Filtering a set of items, based on a set of properties that can be verified by humans, is a common application of CrowdSourcing. When the workers are error-prone, each item is presented to multiple users, to limit the probability of misclassification. Since the Crowd is a relatively expensive resource, minimizing the number of questions per item may naturally result in big savings. Several algorithms to address this minimization problem have been presented in the CrowdScreen framework by Parameswaran et al. However, those algorithms do not scale well and therefore cannot be used in scenarios where high accuracy is required in spite of high user error rates. The goal of this paper is thus to devise algorithms that can cope with such situations. To achieve this, we provide new theoretical insights to the problem, then use them to develop a new efficient algorithm. We also propose novel optimizations for the algorithms of CrowdScreen that improve their scalability. We complement our theoretical study by an experimental evaluation of the algorithms on a large set of synthetic parameters as well as real-life crowdsourcing scenarios, demonstrating the advantages of our solution.

We describe the first large scale analysis of gene translation that is based on a model that takes into account the physical and dynamical nature of this process. The Ribosomal Flow Model (RFM) predicts fundamental features of the translation process, including translation rates, protein abundance levels, ribosomal densities and the relation between all these variables, better than alternative ('non-physical') approaches. In addition, we show that the RFM can be used for accurate inference of various other quantities including genes' initiation rates and translation costs. These quantities could not be inferred by previous predictors. We find that increasing the number of available ribosomes (or equivalently the initiation rate) increases the genomic translation rate and the mean ribosome density only up to a certain point, beyond which both saturate. Strikingly, assuming that the translation system is tuned to work at the pre-saturation point maximizes the predictive power of the model with respect to experimental data. This result suggests that in all organisms that were analyzed (from bacteria to Human), the global initiation rate is optimized to attain the pre-saturation point. The fact that similar results were not observed for heterologous genes indicates that this feature is under selection. Remarkably, the gap between the performance of the RFM and alternative predictors is strikingly large in the case of heterologous genes, testifying to the model's promising biotechnological value in predicting the abundance of heterologous proteins before expressing them in the desired host.

One of the major challenges in the field of neurally driven evolved autonomous agents is deciphering the neural mechanisms underlying their behavior. Aiming at this goal, we have developed the multi-perturbation Shapley value analysis (MSA)--the first axiomatic and rigorous method for deducing causal function localization from multiple-perturbation data, substantially improving on earlier approaches. Based on fundamental concepts from game theory, the MSA provides a formal way of defining and quantifying the contributions of network elements, as well as the functional interactions between them. The previously presented versions of the MSA require full knowledge (or at least an approximation) of the network's performance under all possible multiple perturbations, limiting their applicability to systems with a small number of elements. This article focuses on presenting new scalable MSA variants, allowing for the analysis of large complex networks in an efficient manner, including large-scale neurocontrollers. The successful operation of the MSA along with the new variants is demonstrated in the analysis of several neurocontrollers solving a food foraging task, consisting of up to 100 neural elements.

The claim that genetic properties of neurons significantly influence their synaptic network structure is a common notion in neuroscience. The nematode Caenorhabditis elegans provides an exciting opportunity to approach this question in a large-scale quantitative manner. Its synaptic connectivity network has been identified, and, combined with cellular studies, we currently have characteristic connectivity and gene expression signatures for most of its neurons. By using two complementary analysis assays we show that the expression signature of a neuron carries significant information about its synaptic connectivity signature, and identify a list of putative genes predicting neural connectivity. The current study rigorously quantifies the relation between gene expression and synaptic connectivity signatures in the C. elegans nervous system and identifies subsets of neurons where this relation is highly marked. The results presented and the genes identified provide a promising starting point for further, more detailed computational and experimental investigations.

Perturbation studies, in which functional performance is measured after deletion, mutation, or lesion of elements of a biological system, have been traditionally employed in many fields in biology. The vast majority of these studies have been qualitative and have employed single perturbations, often resulting in little phenotypic effect. Recently, newly emerging experimental techniques have allowed researchers to carry out concomitant multi-perturbations and to uncover the causal functional contributions of system elements. This study presents a rigorous and quantitative multi-perturbation analysis of gene knockout and neuronal ablation experiments. In both cases, a quantification of the elements' contributions, and new insights and predictions, are provided. Multi-perturbation analysis has a potentially wide range of applications and is gradually becoming an essential tool in biology.

This letter presents the multi-perturbation Shapley value analysis (MSA), an axiomatic, scalable, and rigorous method for deducing causal function localization from multiple perturbations data. The MSA, based on fundamental concepts from game theory, accurately quantifies the contributions of network elements and their interactions, overcoming several shortcomings of previous function localization approaches. Its successful operation is demonstrated in both the analysis of a neurophysiological model and of reversible deactivation data. The MSA has a wide range of potential applications, including the analysis of reversible deactivation experiments, neuronal laser ablations, and transcranial magnetic stimulation "virtual lesions," as well as in providing insight into the inner workings of computational models of neurophysiological systems.

This article presents a new approach to the important challenge of localizing function in a neurocontroller. The approach is based on the basic functional contribution analysis (FCA) presented earlier, which assigns contribution values to the elements of the network, such that the ability to predict the network's performance in response to multi-unit lesions is maximized. These contribution values quantify the importance of each element to the tasks the agent performs. Here we present a generalization of the basic FCA to high-dimensional analysis, using high-order compound elements. Such elements are composed of conjunctions of simple elements. Their usage enables the explicit expression of sets of neurons or synapses whose contributions are interdependent, a prerequisite for localizing the function of complex neurocontrollers. High-dimensional FCA is shown to significantly improve on the accuracy of the basic analysis, to provide new insights concerning the main subsets of simple elements in the network that interact in a complex nonlinear manner, and to systematically reveal the types of interactions that characterize the evolved neurocontroller.

