Miracle-dz/UniFAR-FTUs huggingface dataset:
Models in animal collective decision-making: information uncertainty and conflicting preferences

Collective decision-making plays a central part in the lives of many social animals. Two important factors that influence collective decision-making are information uncertainty and conflicting preferences. Here, I bring together, and briefly review, basic models relating to animal collective decision-making in situations with information uncertainty and in situations with conflicting preferences between group members. The intention is to give an overview about the different types of modelling approaches that have been employed and the questions that they address and raise. Despite the use of a wide range of different modelling techniques, results show a coherent picture, as follows. Relatively simple cognitive mechanisms can lead to effective information pooling. Groups often face a trade-off between decision accuracy and speed, but appropriate fine-tuning of behavioural parameters could achieve high accuracy while maintaining reasonable speed. The right balance of interdependence and independence between animals is crucial for maintaining group cohesion and achieving high decision accuracy. In conflict situations, a high degree of decision-sharing between individuals is predicted, as well as transient leadership and leadership according to needs and physiological status. Animals often face crucial trade-offs between maintaining group cohesion and influencing the decision outcome in their own favour. Despite the great progress that has been made, there remains one big gap in our knowledge: how do animals make collective decisions in situations when information uncertainty and conflict of interest operate simultaneously?
Rab11 facilitates cross-talk between autophagy and endosomal pathway through regulation of Hook localization

During autophagy, double-membrane autophagosomes deliver sequestered cytoplasmic content to late endosomes and lysosomes for degradation. The molecular mechanism of autophagosome maturation is still poorly characterized. The small GTPase Rab11 regulates endosomal traffic and is thought to function at the level of recycling endosomes. We show that loss of Rab11 leads to accumulation of autophagosomes and late endosomes in Drosophila melanogaster. Rab11 translocates from recycling endosomes to autophagosomes in response to autophagy induction and physically interacts with Hook, a negative regulator of endosome maturation. Hook anchors endosomes to microtubules, and we show that Rab11 facilitates the fusion of endosomes and autophagosomes by removing Hook from mature late endosomes and inhibiting its homodimerization. Thus induction of autophagy appears to promote autophagic flux by increased convergence with the endosomal pathway.
New Insights on Interstellar Gas-Phase Iron

In this paper we report on the gas-phase abundance of singly ionized iron (Fe II) for 51 lines of sight, using data from FUSE. Fe II column densities are derived by measuring the equivalent widths of several UV absorption lines and subsequently fitting those to a curve of growth. Our derivation of Fe II column densities and abundances creates the largest sample of iron abundances in moderately to highly reddened lines of sight explored with FUSE, lines of sight that are on average more reddened than lines of sight in previous Copernicus studies. We present three major results. First, we observe the well-established correlation between iron depletion and ⟨nH⟩ and also find trends between iron depletion and other line-of-sight parameters [e.g., f(H2), EB-V, and AV], and we examine the significance of these trends. Of note, a few of our lines of sight probe larger densities than previously explored and we do not see significantly enhanced depletion effects. Second, we present two detections of an extremely weak Fe II line at 1901.773 Å in the archival STIS spectra of two lines of sight (HD 24534 and HD 93222). We compare these detections to the column densities derived through FUSE spectra and comment on the line's f-value and utility for future studies of Fe II. Finally, we present strong anecdotal evidence that the Fe II f-values derived empirically through FUSE data are more accurate than previous values that have been theoretically calculated, with the probable exception of f1112.
Interleukin-6 Gene −174G>C and −572G>C Promoter Polymorphisms Are Strong Predictors of Plasma Interleukin-6 Levels After Coronary Artery Bypass Surgery

