Miracle-dz/UniFAR-FTUs huggingface dataset:
The genetic basis of adaptive melanism in pocket mice

Identifying the genes underlying adaptation is a major challenge in evolutionary biology. Here, we describe the molecular changes underlying adaptive coat color variation in a natural population of rock pocket mice, Chaetodipus intermedius. Rock pocket mice are generally light-colored and live on light-colored rocks. However, populations of dark (melanic) mice are found on dark lava, and this concealing coloration provides protection from avian and mammalian predators. We conducted association studies by using markers in candidate pigmentation genes and discovered four mutations in the melanocortin-1-receptor gene, Mc1r, that seem to be responsible for adaptive melanism in one population of lava-dwelling pocket mice. Interestingly, another melanic population of these mice on a different lava flow shows no association with Mc1r mutations, indicating that adaptive dark color has evolved independently in this species through changes at different genes.
Distributed Energy Trading: The Multiple-Microgrid Case

In this paper, a distributed convex optimization framework is developed for energy trading between islanded microgrids. More specifically, the problem consists of several islanded microgrids that exchange energy flows by means of an arbitrary topology. Due to scalability issues and in order to safeguard local information on cost functions, a subgradient-based cost minimization algorithm that converges to the optimal solution in a practical number of iterations and with limited communication overhead is proposed. Furthermore, this approach allows for a very intuitive economics interpretation that explains the algorithm iterations in terms of a “supply-demand model” and “market clearing. ” Numerical results are given in terms of the convergence rate of the algorithm and the attained costs for different network topologies.
In-Group and Out-Group Membership Mediates Anterior Cingulate Activation to Social Exclusion

Functional magnetic resonance imaging was employed to examine sensitivity to social exclusion in three conditions: same-race, other-race, and self-resembling faces. The anterior cingulate cortex (ACC), specifically the dorsal ACC, has been targeted as a key substrate in the physical and social pain matrix and was hypothesized to regulate activation response to various facial conditions. We show that participants demonstrated greatest ACC activation when being excluded by self-resembling and same-race faces, relative to other-race faces. Additionally, participants expressed greater distress and showed increased ACC activation as a result of exclusion in the same-race condition relative to the other-race condition. A positive correlation between implicit racial bias and activation in the amygdala was also evident. Implicit attitude about other-race faces partly explains levels of concern about exclusion by out-group individuals. These findings suggest that individuals are more distressed and their brain (i.e. neural alarm system) responds with greater activation when being excluded by individuals whom they are more likely to share group membership with.
Imagery encoding and false recognition errors: Examining the role of imagery process and imagery content on source misattributions

Imagery encoding effects on source-monitoring errors were explored using the Deese-Roediger-McDermott paradigm in two experiments. While viewing thematically related lists embedded in mixed picture/word presentations, participants were asked to generate images of objects or words (Experiment 1) or to simply name the items (Experiment 2). An encoding task intended to induce spontaneous images served as a control for the explicit imagery instruction conditions (Experiment 1). On the picture/word source-monitoring tests, participants were much more likely to report “seeing” a picture of an item presented as a word than the converse particularly when images were induced spontaneously. However, this picture misattribution error was reversed after generating images of words (Experiment 1) and was eliminated after simply labelling the items (Experiment 2). Thus source misattributions were sensitive to the processes giving rise to imagery experiences (spontaneous vs deliberate), the kinds of images generated (object vs word images), and the ways in which materials were presented (as pictures vs words).
Aquaporin-3-dependent cell migration and proliferation during corneal re-epithelialization.

PURPOSE To determine a role for the water- and glycerol-transporting protein aquaporin-3 (AQP3) in mammalian corneal epithelium, where it is expressed but has no known function. METHODS Corneal epithelial water and glycerol permeabilities were measured in living wild-type and AQP3-null mice using calcein fluorescence-quenching and 14C-glycerol-uptake assays, respectively. After removal of the corneal epithelium by scraping, re-epithelialization was followed by fluorescein staining. The contribution of AQP3-facilitated cell migration to corneal re-epithelialization was assessed using an organ culture model, in which initial resurfacing results from epithelial cell migration, as shown by BrdU analysis and 5-fluorouracil insensitivity, and by scratch wound assay using primary cultures of corneal epithelial cells from wild-type versus AQP3-null mice. Involvement of AQP3 in epithelial cell proliferation was investigated by morphometric and BrdU analysis of histologic sections, and by measurement of [3H]thymidine uptake in primary cultures of corneal epithelial cells. RESULTS AQP3 deficiency did not alter corneal epithelial thickness, morphology, or glycerol content, though both water and glycerol permeabilities were reduced. Time to corneal re-epithelialization in vivo was significantly delayed in AQP3-null mice compared to wild-type mice. Delays were also found in organ and primary cultures, demonstrating a distinct defect in cell migration arising from AQP3 deletion. Delayed restoration of full-thickness epithelia of AQP3-null mice over days after scraping suggested a separate defect in epithelial cell proliferation, which was confirmed by reduction in proliferating BrdU-positive cells in AQP3-deficient mice during healing, and by reduced proliferation in primary cultures of corneal epithelial cells from AQP3-null mice. CONCLUSIONS The significant impairment in corneal re-epithelialization in AQP3-deficient mice results from distinct defects in corneal epithelial cell migration and proliferation. The results provide evidence for involvement of an aquaporin in cell proliferation and suggest AQP3 induction as a possible therapy to accelerate the resurfacing of corneal defects.
Biofilm growth mode promotes maximum carrying capacity and community stability during product inhibition syntrophy

