A hypothetical explanation of congenital nystagmus

Congenital nystagmus (CN) is a conjugate, rhythmic, eye movement disorder characterized by a wide variety of waveforms ranging from jerk to pendular types. No detailed mechanisms have been proposed to explain the generation of the CN wave-form This paper proposes a hypothetical mechanism for CN, and shows with computer simulations that a model based on this hypothesis can account for a variety of disparate waveforms. The basis of this model is a gaze-holding network, or neural integrator, that has both position and velocity feedback loops. The signals carried in these loops could arise from either afference or efference. In normal subjects, the position feedback would be positive and the velocity feedback would be negative. Both would help to increase the time constant of an imperfect neural integrator in the brain stem. We propose that in patients with CN the sign of the velocity pathway is reversed, making the neural integrator unstable. This instability could manifest as many different CN waveforms, depending on the direction and velocity of post-saccadic ocular drift and actions of nonlinearities within the position and velocity feedback loops. Thus a single underlying abnormality may be responsible for a variety of CN waveforms.     

A third explanation for female infanticide

Two directly opposed explanations for the distribution of female infanticide across cultures have recently appeared. Divale and Harris propose to explain this practice as part of a system which reduces population growth. Dickemann says that the practice serves to increase reproductive success. I criticize each of these explanations and propose a third which depends on the technoecological and economic constraints given precedence by Harris and Divale, combined with the insights of sexual selection which are central to Dickemann's account.     

A statistical explanation of MaxEnt for ecologists

MaxEnt is a program for modelling species distributions from presence‐only species records. This paper is written for ecologists and describes the MaxEnt model from a statistical perspective, making explicit links between the structure of the model, decisions required in producing a modelled distribution, and knowledge about the species and the data that might affect those decisions. To begin we discuss the characteristics of presence‐only data, highlighting implications for modelling distributions. We particularly focus on the problems of sample bias and lack of information on species prevalence. The keystone of the paper is a new statistical explanation of MaxEnt which shows that the model minimizes the relative entropy between two probability densities (one estimated from the presence data and one, from the landscape) defined in covariate space. For many users, this viewpoint is likely to be a more accessible way to understand the model than previous ones that rely on machine learning concepts. We then step through a detailed explanation of MaxEnt describing key components (e.g. covariates and features, and definition of the landscape extent), the mechanics of model fitting (e.g. feature selection, constraints and regularization) and outputs. Using case studies for a Banksia species native to south‐west Australia and a riverine fish, we fit models and interpret them, exploring why certain choices affect the result and what this means. The fish example illustrates use of the model with vector data for linear river segments rather than raster (gridded) data. Appropriate treatments for survey bias, unprojected data, locally restricted species, and predicting to environments outside the range of the training data are demonstrated, and new capabilities discussed. Online appendices include additional details of the model and the mathematical links between previous explanations and this one, example code and data, and further information on the case studies.     

A new explanation of the glitch phenomenon

Summary We consider a discrete model for asynchronous circuits and show that, under very mild restrictions, this model excludes the existence of glitch-free arbiters. This result contradicts a long standing conjecture that the nonexistence of glitch-free arbiters is due to the continuous nature of such circuits.Work supported in part by Office of Naval Research Contract N00014-89-J-1913     

A theoretical explanation of the Piper-Steenbjerg effect

The relation between plant yield and plant nutrient concentration is sometimes found to be negative, a phenomenon called the Piper-Steenbjerg (PS) effect. A model was used to examine the underlying causes of the PS effect, and the conditions under which it is most likely to occur. The model uses the nutrient productivity concept for plant growth and a nutrient uptake equation in which root growth rate and external nutrient concentration determine the uptake rate. The study suggests that the PS effect occurs when the fast growth of plants grown in an initially higher nutrient medium eventually leads to a more rapid depletion of external nutrients than the slow growth of plants grown in an initially lower nutrient medium. The fast growth of plants combined with a rapid decrease of nutrient uptake leads to a fall in plant nutrient concentration. When these large plants with very low nutrient concentrations are compared with the smaller, slow-growing plants, a PS effect may be found depending on the time at which the plants are harvested, and on the range of initial values of the external nutrient content. When it occurs, the effect is greatest when the depletion volume per unit new root (V_d) is lowest, and when the mobility of nutrients in the medium is highest (α=1). The results are sufficiently general to apply to a variety of nutrients, plant species and growth media.     

A semantic explanation for the External Argument Generalization

-Er nominals usually obey the External Argument Generalization: the argument of the nominal receives the thematic role that the verb assigns to its external argument. I argue that this syntactic generalization, as well as the exceptions to it, can be explained by semantics.Specifically, -er nominals usually express properties that are inherent in the subject; I argue that they therefore belong to the class of expressions that express such properties—dynamic modals. Crucially, dynamic modals are subject oriented; hence, the proposal that -er nominals are dynamic modals naturally provides an account of the External Argument Generalization.     

Conjecture and explanation: A reply to Reydon

Reydon (2012) comments on my account of how-possibly explanation (Forber, 2010). I distinguish between three types of explanation (global how-possibly, local how-possibly, and how actually) and argue that these distinctions track various roles explanations play in evolutionary biology. While Reydon accepts the distinctions, he questions whether the two different types of how-possibly explanation count as genuine explanations. He summarizes his analysis with a slogan: “global how-possibly explanations are explanations but not how-possibly; local explanations are how-possibly but not explanations.” Reydon’s commentary raises a number of insightful points, and I will not be able to address them all. Instead, after clarifying certain points in my original paper (4 1), I will respond to Reydon’s slogan by addressing whether global how-possibly explanations should count as explaining how possible (4 2), and what (so-called) local how-possibly explanations are, if not explanations (4 3).     

