The Recognition Signal Hypothesis for the Adaptive Evolution of Religion

Recent research on the evolution of religion has focused on whether religion is an unselected by-product of evolutionary processes or if it is instead an adaptation by natural selection. Adaptive hypotheses for religion include direct fitness benefits from improved health and indirect fitness benefits mediated by costly signals and/or cultural group selection. Herein, I propose that religious denominations achieve indirect fitness gains for members through the use of ecologically arbitrary beliefs, rituals, and moral rules that function as recognition markers of cultural inheritance analogous to kin and species recognition of genetic inheritance in biology. This recognition signal hypotheses could act in concert with either costly signaling or cultural group selection to produce evolutionarily altruistic behaviors within denominations. Using a cultural phylogenetic analysis, I show that a large set of religious behaviors among extant Christian denominations supports the prediction of the recognition signal hypothesis that characters change more frequently near historical schisms. By incorporating demographic data into the model, I show that more-distinctive denominations, as measured through dissimilar characteristics, appear to be protected from intrusion by nonmembers in mixed-denomination households, and that they may be experiencing greater biological growth of their populations even in the present day.     

Ecological Thresholds in the Savanna Landscape: Developing a Protocol for Monitoring the Change in Composition and Utilisation of Large Trees

Background

Acquiring greater understanding of the factors causing changes in vegetation structure - particularly with the potential to cause regime shifts - is important in adaptively managed conservation areas. Large trees (≥5 m in height) play an important ecosystem function, and are associated with a stable ecological state in the African savanna. There is concern that large tree densities are declining in a number of protected areas, including the Kruger National Park, South Africa. In this paper the results of a field study designed to monitor change in a savanna system are presented and discussed.

Methodology/Principal Findings

Developing the first phase of a monitoring protocol to measure the change in tree species composition, density and size distribution, whilst also identifying factors driving change. A central issue is the discrete spatial distribution of large trees in the landscape, making point sampling approaches relatively ineffective. Accordingly, fourteen 10 m wide transects were aligned perpendicular to large rivers (3.0–6.6 km in length) and eight transects were located at fixed-point photographic locations (1.0–1.6 km in length). Using accumulation curves, we established that the majority of tree species were sampled within 3 km. Furthermore, the key ecological drivers (e.g. fire, herbivory, drought and disease) which influence large tree use and impact were also recorded within 3 km.

Conclusions/Significance

The technique presented provides an effective method for monitoring changes in large tree abundance, size distribution and use by the main ecological drivers across the savanna landscape. However, the monitoring of rare tree species would require individual marking approaches due to their low densities and specific habitat requirements. Repeat sampling intervals would vary depending on the factor of concern and proposed management mitigation. Once a monitoring protocol has been identified and evaluated, the next stage is to integrate that protocol into a decision-making system, which highlights potential leading indicators of change. Frequent monitoring would be required to establish the rate and direction of change. This approach may be useful in generating monitoring protocols for other dynamic systems.     

The Hypothesis of a Genetic Protolanguage: an Epistemological Investigation

Progress in molecular biology has revealed profound relations between linguistic and genomic sciences, mainly through advances in bioinformatics. The structural symmetries between biochemical and verbal syntaxes raise the question of their origins: did they emerge independently, or did one arise from the other? Does the genetic code contain the traces of a protolanguage, a universal grammar whose gradual evolution and successive mutations progressively led to the polymorphism of natural languages? To explore this question, we review the isomorphism of the genetic code and verbal codes from lexical, syntactic, semantic and pragmatic standpoints. We discuss the limits of these symmetries and their anthropomorphic connotations. We observe the gradual evolution of species and languages according to parallel mechanisms, and the genetic roots of the physiology of language. In conclusion, we hypothesize that human observers may not be projecting linguistic frameworks onto genomic structures. Rather, it could be their linguistic faculties that reflect the grammatical structure of genetic code.     