Sulfate-reducing bacteria (SRB) can interact syntrophically with other community members in the absence of sulfate, and interactions with hydrogen-consuming methanogens are beneficial when these archaea consume potentially inhibitory H2 produced by the SRB. A dual continuous culture approach was used to characterize population structure within a syntrophic biofilm formed by the SRB Desulfovibrio vulgaris Hildenborough and the methanogenic archaeum Methanococcus maripaludis. Under the tested conditions, monocultures of D. vulgaris formed thin, stable biofilms, but monoculture M. maripaludis did not. Microscopy of intact syntrophic biofilm confirmed that D. vulgaris formed a scaffold for the biofilm, while intermediate and steady-state images revealed that M. maripaludis joined the biofilm later, likely in response to H2 produced by the SRB. Close interactions in structured biofilm allowed efficient transfer of H2 to M. maripaludis, and H2 was only detected in cocultures with a mutant SRB that was deficient in biofilm formation (ΔpilA). M. maripaludis produced more carbohydrate (uronic acid, hexose, and pentose) as a monoculture compared to total coculture biofilm, and this suggested an altered carbon flux during syntrophy. The syntrophic biofilm was structured into ridges (∼300 × 50 μm) and models predicted lactate limitation at ∼50 μm biofilm depth. The biofilm had structure that likely facilitated mass transfer of H2 and lactate, yet maximized biomass with a more even population composition (number of each organism) when compared to the bulk-phase community. Total biomass protein was equivalent in lactate-limited and lactate-excess conditions when a biofilm was present, but in the absence of biofilm, total biomass protein was significantly reduced. The results suggest that multispecies biofilms create an environment conducive to resource sharing, resulting in increased biomass retention, or carrying capacity, for cooperative populations.
A Low-Power Integrated Circuit for a Wireless 100-Electrode Neural Recording System

Recent work in field of neuroprosthetics has demonstrated that by observing the simultaneous activity of many neurons in specific regions of the brain, it is possible to produce control signals that allow animals or humans to drive cursors or prosthetic limbs directly through thoughts. As neuroprosthetic devices transition from experimental to clinical use, there is a need for fully-implantable amplification and telemetry electronics in close proximity to the recording sites. To address these needs, we developed a prototype integrated circuit for wireless neural recording from a 100-channel microelectrode array. The design of both the system-level architecture and the individual circuits were driven by severe power constraints for small implantable devices; chronically heating tissue by only a few degrees Celsius leads to cell death. Due to the high data rate produced by 100 neural signals, the system must perform data reduction as well. We use a combination of a low-power ADC and an array of "spike detectors" to reduce the transmitted data rate while preserving critical information. The complete system receives power and commands (at 6.5 kb/s) wirelessly over a 2.64-MHz inductive link and transmits neural data back at a data rate of 330 kb/s using a fully-integrated 433-MHz FSK transmitter. The 4.7times5. 9 mm2 chip was fabricated in a 0.5-mum 3M2P CMOS process and consumes 13.5 mW of power. While cross-chip interference limits performance in single-chip operation, a two-chip system was used to record neural signals from a Utah Electrode Array in cat cortex and transmit the digitized signals wirelessly to a receiver
Adaptive probabilistic neural coding from deterministic spiking neurons: analysis from first principles

