The EVF Model: A Novel Framework for Understanding Gambling and, by Extension, Poker

There are several senses in which the term gambling is used. All have liabilities, problems that have muddied the waters in scientific research, generated conflicting legal decisions, compromised debates over ethical and moral issues, and have led to uneven legislation. Here, a novel framework for the term is offered, based on two continuous variables: a) the Expected Value (EV) of any arbitrary game and, b) the inherent Flexibility (F) of that game. This EVF model produces a classification system for all the enterprises that can or have been called gambling. It is one that allows for more measured decisions to be made and provides a more coherent platform on which to deliberate the many significant issues that have been raised over the years. It also permits a sensible answer to the question of the nature of games like the stock market, opening a small business, and especially, poker

Caterpillars, consciousness and the origins of mind

A novel framework for the origins of consciousness and mind, the Cellular Basis of Consciousness (CBC), is presented. The model is based on a simple, perhaps radical axiom: subjectivity is an inherent feature of particular kinds of organic form. Experiential states, including those denoted as mind and consciousness, are present in the most primitive species. The model has several conceptual and empirical virtues, among them: (a) it (re)solves the problem of how minds are created by brains ─ also known as the Hard Problem (Chalmers 1995) ─ by revealing that the apparent difficulty results from a category error, (b) it redirects the search for the origins of mind from complex neural structures to foundational biomechanical ones, and (c) it reformulates the long-term research focus from looking for miracle moments where a brain is suddenly capable of making a mind to discovering how complex and sophisticated cognitive, emotional and behavioral functions evolve from more primitive ones

What if all animals are sentient?

Birch develops a useful framework for determining when the Animal Sentience Precautionary Principle (ASPP) should be invoked. He rightly notes that there is a lack of agreement among social scientists, ethicists, and legislators even about whether the precautionary principle is useful, let alone when and how it should be implemented. His proposal is to establish a kind of cognitive threshold, and only when an animal shows a sufficient level of sentience would the ASPP be appropriate. From the point of view of the Cellular Basis of Consciousness model (Reber, 2016), all animals are sentient. If correct, the problems Birch identifies need to be confronted from a different perspective

Resolving the hard problem and calling for a small miracle

With the exception of the commentary by Key, the commentaries on Reber have a common feature: the commenters feel, with varying levels of enthusiasm, that there is at least some virtue in the core assumption of the Cellular Basis of Consciousness (CBC) theory that consciousness (or subjectivity or sentience) accompanies the earliest forms of life. The model has two important entailments: (a) it resolves the (in)famous Hard Problem by redirecting the search for the biochemical foundations of sentience away from human consciousness; and (b) it reduces the need for an emergentist miracle to a far simpler scale than is currently assumed. The CBC is grounded in classical principles of evolutionary biology, which it shares with allied areas of research on emotion, learning, memory and perception

To identify all the relevant factors is to explain feeling

Several additional comments on Reber (2016a) have appeared. Like those addressed in Reber (2016b), they reflect points of agreement and disagreement on various elements of my Cellular Basis of Consciousness (CBC) model. Some, however, seem to have missed key points. I\u27m willing to take some responsibility for this. Perhaps I was not clear about some of the more radical points of the model. Hopefully the case-by-case review here will help

Sentient plants? Nervous minds?

The commentaries by Calvo (2018) and Mallatt & Feinberg (2017) on my 2016 target branch out from a common conceptual node like forks in a road. Calvo criticizes me for not acknowledging that plants too are likely to be sentient and claims I have fallen into the kind of category error of which I accuse others ─ a zoocentric bias that fails to grant consciousness to flora. Mallatt & Feinberg maintain that I\u27ve gone too far in granting sentience to any species that lacks a nervous system. Calvo makes some good points but there are other issues concerning plant sentience such as metabolic cost and ethical implications. Mallatt & Feinberg take me to task for failing to provide supporting data. They are right, and a partial remedy is offered. They also imply that I have misunderstand basic principles of evolutionary biology. I think they have misunderstood my position

The effect of substituted benzene dicarboxylic acid linkers on the optical band gap energy and magnetic coupling in manganese trimer metal organic frameworks

We have systematically studied a series of eight metal-organic frameworks (MOFs) in which the secondary building unit is a manganese trimer cluster, and the linkers are differently substituted benzene dicarboxylic acids (BDC). The optical band gap energy of the compounds vary from 2.62 eV to 3.57 eV, and theoretical studies find that different functional groups result in new states in the conduction band, which lie in the gap and lower the optical band gap energy. The optical absorption between the filled Mn 3d states and the ligands is weak due to minimal overlap of the states, and the measured optical band gap energy is due to transitions on the BDC linker. The Mn atoms in the MOFs have local moments of 5 mu B, and selected MOFs are found to be antiferromagnetic, with weak coupling between the cluster units, and paramagnetic above 10 K

Mitogen- and Stress-Activated Kinase 1 (MSK1) Regulates Cigarette Smoke-Induced Histone Modifications on NF-κB-dependent Genes

Cigarette smoke (CS) causes sustained lung inflammation, which is an important event in the pathogenesis of chronic obstructive pulmonary disease (COPD). We have previously reported that IKKα (I kappaB kinase alpha) plays a key role in CS-induced pro-inflammatory gene transcription by chromatin modifications; however, the underlying role of downstream signaling kinase is not known. Mitogen- and stress-activated kinase 1 (MSK1) serves as a specific downstream NF-κB RelA/p65 kinase, mediating transcriptional activation of NF-κB-dependent pro-inflammatory genes. The role of MSK1 in nuclear signaling and chromatin modifications is not known, particularly in response to environmental stimuli. We hypothesized that MSK1 regulates chromatin modifications of pro-inflammatory gene promoters in response to CS. Here, we report that CS extract activates MSK1 in human lung epithelial (H292 and BEAS-2B) cell lines, human primary small airway epithelial cells (SAEC), and in mouse lung, resulting in phosphorylation of nuclear MSK1 (Thr581), phospho-acetylation of RelA/p65 at Ser276 and Lys310 respectively. This event was associated with phospho-acetylation of histone H3 (Ser10/Lys9) and acetylation of histone H4 (Lys12). MSK1 N- and C-terminal kinase-dead mutants, MSK1 siRNA-mediated knock-down in transiently transfected H292 cells, and MSK1 stable knock-down mouse embryonic fibroblasts significantly reduced CS extract-induced MSK1, NF-κB RelA/p65 activation, and posttranslational modifications of histones. CS extract/CS promotes the direct interaction of MSK1 with RelA/p65 and p300 in epithelial cells and in mouse lung. Furthermore, CS-mediated recruitment of MSK1 and its substrates to the promoters of NF-κB-dependent pro-inflammatory genes leads to transcriptional activation, as determined by chromatin immunoprecipitation. Thus, MSK1 is an important downstream kinase involved in CS-induced NF-κB activation and chromatin modifications, which have implications in pathogenesis of COPD

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.