Interleukin-6 (IL-6) synthesized in response to diverse stimuli may play an important role in bridging the inflammatory and atherosclerotic processes. The acute-phase response after coronary artery bypass graft surgery (CABG) is associated with the induction and release of cytokines, such as IL-6. We have examined the effect of common polymorphisms in the IL-6 gene promoter (−174G>C, −572G>C, and −597G>A) on IL-6 levels after elective CABG. DNA extracted from the peripheral blood of 127 patients was amplified by polymerase chain reaction. IL-6 genotypes were resolved by gel electrophoresis after restriction enzyme digestion. Serum IL-6 was measured before surgery and in serial samples at 6, 24, 48, and 72 hours after CABG. Genotype distribution was as expected for a population in Hardy-Weinberg equilibrium for all polymorphisms. Rare allele frequencies (±95% CIs) were similar to those reported previously: −597A 0.36 (0.30 to 0.42), −572C 0.07 (0.04 to 0.10), and −174C 0.37 (0.31 to 0.43). The −174G>C and −597G>A genotypes were in strong allelic association (&Dgr;=0.97, P <0.001). Baseline IL-6 levels did not significantly differ between patients with different genotypes for any polymorphism. However, 6 hours after CABG, peak IL-6 levels were significantly higher (P =0.03) in carriers of the −572C allele than in those of the −572GG genotype (355±67 versus 216±13 pg/mL, respectively) and in those with genotype −174CC compared with −174G allele carriers (287±31 versus 227±15 pg/mL, respectively;P =0.04). These effects remained statistically significant after adjusting for possible confounders, including age, sex, smoking, duration of cardiopulmonary bypass, aortic cross-clamp time, and total duration of surgery. These data demonstrate that IL-6 promoter polymorphisms influence peak IL-6 production after CABG, suggesting that these polymorphisms, which are functional in vitro, are also functional in vivo, suggesting a genetic influence on IL-6 levels after acute severe injury.
Hemolytic reactions produced in dogs by transfusion of incompatible dog blood and plasma; renal aspects following whole blood transfusions.

By LAWRENCE E. YOUNG, M.D., DONALD M. ERVIN, M.D., AND CHARLES L. YUILE, M.D. H EMOLYTIC transfusion reactions occur more frequently than is generally appreciated and their incidence can be expected to increase for some time as the distribution of blood is facilitated. Many are doubtless overlooked because the outward manifestations may not be particularly striking, especially in anesthetized patients and in certain recipients transfused with plasma or with blood from universal donors. Despite the increasing importance of such reactions, their pathologic physiology remains poorly understood and cannot be adequately explored in human subjects. Consideration of these facts stimulated the authors to make observations on planned hemolytic reactions in dogs with the hope that the results might find general application in the field of immuno-hematology, and that they might throw light on the behavior of the kidney when subjected to certain types of insult. The purpose of this paper is to describe preliminary serologic and hematologic observations on reactions produced in dogs by transfusion of incompatible whole blood and plasma. Typical experiments are cited to illustrate the usefulness of iso-immune systems in the dog in making quantitative studies of hemolytic phenomena. Alterations in renal physiology observed during these experiments are described in an accompanying report. ’
The costs of avian brood parasitism explain variation in egg rejection behaviour in hosts

Many bird species can reject foreign eggs from their nests. This behaviour is thought to have evolved in response to brood parasites, birds that lay their eggs in the nest of other species. However, not all hosts of brood parasites evict parasitic eggs. In this study, we collate data from egg rejection experiments on 198 species, and perform comparative analyses to understand the conditions under which egg rejection evolves. We found evidence, we believe for the first time in a large-scale comparative analysis, that (i) non-current host species have rejection rates as high as current hosts, (ii) egg rejection is more likely to evolve when the parasite is relatively large compared with its host and (iii) egg rejection is more likely to evolve when the parasite chick evicts all the host eggs from the nest, such as in cuckoos. Our results suggest that the interactions between brood parasites and their hosts have driven the evolution of egg rejection and that variation in the costs inflicted by parasites is fundamental to explaining why only some host species evolve egg rejection.
Disproportional Control Rights and the Bonding Role of Debt