The Roles of Chemokines in Rabies Virus Infection: Overexpression May Not Always Be Beneficial

It was found previously that induction of innate immunity, particularly chemokines, is an important mechanism of rabies virus (RABV) attenuation. To evaluate the effect of overexpression of chemokines on RABV infection, chemokines macrophage inflammatory protein 1α (MIP-1α), RANTES, and IP-10 were individually cloned into the genome of attenuated RABV strain HEP-Flury. These recombinant RABVs were characterized in vitro for growth properties and expression of chemokines. It was found that all the recombinant viruses grew as well as the parent virus, and each of the viruses expressed the intended chemokine in a dose-dependent manner. When these viruses were evaluated for pathogenicity in the mouse model, it was found that overexpression of MIP-1α further decreased RABV pathogenicity by inducing a transient innate immune response. In contrast, overexpression of RANTES or IP-10 increased RABV pathogenicity by causing neurological diseases, which is due to persistent and high-level expression of chemokines, excessive infiltration and accumulation of inflammatory cells in the central nervous system, and severe enhancement of blood-brain barrier permeability. These studies indicate that overexpression of chemokines, although important in controlling virus infection, may not always be beneficial to the host.Rabies virus (RABV) is a negative-strand RNA virus belonging to the Rhabidoviridae family, genus Lyssavirus, which causes rabies (fatal encephalomyelitis) in many species of mammals (5). More than 55,000 humans die of rabies each year worldwide (26). Once clinical signs develop, rabies is always fatal (12, 53). Despite the lethality of rabies, only mild inflammation and little neuronal destruction were observed in the central nervous system (CNS) of rabies patients (31, 32). Adaptation of wild-type (wt) RABV in laboratory animals and/or cell culture leads to attenuation in phenotype, and laboratory-adapted RABVs have been used for vaccine development (1, 10). To delineate the mechanism(s) of RABV attenuation, previous studies compared the host responses to infection with either laboratory-attenuated or wt RABV (52). It was found that laboratory-attenuated RABV induced extensive inflammation, apoptosis, and neuronal degeneration, as well as induction of expression of innate immune genes in the CNS; however, wt RABV caused little or no neuronal damage and avoided the activation of expression of innate molecule genes. Other investigators also reported the induction of innate immunity in mice or neuronal cells infected with laboratory-attenuated viruses (20, 33, 37). The mostly upregulated genes in the innate immune responses after infection with attenuated RABV include genes encoding for inflammatory chemokines and type I interferon (IFN) as well as IFN-related proteins (20, 33, 378). Further studies have shown that the expression of chemokines (mRNA and proteins), particularly macrophage inflammatory protein 1α (MIP-1α; CCL3), RANTES (CCL5), and IP-10 (CXCL10), correlates with the infiltration of inflammatory cells and enhancement of blood-brain barrier (BBB) permeability (23).Chemokines are a group of small (∼8- to 14-kDa), basic, structurally related molecules that can attract inflammatory cells along concentration gradients and enhance leukocyte-endothelial cell interactions (55). The tertiary structure of chemokines is highly conserved; they contain at least four cysteine residues that form two disulfide bonds (50). Chemokines have been divided into major subfamilies on the basis of the arrangement of the two N-terminal cysteine residues, CC and CXC. CC chemokines act primarily upon monocytes, whereas CXC family members are specific for neutrophils and lymphocytes (14). Chemokines regulate cell trafficking of various types of leukocytes through interactions with G-protein-coupled receptors with seven transmembrane regions (55). Most chemokine receptors are stimulated by more than one chemokine, and one ligand can bind to more than one receptor (50). This combination of redundancy and promiscuity might act as a safety factor to ensure adequate host defenses (15, 30). Chemokines have direct antiviral activities and/or recruit inflammatory cells to the site of infection to kill virus or virus-infected cells (30, 34). However, due to their ability to direct migration of inflammatory cells, overexpression of chemokines may have detrimental effects, especially in the process of autoimmune inflammation. In an experimental autoimmune encephalomyelitis model, IP-10, monocyte chemoattractant protein 1 (MCP-1), and MIP-1α were strongly upregulated (14). Administration of anti-IP-10 antibody decreased disease incidence and severity and the infiltration of mononuclear cells into the CNS (11).In the present study, the roles of chemokines in RABV infection were further investigated by cloning and expressing MIP-1α, RANTES, and IP-10 in the genome of the RABV HEP-Flury strain. It was found that overexpression of MIP-1α decreased the pathogenicity by inducing transient expression of chemokines and infiltration of inflammatory cells into the CNS. In contrast, recombinant RABV expressing RANTES and IP-10 induced persistent and high-level expression of chemokines and extensive infiltration of inflammatory cells into the CNS, causing neurological diseases and death.     

