Columbia University Medical Center

New York City, NY, United States

Columbia University Medical Center

New York City, NY, United States
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St-Onge M.-P.,Columbia University Medical Center
Obesity Reviews | Year: 2017

Short sleep duration has been associated with obesity in numerous epidemiological studies. However, such association studies cannot establish evidence of causality. Clinical intervention studies, on the other hand, can provide information on a causal effect of sleep duration on markers of weight gain: energy intake and energy expenditure. Herein is an overview of the science related to the impact of sleep restriction, in the context of clinical intervention studies, on energy intake, energy expenditure and body weight. Additionally, studies that evaluate the impact of sleep restriction on weight loss and the impact of sleep extension on appetite are discussed. Information to date suggests that weight management is hindered when attempted in the context of sleep restriction, and the public should be made aware of the negative consequences of sleep restriction for weight regulation. © 2017 World Obesity Federation


Shenoy K.V.,Stanford University | Sahani M.,Stanford University | Sahani M.,University College London | Churchland M.M.,Columbia University Medical Center
Annual Review of Neuroscience | Year: 2013

Our ability to move is central to everyday life. Investigating the neural control of movement in general, and the cortical control of volitional arm movements in particular, has been a major research focus in recent decades. Studies have involved primarily either attempts to account for single-neuron responses in terms of tuning for movement parameters or attempts to decode movement parameters from populations of tuned neurons. Even though this focus on encoding and decoding has led to many seminal advances, it has not produced an agreed-upon conceptual framework. Interest in understanding the underlying neural dynamics has recently increased, leading to questions such as how does the current population response determine the future population response, and to what purpose? We review how a dynamical systems perspective may help us understand why neural activity evolves the way it does, how neural activity relates to movement parameters, and how a unified conceptual framework may result. Copyright © 2013 by Annual Reviews. All rights reserved.


Requarth T.,Columbia University Medical Center | Sawtell N.B.,Columbia University Medical Center
Current Opinion in Neurobiology | Year: 2011

This review focuses on recent progress in understanding mechanisms for filtering self-generated sensory signals in cerebellum-like circuits in fish and mammals. Recent in vitro studies in weakly electric gymnotid fish have explored the interplay among anti-Hebbian plasticity, synaptic dynamics, and feedforward inhibition in canceling self-generated electrosensory inputs. Studies of the mammalian dorsal cochlear nucleus have revealed multimodal integration and anti-Hebbian plasticity, suggesting that this circuit may adaptively filter incoming auditory information. In vivo studies in weakly electric mormryid fish suggest a key role for granule cell coding in sensory filtering. The clear links between synaptic plasticity and systems level sensory filtering in cerebellum-like circuits may provide insights into hypothesized adaptive filtering functions of the cerebellum itself. © 2011 Elsevier Ltd.


Friedman D.,Columbia University Medical Center
Frontiers in Behavioral Neuroscience | Year: 2013

A cardinal feature of older-adult cognition is a decline, relative to the young, in the encoding and retrieval of personally relevant events, i.e., episodic memory (EM). A consensus holds that familiarity, a relatively automatic feeling of knowing that can support recognition-memory judgments, is preserved with aging. By contrast, recollection, which requires the effortful, strategic recovery of contextual detail, declines as we age. Over the last decade, event-related brain potential (ERPs) have become increasingly important tools in the study of the aging of EM, because a few, well-researched EM effects have been associated with the cognitive processes thought to underlie successful EM performance. EM effects are operationalized by subtracting the ERPs elicited by correctly rejected, new items from those to correctly recognized, old items. Although highly controversial, the mid-frontal effect (a positive component between ~300 and 500 ms, maximal at fronto-central scalp sites) is thought to reflect familiarity-based recognition. A positivity between ~500 and 800 ms, maximal at left-parietal scalp, has been labeled the left-parietal EM effect. A wealth of evidence suggests that this brain activity reflects recollection-based retrieval. Here, I review the ERP evidence in support of the hypothesis that familiarity is maintained while recollection is compromised in older relative to young adults. I consider the possibility that the inconsistency in findings may be due to individual differences in performance, executive function, and quality of life indices, such as socio-economic status. © 2013 Friedman.


Sawtell N.B.,Columbia University Medical Center
Annual Review of Physiology | Year: 2017

Perception of the environment requires differentiating between external sensory inputs and those that are self-generated. Some of the clearest insights into the neural mechanisms underlying this process have come from studies of the electrosensory systems of fish. Neurons at the first stage of electrosensory processing generate negative images of the electrosensory consequences of the animal's own behavior. By canceling out the effects of predictable, self-generated inputs, negative images allow for the selective encoding of unpredictable, externally generated stimuli. Combined experimental and theoretical studies of electrosensory systems have led to detailed accounts of how negative images are formed at the level of synaptic plasticity rules, cells, and circuits. Here, I review these accounts and discuss their implications for understanding how predictions of the sensory consequences of behavior may be generated in other sensory structures and the cerebellum. © Copyright 2017 by Annual Reviews. All rights reserved.


