Naturalized Panpsychism: An Alternative to Fundamentalist Physicalism and Supernaturalism

A central problem in the mind-body debate is the generation problem: how consciousness occurs in a universe understood as primarily non-conscious. This problem is particularly bothersome for physicalists. I argue that the generation problem stems from a non-critical presupposition about the nature of reality, namely, that the mental is an exception in the universe, a non-fundamental property. I call this presupposition mental specialism. Despite the fact that mental specialism dogmatically ingrained in the debate, there has been little reason offered either to accept or reject it. And doing so would dissolve the generation problem. But rejecting mental specialism, though it would dissolve the generation problem, would mean accepting another anathema presupposition: panpsychism. The resistance to panpsychism stems from the perception that panpsychism runs counter to science, that it is based on dogmatic metaphysical (even transcendental) arguments, and that it entails doctrines that cannot be accepted by science, such as mysteriousness. This perception is misguided and here I argue that a naturalized panpsychism, one that does not run contrary to science in these ways, can be developed and defended. I argue that consciousness emerges from proto-consciousness, the fundamental property that is disposed to give rise to consciousness. Proto-consciousness is not an arbitrarily posited property; following an important contemporary approach in neuroscience (the integrated information account), I understand proto-consciousness as information. The thesis that consciousness emerges from proto-consciousness elicits a fatal problem with panpsychic theories, the combination problem. This problem is how to account for higher-order conscious properties emerging from proto-conscious properties. I solve the combination problem that by adopting Giuolio Tononi’s Integrated Information Theory of Consciousness and demonstrating emerging higher-order conscious properties just is a system integrating information. Thus information is the fundamental property that, when integrated in a system such as a human being, is consciousness. Proto-consciousness is thus a natural property and the formulated panpsychic theory based upon information is a naturalized panpsychism

Sensitive Coverage Saves Lives: Improving media portrayal of suicidal behaviour

The report outlines the results of consultations with journalists, suicide prevention agencies and mental health groups conducted by the journalism ethics charity MediaWise. It makes recommendations for action by media organisations and suicide prevention agencies

Evolutionary and functional relationships within the DJ1 superfamily

BACKGROUND: Inferences about protein function are often made based on sequence homology to other gene products of known activities. This approach is valuable for small families of conserved proteins but can be difficult to apply to large superfamilies of proteins with diverse function. In this study we looked at sequence homology between members of the DJ-1/ThiJ/PfpI superfamily, which includes a human protein of unclear function, DJ-1, associated with inherited Parkinson's disease. RESULTS: DJ-1 orthologs in a variety of eukaryotic species cluster together in a single group. The most closely related group is the bacterial ThiJ genes. These are kinases involved in the biosynthesis of thiamine, a function that has been dispensed with evolutionarily in most eukaryotes where thiamine is an essential nutrient. The similarity with other characterized members of the superfamily, including proteases, is more remote. This is congruent with the recently solved crystal structures that fail to demonstrate the presence of a catalytic triad required for protease activity. CONCLUSION: DJ-1 may have evolved from the bacterial gene encoding ThiJ kinase. However, as this function has been dispensed with in eukaryotes it appears that the gene has been co-opted for another function

Snca and Bdnf gene expression in the VTA and raphe nuclei of midbrain in chronically victorious and defeated male mice

The study aimed to analyze the mRNA levels of Snca and Bdnf genes in the ventral tegmental area (VTA) and raphe nuclei of the midbrain in male mice that had each won or defeated 20 encounters in daily agonistic interactions. Groups of animals that had the same winning and losing track record followed by a no-fight period for 14 days were also studied. Snca mRNA levels were increased in the raphe nuclei in the losers and in the VTA of the winners. After fighting deprivation Snca mRNA levels were decreased to the control level in both groups. Snca mRNA levels were similar to the control level in the VTA of the losers and in the raphe nuclei of the winners. However Snca gene expression was increased in these areas after no-fight period in the winners and losers in comparison with respective mRNA levels in the undeprived animals. Significant positive correlations were found between the mRNA levels of Snca and Bdnf genes in the raphe nuclei. It was concluded, that social experience affects Snca gene expression depending on brain areas and functional activity of monoaminergic systems in chronically victorious or defeated mice

Public health care resource allocation and the rule of rescue

In health care, a tension sometimes arises between the injunction to do as much good as possible with scarce resources and the injunction to rescue identifiable individuals in immediate peril, regardless of cost (the "Rule of Rescue". This tension can generate serious ethical and political difficulties for public policy makers faced with making explicit decisions about the public funding of controversial health technologies, such as costly new cancer drugs. In this paper we explore the appropriate role of the Rule of Rescue in public resource allocation decisions. We consider practical approaches to operationalising the Rule of Rescue from Australia and the UK before examining the relevance of individual moral imperatives to public policy making. We conclude that, whilst public policy makers in a humane society should facilitate exceptional departures from a cost effectiveness norm in clinical decisions about identified individuals, it is not so obvious that they should, as a matter of national public policy, except any one group of unidentified individuals within society from the rules of opportunity cost at the expense of all others

