What Does Economics Assume About People’s Knowledge? Who knows?

The purpose of the paper is to explore, from an assessment viewpoint, the ideas below. Economics, as a social science, has always considered sets of individuals with assumed characteristics, namely the level of knowledge, although in an implicit way in most of the cases. In this sense, an influential approach in Economics assumed that society, as a global set of individuals, was characterised by a certain level of knowledge that, indeed, could be associated with the one of its representative agent. In fact, an attentive recall of the evolution of these matters in Economics will immediately recognise that, since the very first economic models of the government, it was assumed that the level of knowledge of society, represented by a set of voters, was not the same as the one of the agent being elected, i.e. the government. The irrelevance of the difference in the level of knowledge of economic agents was soon abandoned after some seminal works of Hayek and Friedman. More recently, the viewpoint of Economics has changed by focusing on the characteristics (e.g. knowledge) of individuals, who may interact in sub-sets of society. From this point of view is clearly relevant, given the close connection with the assumed level of knowledge, to distinguish the adaptive behaviour from the rational one, as well as the full rational from the bounded rationality behaviour by people. Quite recent developments in the Economics of Knowledge, i.e. the so-called learning models, have been considered as more realistic approaches to model the process by which individuals acquire knowledge, for instance from other individuals that are, themselves, acquiring knowledge

Creative destruction in science

Drawing on the concept of a gale of creative destruction in a capitalistic economy, we argue that initiatives to assess the robustness of findings in the organizational literature should aim to simultaneously test competing ideas operating in the same theoretical space. In other words, replication efforts should seek not just to support or question the original findings, but also to replace them with revised, stronger theories with greater explanatory power. Achieving this will typically require adding new measures, conditions, and subject populations to research designs, in order to carry out conceptual tests of multiple theories in addition to directly replicating the original findings. To illustrate the value of the creative destruction approach for theory pruning in organizational scholarship, we describe recent replication initiatives re-examining culture and work morality, working parents\u2019 reasoning about day care options, and gender discrimination in hiring decisions. Significance statement It is becoming increasingly clear that many, if not most, published research findings across scientific fields are not readily replicable when the same method is repeated. Although extremely valuable, failed replications risk leaving a theoretical void\u2014 reducing confidence the original theoretical prediction is true, but not replacing it with positive evidence in favor of an alternative theory. We introduce the creative destruction approach to replication, which combines theory pruning methods from the field of management with emerging best practices from the open science movement, with the aim of making replications as generative as possible. In effect, we advocate for a Replication 2.0 movement in which the goal shifts from checking on the reliability of past findings to actively engaging in competitive theory testing and theory building. Scientific transparency statement The materials, code, and data for this article are posted publicly on the Open Science Framework, with links provided in the article

Specific inhibition of protein disulphide reductase activity of a 60kda rat liver protein by adenine nucleotides

A 60 kda protein which catalysed the reduction of DTN\u27B, 5.5\u27-dithio-bis(2 nitrobenzoic acid), in an NADPH-dependent manner was purified to single-band homogeneity from rat liver. Amino-terminal sequencing of the first twentyfive amino acids of the protein showed an overall sequence homology of over eighty percent with thioredoxin reductase purified from human placenta. In the presence of thioredoxin obtained either from plant or mammalian origin, the purified protein catalysed the reduction of the interchain disulphides of mouse immunoglobulin G. This protein disulphide reductase activity of the protein was inhibited by millimolar levels of adenosine tri- and di-phosphate in a metallic cation-independent manner. Adenosine monophosphate did not inhibit the reaction. Other nucleotides such as Uridine tri-, di- and monophosphates, Guanosine tri -, di- and monophosphates, Cytosine tri- and monophosphates also did not have any inhibitory effects. None of the above nucleotides affect the enzyme activity of the protein when DTNB was used as the substrate, indicating that both ATP or ADP did not cause an inactivation of catalytic site. Our results suggest that the purified 60kda protien is thioredoxin reductase. This is the first demonstration that both ATP and ADP, which occur in cells at millimolar quantities, can inhibit the protein disulphide reductase activity of the thioredoxin reductase/thioredoxin couple. This may represent a potential regulatory mechanism for the reduction of intracellular protein disulphides