A theoretical explanation of “Concomitant resistance”

Concomitant resistance is a tumor growth dynamic which results when the growth of a second tumor implant is inhibited by the presence of the first. Recently, we modeled tumor growth in the presence of a regenerating liver after partial hepatectomy (Michelson and Leith,Bull. Math. Biol. 57, 345–366, 1995), with an interlocking pair of growth control triads to account for the accelerated growth observed in both tissues. We also modeled tumor dormancy and recurrence as a dynamic equilibrium achieved between proliferating and quiescent subpopulations. In this paper those studies are extended to initially model the concomitant resistance case. Two interlocking model systems are proposed. In one an interactive competition between the tumor implants is described, while in the other purely proportional growth inhibition is described. The equilibria and dynamics of each system when the coefficients are held constant are presented for three subcases of model parameters. We show that the dynamic called concomitant resistance can be real or apparent, and that if the model coefficients are held constant, the only way to truly achieve concomitant resistance is by forcing one of the tumors into total quiescence. If this is the true state of the inhibited implant, then a non-constant recruitment signal is required to insure regrowth when the inhibitor mass is excised. We compare these theoretical results to a potential explanation of the phenomenon provided by Prehn (Cancer Res. 53, 3266–3269, 1993).     

A plausible explanation for heart rates in mammals

We consider a simple model to give a plausible mechanical explanation of what are the actual resting heart rates of mammals optimized for. We study what is the optimal frequency for a viscoelastic fluid circulating in a pulsatile way through a network of tubes and conclude that the heart rate is not optimized to transport blood through the whole net. Rather, actual resting heart rates of mammals happen at frequencies that optimize flow in vessels of radii that correspond to large arteries, which bring oxygenated blood rapidly far away from the heart, towards head and limbs. Our results for the optimal frequencies, obtained using observed radii of femoral arteries in mammals, agree best with the heart rates observed. We find a theoretical allometric relation between optimal flow frequency and radius: ν∼R⁻¹. This one, agrees with the exponent obtained when plotting observed heart rates versus radii of both, femoral arteries and carotids in mammals of different sizes, from mice to horses.     

Viability explanation

This article deals with a type of functional explanation, viability explanation, that has been overlooked in recent philosophy of science. Viability explanations relate traits of organisms and their environments in terms of what an individual needs to survive and reproduce. I show that viability explanations are neither causal nor historical and that, therefore, they should be accounted for as a distinct type of explanation.The investigations for this paper were supported by the Foundation for Philosophical Research (SWON), which is subsidized by the Netherlands Organization for Scientific Research (NWO). I am grateful to Theo Kuipers and Ton Derksen for their useful comments on early versions, to Josje Lodder for improving my logic, and to Jaap van Brakel for his help in structuring this article.     

Epitope-dependent inhibition of T cell activation by the Ea transgene: an explanation for transgene-mediated protection from murine lupus

A high level expression of the Ea(d) transgene encoding the I-E alpha-chain is highly effective in the suppression of lupus autoantibody production in mice. To explore the possible modulation of the Ag-presenting capacity of B cells as a result of the transgene expression, we assessed the ability of the transgenic B cells to activate Ag-specific T cells in vitro. By using four different model Ag-MHC class II combinations, this analysis revealed that a high transgene expression in B cells markedly inhibits the activation of T cells in an epitope-dependent manner, without modulation of the I-E expression. The transgene-mediated suppression of T cell responses is likely to be related to the relative affinity of peptides derived from transgenic I-E alpha-chains (Ealpha peptides) vs antigenic peptides to individual class II molecules. Our results support a model of autoimmunity prevention based on competition for Ag presentation, in which the generation of large amounts of Ealpha peptides with high affinity to I-A molecules decreases the use of I-A for presentation of pathogenic self-peptides by B cells, thereby preventing excessive activation of autoreactive T and B cells.     

Striola magica. A functional explanation of otolith geometry

Otolith end organs of vertebrates sense linear accelerations of the head and gravitation. The hair cells on their epithelia are responsible for transduction. In mammals, the striola, parallel to the line where hair cells reverse their polarization, is a narrow region centered on a curve with curvature and torsion. It has been shown that the striolar region is functionally different from the rest, being involved in a phasic vestibular pathway. We propose a mathematical and computational model that explains the necessity of this amazing geometry for the striola to be able to carry out its function. Our hypothesis, related to the biophysics of the hair cells and to the physiology of their afferent neurons, is that striolar afferents collect information from several type I hair cells to detect the jerk in a large domain of acceleration directions. This predicts a mean number of two calyces for afferent neurons, as measured in rodents. The domain of acceleration directions sensed by our striolar model is compatible with the experimental results obtained on monkeys considering all afferents. Therefore, the main result of our study is that phasic and tonic vestibular afferents cover the same geometrical fields, but at different dynamical and frequency domains.     

树木年轮δ13C含量幼龄效应的定量化探讨

从实验测得的林内外Ci/Ca差值出发,根据已有定量方程,对树木年轮δ     

A base-centred explanation of the B-to-A transition in DNA

In the traditional view, the bistable feature responsible for the switch between the B and A forms of DNA was the sugar-phosphate backbone. Several recent assays of the sequence-dependent structure of DNA are not compatible with that hypothesis. Here we show that certain kinds of base-pair step, mainly those of the pyrimidine-purine variety, can stack in a “bistable” fashion so as to produce one of two overall helix shapes A or B. Further, we suggest that the passive, elastic stiffness of the backbone is responsible for communicating the stacking configuration from bistable steps to their “neutral” neighbours. The role of water molecules, in stabilizing the B form of DNA over the A, may simply be to form hydrogen-bonded bridges with the minor-groove edges of neutral steps in the B configuration.