AdaptivSearch: A Novel Iterative Algorithm for the Generation of n-dimensional Hypersurfaces Using an Adaptive Numerical Strategy

AdaptivSearch is the first adaptive strategy based algorithm for the rational and economical construction of n-dimensional hypersurfaces. AdaptivSearch works iteratively: At each step it parcels out the definition range into several triangles, evaluates the worst according to a built-in error criterion, and refines the approximation to the unknown function by choosing the barycenter of this partial area as the node to be calculated next. Based upon the error criterion, AdaptivSearch selectively approaches those parts of the hypersurface in which the curvature exhibits the strongest changes. Some examples of AdaptivSearch applications for both analytical functions and chemical model surfaces are given in order to demonstrate the behavior of the algorithm. These show its broad applicability and the usefulness, especially for chemical problems.     

Testing an Adaptive Hypothesis Through Context-Dependence: Effects of Water Depth on Foraging Behaviour in Three Species of Garter Snakes

Adaptive hypotheses based on interspecific comparisons can be tested by evaluating the context‐dependence of the behaviour of individual organisms. Drummond (Behaviour, 86, 1983, 1) categorized garter snake species (Thamnophis) as terrestrial–aquatic generalists or aquatic specialists based on diet and aquatic foraging behaviour. He hypothesized that the characteristic foraging behaviours of aquatic specialists – including frequent crawling on the underwater substrate and a high rate of underwater predatory strikes – are adaptations for feeding on relatively widely dispersed aquatic prey. Drummond's hypothesis based on interspecific comparisons suggests that individual snakes might change their foraging in the direction of aquatic specialist behaviour with an increase in water depth (which increases prey dispersion). I tested this prediction through laboratory observations of Mexican Pacific lowlands garter snakes (T. validus) feeding on minnows in shallow (2 cm) and deep (3–7 cm) water. Members of this species are appropriate subjects because they are ecologically intermediate between the generalists and aquatic specialists studied by Drummond, and thus might be expected to show more variation in aquatic foraging behaviour than those species. T. validus showed significantly higher frequencies of crawling on the underwater substrate and of underwater strikes in the deep water than in the shallow water; i.e. increased water depth shifted the behaviour of these snakes toward that of aquatic specialists, thus supporting Drummond's hypothesis. Individuals of an aquatic specialist species, the narrow‐headed garter snake (T. rufipunctatus), showed less pronounced changes in behaviour with increased water depth. Western ribbon snakes (T. proximus), which feed primarily at the land–water interface (and are expected to act like terrestrial–aquatic generalists), typically refused to feed in deep water. Interspecific differences in underwater visual acuity may underly the behavioural differences among the three species by determining whether changes in foraging behaviour with water depth are advantageous. Information on phylogenetic relationships suggests that the facultative behaviour of T. validus may represent an intermediate stage in the evolution of aquatic specialization.     

Interpretation of Genetic Association Studies: Markers with Replicated Highly Significant Odds Ratios May Be Poor Classifiers

Recent successful discoveries of potentially causal single nucleotide polymorphisms (SNPs) for complex diseases hold great promise, and commercialization of genomics in personalized medicine has already begun. The hope is that genetic testing will benefit patients and their families, and encourage positive lifestyle changes and guide clinical decisions. However, for many complex diseases, it is arguable whether the era of genomics in personalized medicine is here yet. We focus on the clinical validity of genetic testing with an emphasis on two popular statistical methods for evaluating markers. The two methods, logistic regression and receiver operating characteristic (ROC) curve analysis, are applied to our age-related macular degeneration dataset. By using an additive model of the CFH, LOC387715, and C2 variants, the odds ratios are 2.9, 3.4, and 0.4, with p-values of 10⁻¹³, 10⁻¹³, and 10⁻³, respectively. The area under the ROC curve (AUC) is 0.79, but assuming prevalences of 15%, 5.5%, and 1.5% (which are realistic for age groups 80 y, 65 y, and 40 y and older, respectively), only 30%, 12%, and 3% of the group classified as high risk are cases. Additionally, we present examples for four other diseases for which strongly associated variants have been discovered. In type 2 diabetes, our classification model of 12 SNPs has an AUC of only 0.64, and two SNPs achieve an AUC of only 0.56 for prostate cancer. Nine SNPs were not sufficient to improve the discrimination power over that of nongenetic predictors for risk of cardiovascular events. Finally, in Crohn''s disease, a model of five SNPs, one with a quite low odds ratio of 0.26, has an AUC of only 0.66. Our analyses and examples show that strong association, although very valuable for establishing etiological hypotheses, does not guarantee effective discrimination between cases and controls. The scientific community should be cautious to avoid overstating the value of association findings in terms of personalized medicine before their time.     

