ABSTRACT
Homelessness is a costly and traumatic condition that affects hundreds of thousands of people each year in the U.S. alone. Most homeless programs focus on assisting people experiencing homelessness, but research has shown that predicting and preventing homelessness can be a more cost-effective solution. Of the few studies focused on predicting homelessness, most focus on people already seeking assistance; however, these methods necessarily cannot identify those not actively seeking assistance. Providing aid before conditions become dire may better prevent homelessness. Few methods exist to predict homelessness on the general population, and these methods use health and criminal history information, much of which may not be available or timely. We hypothesize that recent financial health information based on utility payment history is useful in predicting homelessness. In particular, we demonstrate the value of utility customer billing records to predict homelessness using logistic regression models based on this data. The performance of these models is comparable to other studies, suggesting such an approach could be productionalized due to the ubiquity and timeliness of this type of data. Our results suggest that utility billing records would have value for screening a broad section of the general population to identify those at risk of homelessness.
Subject(s)
Ill-Housed Persons , Humans , Social Problems , Logistic ModelsABSTRACT
In this paper, we present a multi-layer, activity-dependent model for the joint development of ocular dominance (OD) columns and cytochrome oxidase (CO) blobs in primate V1. For simplicity, we focus on layers 4C and 2/3 with both layers receiving direct thalamic inputs and layer 4C sending vertical projections to layer 2/3. Both the thalamic and the vertical connections are taken to be modifiable by activity. Using a correlation-based Hebbian learning rule with subtractive normalization, we show how the formation of an OD map in layer 4C is inherited by layer 2/3 via the vertical projections. Competition between these feedforward projections and the direct thalamic input to layer 2/3 then results in the formation of CO blobs superimposed upon the ocular dominance map. The spacing of the OD columns is determined by the spatial profile of the intralaminar connections within layer 4, while the spacing of CO blobs depends both on the width of the OD columns inherited from layer 4 and the spatial distribution of intralaminar connections within the superficial layer. The resulting CO blob distribution is shown to be consistent with experimental data. In addition, we numerically simulate monocular deprivation and find that while the CO blob distribution is unaltered, the OD pattern undergoes modification. The OD stripes of the deprived eye narrow, whereas the OD stripes for the remaining open eye widen.
Subject(s)
Dominance, Ocular , Visual Cortex , Animals , Visual Cortex/metabolism , Electron Transport Complex IV/metabolism , Primary Visual Cortex , ThalamusABSTRACT
This review addresses the present state of single-cell models of the firing pattern of midbrain dopamine neurons and the insights that can be gained from these models into the underlying mechanisms for diseases such as Parkinson's, addiction, and schizophrenia. We will explain the analytical technique of separation of time scales and show how it can produce insights into mechanisms using simplified single-compartment models. We also use morphologically realistic multicompartmental models to address spatially heterogeneous aspects of neural signaling and neural metabolism. Separation of time scale analyses are applied to pacemaking, bursting, and depolarization block in dopamine neurons. Differences in subpopulations with respect to metabolic load are addressed using multicompartmental models.
Subject(s)
Action Potentials/physiology , Dopaminergic Neurons/physiology , Mesencephalon/cytology , Models, Neurological , Animals , Humans , Mesencephalon/pathology , Parkinson Disease/pathology , Schizophrenia/pathology , Substance-Related Disorders/pathologyABSTRACT
Tobacco use is a major public health problem. Nicotine acts on widely distributed nicotinic acetylcholine receptors (nAChRs) in the brain and excites dopamine (DA) neurons in the ventral tegmental area (VTA). The elicited increase of DA neuronal activity is thought to be an important mechanism for nicotine reward and subsequently the transition to addiction. However, the current understanding of nicotine reward is based predominantly on the data accumulated from in vitro studies, often from VTA slices. Isolated VTA slices artificially terminate communications between neurons in the VTA and other brain regions that may significantly alter nicotinic effects. Consequently, the mechanisms of nicotinic excitation of VTA DA neurons under in vivo conditions have received only limited attention. Building upon the existing knowledge acquired in vitro, it is now time to elucidate the integrated mechanisms of nicotinic reward on intact systems that are more relevant to understanding the action of nicotine or other addictive drugs. In this review, we summarize recent studies that demonstrate the impact of prefrontal cortex (PFC) on the modulation of VTA DA neuronal function and nicotine reward. Based on existing evidence, we propose a new hypothesis that PFC-VTA functional coupling serves as an integration mechanism for nicotine reward. Moreover, addiction may develop due to nicotine perturbing the PFC-VTA coupling and thereby eliminating the PFC-dependent cognitive control over behavior.
