SECURITIES—DEMOCRATIZING EQUITY MARKETS WITH AND WITHOUT EXPLOITATION: ROBINHOOD, GAMESTOP, HEDGE FUNDS, GAMIFICATION, HIGH FREQUENCY TRADING, AND MORE

The stock trading frenzy of January 2021 brought a relatively new player in the securities markets into public consciousness—the platforms offering no- or low-commission trading that seek to appeal to young and less-experienced investors with a “fun” if not “delightful” user experience. Most prominent among these new brokers is Robinhood, with a slick mobile phone app, which claims that its platform will “democratize finance” by making investing cheaper and easier for the masses who have been looked down upon and locked out by the wealthy elites of Wall Street. However, Robinhood’s claims of “democratization” have all the hallmarks of manipulation and exploitation, making Robinhood’s founders multibillionaires while many of its retail customers suffer financial ruin. That is because platforms like Robinhood take arguably legal kickbacks for routing their customer orders—known as payment for order flow—to high frequency trading firms which execute those orders, almost always in dark, off-exchange venues. To maximize those kickbacks, Robinhood’s mobile trading app is gamified via predatory digital engagement practices to disarm its customers’ financial self-defense mechanisms and prompt as much frequent and risky trading as possible. Such trading behavior has been shown to be highly detrimental to retail investors, and indeed many of Robinhood’s customers have been harmed by engaging in such practices, some grievously. The result is that, unlike the legend of Robin Hood stealing from the rich and giving to the poor, the Robinhoods of the world are taking from the less experienced and enriching themselves and their fellow Wall Street billionaires. But it does not have to be this way. Finance can be genuinely democratized (easier access, lower costs, user-friendly financial tools, etc.) and trading can be demystified in ways that facilitate wealth creation rather than wealth extraction. However, for that to happen, regulators must enforce existing laws and rules against illegal conduct and impose meaningful penalties on individual corporate officers that punish and deter. Regulators must also enact new rules to prohibit, for example, predatory digital engagement practices. Once the highly profitable lawbreakers and predators are shut down, the financial industry can focus on serving Main Street investors rather than exploiting them to enrich Wall Street

Effects of gravity on gas-loaded variable conductance heat pipes

The effects of gravity on the operation of gas-loaded variable conductance heat pipes have been investigated. Experimental results have been obtained for three heat pipes (1.6 cm, 2.5 cm and 5 cm diameter) operating with methanol or Freon 113 as the working fluid and krypton or helium as the control gas. Results show that gravity tends to distort the axial temperature profiles on the small diameter pipe. For the large diameter pipe gravity has the effect of causing a stratification of the working fluid and non-condensible gas. These results seem to indicate that in certain cases the presently available design procedure will have to be modified to account for the effects of gravity on variable conductance heat pipe operation. (Author)supported by the National Science Foundation, Heat Transfer Program, Washington, D.C.http://archive.org/details/effectsofgravity00kellNSF Grant #AG-496N

The Repressors of mTORC1 Signaling, REDD1 and REDD2, Are Induced in Immobilized Rat Skeletal Muscle

Please view abstract in the attached PDF file

GlxA is a new structural member of the radical copper oxidase family and is required for glycan deposition at hyphal tips and morphogenesis of <i>Streptomyces lividans</i>

Streptomyces lividans displays a distinct dependence on copper to fully initiate morphological development. Evidence has accumulated to implicate the participation of an extracytoplasmic cuproenzyme in morphogenesis. In the present study, we show that GlxA fulfils all criteria to be that cuproenzyme. GlxA is membrane associated and has an active site consisting of a mononuclear copper and a cross-linked Y-C cofactor. The domain organization of the tertiary structure defines GlxA as a new structural member of the mono-copper oxidase family, with copper co-ordination geometry similar to, but spectroscopically distinct from fungal galactose oxidase (Gox). EPR spectroscopy reveals that the oxidation of cupric GlxA generates a protein radical residing on the Y-C cross-link. A variety of canonical Gox substrates (including D-galactose) were tested but none were readily turned over by GlxA. A glxA null-mutant leads to loss of glycan accumulation at hyphal tips and consequently a drastically changed morphology both on solid substrates and in liquid-grown environments, a scenario similarly observed in the absence of the neighbouring glycan synthase CslA (cellulase synthase-like protein). In addition the glxA mutant has lost the stimulation of development by copper, supporting a model whereby the enzymatic action of GlxA on the glycan is required for development and morphology. From a biotechnology perspective, the open mycelium morphology observed with the glxA mutant in submerged culture has implications for use as an enzyme production host.</jats:p