We examine how firms’ capital structure choices vary with the presence of dual-class ownership and the degree of disproportional control associated with it. We document that, compared to a propensity-matched sample of single-class firms, dual-class firms have higher leverage, greater propensity to issue private debt, more long-term debt, and greater reliance on financial covenants. Within our dual-class sample, the use of debt financing increases with the degree of disproportional control via voting rights or board election rights. This evidence is consistent with controlling insiders bonding against the agency problems associated with dual-class ownership through their capital structure choices. Also consistent with this view, we document that leverage attenuates (and ultimately reverses) the adverse effect of dual-class status on Tobin’s q and cost of equity capital, and is associated with increased institutional investment in dual-class firms. Taken together, our evidence suggests that debt plays a governance role and disciplines insiders in dual-class firms.
Uridine 5′-Triphosphate Promotes In Vitro Schwannoma Cell Migration through Matrix Metalloproteinase-2 Activation

In response to peripheral nerve injury, Schwann cells adopt a migratory phenotype and modify the extracellular matrix to make it permissive for cell migration and axonal re-growth. Uridine 5′-triphosphate (UTP) and other nucleotides are released during nerve injury and activate purinergic receptors expressed on the Schwann cell surface, but little is known about the involvement of purine signalling in wound healing. We studied the effect of UTP on Schwannoma cell migration and wound closure and the intracellular signaling pathways involved. We found that UTP treatment induced Schwannoma cell migration through activation of P2Y2 receptors and through the increase of extracellular matrix metalloproteinase-2 (MMP-2) activation and expression. Knockdown P2Y2 receptor or MMP-2 expression greatly reduced wound closure and MMP-2 activation induced by UTP. MMP-2 activation evoked by injury or UTP was also mediated by phosphorylation of all 3 major mitogen-activated protein kinases (MAPKs): JNK, ERK1/2, and p38. Inhibition of these MAPK pathways decreased both MMP-2 activation and cell migration. Interestingly, MAPK phosphorylation evoked by UTP exhibited a biphasic pattern, with an early transient phosphorylation 5 min after treatment, and a late and sustained phosphorylation that appeared at 6 h and lasted up to 24 h. Inhibition of MMP-2 activity selectively blocked the late, but not the transient, phase of MAPK activation. These results suggest that MMP-2 activation and late MAPK phosphorylation are part of a positive feedback mechanism to maintain the migratory phenotype for wound healing. In conclusion, our findings show that treatment with UTP stimulates in vitro Schwannoma cell migration and wound repair through a MMP-2-dependent mechanism via P2Y2 receptors and MAPK pathway activation.
High on-treatment platelet reactivity and P2Y12 antagonists in clinical trials

Summary Dual antiplatelet therapy with aspirin and clopidogrel in patients undergoing percutaneous coronary intervention (PCI) and in patients with acute coronary syndromes (ACS) has substantially decreased the rate of cardiovascular events. Within the past decade, the variability in pharmacodynamic response as well as the moderate antiplatelet efficacy of clopidogrel has raised major concerns, since high on-clopidogrel platelet reactivity has consistently been associated with increased risk for ischaemic events in PCI patients. The variability in response could be linked to genetic polymorphisms impacting on activity of cytochrome P450 enzymes as well as clinical and demographic variables, but, taken together, factors identified so far can explain only up to approximately 12% of this variability in adenosine diphosphate-induced platelet aggregation on clopidogrel. Regulatory agencies as well as major cardiac societies suggest the use of other anti-platelet medications or alternative dosing strategies for clopidogrel in patients with reduced effectiveness of clopidogrel. This review will focus on the current status of alternate strategies for more sufficient suppression of high platelet reactivity.
A Hundred Cases of Suicide: Clinical Aspects

Historically, doctors have not always acknowledged that they have an obligation to prevent suicide, partly because they shared the prevalent idea that most suicides were caused by moral crises, no concern of theirs—and indeed suicide was a criminal matter until quite recently; but more, perhaps, because a fatalism has characterized their attitudes to its prevention, even where the suicide was clearly suffering from mental illness. Yet two recent American studies have shown more than 90 per cent of suicides to be mentally ill before their death (17, 8); this finding and the familiar clinical observation that suicidal thoughts disappear when the illness is successfully treated provide a strong case for a medical policy of prevention.
Ecology Drives the Distribution of Specialized Tyrosine Metabolism Modules in Fungi