Subject(s)
Nicotine/pharmacology , Prefrontal Cortex/physiology , Receptors, Nicotinic/metabolism , Ventral Tegmental Area/physiology , Gene Expression Regulation , Humans , Receptors, Nicotinic/geneticsABSTRACT
Mitochondria have long been known to sequester cytosolic Ca(2+) and even to shape intracellular patterns of endoplasmic reticulum-based Ca(2+) signaling. Evidence suggests that the mitochondrial network is an excitable medium which can demonstrate independent Ca(2+) induced Ca(2+) release via the mitochondrial permeability transition. The role of this excitability remains unclear, but mitochondrial Ca(2+) handling appears to be a crucial element in diverse diseases as diabetes, neurodegeneration and cardiac dysfunction that also have bioenergetic components. In this paper, we extend the modular Magnus-Keizer computational model for respiration-driven Ca(2+) handling to include a permeability transition based on a channel-like pore mechanism. We demonstrate both excitability and Ca(2+) wave propagation accompanied by depolarizations qualitatively similar to those reported in cell and isolated mitochondria preparations. These waves depend on the energy state of the mitochondria, as well as other elements of mitochondrial physiology. Our results support the concept that mitochondria can transmit state dependent signals about their function across the mitochondrial network. Our model provides the tools for predictions about the internal physiology that leads to this qualitatively different Ca(2+) excitability seen in mitochondria.
Subject(s)
Calcium Signaling , Calcium/metabolism , Computer Simulation , Ion Channel Gating/physiology , Mitochondrial Membrane Transport Proteins/metabolism , Models, Biological , Buffers , Cytosol/metabolism , Glucose/metabolism , Hydrogen-Ion Concentration , Mitochondria/metabolism , Mitochondrial Permeability Transition Pore , Protons , Time FactorsABSTRACT
We present a developmental model of ocular dominance column formation that takes into account the existence of an array of intrinsically specified cytochrome oxidase blobs. We assume that there is some molecular substrate for the blobs early in development, which generates a spatially periodic modulation of experience-dependent plasticity. We determine the effects of such a modulation on a competitive Hebbian mechanism for the modification of the feedforward afferents from the left and right eyes. We show how alternating left and right eye dominated columns can develop, in which the blobs are aligned with the centers of the ocular dominance columns and receive a greater density of feedforward connections, thus becoming defined extrinsically. More generally, our results suggest that the presence of periodically distributed anatomical markers early in development could provide a mechanism for the alignment of cortical feature maps.
Subject(s)
Cerebral Cortex/growth & development , Dominance, Cerebral/physiology , Dominance, Ocular/physiology , Models, Neurological , Nerve Net/physiology , Animals , Computer Simulation , HumansABSTRACT
We derive an activity-based developmental model of ocular dominance column formation in primary visual cortex that takes into account cortical growth. The resulting evolution equation for the densities of feedforward afferents from the two eyes exhibits a sequence of pattern forming instabilities as the size of the cortex increases. We use linear stability analysis to investigate the nature of the transitions between successive patterns in the sequence. We show that these transitions involve the splitting of existing ocular dominance (OD) columns, such that the mean width of an OD column is approximately preserved during the course of development. This is consistent with recent experimental observations of postnatal growth in cat.