Joe Rogan Experience #2255 - Mark Zuckerberg

https://epublications.marquette.edu/zuckerberg_files_videos/1455/thumbnail.jp

Role for Astrocytes in Complex Cognition: An Evolutionary, Behavioral and Computational Perspective

The human brain has more computational power than modern supercomputers by utilizing only a few signaling systems, rendering it the most efficient computational device ever created. Evolution, though not prospective, has iteratively constructed neural networks of increasing complexity that have ultimately endowed humans with extraordinary cognitive abilities. Through an evolutionary lens, there is a clear correlation between organismal sophistication and network signaling complexity Astrocytes, a non-neuronal cell that makes up approximately half the cells in the human brain, show dramatic increases in morphological and signaling complexity in higher-order species. This co-evolution is likely not coincidental but rather represents the development of sophisticated communication hubs that enhance network computation. Notably, system xc- (Sxc), a cystine-glutamate antiporter expressed predominantly on astrocytes, appears almost exclusively in vertebrate species. Additionally, the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) signaling system experienced rapid functional enhancement in early mammals. These parallel evolutionary trends in signaling complexity warrant investigation into potential mechanistic connections between these network-enhancing developments. In this dissertation, I employ an interdisciplinary approach integrating molecular evolution, neuroscience, and computational engineering to uncover astrocytic involvement in higher-order cognition. I demonstrate that the neuropeptide PACAP attenuates drug-seeking behavior through pathway- and cell-specific mechanisms, revealing Sxc as a critical regulatory mediator for PACAP-induced recruitment of astrocytes within glutamate signaling networks. To understand the specific role that Sxc plays in controlling drug-seeking, I dissect this complex behavior into its constitutive parts, categorizing them as evolutionarily conserved and phylogenetic recent cognitive functions. These findings suggest that Sxc plays a discrete role in behaviors requisite of complex cognitive signaling and displays a temporal-specific reliance in learning acquisition but not maintenance. Based on these findings, I propose a novel hypothesis for cognitive evolution: coordinated co-evolution of molecular proteins within glutamate signaling networks drove the expansion of cognitive complexity. Collectively, this work introduces a paradigm-shifting approach for understanding network communication with transformative implications for both molecular medicine and artificial intelligence

Peroxi-Electrocoagulation for PFAS Mitigation: The Impact of Water Quality and Dissolved Organic Matter on Removal Pathways

The recent addition of per- and polyfluoroalkyl substances (PFAS) to the National Primary Drinking Water Regulation per- has increased the need for research on PFAS treatment technologies for water and wastewater. Electrochemical treatment processes have been widely investigated for PFAS removal. Peroxi-electrocoagulation (electrocoagulation paired with hydrogen peroxide (EC:H2O2)) was evaluated as a novel water treatment process for PFAS mitigation due to the multimechanistic removal pathways that can proceed during treatment, including chemical degradation via oxidation, and physical separation pathways such as sorption to flocs, flotation layer accumulation, and foam fractionation. This work investigated the impacts of varying water quality conditions and dissolved organic matter (DOM) composition on PFAS mitigation efficacy and the corresponding removal pathways. Sources of DOM were an additional point of focus to provide insight into the role of DOM characteristics (i.e., aromaticity, molecular weight) on the fate of PFAS in EC:H2O2. This aim was studied by conducting EC:H2O2 with five different types of DOM (including humic acid, fulvic acid, oxalic acid, salicylic acid, and one natural river DOM). EC:H2O2 was effective as a PFAS mitigation technology using a bicarbonate electrolyte matrix and different types of DOM (including reference DOM and natural DOM). Generally, PFAS removal was higher at pH 3 compared to pH 6.3, ostensibly due to enhanced oxidant yield, interactions between iron and PFAS, and foam formation. At pH 3, oxidation was a key route of removal for the carboxylic acids including perfluorooctanoic acid (PFOA) and 5:3 fluorotelomer carboxylic acid (5:3 FTCA). A combination of chemical degradation and physical separation processes contributed to the removal of sulfonic acids including 6:2 fluorotelomer sulfonic acid (6:2 FTS) and perfluorooctanesulfonic acid (PFOS). However, in the presence of DOM, especially the \u3c 1 kDa low molecular weight and low aromatic autochthonous components, PFAS were more readily removed via physical sorption to the flotation layer, potentially due to the formation of DOM-iron-PFAS complexes. Regarding engineering applications, EC:H2O2 may have limited feasibility for PFAS mitigation in drinking water due to the highly acidic pH conditions needed and the release of metals during treatment. Accordingly, EC:H2O2 may better serve as a pretreatment and foam fractionation technology for higher strength wastewaters (such as membrane concentrates and industrial wastewaters) prior to more dedicated liquid-stream destructive technologies such as electrooxidation or supercritical water oxidation

Response to Michael Conway’s Review of \u3cem\u3eMaurice Blondel on the Supernatural in Human Action: Sacrament and Superstition\u3c/em\u3e (Boston & Leiden: Brill, 2017) by Cathal Doherty SJ.

This is a brief response (1000 words) to Michael A. Conway’s lengthy book review in Irish Theological Quarterly, Vol. 84, No. 2 (May 2019): 212–218

Mitochondrial Reactive Oxygen Species Production in Lungs of Rats With Different Susceptibilities to Hyperoxia-Induced Acute Lung Injury

Adult rats exposed to hyperoxia (\u3e95 % O2) die within 60–72 h from respiratory failure. However, when preconditioned with either \u3e95 % O2 for 48 h followed by 24 h in room air (H-T) or 60 % O2 for 7 days (H-S), they acquire tolerance or susceptibility to hyperoxia, respectively. The aim was to quantify H2O2 production rate and identify sources in isolated lung mitochondria and isolated perfused lungs (IPLs) of normoxia, H-T, and H-S rats. Mitochondria were isolated from lungs, and H2O2 production rates were quantified in the presence of pyruvate-malate or succinate, with and without inhibitors of mitochondrial complex I (CI), complex II (CII), and/or H2O2 scavenging systems. Lung rate of H2O2 release was quantified in IPLs with and without CII inhibitor. Results from isolated mitochondria show that CII is the main H2O2 source, and that both H2O2 production rate and scavenging capacity were ~48 % lower in H-S mitochondria compared to normoxia. Results from IPLs show that CII is also the dominant H2O2 source from lung tissue, and that H2O2 release rate was lower in H-T lungs compared to normoxia and H-S lungs. These results suggest that for H-S rats, both mitochondrial rate of H2O2 production and scavenging capacity were significantly lower than those in normoxia mitochondria and may contribute to their increased hyperoxia susceptibility. The lower H2O2 release rate from H-T IPLs, along with no change in mitochondrial H2O2 production rate, is consistent with higher antioxidant capacity in the lungs of H-T rats, which may contribute to their hyperoxia tolerance