Gene clusters encoding accessory or environmentally specialized metabolic pathways likely play a significant role in the evolution of fungal genomes. Two such gene clusters encoding enzymes associated with the tyrosine metabolism pathway (KEGG #00350) have been identified in the filamentous fungus Aspergillus fumigatus. The l-tyrosine degradation (TD) gene cluster encodes a functional module that facilitates breakdown of the phenolic amino acid, l-tyrosine through a homogentisate intermediate, but is also involved in the production of pyomelanin, a fungal pathogenicity factor. The gentisate catabolism (GC) gene cluster encodes a functional module likely involved in phenolic compound degradation, which may enable metabolism of biphenolic stilbenes in multiple lineages. Our investigation of the evolution of the TD and GC gene clusters in 214 fungal genomes revealed spotty distributions partially shaped by gene cluster loss and horizontal gene transfer (HGT). Specifically, a TD gene cluster shows evidence of HGT between the extremophilic, melanized fungi Exophiala dermatitidis and Baudoinia compniacensis, and a GC gene cluster shows evidence of HGT between Sordariomycete and Dothideomycete grass pathogens. These results suggest that the distribution of specialized tyrosine metabolism modules is influenced by both the ecology and phylogeny of fungal species.
The cell-surface marker MTS24 identifies a novel population of follicular keratinocytes with characteristics of progenitor cells

We describe a novel murine progenitor cell population localised to a previously uncharacterised region between sebaceous glands and the hair follicle bulge, defined by its reactivity to the thymic epithelial progenitor cell marker MTS24. MTS24 labels a membrane-bound antigen present during the early stages of hair follicle development and in adult mice. MTS24 co-localises with expression of α6-integrin and keratin 14, indicating that these cells include basal keratinocytes. This novel population does not express the bulge-specific stem cell markers CD34 or keratin 15, and is infrequently BrdU label retaining. MTS24-positive and -negative keratinocyte populations were isolated by flow cytometry and assessed for colony-forming efficiency. MTS24-positive keratinocytes exhibited a two-fold increase in colony formation and colony size compared to MTS24-negative basal keratinocytes. In addition, both the MTS24-positive and CD34-positive subpopulations were capable of producing secondary colonies after serial passage of individual cell clones. Finally, gene expression profiles of MTS24 and CD34 subpopulations were compared. These results showed that the overall gene expression profile of MTS24-positive cells resembles the pattern previously reported in bulge stem cells. Taken together, these data suggest that the cell-surface marker MTS24 identifies a new reservoir of hair follicle keratinocytes with a proliferative capacity and gene expression profile suggestive of progenitor or stem cells.
Sandpile on scale-free networks.

We investigate the avalanche dynamics of the Bak-Tang-Wiesenfeld sandpile model on scale-free (SF) networks, where the threshold height of each node is distributed heterogeneously, given as its own degree. We find that the avalanche size distribution follows a power law with an exponent tau. Applying the theory of the multiplicative branching process, we obtain the exponent tau and the dynamic exponent z as a function of the degree exponent gamma of SF networks as tau=gamma divided by (gamma-1) and z=(gamma-1) divided by (gamma-2) in the range 23, with a logarithmic correction at gamma=3. The analytic solution supports our numerical simulation results. We also consider the case of a uniform threshold, finding that the two exponents reduce to the mean-field ones.
The V beta repertoire of mouse gut homodimeric alpha CD8+ intraepithelial T cell receptor alpha/beta + lymphocytes reveals a major extrathymic pathway of T cell differentiation

