Artificial Intelligence & Artificial Prices: Safeguarding Securities Markets from Manipulation by Non-Human Actors

Securities traders are currently competing to use Artificial Intelligence (A.I.) in order to make more profitable decisions in the marketplace. While A.I. provides superior abilities in recognizing market patterns, its complexity can obscure its decision-making process beyond human comprehension. Problematically, the current securities laws prohibiting manipulation of securities prices rest liability for violations on a trader’s intent. In order to prepare for A.I. market participants, both courts and regulators need to accept that human concepts of decision-making will be inadequate in regulating A.I. behavior. However, the wealth of case law in the market manipulation doctrine need not be cast aside. Industry regulators should instead require A.I. users to harness the power of their machines to provide meaningful feedback in order to both detect potential manipulations and create evidentiary records in the event that allegations of A.I. manipulation arise

Cytoskeletal dynamics in and traumatic injury of cerebellar and hippocampal neurons

__Abstract__ This thesis addresses two separate, yet overlapping, physiological processes, namely traumatic brain injury (TBI) and microtubule (MT) dynamics, primarily through the use of cultured cells derived from embryonic mice. The difficulties which arise through the experimental study of these processes, either in brain slices or in the whole animal, can be partially circumvented by using various in vitro systems to tease out the factors contributing to, and the mechanisms behind, these complex phenomena. Here, focus is given to cell cultures derived from two different brain regions, the hippocampus and the cerebellum, reviewed in this Chapter. In addition, the Introduction describes cell culture protocols, and neuronal cytoarchitecture in the hippocampus and the cerebellum, before relating these findings to glutamate-mediated cell death, particularly in cerebellar Purkinje cells (PCs). The effects of "excitotoxicity" are identified in these cells at the level of the dendritic spine and the MTs of the neuronal cytoskeleton. Alterations in both cultured PCs and hippocampal neurons are also described in relation to traumatic injury and to Williams Syndrome (WS), a rare genetic disorder. This initial portion provides a theoretical framework for the experimental studies contained in the successive chapters. In Chapter 2, cultured cells are injured using an in vitro model of stretch-induced injury. With this model, the cellular sequelae of trauma are examined in hippocampal and cerebellar cells. Several questions are asked: 1) What are the effects of increasing degrees of stretch on these cells? 2) What are the similarities and differences between neurons and glia in response to stretch injury? 3) What are the similarities and differences between hippocampal and cerebellar cells in response to stretch injury? 4) What is the relationship between TBI and glutamate-mediated excitotoxicity? and 5) What are the potential correlates among stretch injury in vitro, experimental injury to animals in vivo, and clinical TBI? Chapter 3 is concerned with the activity ofMT plus-end binding proteins, namely end-binding protein 3 (EB3) and cytoplasmic linker protein of 115 k.Da (CLIP-115), in neurons. First, cultured hippocampal and cerebellar cells are made to express EB3 tagged with green fluorescent protein (GFP) in order to image and quantify the activity of MTs in neurons and glia. Second, hippocampal brain slices from adult CLIP-115 homozygous (knockout, or KO) mice are examined in order to quantify the cellular effects of this genetic deletion. Several questions are asked: 1) What is the role of plus-end binding proteins in neurons, especially as compared to glia or to other non-neuronal cells? 2) What are the similarities and differences in the velocities of growing MTs in hippocampal neurons and glia, and in cerebellar PCs and glia? 3) What happens to MT growth velocities, and other dynamic processes, when cultured cells derived from CLIP-115 KO mice are made to express EB3-GFP? 4) What are the effects of the deletion of CLIP-115 on dendritic and spine morphologies in the adult mouse hippocampus? and 5) What are the implications of altered MT dynamics for patients with WS? Lastly, Chapter 4 presents concluding remarks and implications of the present data. Here future studies are highlighted that utilize in vitro preparations for the combined study of cytoskeletal dynamics and traumatic injury

Az eutanázia megítélése a 18−19 évesek körében

A nyugati típusú kultúrákra jellemző halálkép változása nyomon követhető. A gyökeres változás a szakirodalom szerint a 20. században történt, mikor számos ok miatt a halál az élet értelmetlen és végleges befejezésének szinonimájává vált. A haldokló ellátása, gondozása a családról az egészségügyi ellátórendszerre tevődött át. A személyes tapasztalat hiánya elsősorban a társas támogatás rendszerét veszélyezteti. Mivel a mai „elöregedő” társadalomban alapvető fontosságú, hogy a szociális kapcsolatok, a család támogató szerepe működőképes legyen, figyelmünket elsősorban a felnövekvő, fiatal korosztály felé kell fordítanunk (Zana, Szabó és Hegedűs, 2008). Napjainkban a fiatalok ugyanis nem találkoznak a halállal, nem beszélnek róla a családban, keveset foglalkoznak vele a mindennapi életük során. Mindez a halál tabu jellegét erősíti, ami, úgy gondolom, szorongáskeltő faktor számukra