A neuron transforms its input into output spikes, and this transformation is the basic unit of computation in the nervous system. The spiking response of the neuron to a complex, time-varying input can be predicted from the detailed biophysical properties of the neuron, modeled as a deterministic nonlinear dynamical system. In the tradition of neural coding, however, a neuron or neural system is treated as a black box and statistical techniques are used to identify functional models of its encoding properties. The goal of this work is to connect the mechanistic, biophysical approach to neuronal function to a description in terms of a coding model. Building from preceding work at the single neuron level, we develop from first principles a mathematical theory mapping the relationships between two simple but powerful classes of models: deterministic integrate-and-fire dynamical models and linear-nonlinear coding models. To do so, we develop an approach for studying a nonlinear dynamical system by conditioning on an observed linear estimator. We derive asymptotic closed-form expressions for the linear filter and estimates for the nonlinear decision function of the linear/nonlinear model. We analytically derive the dependence of the linear filter on the input statistics and we show how deterministic nonlinear dynamics can be used to modulate the properties of a probabilistic code. We demonstrate that integrate-and-fire models without any additional currents can perform perfect contrast gain control, a sophisticated adaptive computation, and we identify the general dynamical principles responsible. We then design from first principles a nonlinear dynamical model that implements gain control. While we focus on the integrate-and-fire models for tractability, the framework we propose to relate LN and dynamical models generalizes naturally to more complex biophysical models.
Neonatal nicotine exposure impairs nicotinic enhancement of central auditory processing and auditory learning in adult rats

Children of women who smoke cigarettes during pregnancy display cognitive deficits in the auditory–verbal domain. Clinical studies have implicated developmental exposure to nicotine, the main psychoactive ingredient of tobacco, as a probable cause of subsequent auditory deficits. To test for a causal link, we have developed an animal model to determine how neonatal nicotine exposure affects adult auditory function. In adult control rats, nicotine administered systemically (0.7 mg/kg, s.c.) enhanced the sensitivity to sound of neural responses recorded in primary auditory cortex. The effect was strongest in cortical layers 3 and 4, where there is a dense concentration of nicotinic acetylcholine receptors (nAChRs) that has been hypothesized to regulate thalamocortical inputs. In support of the hypothesis, microinjection into layer 4 of the nonspecific nAChR antagonist mecamylamine (10 µm) strongly reduced sound‐evoked responses. In contrast to the effects of acute nicotine and mecamylamine in adult control animals, neither drug was as effective in adult animals that had been treated with 5 days of chronic nicotine exposure (CNE) shortly after birth. Neonatal CNE also impaired performance on an auditory‐cued active avoidance task, while having little effect on basic auditory or motor functions. Thus, neonatal CNE impairs nicotinic regulation of cortical function, and auditory learning, in the adult. Our results provide evidence that developmental nicotine exposure is responsible for auditory–cognitive deficits in the offspring of women who smoke during pregnancy, and suggest a potential underlying mechanism, namely diminished function of cortical nAChRs.
Fluvial erosion/transport equation of landscape evolution models revisited

We present a mesoscale erosion/deposition model, which differs from previous landscape evolution models equations by taking explicitly into account a mass balance equation for the streamflow. The geological and hydrological complexity is lumped into two basic fluxes (erosion and deposition) and two averaged parameters (unit width discharge q and stream slope s). The model couples the dynamics of streamflow and topography through a sediment transport length function x(q), which is the average travel distance of a particle in the flow before being trapped on topography. This property reflects a time lag between erosion and deposition, which allows the streamflow not to be instantaneously at capacity. The so-called x-q model may reduce either to transport-limited or to detachment-limited erosion modes depending on x. But it also may not. We show in particular how it does or does not for steady state topographies, long-term evolution, and high-frequency base level perturbations. Apart from the unit width discharge and the settling velocity, the x(q) function depends on a dimensionless number encompassing the way sediment is transported within the streamflow. Using models of concentration profile through the water column, we show the dependency of this dimensionless coefficient on the Rouse number. We discuss how consistent the x-q model framework is with bed load scaling expressions and Einstein's conception of sediment motion.
Epidemic live streaming: optimal performance trade-offs

Several peer-to-peer systems for live streaming have been recently deployed (e.g. CoolStreaming, PPLive, SopCast). These all rely on distributed, epidemic-style dissemination mechanisms. Despite their popularity, the fundamental performance trade-offs of such mechanisms are still poorly understood. In this paper we propose several results that contribute to the understanding of such trade-offs. Specifically, we prove that the so-called random peer, latest useful chunk mechanism can achieve dissemination at an optimal rate and within an optimal delay, up to an additive constant term. This qualitative result suggests that epidemic live streaming algorithms can achieve near-unbeatable rates and delays. Using mean-field approximations, we also derive recursive formulas for the diffusion function of two schemes referred to as latest blind chunk, random peer and latest blind chunk, random useful peer. Finally, we provide simulation results that validate the above theoretical results and allow us to compare the performance of various practically interesting diffusion schemes terms of delay, rate, and control overhead. In particular, we identify several peer/chunk selection algorithms that achieve near-optimal performance trade-offs. Moreover, we show that the control overhead needed to implement these algorithms may be reduced by restricting the neighborhood of each peer without substantial performance degradation.
Immunoglobulins and cellular constituents of the BAL fluid of patients with sulfur mustard gas-induced pulmonary fibrosis.