Why Therapeutic Response May Not Prolong the Life of a Cancer Patient: Selection for Oncogenic Resistance

Most cancers do not respond to chemotherapy. Disappointedly, even objective clinical responses to anticancer therapy often do not translate into improvements in overall survival. To explain the response-survival paradox, it has been pointed out that effective therapy is ineffective against cancer stem cells, which replenish the tumor (causing relapse). In contrast, I discuss that, according to this scenario, patient survival will be prolonged at least by the duration of remission. Furthermore, stem-cell-based relapses will be sensitive to the initial therapy, and in theory cancer could be controlled indefinitely. To explain the paradox, I discuss that effective therapy selects for resistance among proliferating cancer cells. Importantly, mechanisms of resistance can be divided into non-oncogenic (e.g., drug transporters and mutation in drug-targets) and oncogenic (apoptosis and cell cycle dysregulation). The latter is associated with highly aggressive cancer phenotype and, therefore, there is no increase in overall survival. I further suggest that (a) therapeutic response is a prerequisite for successful therapy, (b) resistance can be exploited for therapeutic advantage, (c) each response can be translated into increased survival, and (e) in slow growing tumors, cancer can be stopped without tumor shrinkage. Therapy will control cancer if it can selectively suppress proliferating cancer cells and will improve survival as long as acquired resistance can be exploited.     

Polymerization of Purified Yeast Septins: Evidence That Organized Filament Arrays May Not Be Required for Septin Function

The septins are a family of proteins required for cytokinesis in a number of eukaryotic cell types. In budding yeast, these proteins are thought to be the structural components of a filament system present at the mother–bud neck, called the neck filaments. In this study, we report the isolation of a protein complex containing the yeast septins Cdc3p, Cdc10p, Cdc11p, and Cdc12p that is capable of forming long filaments in vitro. To investigate the relationship between these filaments and the neck filaments, we purified septin complexes from cells deleted for CDC10 or CDC11. These complexes were not capable of the polymerization exhibited by wild-type preparations, and analysis of the neck region by electron microscopy revealed that the cdc10Δ and cdc11Δ cells did not contain detectable neck filaments. These results strengthen the hypothesis that the septins are the major structural components of the neck filaments. Surprisingly, we found that septin dependent processes like cytokinesis and the localization of Bud4p to the neck still occurred in cdc10Δ cells. This suggests that the septins may be able to function in the absence of normal polymerization and the formation of a higher order filament structure.     

My Neighbor: Children's Perception of Agency in Interaction with an Imaginary Agent

Children may treat an invisible entity as a live and thinking entity, known as an imaginary companion (IC). Some researchers suggest that this is simply pretend play, but it is possible that children experience agency in their interactions with ICs. Given the literature on cognitive science and social brain research, we hypothesize that young children may have an agent-perception system that responds to an invisible agent by which they may experience realistic agency in their interactions with ICs. In this study, children were introduced to an invisible agent and an invisible stone. However, they assigned biological and psychological properties to the agent but not the stone. The tendency of assigning such properties was stronger in children with ICs than in those without ICs. These results contribute to our understanding of cognitive and neural development in typical and atypical children.     