Gut intraepithelial lymphocytes (IEL) contain two independent T cell receptor alpha/beta + T cell populations, with different V beta repertoires. In DBA/2 mice (Mlsa, IE+), the CD4+ and heterodimeric alpha/beta CD8+ thymodependent T cell pool shows the same deletion of V beta 6, 8.1, and 11+ cells as found in peripheral lymphoid organs. In contrast, such deletions are not observed in the pool of IEL bearing homodimeric alpha CD8+ chains, in which these V beta families are frequently observed in high amounts. The size of this gut homodimeric alpha CD8+ IEL pool and its different V beta repertoire selection demonstrate the existence of a major extrathymic pathway of T cell differentiation with a gut-restricted localization. The large amount of the thymo-independent, homodimeric alpha CD8+ IEL found in the small bowel may contribute to a first line of defense against exogenous superantigens.
Leucine-Responsive Regulatory Protein Lrp and PapI Homologues Influence Phase Variation of CS31A Fimbriae

ABSTRACT CS31A, a K88-related surface antigen specified by the clp operon, is a member of the type P family of adhesive factors and plays a key role in the establishment of disease caused by septicemic and enterotoxigenic Escherichia coli strains. Its expression is under the control of methylation-dependent transcriptional regulation, for which the leucine-responsive regulatory protein (Lrp) is essential. CS31A is preferentially in the OFF state and exhibits distinct regulatory features compared to the regulation of other P family members. In the present study, surface plasmon resonance and DNase I protection assays showed that Lrp binds to the distal moiety of the clp regulatory region with low micromolar affinity compared to its binding to the proximal moiety, which exhibits stronger, nanomolar affinity. The complex formation was also influenced by the addition of PapI or FooI, which increased the affinity of Lrp for the clp distal and proximal regions and was required to induce phase variation. The influence of PapI or FooI, however, was predominantly associated with a more complete shutdown of clp expression, in contrast to what has previously been observed with AfaF (a PapI ortholog). Taken together, these results suggest that the preferential OFF state observed in CS31A cells is mainly due to the weak interaction of the leucine-responsive regulatory protein with the clp distal region and that the PapI homolog favors the OFF phase. Within the large repertoire of fimbrial variants in the P family, our study illustrates that having a fimbrial operon that lacks its own PapI ortholog allows it to be more flexibly regulated by other orthologs in the cell.
DNA photorepair in echinoid embryos: effects of temperature on repair rate in Antarctic and non-Antarctic species

SUMMARY To determine if an Antarctic species repairs DNA at rates equivalent to warmer water equivalents, we examined repair of UV-damaged DNA in echinoid embryos and larvae. DNA repair by photoreactivation was compared in three species Sterechinus neumayeri (Antarctica), Evechinus chloroticus (New Zealand) and Diadema setosum (Tropical Australia) spanning a latitudinal gradient from polar (77.86°S) to tropical (19.25°S) environments. We compared rates of photoreactivation as a function of ambient and experimental temperature in all three species, and rates of photoreactivation as a function of embryonic developmental stage in Sterechinus. DNA damage was quantified from cyclobutane pyrimidine dimer (CPD) concentrations and rates of abnormal embryonic development. This study established that in the three species and in three developmental stages of Sterechinus, photoreactivation was the primary means of removing CPDs, was effective in repairing all CPDs in less than 24 h, and promoted significantly higher rates of normal development in UV-exposed embryos. CPD photorepair rate constant (k) in echinoid embryos ranged from 0.33 to 1.25 h-1, equating to a time to 50% repair of between 0.6 and 2.1 h and time to 90%repair between 3.6 and 13.6 h. We observed that experimental temperature influenced photoreactivation rate. In Diadema plutei, the photoreactivation rate constant increased from k=0.58 h-1 to 1.25 h-1, with a Q10=2.15 between 22°C and 32°C. When compared among the three species across experimental temperatures (-1.9 to 32°C), photoreactivation rates vary with a Q10=1.39. Photoreactivation rates were examined in three developmental stages of Sterechinus embryos, and while not significantly different, repair rates tended to be higher in the younger blastula and gastrula stages compared with later stage embryos. We concluded that photoreactivation is active in the Antarctic Sterechinus, but at a significantly slower (non-temperature compensated) rate. The low level of temperature compensation in photoreactivation may be one explanation for the relatively high sensitivity of Antarctic embryos to UV-R in comparison with non-Antarctic equivalents.