Visualization of microtubule growth in cultured neurons via the use of EB3-GFP (end-binding protein 3-green fluorescent protein)

Several microtubule binding proteins, including CLIP-170 (cytoplasmic linker protein-170), CLIP-115, and EB1 (end-binding protein 1), have been shown to associate specifically with the ends of growing microtubules in non-neuronal cells, thereby regulating microtubule dynamics and the binding of microtubules to protein complexes, organelles, and membranes. When fused to GFP (green fluorescent protein), these proteins, which collectively are called +TIPs (plus end tracking proteins), also serve as powerful markers for visualizing microtubule growth events. Here we demonstrate that e

Models of Traumatic Cerebellar Injury

Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Studies of human TBI demonstrate that the cerebellum is sometimes affected even when the initial mechanical insult is directed to the cerebral cortex. Some of the components of TBI, including ataxia, postural instability, tremor, impairments in balance and fine motor skills, and even cognitive deficits, may be attributed in part to cerebellar damage. Animal models of TBI have begun to explore the vulnerability of the cerebellum. In this paper, we review the clinical presentation, pathogenesis, and putative mechanisms underlying cerebellar damage with an emphasis on experimental models that have been used to further elucidate this poorly understood but important aspect of TBI. Animal models of indirect (supratentorial) trauma to the cerebellum, including fluid percussion, controlled cortical impact, weight drop impact acceleration, and rotational acceleration injuries, are considered. In addition, we describe models that produce direct trauma to the cerebellum as well as those that reproduce specific components of TBI including axotomy, stab injury, in vitro stretch injury, and excitotoxicity. Overall, these models reveal robust characteristics of cerebellar damage including regionally specific Purkinje cell injury or loss, activation of glia in a distinct spatial pattern, and traumatic axonal injury. Further research is needed to better understand the mechanisms underlying the pathogenesis of cerebellar trauma, and the experimental models discussed here offer an important first step toward achieving that objective

Alcohol significantly lowers the seizure threshold in mice when co-administered with bupropion hydrochloride

<p>Abstract</p> <p>Background</p> <p>Bupropion HCl is a widely used antidepressant that is known to cause seizures in a dose-dependent manner. Many patients taking antidepressants will consume alcohol, even when advised not to. Previous studies have not shown any interactions between bupropion HCl and alcohol. However, there have been no previous studies examining possible changes in seizure threshold induced by a combination of alcohol and bupropion HCl.</p> <p>Methods</p> <p>Experimentally naïve female Swiss albino mice (10 per group) received either single doses of bupropion HCl (ranging from 100 mg/kg to 120 mg/kg) or vehicle (0.9% NaCl) by intraperitoneal (IP) injection in a dose volume of 10 ml/kg, and single-dose ethanol alone (2.5 g/kg), or vehicle, 5 min prior to bupropion dosing. The presence or absence of seizures, the number of seizures, the onset, duration and the intensity of seizures were all recorded for 5 h following the administration of ethanol.</p> <p>Results</p> <p>The results show that administration of IP bupropion HCl alone induced seizures in mice in a dose-dependent manner, with the 120 mg/kg dose having the largest effect. The percentage of convulsing mice were 0%, 20%, 30% and 60% in the 0 (vehicle), 100, 110, and 120 mg/kg dose groups, respectively. Pretreatment with ethanol produced a larger bupropion HCl-induced convulsive effect at all the doses (70% each at 100, 110 and 120 mg/kg) and a 10% effect in the ethanol + vehicle only group. The convulsive dose of bupropion HCl required to induce seizures in 50% of mice (CD₅₀), was 116.72 mg/kg for bupropion HCl alone (CI: 107.95, 126.20) and 89.40 mg/kg for ethanol/bupropion HCl (CI: 64.92, 123.10).</p> <p>Conclusion</p> <p>These results show that in mice alcohol lowers the seizure threshold for bupropion-induced seizures. Clinical implications are firstly that there may be an increased risk of seizures in patients consuming alcohol, and secondly that formulations that can release bupropion more readily in alcohol may present additional risks to patients.</p