The Striatal Transporter for Dopamine in the Rat May Be Kinetically Up-Regulated Following 3 Weeks of Withdrawal from Cocaine Self-Administration

Abstract: Rotating disk electrode voltammetry was used to measure the inwardly directed V_max and K_m of dopamine with its transporter in striatal suspensions prepared from nonhandled control rats, rats that had been trained to self-administer cocaine for 20 days (at 26 mg/day per rat) via a jugular catheter and subsequently withdrawn for 3 weeks, and rats that had received saline (155 mM NaCl) via a jugular catheter on the same schedule as the rats that had received cocaine. Because a limited number of animals was available from the self-administration procedure, the velocity of dopamine transport as a function of [dopamine] was measured by incremental addition of dopamine to a given striatal preparation. In nonhandled controls the values of V_max, K_m, and turnover, observed in this experimental paradigm, were increased relative to results obtained in studies of the velocity-[dopamine] relationship where dopamine was added to suspensions, one concentration per suspension. The kinetics of the association of dopamine with the transporter were unchanged. The V_max to K_m ratios obtained in the two experiments were statistically indistinguishable, suggesting that the two types of experiments probe the same transporter. Also, the increased velocity observed in the experiment involving sequential additions to the same preparation is evidence of trans acceleration, suggesting that the movement of dopamine across the membrane is carrier mediated as opposed to being mediated via channels or pores and that the rate-limiting step in inwardly directed transport is the reorientation of the unloaded transporter from the inwardly to the outwardly facing forms. Saline-treated rats in the self-administration paradigm exhibited kinetic parameters of transport indistinguishable from those observed in nonhandled controls. In contrast, V_max and K_m of the transporter were increased in suspensions prepared from rats that self-administered cocaine and were withdrawn for 3 weeks, relative to saline-treated and nonhandled animals. Combined, these results suggest that the striatal uptake of dopamine is mediated by a transporter and that it is kinetically up-regulated following withdrawal from repeated cocaine administered in a self-administration paradigm.     

Role of the Golgi Apparatus in the Blood-Brain Barrier: Golgi Protection May Be a Targeted Therapy for Neurological Diseases

The blood-brain barrier (BBB) protects the brain from toxic material in the blood, provides nutrients for brain tissues, and screens harmful substances from the brain. The specific brain microvascular endothelial cells (BMVECs), tight junction between endothelial cells, and astrocytes ensure proper function of the central nervous system (CNS). Pathological factors disrupt the integrity of the BBB by destroying the normal function of endothelial cells and decreasing the production of tight junction proteins or the expression of proteins specifically localized on astrocytes. Interestingly, fragmentation of the Golgi apparatus is observed in neurological diseases and is involved in the destruction of the BBB function. The Golgi acts as a processing center in which proteins are transported after being processed in the endoplasmic reticulum. Besides reprocessing, classifying, and packaging proteins, the Golgi apparatus (GA) also acts as a signaling platform and calcium pool. In this review, we summarized the current literature on the potential relationship between the Golgi and endothelial cells, tight junction, and astrocytes. The normal function of the BBB is maintained as long as the normal function and morphology of the GA are not disturbed. Furthermore, we speculate that protecting the Golgi may be a novel therapeutic approach to protect the BBB and treat neurological diseases due to BBB dysfunction.     

The Senescence Hypothesis of Disease Progression in Alzheimer Disease: an Integrated Matrix of Disease Pathways for FAD and SAD

Alzheimer disease (AD) is a progressive, neurodegenerative disease characterised in life by cognitive decline and behavioural symptoms and post-mortem by the neuropathological hallmarks including the microtubule-associated protein tau-reactive tangles and neuritic plaques and amyloid-beta-protein-reactive senile plaques. Greater than 95 % of AD cases are sporadic (SAD) with a late onset and <5 % of AD cases are familial (FAD) with an early onset. FAD is associated with various genetic mutations in the amyloid precursor protein (APP) and the presenilins (PS)1 and PS2. As yet, no disease pathway has been fully accepted and there are no treatments that prevent, stop or reverse the cognitive decline associated with AD. Here, we review and integrate available environmental and genetic evidence associated with all forms of AD. We present the senescence hypothesis of AD progression, suggesting that factors associated with AD can be seen as partial stressors within the matrix of signalling pathways that underlie cell survival and function. Senescence pathways are triggered when stressors exceed the cells ability to compensate for them. The APP proteolytic system has many interactions with pathways involved in programmed senescence and APP proteolysis can both respond to and be driven by senescence-associated signalling. Disease pathways associated with sporadic disease may be different to those involving familial genetic mutations. The interpretation we provide strongly points to senescence as an additional underlying causal process in dementia progression in both SAD and FAD via multiple disease pathways.     

I Foresee My Life: The Ritual Performance of Autobiography in an Amazonian Community

I Foresee My Life: The Ritual Performance of Autobiography in an Amazonian Community . Suzanne Oakdale. Lincoln: University of Nebraska Press, 2006. 206 pp.     