STUDY OBJECTIVE The acute heavy exposure to sulfur mustard gas can lead to pulmonary fibrosis (PF). This study was performed to determine the cellular and protein content of BAL fluid in 24 patients with sulfur mustard gas-induced PF. PATIENTS Twenty-four veterans with sulfur mustard gas-induced PF and 18 nonexposed veterans serving as control subjects were enrolled into the study. MEASUREMENTS Chest roentgenograms, pulmonary function tests (PFTs), tests for carbon monoxide diffusing capacity of the lung (DLCO), high-resolution CT scans of the chest, BAL via fiberoptic bronchoscopy, analyses of BAL fluids for cellular and protein constituents, and determinations of serum albumin and Ig levels were performed in all cases. A transbronchial lung biopsy was done in all patients following BAL. RESULTS Neutrophilic alveolitis was the predominant feature. Neutrophils (p = 0.0001) and eosinophils (p = 0.0001) were the predominant cell types in the BAL fluid of patients with PF. There was a strong correlation between the BAL fluid neutrophil count (p = 0.76; p = 0.0003) or its percentage (p = 0.77; p = 0.0003) and the degree of fibrosis. Of the BAL fluid Ig levels, only the IgG level in the study group was significantly higher than the IgG level of the control group (p = 0.0001). Of the PFT physiologic parameters, only the percentage of DLCO showed a significant correlation with the degree of fibrosis (p = -0.76; p < 0.001). CONCLUSION The cellular constituents of BAL fluid in patients with sulfur mustard gas-induced PF are very similar to the cellular constituents seen in patients with idiopathic PF, and this finding indicates the presence of an ongoing active alveolitis in PF.
Induction of STAT1 Phosphorylation at Serine 727 and Expression of Proinflammatory Cytokines by Porcine Reproductive and Respiratory Syndrome Virus

Porcine reproductive and respiratory syndrome virus (PRRSV) is a viral pathogen that causes acute respiratory illnesses in young pigs. Since 1987, PRRSV has contributed substantial economic losses to the swine industry. Elevation of proinflammatory cytokines in PRRSV-infected pigs is thought to contribute to PRRSV pathogenesis. In this study, PRRSV VR-2385, a Type 2 strain with moderate virulence, was found to induce phosphorylation of signal transducer and activator of transcription 1 (STAT1) at serine 727 (pSTAT1-S727) in MARC-145 cells. No phosphorylated STAT1 at tyrosine 701 was detected, which indicates that the pSTAT1-S727 elevation was interferon-independent. The PRRSV-induced pSTAT1-S727, however, was dose-dependent and its levels increased with infection time. IngelVac PRRS MLV strain had a minimal effect on pSTAT1-S727. Compared to MLV-infected cells, VR-2385 infection caused significantly higher level of expression of proinflammatory cytokines, including interleukin 1 beta (IL-1beta) and IL-8. The VR-2385-induced pSTAT1-S727 and cytokine expression were reduced after SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), or methylthioadenosine (MTA), a methyl transferase inhibitor, was added to the cells. The SB203580 and MTA-mediated inhibition suggested that the virus-induced pSTAT1-S727 was dependent on p38 MAPK pathway. In primary porcine alveolar macrophages (PAMs), VR-2385 also induced pSTAT1-S727 and expression of proinflammatory cytokines and chemokines, including IL-1beta, IL-8, chemokine ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 10 (CXCL10). Similarly, SB203580 treatment of PAM cells blocked the elevation of pSTAT1-S727 and cytokine expression. Overexpression of individual viral proteins showed that non-structural protein 12 (nsp12) was able to induce elevation of pSTAT1-S727 and the expression of IL-1β and IL-8. These results indicated that PRRSV VR-2385 induces pSTAT1-S727 and the expression of proinflammatory cytokines, which contributes to the insight of PRRSV pathogenesis.
Factors of the Psychopathic Personality Inventory

Psychopathy is a personality disorder that includes interpersonal-affective and antisocial deviance features. The Psychopathic Personality Inventory (PPI) contains two underlying factors (fearless dominance and impulsive antisociality) that may differentially tap these two sets of features. In a mixed-gender sample of undergraduates and prisoners, we found that PPI fearless dominance was related to low Behavioral Inhibition System activity, high Behavioral Activation System (BAS) activity, expert prototype psychopathy scores, and primary psychopathy. Impulsive antisociality was related to high BAS activity and all psychopathy measures. High Extraversion and Openness and low Neuroticism and Agreeableness predicted fearless dominance, whereas high Neuroticism and low Agreeableness and Conscientiousness predicted impulsive antisociality. Although low levels of Agreeableness predicted both PPI factors, their differential relations with other five-factor model traits highlight differences in the way psychopathy manifests itself. Consistent with movements toward assessing personality disorder using the five-factor model, the authors report regression-based equations for the clinical assessment of these psychopathy dimensions using the NEO Personality Inventory—Revised (NEO-PI-R).