Combating catastrophic forgetting with developmental compression

Generally intelligent agents exhibit successful behavior across problems in several settings. Endemic in approaches to realize such intelligence in machines is catastrophic forgetting: sequential learning corrupts knowledge obtained earlier in the sequence, or tasks antagonistically compete for system resources. Methods for obviating catastrophic forgetting have sought to identify and preserve features of the system necessary to solve one problem when learning to solve another, or to enforce modularity such that minimally overlapping sub-functions contain task specific knowledge. While successful, both approaches scale poorly because they require larger architectures as the number of training instances grows, causing different parts of the system to specialize for separate subsets of the data. Here we present a method for addressing catastrophic forgetting called developmental compression. It exploits the mild impacts of developmental mutations to lessen adverse changes to previously-evolved capabilities and `compresses' specialized neural networks into a generalized one. In the absence of domain knowledge, developmental compression produces systems that avoid overt specialization, alleviating the need to engineer a bespoke system for every task permutation and suggesting better scalability than existing approaches. We validate this method on a robot control problem and hope to extend this approach to other machine learning domains in the future

Data-driven PDE discovery with evolutionary approach

The data-driven models allow one to define the model structure in cases when a priori information is not sufficient to build other types of models. The possible way to obtain physical interpretation is the data-driven differential equation discovery techniques. The existing methods of PDE (partial derivative equations) discovery are bound with the sparse regression. However, sparse regression is restricting the resulting model form, since the terms for PDE are defined before regression. The evolutionary approach described in the article has a symbolic regression as the background instead and thus has fewer restrictions on the PDE form. The evolutionary method of PDE discovery (EPDE) is described and tested on several canonical PDEs. The question of robustness is examined on a noised data example

Preferential utilization of NADPH as the endogenous electron donor for NAD(P)H:quinone oxidoreductase 1 (NQO1) in intact pulmonary arterial endothelial cells

The goal was to determine whether endogenous cytosolic NAD(P)H:quinone oxidoreductase 1 (NQO1) preferentially uses NADPH or NADH in intact pulmonary arterial endothelial cells in culture. The approach was to manipulate the redox status of the NADH/NAD+ and NADPH/NADP+ redox pairs in the cytosolic compartment using treatment conditions targeting glycolysis and the pentose phosphate pathway alone or with lactate, and to evaluate the impact on the intact cell NQO1 activity. Cells were treated with 2-deoxyglucose, iodoacetate, or epiandrosterone in the absence or presence of lactate, NQO1 activity was measured in intact cells using duroquinone as the electron acceptor, and pyridine nucleotide redox status was measured in total cell KOH extracts by high-performance liquid chromatography. 2-Deoxyglucose decreased NADH/NAD+ and NADPH/NADP+ ratios by 59 and 50%, respectively, and intact cell NQO1 activity by 74%; lactate restored NADH/NAD+, but not NADPH/NADP+ or NQO1 activity. Iodoacetate decreased NADH/NAD+ but had no detectable effect on NADPH/NADP+ or NQO1 activity. Epiandrosterone decreased NQO1 activity by 67%, and although epiandrosterone alone did not alter the NADPH/NADP+ or NADH/NAD+ ratio, when the NQO1 electron acceptor duroquinone was also present, NADPH/NADP+ decreased by 84% with no impact on NADH/NAD+. Duroquinone alone also decreased NADPH/NADP+ but not NADH/NAD+. The results suggest that NQO1 activity is more tightly coupled to the redox status of the NADPH/NADP+ than NADH/NAD+ redox pair, and that NADPH is the endogenous NQO1 electron donor. Parallel studies of pulmonary endothelial transplasma membrane electron transport (TPMET), another redox process that draws reducing equivalents from the cytosol, confirmed previous observations of a correlation with the NADH/NAD+ ratio

Characterization of theThreshold for NAD(P)H:quinone Oxidoreductase Activity in Intact Sulforaphane-treated Pulmonary Arterial Endothelial Cells