Impulse balance and framing effects in threshold public good games

In this paper, we revisit the evidence for framing effects in threshold public good games. Our particular focus is on why the probability of providing the public good appears to be higher in positive, give frames compared with negative, take frames. We show that the impulse balance theory can explain this effect. We also report a new experiment designed to test the predictions of the impulse balance theory. The results of the experiment fit well, both in quantitative and qualitative terms, with our predictions.</p

Waiting times and socioeconomic status: evidence from England

Waiting times for elective surgery, like hip replacement, are often referred to as an equitable rationing mechanism in publicly-funded healthcare systems because access to care is not based on socioeconomic status. Previous work has established that that this may not be the case and there is evidence of inequality in NHS waiting times favouring patients living in the least deprived neighbourhoods in England. We advance the literature by explaining variations of inequalities in waiting times in England in four different ways. First, we ask whether inequalities are driven by education rather than income. Our analysis shows that education and income deprivation have distinct effects on waiting time. Patients in the first quintile with least deprivation in education wait 9% less than patients in the second quintile and 14% less than patients in the third-to-fifth quintile. Patients in the fourth and fifth most income-deprived quintile wait about 7% longer than patients in the least deprived quintile. Second, we investigate whether inequalities arise "across" hospitals or "within" the hospital. The analysis provides evidence that most inequalities occur within hospitals rather than across hospitals. Moreover, failure to control for hospital fixed effects results in underestimation of the income gradient. Third, we explore whether inequalities arise across the entire waiting time distribution. Inequalities between better educated patients and other patients occur over large part of the waiting time distribution. Moreover we find that the education gradient becomes smaller for very long waiting. Fourth, we investigate whether the gradient may reflect the fact that patients with higher socioeconomic status have a different severity as proxied through a range of types and the number of diagnoses (in addition to age and gender) compared to those with lower socioeconomic status. We find no evidence that differences in severity explain the social gradient in waiting times

Public health care resource allocation and the rule of rescue

In health care, a tension sometimes arises between the injunction to do as much good as possible with scarce resources and the injunction to rescue identifiable individuals in immediate peril, regardless of cost (the "Rule of Rescue". This tension can generate serious ethical and political difficulties for public policy makers faced with making explicit decisions about the public funding of controversial health technologies, such as costly new cancer drugs. In this paper we explore the appropriate role of the Rule of Rescue in public resource allocation decisions. We consider practical approaches to operationalising the Rule of Rescue from Australia and the UK before examining the relevance of individual moral imperatives to public policy making. We conclude that, whilst public policy makers in a humane society should facilitate exceptional departures from a cost effectiveness norm in clinical decisions about identified individuals, it is not so obvious that they should, as a matter of national public policy, except any one group of unidentified individuals within society from the rules of opportunity cost at the expense of all others

Macrophage Activation Redirects Yersinia-Infected Host Cell Death from Apoptosis to Caspase-1-Dependent Pyroptosis

Infection of macrophages by Yersinia species results in YopJ-dependent apoptosis, and naïve macrophages are highly susceptible to this form of cell death. Previous studies have demonstrated that macrophages activated with lipopolysaccharide (LPS) prior to infection are resistant to YopJ-dependent cell death; we found this simultaneously renders macrophages susceptible to killing by YopJ− Yersinia pseudotuberculosis (Yptb). YopJ− Yptb-induced macrophage death was dependent on caspase-1 activation, resulting in rapid permeability to small molecules, followed by membrane breakdown and DNA damage, and accompanied by cleavage and release of proinflammatory interleukin-18. Induction of caspase-1-dependent death, or pyroptosis, required the bacterial type III translocon but none of its known translocated proteins. Wild-type Yptb infection also triggered pyroptosis: YopJ-dependent activation of proapoptotic caspase-3 was significantly delayed in activated macrophages and resulted in caspase-1-dependent pyroptosis. The transition to susceptibility was not limited to LPS activation; it was also seen in macrophages activated with other Toll-like receptor (TLR) ligands and intact nonviable bacteria. Yptb infection triggered macrophage activation and activation of caspase-1 in vivo. Y. pestis infection of activated macrophages also stimulated caspase-1 activation. These results indicate that host signaling triggered by TLR and other activating ligands during the course of Yersinia infection redirects both the mechanism of host cell death and the downstream consequences of death by shifting from noninflammatory apoptosis to inflammatory pyroptosis

Regulation of LRRK2 Stability by the E3 Ubiquitin Ligase CHIP

Dominantly inherited mutations in the leucine-rich repeat kinase 2 gene (LRRK2) are the most common cause of familial Parkinson's disease (PD) and have also been identified in individuals with sporadic PD. Although the exact cellular function of LRRK2 remains unknown, most PD-linked mutations appear to be toxic to cells in culture via mechanisms that depend on the kinase activity of LRRK2 or on the formation of cytoplasmic inclusions. Here we show that the E3 ubiquitin ligase CHIP physically associates with LRRK2 and regulates the cellular abundance of LRRK2. We further show that LRRK2 forms a complex with overexpressed and endogenous CHIP and Hsp90. Our data indicates that the destabilization of LRRK2 by CHIP is due to ubiquitination and proteasome-dependent degradation. Hsp90 can attenuate CHIP-mediated degradation and this can be blocked by the Hsp90 inhibitor geldanamycin. These findings provide important insight into the cellular regulation of LRRK2 stability and may lead to the development of therapeutics to treat PD based on controlling LRRK2 stability