Facilitative-Competitive Interactions in an Old-Growth Forest: The Importance of Large-Diameter Trees as Benefactors and Stimulators for Forest Community Assembly

The role of competition in tree communities is increasingly well understood, while little is known about the patterns and mechanisms of the interplay between above- and belowground competition in tree communities. This knowledge, however, is crucial for a better understanding of community dynamics and developing adaptive near-natural management strategies. We assessed neighbourhood interactions in an unmanaged old-growth European beech (Fagus sylvatica) forest by quantifying variation in the intensity of above- (shading) and belowground competition (crowding) among dominant and co-dominant canopy beech trees during tree maturation. Shading had on average a much larger impact on radial growth than crowding and the sensitivity to changes in competitive conditions was lowest for crowding effects. We found that each mode of competition reduced the effect of the other. Increasing crowding reduced the negative effect of shading, and at high levels of shading, crowding actually had a facilitative effect and increased growth. Our study demonstrates that complementarity in above- and belowground processes enable F. sylvatica to alter resource acquisition strategies, thus optimising tree radial growth. As a result, competition seemed to become less important in stands with a high growing stock and tree communities with a long continuity of anthropogenic undisturbed population dynamics. We suggest that growth rates do not exclusively depend on the density of potential competitors at the intraspecific level, but on the conspecific aggregation of large-diameter trees and their functional role for regulating biotic filtering processes. This finding highlights the potential importance of the rarely examined relationship between the spatial aggregation pattern of large-diameter trees and the outcome of neighbourhood interactions, which may be central to community dynamics and the related forest ecosystem services.     

A 21-Day of Adjunctive Corticosteroid Use May Not Be Necessary for HIV-1-Infected Pneumocystis Pneumonia with Moderate and Severe Disease

Background

The current guidelines recommend 21-day adjunctive corticosteroid therapy for HIV-1-infected pneumocystis pneumonia patients (HIV-PCP) with moderate-to-severe disease. Whether shorter adjunctive corticosteroid therapy is feasible in such patients is unknown.

Methods

We conducted a retrospective study to elucidate the proportion of patients with moderate and severe HIV-PCP who required adjunctive corticosteroid therapy for 21 days. The enrollment criteria included HIV-PCP that fulfilled the current criteria for 21-day corticosteroid therapy; PaO₂ on room air of <70mmHg or A-aDO₂ ≥35 mmHg.

Results

The median duration of corticosteroid therapy in the 73 study patients was 13 days (IQR 9–21). Adjunctive corticosteroid therapy was effective and discontinued within 10 and 14 days in 30% and 60% of the patients, respectively. Only 9% of the patients with moderate HIV-PCP (n = 22, A-aDO₂ 35–45 mmHg) received steroids for >14 days, whereas 35% of the patients with severe HIV-PCP (n = 51, A-aDO₂ ≥45 mmHg) required corticosteroid therapy for ≥21 days. Four (13%) of the severe cases died, whereas no patient with moderate disease died. Among patients with severe HIV-PCP, discontinuation of corticosteroid therapy within 14 days correlated significantly with higher baseline CD4 (p = 0.049).

Conclusion

Shorter adjunctive corticosteroid therapy was clinically effective and adjunctive corticosteroid could be discontinued within 14 days in 60% of moderate-to-severe HIV-PCP and 90% of moderate cases.     

The Origin of Cladocera (Crustacea,Branchiopoda): A New Understanding of an Old Hypothesis

Comparative analysis of the ontogeny of representatives of two sister taxa (Cladocera and Cyclestherida) showed that the paedomorphic morphology of cladocerans (the small number of thoracic segments and segments of branches of antennae II, and the reduction of the carapace) was caused by the cessation of development of the somatic structures at early larval stages of ontogeny. It is demonstrated that this stop is not associated with the accelerated development of the reproductive system (progenesis), since it takes place long prior to the beginning of reproduction. In accordance with this fact, the past hypotheses that cladocerans evolved from the reproducing larvae of the ancestral form or that they are early maturing metanauplii should be recognized as erroneous. Cyclestheria. The origin of Cladocera from a Cyclestheria-like ancestor should be regarded as neotenic, taking into consideration the extended interpretation of this term.