Effectiveness of multiple pre-ischemia electro-acupuncture on attenuating lipid peroxidation induced by cerebral ischemia in adult rats

Free radicals induced by cerebral ischemia-reperfusion injury can trigger lipid peroxidation, leading to the production of malondialdehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE). Post-ischemia electroacupuncture (EA) therapy was able to reduce extent of lipid peroxidation. However, the effect of pre-ischemic EA therapy has not been reported. In this study, we aim to investigate the effectiveness of pre-ischemic EA therapy on lipid peroxidation in the rat ischemic injury model. Four groups of Sprague-Dawley rats were designed: Placebo group (without EA therapy), NA group (EA therapy on non-acupoint), GB20 group (EA therapy on Fengchi), and ST36 group (EA therapy on Zusanli). Half of each group (n = 6) received 30-minute EA therapy for 3 times and the other half group for 18 times before the occlusion of right middle cerebral artery. Right brains were taken for determination of concentration of MDA and the total of MDA plus 4-HNE. We found that multiple pre-ischemia EA therapy at either GB20 or ST36 can effectively reduce the amount of MDA produced after MCA occlusion. However, this reduction was not observed in the total amount of MDA and 4-HNE. In conclusion, pre-ischemia EA can partly regulate the lipid peroxidation in cerebral ischemia, where both GB20 and ST36 have a similar beneficial effectiveness

Electroacupuncture reduces the extent of lipid peroxidation by increasing superoxide dismutase and glutathione peroxidase activities in ischemic-reperfused rat brains

Reactive oxygen species can be scavenged by superoxide dismutase (SOD) and glutathione peroxidase (GPx). During ischemia-reperfusion, the normal functioning of these antioxidant enzymes may be insufficient for the prevention of oxidant-induced peroxidation of membrane lipids and hence cerebral infarction. We therefore investigated whether electroacupuncture (EA) treatment at Fengchi points in post-ischemic rats could increase the antioxidant enzyme activities and thereby reduce the extent of lipid peroxidation. The results indicated that while EA did not alter the antioxidant enzyme activities in non-ischemic normal rat brains, ischemia-reperfusion caused significant increases in SOD and GPx activities. EA treatment further increased the antioxidant enzyme activities in ischemic-reperfused brain tissues, with a concomitant decrease in the extent of lipid peroxidation. Our finding suggests that EA treatment at Fengchi reduced the extent of lipid peroxidation in ischemic-reperfused rat brains, possibly by increasing the activities of SOD and GPx

Electro-acupuncture potentiates the disulphide-reducing activities of thioredoxin system by increasing thioredoxin expression in ischemia-reperfused rat brains

Reactive oxygen species can directly affect the conformation and activity of sulfhydryl-containing proteins by oxidation of their thiol moiety. During the process of ischemia-reperfusion, the thioredoxin (Trx) system (consisting of thioredoxin reductase (TR), Trx and NADPH) prevents susceptible proteins from this oxidative modification. Oxidative damage is one of the most damaging stress in ischemia. If oxidative stress could be minimized, the damage occurred will be minimized accordingly. We therefore investigated whether electroacupuncture (EA) treatment at Fengchi (GB20) or Zusanli (ST36) acupoints in post-ischemic rats could increase TR-related activities and Trx expression which would translate into maintaining the intact thiol moiety of susceptible proteins in the surrounding. Our results indicated that EA treatment at either acupoint increased the Trx expression in ischemic-reperfused brain tissues. Induced Trx expressed levels gradually increased from post-ischemia day 1 to day 4. Statistical analysis revealed that there was no observable difference in the effect of EA treatment at GB20 and ST36. Sham EA treatment did not induce any Trx expression. EA at either acupoint did not alter TR activities in both non-ischemic and ischemic-reperfused rat brains. Taken overall, our finding suggests that EA treatment at GB20 or ST36 could increase Trx expression which could minimize oxidative modifications of thiol groups of surrounding proteins