The recoding of diverse sensory and motor signals by granule cells (GCs) is probably critical for the function of cerebellar circuits, yet the nature of these transformations and their significance for cerebellar information processing remain poorly understood. In cerebellum-like structures in fish, anti-Hebbian plasticity at parallel fiber synapses generates " negative images" that act to cancel predictable patterns of electrosensory input. Here I test the hypothesis that GCs enhance the capacity of Purkinje-like cells to generate specific negative images by selectively encoding combinations of sensory and motor signals. Using in vivo whole-cell recordings, I show (1) that a subset of GCs integrate sensory and motor signals conveyed by distinct mossy fiber classes and (2) that Purkinje-like cells exhibit plastic changes specific to the combinations of signals that individual GCs encode. Consistent with influential theories of cerebellar function, these findings suggest that selective GC output enhances the capacity of Purkinje-like cells to acquire selectivity through associative plasticity. © 2010 Elsevier Inc.


Di Paolo G.,Columbia University Medical Center | Kim T.-W.,Columbia University Medical Center
Nature Reviews Neuroscience | Year: 2011

Lipid-mediated signalling regulates a plethora of physiological processes, including crucial aspects of brain function. In addition, dysregulation of lipid pathways has been implicated in a growing number of neurodegenerative disorders, such as Alzheimer's disease (AD). Although much attention has been given to the link between cholesterol and AD pathogenesis, growing evidence suggests that other lipids, such as phosphoinositides and phosphatidic acid, have an important role. Regulators of lipid metabolism (for example, statins) are a highly successful class of marketed drugs, and exploration of lipid dysregulation in AD and identification of novel therapeutic agents acting through relevant lipid pathways offers new and effective options for the treatment of this devastating disorder. © 2011 Macmillan Publishers Limited. All rights reserved.


Lasorella A.,Columbia University Medical Center | Benezra R.,Sloan Kettering Cancer Center | Iavarone A.,Columbia University Medical Center
Nature Reviews Cancer | Year: 2014

Inhibitor of DNA binding (ID) proteins are transcriptional regulators that control the timing of cell fate determination and differentiation in stem and progenitor cells during normal development and adult life. ID genes are frequently deregulated in many types of human neoplasms, and they endow cancer cells with biological features that are hijacked from normal stem cells. The ability of ID proteins to function as central 'hubs' for the coordination of multiple cancer hallmarks has established these transcriptional regulators as therapeutic targets and biomarkers in specific types of human tumours. © 2014 Macmillan Publishers Limited.


Kim T.-W.,Columbia University Medical Center
Neurotherapeutics | Year: 2015

Alzheimer’s disease (AD) is the most common cause of dementia and represents one of the highest unmet needs in medicine today. Drug development efforts for AD have been encumbered by largely unsuccessful clinical trials in the last decade. Drug repositioning, a process of discovering a new therapeutic use for existing drugs or drug candidates, is an attractive and timely drug development strategy especially for AD. Compared with traditional de novo drug development, time and cost are reduced as the safety and pharmacokinetic properties of most repositioning candidates have already been determined. A majority of drug repositioning efforts for AD have been based on positive clinical or epidemiological observations or in vivo efficacy found in mouse models of AD. More systematic, multidisciplinary approaches will further facilitate drug repositioning for AD. Some experimental approaches include unbiased phenotypic screening using the library of available drug collections in physiologically relevant model systems (e.g. stem cell-derived neurons or glial cells), computational prediction and selection approaches that leverage the accumulating data resulting from RNA expression profiles, and genome-wide association studies. This review will summarize several notable strategies and representative examples of drug repositioning for AD. © 2014, The American Society for Experimental NeuroTherapeutics, Inc.


Tang P.,Columbia University Medical Center
Journal of the American Academy of Orthopaedic Surgeons | Year: 2011

The ulnar and radial collateral ligaments are primary stabilizers of the thumb metacarpophalangeal (MP) joint. Injury to these ligaments can lead to instability and disability. Stress testing is essential to establish the diagnosis. Complete tear is diagnosed on physical examination when the proximal phalanx of the thumb can be angulated ulnarly or radially on the metacarpal head by 30° to 35° with the MP joint in either zero degrees of extension or 30° of flexion. Lack of a firm end point or angulation measuring >15° on stress testing compared with the contralateral thumb MP joint are also indicative of complete tear. Partial ligament injuries may be managed nonsurgically, but complete tears are usually managed surgically. Various techniques are used to reattach the ligament to bone, including suture anchors and, less commonly, repair of midsubstance tears. Options for managing chronic injuries include ligament repair, ligament reconstruction with a free tendon graft, and arthrodesis of the MP joint.

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