This article presents a general approach for employing lesion analysis to address the fundamental challenge of localizing functions in a neural system. We describe functional contribution analysis (FCA), which assigns contribution values to the elements of the network such that the ability to predict the network's performance in response to multilesions is maximized. The approach is thoroughly examined on neurocontroller networks of evolved autonomous agents. The FCA portrays a stable set of neuronal contributions and accurate multilesion predictions that are significantly better than those obtained based on the classical single lesion approach. It is also used for a detailed synaptic analysis of the neurocontroller connectivity network, delineating its main functional backbone. The FCA provides a quantitative way of measuring how the network functions are localized and distributed among its elements. Our results question the adequacy of the classical single lesion analysis traditionally used in neuroscience and show that using lesioning experiments to decipher even simple neuronal systems requires a more rigorous multilesion analysis.

In this article we revisit the classical neuroscience paradigm of Hebbian learning. We find that it is difficult to achieve effective associative memory storage by Hebbian synaptic learning, since it requires network-level information at the synaptic level or sparse coding level. Effective learning can yet be achieved even with nonsparse patterns by a neuronal process that maintains a zero sum of the incoming synaptic efficacies. This weight correction improves the memory capacity of associative networks from an essentially bounded one to a memory capacity that scales linearly with network size. It also enables the effective storage of patterns with multiple levels of activity within a single network. Such neuronal weight correction can be successfully carried out by activity-dependent homeostasis of the neuron's synaptic efficacies, which was recently observed in cortical tissue. Thus, our findings suggest that associative learning by Hebbian synaptic learning should be accompanied by continuous remodeling of neuronally driven regulatory processes in the brain.

We introduce a novel algorithm, termed PPA (Performance Prediction Algorithm), that quantitatively measures the contributions of elements of a neural system to the tasks it performs. The algorithm identifies the neurons or areas which participate in a cognitive or behavioral task, given data about performance decrease in a small set of lesions. It also allows the accurate prediction of performances due to multi-element lesions. The effectiveness of the new algorithm is demonstrated in two models of recurrent neural networks with complex interactions among the ele(cid:173) ments. The algorithm is scalable and applicable to the analysis of large neural networks. Given the recent advances in reversible inactivation techniques, it has the potential to significantly contribute to the under(cid:173) standing of the organization of biological nervous systems, and to shed light on the long-lasting debate about local versus distributed computa(cid:173) tion in the brain.

Human and animal studies show that mammalian brains undergo massive synaptic pruning during childhood, losing about half of the synapses by puberty. We have previously shown that maintaining the network performance while synapses are deleted requires that synapses be properly modified and pruned, with the weaker synapses removed. We now show that neuronal regulation, a mechanism recently observed to maintain the average neuronal input field of a postsynaptic neuron, results in a weight-dependent synaptic modification. Under the correct range of the degradation dimension and synaptic upper bound, neuronal regulation removes the weaker synapses and judiciously modifies the remaining synapses. By deriving optimal synaptic modification functions in an excitatory-inhibitory network, we prove that neuronal regulation implements near-optimal synaptic modification and maintains the performance of a network undergoing massive synaptic pruning. These findings support the possibility that neural regulation complements the action of Hebbian synaptic changes in the self-organization of the developing brain.

Research with humans and primates shows that the developmental course of the brain involves synaptic overgrowth followed by marked selective pruning. Previous explanations have suggested that this intriguing, seemingly wasteful phenomenon is utilized to remove, "erroneous" synapses. We prove that this interpretation is wrong if synapses are Hebbian. Under limited metabolic energy resources restricting the amount and strength of synapses, we show that memory performance is maximized if synapses are first overgrown and then pruned following optimal "minimal-value" deletion. This optimal strategy leads to interesting insights concerning childhood amnesia.

We analyze in detail the performance of a Hamming network classifying inputs that are distorted versions of one of its m stored memory patterns, each being a binary vector of length n. It is shown that the activation function of the memory neurons in the original Hamming network may be replaced by a simple threshold function. By judiciously determining the threshold value, the "winner-take-all" subnet of the Hamming network (known to be the essential factor determining the time complexity of the network's computation) may be altogether discarded. For m growing exponentially in n, the resulting threshold Hamming network correctly classifies the input pattern in a single iteration, with probability approaching 1.

Let $(p_1 ,p_2 , \cdots ,p_n )$ be a probability distribution, $\pi = (\pi _1 ,\pi _2 , \cdots ,\pi _n )$ be a permutation of $1,2, \cdots ,n$ and $X_1 ,X_2 , \cdots ,X_k $ be k independent and identically distributed random variables with distribution $P(X = i) = p\pi _i $. It is known that the organ pipe permutation $\pi ^ * $ makes the range \[ D(k,\pi ) = \max\limits_{1 \leqq j \leqq k} X_i - \min\limits_{1 \leqq j \leqq k} X_i \]a stochastic minimum for $k = 2$ (P. P. Bergmans, Information and Control, 20 (1972), pp. 331–350), and minimal on the average for general k (J. R. Bitner and C. K. Wong, 8 (1979), pp. 479–498). We prove the stochastic minimality for general k and study a natural extension of the organ pipe permutation that is optimal when certain constraints are placed on the possible choices of $\pi $.