interestingly, we have shown that the activation of these channels may be sensitized by co-incident NMDA receptor activation, suggesting a potential contribution of TRPM2 to synaptic transmission. Using hippocampal cultures and slices from TRPM2 null mice we demonstrate that the loss of these channels selectively impairs NMDAR-dependent long-term depression (LTD) while sparing long-term potentiation. Impaired LTD resulted from an inhibition of GSK-3β, through increased phosphorylation, and a reduction in the expression of PSD95 and AMPARs. Notably, LTD could be rescued in TRPM2 null mice by recruitment of GSK-3β signaling following dopamine D2 receptor stimulation. We propose that TRPM2 channels play a key role in hippocampal synaptic plasticity