Oligosaccharyltransferase Inhibition Induces Senescence in RTK-Driven Tumor Cells

Asparagine (N)-linked glycosylation is a protein modification critical for glycoprotein folding, stability, and cellular localization. To identify small molecules that inhibit new targets in this biosynthetic pathway, we initiated a cell-based high throughput screen and lead compound optimization campaign that delivered a cell permeable inhibitor (NGI-1). NGI-1 targets the oligosaccharyltransferase (OST), a hetero-oligomeric enzyme that exists in multiple isoforms and transfers oligosaccharides to recipient proteins. In non-small cell lung cancer cells NGI-1 blocks cell surface localization and signaling of the EGFR glycoprotein, but selectively arrests proliferation in only those cell lines that are dependent on EGFR (or FGFR) for survival. In these cell lines OST inhibition causes cell cycle arrest accompanied by induction of p21, autofluorescence, and changes in cell morphology; all hallmarks of senescence. These results identify OST inhibition as a potential therapeutic approach for treating receptor tyrosine kinase-dependent tumors and provides a chemical probe for reversibly regulating N-linked glycosylation in mammalian cells

Widespread Polymorphism in the Positions of Stop Codons in Drosophila melanogaster

The mechanisms underlying evolutionary changes in protein length are poorly understood. Protein domains are lost and gained between species and must have arisen first as within-species polymorphisms. Here, we use Drosophila melanogaster population genomic data combined with between species divergence information to understand the evolutionary forces that generate and maintain polymorphisms causing changes in protein length in D. melanogaster. Specifically, we looked for protein length variations resulting from premature termination codons (PTCs) and stop codon losses (SCLs). We discovered that 438 genes contained polymorphisms resulting in truncation of the translated region (PTCs) and 119 genes contained polymorphisms predicted to lengthen the translated region (SCLs). Stop codon polymorphisms (SCPs) (especially PTCs) appear to be more deleterious than other polymorphisms, including protein amino acid changes. Genes harboring SCPs are in general less selectively constrained, more narrowly expressed, and enriched for dispensable biological functions. However, we also observed exceptional cases such as genes that have multiple independent SCPs, alleles that are shared between D. melanogaster and Drosophila simulans, and high-frequency alleles that cause extreme changes in gene length. SCPs likely have an important role in the evolution of these genes

Ecosystem Overfishing in the Ocean

Fisheries catches represent a net export of mass and energy that can no longer be used by trophic levels higher than those fished. Thus, exploitation implies a depletion of secondary production of higher trophic levels (here the production of mass and energy by herbivores and carnivores in the ecosystem) due to the removal of prey. The depletion of secondary production due to the export of biomass and energy through catches was recently formulated as a proxy for evaluating the ecosystem impacts of fishing–i.e., the level of ecosystem overfishing. Here we evaluate the historical and current risk of ecosystem overfishing at a global scale by quantifying the depletion of secondary production using the best available fisheries and ecological data (i.e., catch and primary production). Our results highlight an increasing trend in the number of unsustainable fisheries (i.e., an increase in the risk of ecosystem overfishing) from the 1950s to the 2000s, and illustrate the worldwide geographic expansion of overfishing. These results enable to assess when and where fishing became unsustainable at the ecosystem level. At present, total catch per capita from Large Marine Ecosystems is at least twice the value estimated to ensure fishing at moderate sustainable levels

Is REDD1 a Metabolic Éminence Grise?

Regulated in development and DNA damage response 1 (REDD1) has been functionally linked to the control of diverse cellular processes due, at least in part, to its ability to repress mammalian or mechanistic Target of Rapamycin (mTOR) Complex-1 (mTORC1), a key protein complex controlled by hormonal and nutrient cues. Notably, emerging evidence suggests that REDD1 also regulates several pathways involved in modulating energy balance and metabolism. Herein, we discuss evidence implicating REDD1 as a key modulator of insulin action and metabolic function, including its potential contribution to mitochondrial biology and pancreatic islet function. Collectively, the available evidence suggests that REDD1 has a more prominent role in energy homeostasis than was previously thought, and implicates REDD1 as a potential therapeutic target for treatment of metabolic disorders