Treatment of bovine pulmonary arterial endothelial cells in culture with the phase II enzyme inducer sulforaphane (5 μM, 24 h; sulf-treated) increased cell-lysate NAD(P)H:quinone oxidoreductase (NQO1) activity by 5.7 ± 0.6 (mean ± SEM)-fold, but intact-cell NQO1 activity by only 2.8 ± 0.1-fold compared to control cells. To evaluate the hypothesis that the threshold for sulforaphane-induced intact-cell NQO1 activity reflects a limitation in the capacity to supply NADPH at a sufficient rate to drive all the induced NQO1 to its maximum activity, total KOH-extractable pyridine nucleotides were measured in cells treated with duroquinone to stimulate maximal NQO1 activity. NQO1 activation increased NADP+ in control and sulf-treated cells, with the effect more pronounced in the sulf-treated cells, in which the NADPH was also decreased. Glucose-6-phosphate dehydrogenase (G-6-PDH) inhibition partially blocked NQO1 activity in control and sulf-treated cells, but G-6-PDH overexpression via transient transfection with the human cDNA alleviated neither the restriction on intact sulf-treated cell NQO1 activity nor the impact on the NADPH/NADP+ ratios. Intracellular ATP levels were not affected by NQO1 activation in control or sulf-treated cells. An increased dependence on extracellular glucose and a rightward shift in the Km for extracellular glucose were observed in NQO1-stimulated sulf-treated vs control cells. The data suggest that glucose transport in the sulf-treated cells may be insufficient to support the increased metabolic demand for pentose phosphate pathway-generated NADPH as an explanation for the NQO1 threshold

Multi-layered Spectral Formation in SNe Ia Around Maximum Light

We use the radiative transfer code PHOENIX to study the line formation of the wavelength region 5000-7000 Angstroms. This is the region where the SNe Ia defining Si II feature occurs. This region is important since the ratio of the two nearby silicon lines has been shown to correlate with the absolute blue magnitude. We use a grid of LTE synthetic spectral models to investigate the formation of line features in the spectra of SNe Ia. By isolating the main contributors to the spectral formation we show that the ions that drive the spectral ratio are Fe III, Fe II, Si II, and S II. While the first two strongly dominate the flux transfer, the latter two form in the same physical region inside of the supernova. We also show that the naive blackbody that one would derive from a fit to the observed spectrum is far different than the true underlying continuum.Comment: 35 pages, 15 figures, ApJ (2008) 684 in pres

State-Dependent Computation Using Coupled Recurrent Networks

Although conditional branching between possible behavioral states is a hallmark of intelligent behavior, very little is known about the neuronal mechanisms that support this processing. In a step toward solving this problem, we demonstrate by theoretical analysis and simulation how networks of richly interconnected neurons, such as those observed in the superficial layers of the neocortex, can embed reliable, robust finite state machines. We show how a multistable neuronal network containing a number of states can be created very simply by coupling two recurrent networks whose synaptic weights have been configured for soft winner-take-all (sWTA) performance. These two sWTAs have simple, homogeneous, locally recurrent connectivity except for a small fraction of recurrent cross-connections between them, which are used to embed the required states. This coupling between the maps allows the network to continue to express the current state even after the input that elicited that state iswithdrawn. In addition, a small number of transition neurons implement the necessary input-driven transitions between the embedded states. We provide simple rules to systematically design and construct neuronal state machines of this kind. The significance of our finding is that it offers a method whereby the cortex could construct networks supporting a broad range of sophisticated processing by applying only small specializations to the same generic neuronal circuit

Evolving Spatially Aggregated Features from Satellite Imagery for Regional Modeling

Satellite imagery and remote sensing provide explanatory variables at relatively high resolutions for modeling geospatial phenomena, yet regional summaries are often desirable for analysis and actionable insight. In this paper, we propose a novel method of inducing spatial aggregations as a component of the machine learning process, yielding regional model features whose construction is driven by model prediction performance rather than prior assumptions. Our results demonstrate that Genetic Programming is particularly well suited to this type of feature construction because it can automatically synthesize appropriate aggregations, as well as better incorporate them into predictive models compared to other regression methods we tested. In our experiments we consider a specific problem instance and real-world dataset relevant to predicting snow properties in high-mountain Asia

Depleted Energy Charge and Increased Pulmonary Endothelial Permeability Induced by Mitochondrial Complex I inhibition are Mitigated by Coenzyme Q\u3csub\u3e1\u3c/sub\u3e in the Isolated Perfused Rat Lung

Mitochondrial dysfunction is associated with various forms of lung injury and disease that also involve alterations in pulmonary endothelial permeability, but the relationship, if any, between the two is not well understood. This question was addressed by perfusing isolated intact rat lung with a buffered physiological saline solution in the absence or presence of the mitochondrial complex I inhibitor rotenone (20 μM). Compared to control, rotenone depressed whole lung tissue ATP from 5.66±0.46 (SEM) to 2.34±0.15 µmol·g−1 dry lung, with concomitant increases in the ADP:ATP and AMP:ATP ratios. Rotenone also increased lung perfusate lactate (from 12.36±1.64 to 38.62±3.14 µmol·15 min−1 perfusion·g−1 dry lung) and the lactate:pyruvate ratio, but had no detectable impact on lung tissue GSH:GSSG redox status. The amphipathic quinone coenzyme Q1 (CoQ1; 50 μM) mitigated the impact of rotenone on the adenine nucleotide balance, wherein mitigation was blocked by NAD(P)H-quinone oxidoreductase 1 or mitochondrial complex III inhibitors. In separate studies, rotenone increased the pulmonary vascular endothelial filtration coefficient (Kf) from 0.043±0.010 to 0.156±0.037 ml·min−1·cm H2O−1·g−1 dry lung, and CoQ1 protected against the effect of rotenone on Kf. A second complex I inhibitor, piericidin A, qualitatively reproduced the impact of rotenone on Kf and the lactate:pyruvate ratio. Taken together, the observations imply that pulmonary endothelial barrier integrity depends on mitochondrial bioenergetics as reflected in lung tissue ATP levels and that compensatory activation of whole lung glycolysis cannot protect against pulmonary endothelial hyperpermeability in response to mitochondrial blockade. The study further suggests that low-molecular-weight amphipathic quinones may have therapeutic utility in protecting lung barrier function in mitochondrial insufficiency

Effects of Age and Gender on Physical Performance

Our purpose was to examine the effects of age and gender on physical performance. We assessed a one-hour swimming performance and participation of 4,271 presumably healthy men and women, aged 19–91 years, from the 2001–2003 United States Masters Swimming long-distance (1 h) national competition. The decline in performance with increasing age was found to be quadratic rather than linear. The equation which best fit variation in 1 h swimming distance in meters (m) according to variations in age in years (y) in men was: distance (m) = 4058 + 2.18 age−0.29 age (http://www.acsmmsse.org/pt/re/msse/positionstandards.htm;jsessionid=DiRVACC7YS3mq27s5kV3vwpEVSokmmD1ZJLC7pdnol3KcfoSu0t!1096311956!-949856145!9001!-1), with the same equation for women except that 380 m needed to be subtracted from the calculated value at all ages (about a 10% difference). There was a large overlap in performance between men and women. The overall mean decline in performance with age was about 50% and was parallel in men and women. The mean difference in distance for a 1-year increment in age was −9.7 m at 21 y of age, −21.3 m at 40 y, and −44.5 m at 80 y. Far greater declines of about 96% in numbers participating with advanced age (80 y and over, 4% of peak numbers) were observed than in the 40–49 y age group. In conclusion, the declines in performance were parallel in men and women at all ages, and the 1-year age-related declines in performance were about twice as great at 40 y and more than four-times as great at 80 y than at 20 y of age, with even greater age-related declines in participation being noted for both men and women

The DICE calibration project: design, characterization, and first results

We describe the design, operation, and first results of a photometric calibration project, called DICE (Direct Illumination Calibration Experiment), aiming at achieving precise instrumental calibration of optical telescopes. The heart of DICE is an illumination device composed of 24 narrow-spectrum, high-intensity, light-emitting diodes (LED) chosen to cover the ultraviolet-to-near-infrared spectral range. It implements a point-like source placed at a finite distance from the telescope entrance pupil, yielding a flat field illumination that covers the entire field of view of the imager. The purpose of this system is to perform a lightweight routine monitoring of the imager passbands with a precision better than 5 per-mil on the relative passband normalisations and about 3{\AA} on the filter cutoff positions. The light source is calibrated on a spectrophotometric bench. As our fundamental metrology standard, we use a photodiode calibrated at NIST. The radiant intensity of each beam is mapped, and spectra are measured for each LED. All measurements are conducted at temperatures ranging from 0{\deg}C to 25{\deg}C in order to study the temperature dependence of the system. The photometric and spectroscopic measurements are combined into a model that predicts the spectral intensity of the source as a function of temperature. We find that the calibration beams are stable at the $10^{-4}$ level -- after taking the slight temperature dependence of the LED emission properties into account. We show that the spectral intensity of the source can be characterised with a precision of 3{\AA} in wavelength. In flux, we reach an accuracy of about 0.2-0.5% depending on how we understand the off-diagonal terms of the error budget affecting the calibration of the NIST photodiode. With a routine 60-mn calibration program, the apparatus is able to constrain the passbands at the targeted precision levels.Comment: 25 pages, 27 figures, accepted for publication in A&